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Research on Benfotiamine Clinton Holladay, M.S.Copyright 2003 Clinton HolladayJune 5, 2003A short while ago a group of individuals I know purchased a large amount of benfotiamine and began ingesting it orally. I was urged by these individuals to place some of the research I have been conducting on benfo (benfotiamine) online along with the results of their benfo use. I was asked to do this in a manner that would allow individuals that do not have a background in the health sciences to comprehend it. I will be pursuing a PhD shortly and benfo will be central to my research. I am not a physician and the following information is not intended to be used as medical advice. Advanced glycation endproducts or AGEs are produced by the processing of sugars within the cell. They are one of the primary causes of aging and general wear and tear on your cells. Diabetics age the same way as normal people, but because they often have abnormal levels of sugars in their cells, they age faster. When blood sugar levels are high, certain cells in the body are flooded with glucose, particularly neurons and cells in the eyes and kidneys. Diabetics often suffer from nerve damage, kidney failure, and premature blindness. Numerous researchers have concentrated their efforts on AGE-blocking mechanisms because they would limit the wear and tear on the body’s cells and allow individuals to live longer and healthier, particularly diabetics. Benfo has emerged as the premier AGE inhibitor.Case StudiesIt is important to note that the following case studies are not double-blind controlled studies. Case study #1. Female, early fifties, non-diabetic, suffers from chronic fatigue, depression, and the normal aches and pains that accompany middle age. Her diet is average. She is able to do about two hours of physical labor a day, and she has suffered from depression for years. She has tried numerous treatments for depression including Prozac, and some of them have helped, but none have completely eliminated the depression. Sometimes she aches all over. She was addicted to caffeine for several years, but only consumes it about once a week now. She has high blood pressure, and treats it with Vasotec and also takes Maxide (a diuretic).She ingested 650 mg of benfo once a day for five days and did not notice any difference. On day 6 she doubled the dose to 1300 mg and started to notice a change a few hours later. There was a dramatic increase in stamina and energy. She is now able to do eight hours of physical work each day. She has an extremely heightened sense of well-being and all aspects of the depression have left. She has better clarity of thought, and sleeps better. Previously she would usually wake up two or three times a night. Now she sleeps through the whole night and has said she is in a deeper sleep at night. She has reported being able to control her appetite more. She has reported less shortness of breath. On day 13 she has had no weight change. On day 13 she experienced what felt exactly like a caffeine withdrawal headache. She immediately consumed two cans of mountain dew and the headache did not leave. Previous to this, caffeine had always relieved a headache of this sort for her. At day 14 she still had a headache and the tips of her toes started tingling. She reduced her dose to 650 mg per day once a day on day 14. On day 15 she still had a headache. On day 16 her toes started tingling and the headache left. On day 17 her pinkie started tingling. Her blood pressure has always fluctuated between 120/80 and 150/90. Throughout the treatment her blood pressure has fluctuated like it normally does. She says she feels like she did when she was thirty years old. Comment: The tingling is likely the cause of blood circulating to parts of her body that have not had a great deal of circulation in recent years.Case study #2. Male, mid fifties, non-diabetic. Average diet. Overall health is better than average for his age. He gets indigestion at night and takes Prilosec. He has the normal aches and pains that accompany middle age. When he wakes up in the morning his feet are inflexible, but that would go away after walking on them for about two minutes. After driving for two hours he is stiff when he gets out of his car. Most of the aches and pains and the foot inflexibility appeared in the last five to fifteen years. He began taking 650 mg of benfo once a day. On day 3 nothing hurt when he woke up. By day five all his aches and pains had disappeared. He is no longer stiff when he gets out of his car after driving for two hours. He feels more flexible. He says it has fixed everything that has gone wrong with him in the past fifteen years. He says he feels more cheerful but is not sure if it is because of repair to neurological damage or because his aches and pains are gone. He has reported a greater clarity of thought. He says he feels like he did when he was age 25-40 (he says he felt the same during those years). Up until twelve months ago his blood pressure has been 120/90. For the past twelve months it has averaged 130/120. On day 5 his blood pressure was 120/85 and it has remained consistent every day since then. Now he can only take a fifteen minute nap during the day whereas before he could fall asleep for hours. At night he sleeps better, probably because the aches and pains are gone. His appetite is only about 80% of what it used to be. He has reported increased stamina and energy. Before taking benfo it was getting hard for him to do ten hours of work per day. Now he can do fourteen hours of work per day. He still requires the same amount of sleep at night, but if he does not get his full requirement he doesn’t notice it nearly as much.Comment: The decrease in caloric intake may be because he was lacking an essential nutrient- not enough thiamine? The stiffening of the joints brought on by old age is partly a symptom poor blood circulation. The fact that this individual has become much more flexible is a possible indication of increased circulation.Case study #3. Male, late forties. He has been a type 1 diabetic for twenty years. Average diet. Over the last five years his health has declined more rapidly. He has more aches and pains than the average person because he is diabetic. He aches so much at night that he usually can’t get to sleep unless he takes Ibuprofen. He began taking 650 mg benfo once a day. On day 2 he noticed a decline in the severity of his aches and pains. He still needs the same amount of sleep, but if he doesn’t get his full requirement he doesn’t notice nearly as much. He has had an increase in stamina and energy. He says his stamina has doubled. On day 14 he felt like he did ten years ago, and it keeps improving each day. He is more cheerful, but like #2 he can’t tell if it’s because his aches and pains are gone or if benfo has a neurological effect on him. I will not disclose the brand of benfo which was used because I do not wish to be seen as promoting any particular brand. These case studies will be updated on July 5, 2003 and new ones will be added. The updates will be posted on www.geocities.com/robholladay99/updates.html The following exerpts are from medical journals. The abstracts (summaries) for most of them can be viewed online through the pubmed database, which is a free database most biomedical scientists use. To find pubmed, go to google.com and type in pubmed. Once you’re in pubmed, type in part of the title and you should be able to find the abstract. When typing in the title use "benfotiamine" not "benfo". As an anti-spamming measure, many search engines will not index web pages that list the key search words more than seven times throughout the document, hence this document was modified after it was created . Several things are important to note in the following literature. First of all, not only does benfo stop some effects of aging, it reverses them. Gradually over time people’s neurons quit working because of normal wear and tear. However, when benfo was ingested, not only did the nerve damage stop, some of the damage done through aging was repaired. A strong point is made that benfo is the most bioavailable source of thiamine. This means benfo is better absorbed than other sources of thiamine. Also, high levels of thiamine have analgesic (pain-relieving) effects on animals. In the Russian study the pain level of the patients decreased from 8.2 to 2.3, a decrease of about four hundred percent. Research articles on benfoWada T, Tagaki H, Minakami H, Hamanka W, Okamoto K, Ito, A, Sahashi Y. 1961. A new thiamine derivative, S-benzoylthiamine O-monophosphate. Science 134: 195-196.Benfo “is more easily absorbed in the body than thiamine hydrochloride, and administration results in higher thiamine and cocarboxylase levels in organs; moreover, these levels last for a longer period of time…It does not cause any unfavorable symptom in animals such as thiamine hydrochloride does…The LD50 by oral administration in mice, dd-strain hybrid, weighing 14 to 16g was 15g/kg of body weight”Bitsch R, Wolf M, Moller J, Heuzeroth L, Gruneklee D. Bioavailability assessment of the lipophilic benfo as compared to a water-soluble thiamin derivative. Ann Nutr Metab. 1991;35(5):292-6. “in presence of allicin, the active principle of garlic, the water-soluble thiamin hydrochloride is transformed into a lipid-soluble compound being identified as allithiamine…Ten healthy young men…The volunteers ingested a single dose of 40 mg benfo…Thus, the measured values reveal, when compared with mononitrate, a clearly improved thiamin bioavailability from benfo, due to the more lipophilic properties of this substance or possibly its dephosphorylated metabolite and a more rapid transformation into the physiologically active derivative. This may be of great advantage in the treatment of neurological disorders responding to high thiamin doses and further on in situations when the active intestinal absorbtion mechanisms are impaired”Stracke H, Lindemann A, Federlin K. A benfo-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.“Benfo…was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold...Therapy-specific adverse effects were not seen”Loew D. Pharmacokinetics of thiamine derivatives especially of benfo. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.“The effective form of thiamine, thiamine diphosphate, is an organic compound needed by the organism for vital functions…Due to this peculiarity the conditions for absorbtion of lipid-soluble vitamins differ from those for water-soluble thiamine derivatives. Unlike the latter, allithiamines are absorbed passively, they traverse the intestinal absorption barrier faster and more readily, leading to higher blood and tissue concentrations even when comparatively low doses are given…It therefore fulfills important pharmacodynamic conditions for rational therapy. Due to their greater biovailability and better tissue passage lipid-soluble thiamine analogues like benfo are preferable to water-soluble thiamine derivatives for treatment of various pathological conditions, e.g. cardiomyopathy, Werincke-Korsakow syndrome, and alcoholic or diabetic polyneuropathies…Due to its excellent pharmacokinetic profile and to its excellent tolerability benfo should be preferred in treatment of relevant conditions like neuropathies”Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter CH. Comparative bioavailability of two vitamin B1 preparations: benfo and thiamine mononitrate. Eur J Clin Pharmacol. 1997;52(4):319-20.“a study using equimolar quantities of the two preparations for exact comparison of the bioavailability of benfo and thiamine mononitrate has never been performed. Therfore, the present trial was undertaken…the higher thiamine content in the erythrocytes and the higher thiamine excretion in urine after oral benfo administration are proof of the considerably higher relative bioavailability of benfo than thiamine mononitrate”Simeonov S, Pavlova M, Mitkov M, Mincheva L, Troev D. Therapeutic efficacy of "Milgamma" in patients with painful diabetic neuropathy. Folia Med (Plovdiv). 1997;39(4):5-10.“Forty-Five diabetes patients with painful peripheral polyneuropathy were enrolled in a 3-month observational study comparing the therapeutic efficiacy of Milgamma tablets (benfo)…Statistically significant relief of both background and peak neuropathic pain was achieved in all of the Milgamma-treated patients…No adverse reactions were observed…Our results underscore the importance of Milgamma tablets as an indispensable element in the therapeutic regimen of patients with painful diabetic polyneuropathy”Greb A, Bitsch R. Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther. 1998 Apr;36(4):216-21.“Seven healthy volunteers…a single oral dose of either benfo…fursultiamin…thiaminedisulfide…In this study the allithiamine derivative benfo proved the best bioavailability. Owing to its excellent absorption properties it can be concluded that oral administration of benfo is suitable for therapeutical purposes”Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfo in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.Good review, full-text is available free online. “In bioavailability studies on healthy human subjects, it was shown that absorption of benfo was several times better than that of water-soluble vitamin B1 and that there was a 120-fold higher increase of metabolically active thiamine diphosphate in erythrocytes (Heinrich, 1990)…In animals given dosages that exceeded basic requirements by 100- or 1000-fold thiamine has analgesic and neuroprotective effects(woelk and peeler-Ichakawa, 1985; Jurna, 1988; Reeh, 1988, 1991; Wild, 1988). However, if high levels are to be achieved with oral vitamin B1 treatment, lipid soluble thiamine derivatives or pro-drugs with high bioavailability, such as benfo, are required…320 mg/day during weeks 1 to 4 and 120 mg benfo/day during weeks 5 to 8…Within the 8-week study period, benfo led to a significant improvement of the threshold of vibration perception at the great toe, motor function, and the overall symptom score. Marked improvement occurred in both pain and co-ordination”Sadekov RA, Danilov AB, Vein AM. [Diabetic polyneuropathy treatment by milgamma-100 preparation] Zh Nevrol Psikhiatr Im S S Korsakova. 1998;98(9):30-2. Russian.“benfo…was studied in treatment of diabetic polyneuropathy in 14 patients…After the course of treatment the intensity of pains was decreased according to visual analogous scale on the average from 8.2 to 2.3 scores, the indices of vibratory sensitivity improved significantly as well as the data of cardiovascular tests…The treatment resulted in the improvement of the condition in 93% of the cases” T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine pharmacokinetics by end-stage renal disease (ESRD). Int J Clin Pharmacol Ther. 1999 Sep;37(9):449-55.“20 end-stage renal disease(ESRD) patients…After a single oral dose of 100 mg benfo…ESRD patients may benefit from high-dose thiamine derivatives notwithstanding their chemical form. However, the better absorption and high transfer rate of debenzoylated BTMP (benfo) to TDP (thiamine diphosphate) even at much lower doses compensates for reduced renal excretion and may protect, therefore, against numerous adverse effects of uremia”Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different benfo dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.320, 120, and 150 mg benfo/day was administered to “diabetic patients suffering from painful peripheral diabetic neuropathy. In a 6-week open clinical trial, 36 patients…An overall beneficial therapeutic effect on the neuropathy status was observed in all three groups during the study…The greatest change occurred in the group of patients receiving the high dose of benfo…Metabolic control did not change over the study...Extremely interesting is the result of recent in vitro experiences that thiamine pyrophosphate and pyroxidine inhibit the formation of glycation end products" T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfo. Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.“20 end-stage renal disease (ESRD) patients…After benfo administration, the peak plasma concentration of TDP exceeded that in healthy subjects by 51%...Compared with thiamine nitrate, the oral administration of benfo leads to higher TDP concentrations in erythrocytes accompanied with a significant improvement of the erythrocyte transkelotase activity in ESRD patients”Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M. Benfo is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.“We investigated the hypothesis that benfo, a lipophilic derivative of thiamine, affects replication delay and generation of advanced glycosylation endproducts (AGE) in human umbilical vein endothelial cells cultured in the presence of high glucose…Benfo, a derivative of thiamine with better bioavailability, corrects defective replication and increased AGE generation in endothelial cells cultured in high glucose, to a similar extent as thiamine. These effects may result from normalization of accelerated glycolysis and the consequent decrease in metabolites that are extremely active in generating nonenzymatic protein glycation. The potential role of thiamine administration in the prevention or treatment of vascular complications of diabetes deserves further investigation”Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M, Geyer J, Kopcke W, Sauerland C, Bretzel RG, Federlin KF. Efficacy of benfo versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.“After three months preventative administration of both vitamin B1 preparations NCV (nerve conduction velocity) had increased substantially…It was nearly normal after six months with benfo, while the administration of thiamine nitrate resulted in no further amelioration. NCV was nearly normalized after six months of benfo application but not with thiamine. Furthermore, benfo induced a major inhibition of neural imidazole-type AGE formation and completely prevented diabetes induced glycoxidation products”Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M. Benfo blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.“Our results in both endothelial cells cultured for several days and retinas from rats with nine months of diabetes showed that benfo, a lipid-soluble thiamine derivative, prevents activation of three major pathways involved in hyperglycemia-induced vascular damage: the hexosamine pathway, the intracellular AGE formation pathway and the DAG-PKC pathway…We showed that benfo blocks these pathways of hyperglycemic damage by increasing the activity of transketolase…Administration of benfo for nine months also completely prevented the development of experimental diabetic retinopathy in rats...Thus we conclude that augmentation of transketolase activity is solely responsible for the observed effects of benfo”Comment: This study is very significant because it demonstrates how benfo blocks several other aging mechanisms besides AGE formation. However, I am not yet convinced of the statement that transketolase activity is solely responsible for the observed effects of benfo. The following four studies are located on the Internet but are not yet listed on Medline. To find them, go to google.com and type in part of the titleBergfeld R, Matsumara X. Du, Brownlee M. Benfo prevents the consequences of hyperglycemia-induced mitochondrial overproduction of reactive oxygen species, and experimental diabetic retinopathy.“diabetic rats were treated with benfo (80 mg/kg weight) for 36 weeks…Benfo decreases AGE formation by 60%...These data suggest that treatment with benfo may be an effective approach to prevent the development of diabetic complications”Lin J, Alt A, Liersch J, Bretzel R, Brownlee M, Hammes H. Benfo inhibits intracellular formation of advanced glycation end products in vivo“Here, we studied the effect of benfo, a lipid-soluble thiamine derivative with known AGE-inhibiting properties in vitro on the intracellular formation of (CML) and methylgloxal-derived AGE in red blood cells. Blood was collected from 6 type 1 diabetic patients before and after treatment with 600 mg/day benfo for 28 days…Thiamine derivatives, in particular the lipid-soluble prodrug benfo, are effective inhibitors of intracellular formation of AGE and CML”Stracke H, Werkmann D, Mavrakis K, Federlin K, Kopke W, Sauerland C, Hammes H, Bretzel RG. Influence of vitamin B1 on diabetic neuropathy-studies in streptozotocin-diabetic rats.“we investigated the effects of oral administration of thiamine and benfo on the development of glucose oxidation products in the nerve and on nerve conduction velocity in streptozotocin-diabetic rats…Conclusion: Early treatment with benfo normalizes increased cellular oxidative stress and the reduced nerve conduction velocity”Hammes H, Bretzel, R.G., Federlin, K, Horiuchi S, Niwa T, Stracke H. Benfo inhibits the formation of advanced glycation end products in diabetic rats.“benfo (100 mg/kg x day) and thiamin (70.18 mg/kg x day) administered orally for 6 months…neither benfo nor thiamin treatment affected metabolic control…Benfo administration in diabetic rats induced a major inhibition of neutral imidazolone-type AGE formation and completely prevented diabetes-induced glycoxidation formation. Treatment with thiamin did not affect AGE or CML levels”ThiamineAllithiamines are lipid-soluble sources of thiamine. Benfo is an allithiamine. Thiamine is water-soluble and is also known as vitamin B1.After reviewing the relevant medical literature on thiamine, I have come to conclude that large portions of the population may be thiamine deficient. In addition, many individuals that are not technically thiamine deficient would likely receive benefit from thiamine supplementation. Thiamine deficiency is associated with numerous undesirable medical conditions.Relation of thiamine to heart diseaseShamir R, Dagan O, Abramovitch D, Abramovitch T, Vidne BA, Dinari G. Thiamine deficiency in children with congenital heart disease before and after corrective surgery. JPEN J Parenter Enteral Nutr. 2000 May-Jun;24(3):154-8.Thiamine deficiency “is common in children with congenital heart disease (CHD) referred for corrective surgery both before and after surgery. Our results suggest that neither diuretic treatment nor malnutrition can fully explain the development of TD in these children”Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E, Levy R. [Right heart failure caused by thiamine deficiency (cardiac beriberi)] Presse Med. 2000 Feb 12;29(5):240-1. French.Beaud C, Fuhrman C, Perchet H, Monnet I, Chouaid C, Housset B. [Thiamine deficiency. A cause of cardiac insufficiency not to be ignored] Rev Mal Respir. 1998 Jun;15(3):303-4. French.“Thiamine deficiency is one of the classical causes of high output for heart failure”Okura H, Gohma I, Hatta K, Imanaka T. Thiamine deficiency and pulmonary hypertension in Crow-Fukase syndrome. Intern Med. 1995 Jul;34(7):674-5. “After oral administration of prednisolone and thiamine, echocardiogram showed marked improvement of the pulmonary hypertension”Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc. 1995 May;95(5):541-4. “Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk”Shimon I, Almog S, Vered Z, Seligmann H, Shefi M, Peleg E, Rosenthal T, Motro M, Halkin H, Ezra D. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med. 1995 May;98(5):485-90.“Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy”Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered Z, Ezra D. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med. 1991 Aug;91(2):151-5.”These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements”Relation of thiamine to neurological disordersLonsdale D, Shamberger RJ, Audhya T. Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: a pilot study. Neuroendocrinol Lett. 2002 Aug;23(4):303-8.“Thiamine tetrahydrofurfuryl disulfide appears to have a beneficial clinical effect on some autistic children, since 8 of the 10 children improved clinically”Nakagawasai O, Tadano T, Hozumi S, Taniguchi R, Tan-No K, Esashi A, Niijima F, Kisara K. Characteristics of depressive behavior induced by feeding thiamine-deficient diet in mice.Life Sci. 2001 Jul 27;69(10):1181-91.Ambrose ML, Bowden SC, Whelan G. Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings. Alcohol Clin Exp Res. 2001 Jan;25(1):112-6.“A therapeutic relationship between dose and working memory performance was indicated”Older MW, Dickerson JW. Thiamine and the elderly orthopaedic patient. Age Ageing. 1982 May;11(2):101-7.“In both groups those patients who were noticeably confused after operation were found to have a considerable fall in their thiamine status suggesting this may be a contributory factor to postoperative confusion”Winston AP, son CP, Madira W, Gatward NM, Palmer RL. Prevalence of thiamin deficiency in anorexia nervosa. Int J Eat Disord. 2000 Dec;28(4):451-4.“Fourteen patients (38%) had results in the deficient range; 7 (19%) met the most stringent published criterion for deficiency. Deficiency was not related to duration of eating restraint, frequency of vomiting, or alcohol consumption”Terasawa M, Nakahara T, Tsukada N, Sugawara A, Itokawa Y. The relationship between thiamine deficiency and performance of a learning task in rats. Metab Brain Dis. 1999 Sep;14(3):137-48.“We taught rats to press a lever to escape from the pain of electrical stimulation by learning to turn a switch off… The rats that were fed the thiamine-deficient diet showed a slower response time and a longer running time than the rats fed the normal diet… We found that the thiamine concentration in the blood of the rats in the trained group was significantly higher than that in the group without training”Jimenez-Jimenez FJ, Molina JA, Hernanz A, Fernandez-Vivancos E, de Bustos F, Barcenilla B, Gomez-Escalonilla C, Zurdo M, Berbel A, Villanueva C. Cerebrospinal fluid levels of thiamine in patients with Parkinson's disease. Neurosci Lett. 1999 Aug 13;271(1):33-6.“These results suggest that low CSF free thiamine levels could be related with the risk for PD”Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J. 1997 Dec;74(12):803-8.“Diabetic peripheral neuropathy in Dar es Salaam is associated with thiamine deficiency”Langlais PJ, G, Guo SX, Bondy SC. Increased cerebral free radical production during thiamine deficiency. Metab Brain Dis. 1997 Jun;12(2):137-43.“These findings suggest that increased formation of free radicals occurs during the more acute symptomatic stage of thiamine deficiency and may contribute to the structural damage described in this model of Wernicke's encephalopathy”Easton CJ, Bauer LO. Beneficial effects of thiamine on recognition memory and P300 in abstinent cocaine-dependent patients. Psychiatry Res. 1997 May 30;70(3):165-74. “Thiamine was found to significantly improve recognition accuracy and P300 amplitude, at the midline parietal (Pz) electrode. The improvement was most reliable under conditions of increased memory load”Benton D, Griffiths R, Haller J. Thiamine supplementation mood and cognitive functioning. Psychopharmacology (Berl). 1997 Jan;129(1):66-71. ”An improvement in thiamine status was associated with reports of being more clearheaded, composed and energetic. The taking of thiamine had no influence on memory but reaction times were faster following supplementation”Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's disease. Metab Brain Dis. 1996 Mar;11(1):89-94.”Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100 mg/day had a mild beneficial effect in patients with Alzheimer's disease in a 12-week open trial. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function”Gold M, Chen MF, K. Plasma and red blood cell thiamine deficiency in patients with dementia of the Alzheimer's type. Arch Neurol. 1995 Nov;52(11):1081-6.“A significant proportion of patients with SDAT may have a thiamine deficiency, which may have an impact on cognitive function. Currently used assays may not be adequate to assess thiamine status”Adamolekun B, Eniola A. Thiamine-responsive acute cerebellar ataxia following febrile illness. Cent Afr J Med. 1993 Feb;39(2):40-1. Review.“acute thiamine depletion may be the pathogenetic mechanism for post-pyrexial acute cerebellar ataxia”Ben-Hur T, Wolff E, River Y. [Thiamin deficiency is common in Israel] Harefuah. 1992 Nov 15;123(10):382-4, 436, 435. Hebrew.“Thiamin levels should be determined not only in alcoholics and those with classic B1 deficiency syndromes, but in the routine workup of patients with sensory-motor neuropathy, dementia, gait disorders, cerebellar syndromes and confusional states”Sacks W, Esser AH, Feitel B, Abbott K. Acetazolamide and thiamine: an ancillary therapy for chronic mental illness. Psychiatry Res. 1989 Jun;28(3):279-88.“Overall, 50% of the patients showed improvement on all assessment scales. No untoward effects occurred in these patients…”Relation of thiamine and geriatric patientsSmidt LJ, Cremin FM, Grivetti LE, Clifford AJ. Influence of thiamin supplementation on the health and general well-being of an elderly Irish population with marginal thiamin deficiency. J Gerontol. 1991 Jan;46(1):M16-22.”thiamin-supplemented women experienced significantly increased appetite, energy intake, body weight and general well-being, and decreased fatigue. Thiamin supplementation also tended to reduce daytime sleep time, improve sleep patterns, and increase activity. These data suggest that evaluation of thiamin status is indicated when nonspecific conditions such as anorexia, weight loss, fatigue, depression, and sleep disorders are present in elderly persons”Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels in elder patients admitted through the emergency department. Acad Emerg Med. 2000 Oct;7(10):1156-9.“CONCLUSIONS: Elder nursing home patients seen in the ED and admitted to the hospital are frequently thiamine-deficient”Wilkinson TJ, Hanger HC, Elmslie J, PM, Sainsbury R. The response to treatment of subclinical thiamine deficiency in the elderly. Am J Clin Nutr. 1997 Oct;66(4):925-8.“Only the subjects with persistently low TPP concentrations showed subjective benefits from treatment with improvements in quality of life… There was a trend toward benefits in sleep and energy… Quality of life was enhanced by providing thiamine supplements. Blood pressure and weight were lower after thiamine supplementation”Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte thiamin concentrations in geriatric outpatients. J Am Coll Nutr. 1996 Jun;15(3):231-6.“CONCLUSION: About 50% of geriatric outpatients in this study had low plasma thiamin levels”Nichols HK, Basu TK. Thiamin status of the elderly: dietary intake and thiamin pyrophosphate response. J Am Coll Nutr. 1994 Feb;13(1):57-61.“Average daily thiamin intake was above the recommended requirement… however, almost half of the total study population had TPP effect > 14%, suggesting thiamin deficiency… CONCLUSION: These findings raise questions about the reliability of dietary intake in assessing metabolic availability of thiamin in the elderly”O'Keeffe ST, Tormey WP, Glasgow R, Lavan JN. Thiamine deficiency in hospitalized elderly patients. Gerontology. 1994;40(1):18-24.“Necropsy studies suggest that thiamine deficiency is underdiagnosed in life… There was no difference in anthropometric indices or in the prevalence of other nutrient deficiencies between the two groups. Thiamine deficiency is common in elderly patients admitted to hospital and may contribute to the development of delirium”Iber FL, Blass JP, Brin M, Leevy CM. Thiamin in the elderly--relation to alcoholism and to neurological degenerative disease. Am J Clin Nutr. 1982 Nov;36(5 Suppl):1067-82. Review.“There is no known toxicity for thiamin”Relation of thiamine to diabetesAvena R, Arora S, Carmody BJ, Cosby K, Sidawy AN. Thiamine (Vitamin B1) protects against glucose- and insulin-mediated proliferation of human infragenicular arterial smooth muscle cells. Ann Vasc Surg. 2000 Jan;14(1):37-43.“Vitamin B1 intake may prove important in delaying the atherosclerotic complications of diabetes”La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA, Molinatti GM, Porta M. Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions. Diabetologia. 1996 Nov;39(11):1263-8.Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S, Scheinman M, T. Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells. Surgery. 2001 Nov;130(5):851-8.“The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes”Hassan R, Qureshi H, Zuberi SJ. Effect of thiamine on glucose utilization in hepatic cirrhosis. J Gastroenterol Hepatol. 1991 Jan-Feb;6(1):59-60.“It is therefore suggested that thiamine supplements be given to cirrhotics with hyperglycaemia, to improve glucose utilization”Rindi G, Laforenza U. Thiamine intestinal transport and related issues: recent aspects.Proc Soc Exp Biol Med. 2000 Sep;224(4):246-55. Review.“Thiamine uptake is enhanced by thiamine deficiency, and reduced by thyroid hormone and diabetes”Saito N, Kimura M, Kuchiba A, Itokawa Y. Blood thiamine levels in outpatients with diabetes mellitus. J Nutr Sci Vitaminol (Tokyo). 1987 Dec;33(6):421-30.“From the above findings it was concluded that diabetic outpatients tend to have a low blood thiamine level, with low erythrocyte transketolase activity and high erythrocyte TPP effect, and showed marginal thiamine deficiency” Relation of thiamine to diseaseWallace AE, Weeks WB. Thiamine treatment of chronic hepatitis B infection. Am J Gastroenterol. 2001 Mar;96(3):864-8.”In each case study, thiamine administration was associated with reduction in aminotransferase levels and the fall of HBV DNA to undetectable levels… The relationship between thiamine administration and chronic hepatitis B infection warrants further study. If proven effective in reducing liver damage or inducing remission of the hepatitis B virus in larger trials, thiamine will offer obvious advantages over the current treatments for chronic viral hepatitis B infection”Rossouw JE, Labadarios D, Krasner N, M, R. Red blood cell transketolase activity and the effect of thiamine supplementation in patients with chronic liver disease. Scand J Gastroenterol. 1978;13(2):133-8.“Biochemical evidence of thiamine deficiency was found in 58% of patients with chronic liver disease… high doses of thiamine should be included in the routine nutritional management of patients with severe chronic liver disease”Shoji S, Furuishi K, Misumi S, Miyazaki T, Kino M, Yamataka K. Thiamine disulfide as a potent inhibitor of human immunodeficiency virus (type-1) production. Biochem Biophys Res Commun. 1994 Nov 30;205(1):967-75.” The results suggest that thiamine disulfide may be important for AIDS chemotherapy”Shoji S, Furuishi K, Ogata A, Yamataka K, Tachibana K, Mukai R, Uda A, Harano K, Matsushita S, Misumi S. An allosteric drug, o,o'-bismyristoyl thiamine disulfide, suppresses HIV-1 replication through prevention of nuclear translocation of both HIV-1 Tat and NF-kappa B. Biochem Biophys Res Commun. 1998 Aug 28;249(3):745-53.Butterworth RF, Gaudreau C, Vincelette J, Bourgault AM, Lamothe F, Nutini AM. Thiamine deficiency and Wernicke's encephalopathy in AIDS. Metab Brain Dis. 1991 Dec;6(4):207-12.“we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse… it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex”Haisraeli-Shalish M, Livneh A, Katz J, Doolman R, Sela BA. Recurrent aphthous stomatitis and thiamine deficiency. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Dec;82(6):634-6.” 70 patients with recurrent aphthous stomatitis and in 50 members of a control group… Low levels of vitamin B1 were detected in 49 patients but in only two members of the control group… Our finding suggests an association between thiamine deficiency and recurrent aphthous stomatitis”Engel D. Tropical pyomyositis, a thiamine-deficiency disease. Med Hypotheses. 1981 Mar;7(3):345-52.“it is suggested that thiamine deficiency is an essential contributary factor in producing tropical pyomyositis… Thiamine deficiency induces a biochemical lesion (s) in the pyruvate oxidase system of the muscle, which breaks down its normal resistance to infection and opens the gate to bacterial agents”Krishna S, AM, Supanaranond W, Pukrittayakamee S, ter Kuile F, Tawfiq KM, Holloway PA, White NJ. Thiamine deficiency and malaria in adults from southeast Asia. Lancet. 1999 Feb 13;353(9152):546-9.”12 (52%) of 23 patients with severe malaria and ten (19%) of 54 patients with uncomplicated malaria had alpha values above the normal range (p<0.0001 and p=0.0014, respectively, compared with controls), which indicated severe thiamine deficiency” Pietrzak I, Baczyk K, Mlynarczyk M, Kaczmarek M. [Content of thiamin in plasma and erythrocytes in patients with end stage renal disease] Przegl Lek. 1996;53(5):423-6. Polish.”We suggest the need of thiamine supplementation in ESRD patients especially in those treated by dialysis. The supplementation of thiamine is needed particularly in patients on peritoneal dialysis”Relation of thiamine to other dataHung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. 2001 Nov;38(5):941-7.“We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency”Huang S, Ren G. [Thiamine status of university teacher families in Changsha] Hunan Yi Ke Da Xue Xue Bao. 1998;23(1):27-30. Chinese.“We conclude that those people who take the refined cereals and its products as a staple food, is in the risk of thiamine deficiency”Suzuki M, Itokawa Y. Effects of thiamine supplementation on exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106.“High-dose thiamine (vitamin B1) supplementation (100 mg/day) may be helpful in preventing or accelerating recovery from exercise-induced fatigue… Thiamine supplementation significantly suppressed the increase in blood glucose in the normal thiamine group and significantly decreased the number of complaints shortly after exercise in the subjective fatigue assessment of 30 items”Kimura M, Itokawa Y, Fujiwara M. Cooking losses of thiamin in food and its nutritional significance. J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl 1:S17-24.”The thiamin contents in cooked daily meals were 50-60 percent of the calculated values on an average”Cruickshank AM, Telfer AB, Shenkin A. Thiamine deficiency in the critically ill. Intensive Care Med. 1988;14(4):384-7.“We performed a retrospective study on 158 patients admitted to the Intensive Care Unit who required nutritional support. Patients who survived had significantly higher body thiamine status than those who died”Onodera K, Kisara K, Okabe H, Ogura Y. [studies on the effects of thiamine deficiency on rat testes (author's transl)] Nippon Yakurigaku Zasshi. 1980 Mar;76(2):143-52. Japanese.“In the thiamine deficient group, the seminiferous tubuli of rats having erections had atrophied”Labadarios D, Rossouw JE, McConnell JB, M, R. Thiamine deficiency in fulminant hepatic failure and effects of supplementation. Int J Vitam Nutr Res. 1977;47(1):17-22.“Nine out of 24 patients with acute hepatocellular necrosis leading to fulminant hepatic failure showed biochemical evidence of thiamine deficiency early in the course of their illness”Why haven’t we heard of benfo before? The patent on the manufacture of benfo expired decades ago. Pharmaceutical companies pursue drugs that can be patented so they can have a monopoly and charge 100 times what the drug is worth. They have spent a lot of money on AGE inhibitors that don’t work as well as benfo. Ingestion of benfo may result in the elimination of AGE-protein crosslinks, which are a major constituent of arterial plaque. I am intrigued by the idea that benfo may cause the removal of plaque from the blood vessels, but I am concerned about the rapid manner in which it may cause the removal of plaque from the blood vessels. If the plaque is being removed, a large chunk might break off and cause a stroke or heart attack. If I was older than 60 or if I had a serious problem with high blood pressure I would probably start out by taking very low doses of benfo and gradually increase my dosage. Of course, there are no reports of strokes or heart attacks from benfo in the medical literature, but it’s a thought to consider. My PhD research will mostly consist of double-blind controlled studies on the administration of benfo in normal individuals, diabetics, individuals with high blood pressure, Alzheimer patients etc. I believe the researchers who have investigated benfo to date have been extremely short sighted by not discovering they full potential of benfo in the clinical studies that have already been performed on humans.It is illegal to make claims about benfo and sell it as a dietary supplement unless the claims are based on substantial scientific evidence. The three case studies outlined in this document are not from a double-blind controlled study and FDA regulations would not allow for them to be referred to as substantial scientific evidence. Claims should not be made based on these preliminary findings. For questions or comments email robholladay99@...Since I am not a physician, it would be inappropriate for me to answer emails asking for medical advice.

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Tom, thanks for the great article. I will be starting this form of B1 when I finish my bottle of thiamine. Will keep everyone posted on any benefits I receive. Are you taking this form of B1 and did you find out about it through the Brewer Science Library? White is the educatuional cordinater at the library and publishes a quarterly newslettet. She is a wonderful source of info about ms and other dis-eases in the body. Best Wishes, Kathy

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Research on Benfotiamine Clinton Holladay, M.S.Copyright 2003 Clinton HolladayJune 5, 2003A short while ago a group of individuals I know purchased a large amount of benfotiamine and began ingesting it orally. I was urged by these individuals to place some of the research I have been conducting on benfo (benfotiamine) online along with the results of their benfo use. I was asked to do this in a manner that would allow individuals that do not have a background in the health sciences to comprehend it. I will be pursuing a PhD shortly and benfo will be central to my research. I am not a physician and the following information is not intended to be used as medical advice. Advanced glycation endproducts or AGEs are produced by the processing of sugars within the cell. They are one of the primary causes of aging and general wear and tear on your cells. Diabetics age the same way as normal people, but because they often have abnormal levels of sugars in their cells, they age faster. When blood sugar levels are high, certain cells in the body are flooded with glucose, particularly neurons and cells in the eyes and kidneys. Diabetics often suffer from nerve damage, kidney failure, and premature blindness. Numerous researchers have concentrated their efforts on AGE-blocking mechanisms because they would limit the wear and tear on the body’s cells and allow individuals to live longer and healthier, particularly diabetics. Benfo has emerged as the premier AGE inhibitor.Case StudiesIt is important to note that the following case studies are not double-blind controlled studies. Case study #1. Female, early fifties, non-diabetic, suffers from chronic fatigue, depression, and the normal aches and pains that accompany middle age. Her diet is average. She is able to do about two hours of physical labor a day, and she has suffered from depression for years. She has tried numerous treatments for depression including Prozac, and some of them have helped, but none have completely eliminated the depression. Sometimes she aches all over. She was addicted to caffeine for several years, but only consumes it about once a week now. She has high blood pressure, and treats it with Vasotec and also takes Maxide (a diuretic).She ingested 650 mg of benfo once a day for five days and did not notice any difference. On day 6 she doubled the dose to 1300 mg and started to notice a change a few hours later. There was a dramatic increase in stamina and energy. She is now able to do eight hours of physical work each day. She has an extremely heightened sense of well-being and all aspects of the depression have left. She has better clarity of thought, and sleeps better. Previously she would usually wake up two or three times a night. Now she sleeps through the whole night and has said she is in a deeper sleep at night. She has reported being able to control her appetite more. She has reported less shortness of breath. On day 13 she has had no weight change. On day 13 she experienced what felt exactly like a caffeine withdrawal headache. She immediately consumed two cans of mountain dew and the headache did not leave. Previous to this, caffeine had always relieved a headache of this sort for her. At day 14 she still had a headache and the tips of her toes started tingling. She reduced her dose to 650 mg per day once a day on day 14. On day 15 she still had a headache. On day 16 her toes started tingling and the headache left. On day 17 her pinkie started tingling. Her blood pressure has always fluctuated between 120/80 and 150/90. Throughout the treatment her blood pressure has fluctuated like it normally does. She says she feels like she did when she was thirty years old. Comment: The tingling is likely the cause of blood circulating to parts of her body that have not had a great deal of circulation in recent years.Case study #2. Male, mid fifties, non-diabetic. Average diet. Overall health is better than average for his age. He gets indigestion at night and takes Prilosec. He has the normal aches and pains that accompany middle age. When he wakes up in the morning his feet are inflexible, but that would go away after walking on them for about two minutes. After driving for two hours he is stiff when he gets out of his car. Most of the aches and pains and the foot inflexibility appeared in the last five to fifteen years. He began taking 650 mg of benfo once a day. On day 3 nothing hurt when he woke up. By day five all his aches and pains had disappeared. He is no longer stiff when he gets out of his car after driving for two hours. He feels more flexible. He says it has fixed everything that has gone wrong with him in the past fifteen years. He says he feels more cheerful but is not sure if it is because of repair to neurological damage or because his aches and pains are gone. He has reported a greater clarity of thought. He says he feels like he did when he was age 25-40 (he says he felt the same during those years). Up until twelve months ago his blood pressure has been 120/90. For the past twelve months it has averaged 130/120. On day 5 his blood pressure was 120/85 and it has remained consistent every day since then. Now he can only take a fifteen minute nap during the day whereas before he could fall asleep for hours. At night he sleeps better, probably because the aches and pains are gone. His appetite is only about 80% of what it used to be. He has reported increased stamina and energy. Before taking benfo it was getting hard for him to do ten hours of work per day. Now he can do fourteen hours of work per day. He still requires the same amount of sleep at night, but if he does not get his full requirement he doesn’t notice it nearly as much.Comment: The decrease in caloric intake may be because he was lacking an essential nutrient- not enough thiamine? The stiffening of the joints brought on by old age is partly a symptom poor blood circulation. The fact that this individual has become much more flexible is a possible indication of increased circulation.Case study #3. Male, late forties. He has been a type 1 diabetic for twenty years. Average diet. Over the last five years his health has declined more rapidly. He has more aches and pains than the average person because he is diabetic. He aches so much at night that he usually can’t get to sleep unless he takes Ibuprofen. He began taking 650 mg benfo once a day. On day 2 he noticed a decline in the severity of his aches and pains. He still needs the same amount of sleep, but if he doesn’t get his full requirement he doesn’t notice nearly as much. He has had an increase in stamina and energy. He says his stamina has doubled. On day 14 he felt like he did ten years ago, and it keeps improving each day. He is more cheerful, but like #2 he can’t tell if it’s because his aches and pains are gone or if benfo has a neurological effect on him. I will not disclose the brand of benfo which was used because I do not wish to be seen as promoting any particular brand. These case studies will be updated on July 5, 2003 and new ones will be added. The updates will be posted on www.geocities.com/robholladay99/updates.html The following exerpts are from medical journals. The abstracts (summaries) for most of them can be viewed online through the pubmed database, which is a free database most biomedical scientists use. To find pubmed, go to google.com and type in pubmed. Once you’re in pubmed, type in part of the title and you should be able to find the abstract. When typing in the title use "benfotiamine" not "benfo". As an anti-spamming measure, many search engines will not index web pages that list the key search words more than seven times throughout the document, hence this document was modified after it was created . Several things are important to note in the following literature. First of all, not only does benfo stop some effects of aging, it reverses them. Gradually over time people’s neurons quit working because of normal wear and tear. However, when benfo was ingested, not only did the nerve damage stop, some of the damage done through aging was repaired. A strong point is made that benfo is the most bioavailable source of thiamine. This means benfo is better absorbed than other sources of thiamine. Also, high levels of thiamine have analgesic (pain-relieving) effects on animals. In the Russian study the pain level of the patients decreased from 8.2 to 2.3, a decrease of about four hundred percent. Research articles on benfoWada T, Tagaki H, Minakami H, Hamanka W, Okamoto K, Ito, A, Sahashi Y. 1961. A new thiamine derivative, S-benzoylthiamine O-monophosphate. Science 134: 195-196.Benfo “is more easily absorbed in the body than thiamine hydrochloride, and administration results in higher thiamine and cocarboxylase levels in organs; moreover, these levels last for a longer period of time…It does not cause any unfavorable symptom in animals such as thiamine hydrochloride does…The LD50 by oral administration in mice, dd-strain hybrid, weighing 14 to 16g was 15g/kg of body weight”Bitsch R, Wolf M, Moller J, Heuzeroth L, Gruneklee D. Bioavailability assessment of the lipophilic benfo as compared to a water-soluble thiamin derivative. Ann Nutr Metab. 1991;35(5):292-6. “in presence of allicin, the active principle of garlic, the water-soluble thiamin hydrochloride is transformed into a lipid-soluble compound being identified as allithiamine…Ten healthy young men…The volunteers ingested a single dose of 40 mg benfo…Thus, the measured values reveal, when compared with mononitrate, a clearly improved thiamin bioavailability from benfo, due to the more lipophilic properties of this substance or possibly its dephosphorylated metabolite and a more rapid transformation into the physiologically active derivative. This may be of great advantage in the treatment of neurological disorders responding to high thiamin doses and further on in situations when the active intestinal absorbtion mechanisms are impaired”Stracke H, Lindemann A, Federlin K. A benfo-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.“Benfo…was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold...Therapy-specific adverse effects were not seen”Loew D. Pharmacokinetics of thiamine derivatives especially of benfo. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.“The effective form of thiamine, thiamine diphosphate, is an organic compound needed by the organism for vital functions…Due to this peculiarity the conditions for absorbtion of lipid-soluble vitamins differ from those for water-soluble thiamine derivatives. Unlike the latter, allithiamines are absorbed passively, they traverse the intestinal absorption barrier faster and more readily, leading to higher blood and tissue concentrations even when comparatively low doses are given…It therefore fulfills important pharmacodynamic conditions for rational therapy. Due to their greater biovailability and better tissue passage lipid-soluble thiamine analogues like benfo are preferable to water-soluble thiamine derivatives for treatment of various pathological conditions, e.g. cardiomyopathy, Werincke-Korsakow syndrome, and alcoholic or diabetic polyneuropathies…Due to its excellent pharmacokinetic profile and to its excellent tolerability benfo should be preferred in treatment of relevant conditions like neuropathies”Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter CH. Comparative bioavailability of two vitamin B1 preparations: benfo and thiamine mononitrate. Eur J Clin Pharmacol. 1997;52(4):319-20.“a study using equimolar quantities of the two preparations for exact comparison of the bioavailability of benfo and thiamine mononitrate has never been performed. Therfore, the present trial was undertaken…the higher thiamine content in the erythrocytes and the higher thiamine excretion in urine after oral benfo administration are proof of the considerably higher relative bioavailability of benfo than thiamine mononitrate”Simeonov S, Pavlova M, Mitkov M, Mincheva L, Troev D. Therapeutic efficacy of "Milgamma" in patients with painful diabetic neuropathy. Folia Med (Plovdiv). 1997;39(4):5-10.“Forty-Five diabetes patients with painful peripheral polyneuropathy were enrolled in a 3-month observational study comparing the therapeutic efficiacy of Milgamma tablets (benfo)…Statistically significant relief of both background and peak neuropathic pain was achieved in all of the Milgamma-treated patients…No adverse reactions were observed…Our results underscore the importance of Milgamma tablets as an indispensable element in the therapeutic regimen of patients with painful diabetic polyneuropathy”Greb A, Bitsch R. Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther. 1998 Apr;36(4):216-21.“Seven healthy volunteers…a single oral dose of either benfo…fursultiamin…thiaminedisulfide…In this study the allithiamine derivative benfo proved the best bioavailability. Owing to its excellent absorption properties it can be concluded that oral administration of benfo is suitable for therapeutical purposes”Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfo in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.Good review, full-text is available free online. “In bioavailability studies on healthy human subjects, it was shown that absorption of benfo was several times better than that of water-soluble vitamin B1 and that there was a 120-fold higher increase of metabolically active thiamine diphosphate in erythrocytes (Heinrich, 1990)…In animals given dosages that exceeded basic requirements by 100- or 1000-fold thiamine has analgesic and neuroprotective effects(woelk and peeler-Ichakawa, 1985; Jurna, 1988; Reeh, 1988, 1991; Wild, 1988). However, if high levels are to be achieved with oral vitamin B1 treatment, lipid soluble thiamine derivatives or pro-drugs with high bioavailability, such as benfo, are required…320 mg/day during weeks 1 to 4 and 120 mg benfo/day during weeks 5 to 8…Within the 8-week study period, benfo led to a significant improvement of the threshold of vibration perception at the great toe, motor function, and the overall symptom score. Marked improvement occurred in both pain and co-ordination”Sadekov RA, Danilov AB, Vein AM. [Diabetic polyneuropathy treatment by milgamma-100 preparation] Zh Nevrol Psikhiatr Im S S Korsakova. 1998;98(9):30-2. Russian.“benfo…was studied in treatment of diabetic polyneuropathy in 14 patients…After the course of treatment the intensity of pains was decreased according to visual analogous scale on the average from 8.2 to 2.3 scores, the indices of vibratory sensitivity improved significantly as well as the data of cardiovascular tests…The treatment resulted in the improvement of the condition in 93% of the cases” T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine pharmacokinetics by end-stage renal disease (ESRD). Int J Clin Pharmacol Ther. 1999 Sep;37(9):449-55.“20 end-stage renal disease(ESRD) patients…After a single oral dose of 100 mg benfo…ESRD patients may benefit from high-dose thiamine derivatives notwithstanding their chemical form. However, the better absorption and high transfer rate of debenzoylated BTMP (benfo) to TDP (thiamine diphosphate) even at much lower doses compensates for reduced renal excretion and may protect, therefore, against numerous adverse effects of uremia”Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different benfo dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.320, 120, and 150 mg benfo/day was administered to “diabetic patients suffering from painful peripheral diabetic neuropathy. In a 6-week open clinical trial, 36 patients…An overall beneficial therapeutic effect on the neuropathy status was observed in all three groups during the study…The greatest change occurred in the group of patients receiving the high dose of benfo…Metabolic control did not change over the study...Extremely interesting is the result of recent in vitro experiences that thiamine pyrophosphate and pyroxidine inhibit the formation of glycation end products" T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfo. Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.“20 end-stage renal disease (ESRD) patients…After benfo administration, the peak plasma concentration of TDP exceeded that in healthy subjects by 51%...Compared with thiamine nitrate, the oral administration of benfo leads to higher TDP concentrations in erythrocytes accompanied with a significant improvement of the erythrocyte transkelotase activity in ESRD patients”Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M. Benfo is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.“We investigated the hypothesis that benfo, a lipophilic derivative of thiamine, affects replication delay and generation of advanced glycosylation endproducts (AGE) in human umbilical vein endothelial cells cultured in the presence of high glucose…Benfo, a derivative of thiamine with better bioavailability, corrects defective replication and increased AGE generation in endothelial cells cultured in high glucose, to a similar extent as thiamine. These effects may result from normalization of accelerated glycolysis and the consequent decrease in metabolites that are extremely active in generating nonenzymatic protein glycation. The potential role of thiamine administration in the prevention or treatment of vascular complications of diabetes deserves further investigation”Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M, Geyer J, Kopcke W, Sauerland C, Bretzel RG, Federlin KF. Efficacy of benfo versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.“After three months preventative administration of both vitamin B1 preparations NCV (nerve conduction velocity) had increased substantially…It was nearly normal after six months with benfo, while the administration of thiamine nitrate resulted in no further amelioration. NCV was nearly normalized after six months of benfo application but not with thiamine. Furthermore, benfo induced a major inhibition of neural imidazole-type AGE formation and completely prevented diabetes induced glycoxidation products”Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M. Benfo blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.“Our results in both endothelial cells cultured for several days and retinas from rats with nine months of diabetes showed that benfo, a lipid-soluble thiamine derivative, prevents activation of three major pathways involved in hyperglycemia-induced vascular damage: the hexosamine pathway, the intracellular AGE formation pathway and the DAG-PKC pathway…We showed that benfo blocks these pathways of hyperglycemic damage by increasing the activity of transketolase…Administration of benfo for nine months also completely prevented the development of experimental diabetic retinopathy in rats...Thus we conclude that augmentation of transketolase activity is solely responsible for the observed effects of benfo”Comment: This study is very significant because it demonstrates how benfo blocks several other aging mechanisms besides AGE formation. However, I am not yet convinced of the statement that transketolase activity is solely responsible for the observed effects of benfo. The following four studies are located on the Internet but are not yet listed on Medline. To find them, go to google.com and type in part of the titleBergfeld R, Matsumara X. Du, Brownlee M. Benfo prevents the consequences of hyperglycemia-induced mitochondrial overproduction of reactive oxygen species, and experimental diabetic retinopathy.“diabetic rats were treated with benfo (80 mg/kg weight) for 36 weeks…Benfo decreases AGE formation by 60%...These data suggest that treatment with benfo may be an effective approach to prevent the development of diabetic complications”Lin J, Alt A, Liersch J, Bretzel R, Brownlee M, Hammes H. Benfo inhibits intracellular formation of advanced glycation end products in vivo“Here, we studied the effect of benfo, a lipid-soluble thiamine derivative with known AGE-inhibiting properties in vitro on the intracellular formation of (CML) and methylgloxal-derived AGE in red blood cells. Blood was collected from 6 type 1 diabetic patients before and after treatment with 600 mg/day benfo for 28 days…Thiamine derivatives, in particular the lipid-soluble prodrug benfo, are effective inhibitors of intracellular formation of AGE and CML”Stracke H, Werkmann D, Mavrakis K, Federlin K, Kopke W, Sauerland C, Hammes H, Bretzel RG. Influence of vitamin B1 on diabetic neuropathy-studies in streptozotocin-diabetic rats.“we investigated the effects of oral administration of thiamine and benfo on the development of glucose oxidation products in the nerve and on nerve conduction velocity in streptozotocin-diabetic rats…Conclusion: Early treatment with benfo normalizes increased cellular oxidative stress and the reduced nerve conduction velocity”Hammes H, Bretzel, R.G., Federlin, K, Horiuchi S, Niwa T, Stracke H. Benfo inhibits the formation of advanced glycation end products in diabetic rats.“benfo (100 mg/kg x day) and thiamin (70.18 mg/kg x day) administered orally for 6 months…neither benfo nor thiamin treatment affected metabolic control…Benfo administration in diabetic rats induced a major inhibition of neutral imidazolone-type AGE formation and completely prevented diabetes-induced glycoxidation formation. Treatment with thiamin did not affect AGE or CML levels”ThiamineAllithiamines are lipid-soluble sources of thiamine. Benfo is an allithiamine. Thiamine is water-soluble and is also known as vitamin B1.After reviewing the relevant medical literature on thiamine, I have come to conclude that large portions of the population may be thiamine deficient. In addition, many individuals that are not technically thiamine deficient would likely receive benefit from thiamine supplementation. Thiamine deficiency is associated with numerous undesirable medical conditions.Relation of thiamine to heart diseaseShamir R, Dagan O, Abramovitch D, Abramovitch T, Vidne BA, Dinari G. Thiamine deficiency in children with congenital heart disease before and after corrective surgery. JPEN J Parenter Enteral Nutr. 2000 May-Jun;24(3):154-8.Thiamine deficiency “is common in children with congenital heart disease (CHD) referred for corrective surgery both before and after surgery. Our results suggest that neither diuretic treatment nor malnutrition can fully explain the development of TD in these children”Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E, Levy R. [Right heart failure caused by thiamine deficiency (cardiac beriberi)] Presse Med. 2000 Feb 12;29(5):240-1. French.Beaud C, Fuhrman C, Perchet H, Monnet I, Chouaid C, Housset B. [Thiamine deficiency. A cause of cardiac insufficiency not to be ignored] Rev Mal Respir. 1998 Jun;15(3):303-4. French.“Thiamine deficiency is one of the classical causes of high output for heart failure”Okura H, Gohma I, Hatta K, Imanaka T. Thiamine deficiency and pulmonary hypertension in Crow-Fukase syndrome. Intern Med. 1995 Jul;34(7):674-5. “After oral administration of prednisolone and thiamine, echocardiogram showed marked improvement of the pulmonary hypertension”Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc. 1995 May;95(5):541-4. “Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk”Shimon I, Almog S, Vered Z, Seligmann H, Shefi M, Peleg E, Rosenthal T, Motro M, Halkin H, Ezra D. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med. 1995 May;98(5):485-90.“Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy”Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered Z, Ezra D. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med. 1991 Aug;91(2):151-5.”These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements”Relation of thiamine to neurological disordersLonsdale D, Shamberger RJ, Audhya T. Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: a pilot study. Neuroendocrinol Lett. 2002 Aug;23(4):303-8.“Thiamine tetrahydrofurfuryl disulfide appears to have a beneficial clinical effect on some autistic children, since 8 of the 10 children improved clinically”Nakagawasai O, Tadano T, Hozumi S, Taniguchi R, Tan-No K, Esashi A, Niijima F, Kisara K. Characteristics of depressive behavior induced by feeding thiamine-deficient diet in mice.Life Sci. 2001 Jul 27;69(10):1181-91.Ambrose ML, Bowden SC, Whelan G. Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings. Alcohol Clin Exp Res. 2001 Jan;25(1):112-6.“A therapeutic relationship between dose and working memory performance was indicated”Older MW, Dickerson JW. Thiamine and the elderly orthopaedic patient. Age Ageing. 1982 May;11(2):101-7.“In both groups those patients who were noticeably confused after operation were found to have a considerable fall in their thiamine status suggesting this may be a contributory factor to postoperative confusion”Winston AP, son CP, Madira W, Gatward NM, Palmer RL. Prevalence of thiamin deficiency in anorexia nervosa. Int J Eat Disord. 2000 Dec;28(4):451-4.“Fourteen patients (38%) had results in the deficient range; 7 (19%) met the most stringent published criterion for deficiency. Deficiency was not related to duration of eating restraint, frequency of vomiting, or alcohol consumption”Terasawa M, Nakahara T, Tsukada N, Sugawara A, Itokawa Y. The relationship between thiamine deficiency and performance of a learning task in rats. Metab Brain Dis. 1999 Sep;14(3):137-48.“We taught rats to press a lever to escape from the pain of electrical stimulation by learning to turn a switch off… The rats that were fed the thiamine-deficient diet showed a slower response time and a longer running time than the rats fed the normal diet… We found that the thiamine concentration in the blood of the rats in the trained group was significantly higher than that in the group without training”Jimenez-Jimenez FJ, Molina JA, Hernanz A, Fernandez-Vivancos E, de Bustos F, Barcenilla B, Gomez-Escalonilla C, Zurdo M, Berbel A, Villanueva C. Cerebrospinal fluid levels of thiamine in patients with Parkinson's disease. Neurosci Lett. 1999 Aug 13;271(1):33-6.“These results suggest that low CSF free thiamine levels could be related with the risk for PD”Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J. 1997 Dec;74(12):803-8.“Diabetic peripheral neuropathy in Dar es Salaam is associated with thiamine deficiency”Langlais PJ, G, Guo SX, Bondy SC. Increased cerebral free radical production during thiamine deficiency. Metab Brain Dis. 1997 Jun;12(2):137-43.“These findings suggest that increased formation of free radicals occurs during the more acute symptomatic stage of thiamine deficiency and may contribute to the structural damage described in this model of Wernicke's encephalopathy”Easton CJ, Bauer LO. Beneficial effects of thiamine on recognition memory and P300 in abstinent cocaine-dependent patients. Psychiatry Res. 1997 May 30;70(3):165-74. “Thiamine was found to significantly improve recognition accuracy and P300 amplitude, at the midline parietal (Pz) electrode. The improvement was most reliable under conditions of increased memory load”Benton D, Griffiths R, Haller J. Thiamine supplementation mood and cognitive functioning. Psychopharmacology (Berl). 1997 Jan;129(1):66-71. ”An improvement in thiamine status was associated with reports of being more clearheaded, composed and energetic. The taking of thiamine had no influence on memory but reaction times were faster following supplementation”Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's disease. Metab Brain Dis. 1996 Mar;11(1):89-94.”Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100 mg/day had a mild beneficial effect in patients with Alzheimer's disease in a 12-week open trial. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function”Gold M, Chen MF, K. Plasma and red blood cell thiamine deficiency in patients with dementia of the Alzheimer's type. Arch Neurol. 1995 Nov;52(11):1081-6.“A significant proportion of patients with SDAT may have a thiamine deficiency, which may have an impact on cognitive function. Currently used assays may not be adequate to assess thiamine status”Adamolekun B, Eniola A. Thiamine-responsive acute cerebellar ataxia following febrile illness. Cent Afr J Med. 1993 Feb;39(2):40-1. Review.“acute thiamine depletion may be the pathogenetic mechanism for post-pyrexial acute cerebellar ataxia”Ben-Hur T, Wolff E, River Y. [Thiamin deficiency is common in Israel] Harefuah. 1992 Nov 15;123(10):382-4, 436, 435. Hebrew.“Thiamin levels should be determined not only in alcoholics and those with classic B1 deficiency syndromes, but in the routine workup of patients with sensory-motor neuropathy, dementia, gait disorders, cerebellar syndromes and confusional states”Sacks W, Esser AH, Feitel B, Abbott K. Acetazolamide and thiamine: an ancillary therapy for chronic mental illness. Psychiatry Res. 1989 Jun;28(3):279-88.“Overall, 50% of the patients showed improvement on all assessment scales. No untoward effects occurred in these patients…”Relation of thiamine and geriatric patientsSmidt LJ, Cremin FM, Grivetti LE, Clifford AJ. Influence of thiamin supplementation on the health and general well-being of an elderly Irish population with marginal thiamin deficiency. J Gerontol. 1991 Jan;46(1):M16-22.”thiamin-supplemented women experienced significantly increased appetite, energy intake, body weight and general well-being, and decreased fatigue. Thiamin supplementation also tended to reduce daytime sleep time, improve sleep patterns, and increase activity. These data suggest that evaluation of thiamin status is indicated when nonspecific conditions such as anorexia, weight loss, fatigue, depression, and sleep disorders are present in elderly persons”Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels in elder patients admitted through the emergency department. Acad Emerg Med. 2000 Oct;7(10):1156-9.“CONCLUSIONS: Elder nursing home patients seen in the ED and admitted to the hospital are frequently thiamine-deficient”Wilkinson TJ, Hanger HC, Elmslie J, PM, Sainsbury R. The response to treatment of subclinical thiamine deficiency in the elderly. Am J Clin Nutr. 1997 Oct;66(4):925-8.“Only the subjects with persistently low TPP concentrations showed subjective benefits from treatment with improvements in quality of life… There was a trend toward benefits in sleep and energy… Quality of life was enhanced by providing thiamine supplements. Blood pressure and weight were lower after thiamine supplementation”Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte thiamin concentrations in geriatric outpatients. J Am Coll Nutr. 1996 Jun;15(3):231-6.“CONCLUSION: About 50% of geriatric outpatients in this study had low plasma thiamin levels”Nichols HK, Basu TK. Thiamin status of the elderly: dietary intake and thiamin pyrophosphate response. J Am Coll Nutr. 1994 Feb;13(1):57-61.“Average daily thiamin intake was above the recommended requirement… however, almost half of the total study population had TPP effect > 14%, suggesting thiamin deficiency… CONCLUSION: These findings raise questions about the reliability of dietary intake in assessing metabolic availability of thiamin in the elderly”O'Keeffe ST, Tormey WP, Glasgow R, Lavan JN. Thiamine deficiency in hospitalized elderly patients. Gerontology. 1994;40(1):18-24.“Necropsy studies suggest that thiamine deficiency is underdiagnosed in life… There was no difference in anthropometric indices or in the prevalence of other nutrient deficiencies between the two groups. Thiamine deficiency is common in elderly patients admitted to hospital and may contribute to the development of delirium”Iber FL, Blass JP, Brin M, Leevy CM. Thiamin in the elderly--relation to alcoholism and to neurological degenerative disease. Am J Clin Nutr. 1982 Nov;36(5 Suppl):1067-82. Review.“There is no known toxicity for thiamin”Relation of thiamine to diabetesAvena R, Arora S, Carmody BJ, Cosby K, Sidawy AN. Thiamine (Vitamin B1) protects against glucose- and insulin-mediated proliferation of human infragenicular arterial smooth muscle cells. Ann Vasc Surg. 2000 Jan;14(1):37-43.“Vitamin B1 intake may prove important in delaying the atherosclerotic complications of diabetes”La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA, Molinatti GM, Porta M. Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions. Diabetologia. 1996 Nov;39(11):1263-8.Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S, Scheinman M, T. Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells. Surgery. 2001 Nov;130(5):851-8.“The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes”Hassan R, Qureshi H, Zuberi SJ. Effect of thiamine on glucose utilization in hepatic cirrhosis. J Gastroenterol Hepatol. 1991 Jan-Feb;6(1):59-60.“It is therefore suggested that thiamine supplements be given to cirrhotics with hyperglycaemia, to improve glucose utilization”Rindi G, Laforenza U. Thiamine intestinal transport and related issues: recent aspects.Proc Soc Exp Biol Med. 2000 Sep;224(4):246-55. Review.“Thiamine uptake is enhanced by thiamine deficiency, and reduced by thyroid hormone and diabetes”Saito N, Kimura M, Kuchiba A, Itokawa Y. Blood thiamine levels in outpatients with diabetes mellitus. J Nutr Sci Vitaminol (Tokyo). 1987 Dec;33(6):421-30.“From the above findings it was concluded that diabetic outpatients tend to have a low blood thiamine level, with low erythrocyte transketolase activity and high erythrocyte TPP effect, and showed marginal thiamine deficiency” Relation of thiamine to diseaseWallace AE, Weeks WB. Thiamine treatment of chronic hepatitis B infection. Am J Gastroenterol. 2001 Mar;96(3):864-8.”In each case study, thiamine administration was associated with reduction in aminotransferase levels and the fall of HBV DNA to undetectable levels… The relationship between thiamine administration and chronic hepatitis B infection warrants further study. If proven effective in reducing liver damage or inducing remission of the hepatitis B virus in larger trials, thiamine will offer obvious advantages over the current treatments for chronic viral hepatitis B infection”Rossouw JE, Labadarios D, Krasner N, M, R. Red blood cell transketolase activity and the effect of thiamine supplementation in patients with chronic liver disease. Scand J Gastroenterol. 1978;13(2):133-8.“Biochemical evidence of thiamine deficiency was found in 58% of patients with chronic liver disease… high doses of thiamine should be included in the routine nutritional management of patients with severe chronic liver disease”Shoji S, Furuishi K, Misumi S, Miyazaki T, Kino M, Yamataka K. Thiamine disulfide as a potent inhibitor of human immunodeficiency virus (type-1) production. Biochem Biophys Res Commun. 1994 Nov 30;205(1):967-75.” The results suggest that thiamine disulfide may be important for AIDS chemotherapy”Shoji S, Furuishi K, Ogata A, Yamataka K, Tachibana K, Mukai R, Uda A, Harano K, Matsushita S, Misumi S. An allosteric drug, o,o'-bismyristoyl thiamine disulfide, suppresses HIV-1 replication through prevention of nuclear translocation of both HIV-1 Tat and NF-kappa B. Biochem Biophys Res Commun. 1998 Aug 28;249(3):745-53.Butterworth RF, Gaudreau C, Vincelette J, Bourgault AM, Lamothe F, Nutini AM. Thiamine deficiency and Wernicke's encephalopathy in AIDS. Metab Brain Dis. 1991 Dec;6(4):207-12.“we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse… it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex”Haisraeli-Shalish M, Livneh A, Katz J, Doolman R, Sela BA. Recurrent aphthous stomatitis and thiamine deficiency. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Dec;82(6):634-6.” 70 patients with recurrent aphthous stomatitis and in 50 members of a control group… Low levels of vitamin B1 were detected in 49 patients but in only two members of the control group… Our finding suggests an association between thiamine deficiency and recurrent aphthous stomatitis”Engel D. Tropical pyomyositis, a thiamine-deficiency disease. Med Hypotheses. 1981 Mar;7(3):345-52.“it is suggested that thiamine deficiency is an essential contributary factor in producing tropical pyomyositis… Thiamine deficiency induces a biochemical lesion (s) in the pyruvate oxidase system of the muscle, which breaks down its normal resistance to infection and opens the gate to bacterial agents”Krishna S, AM, Supanaranond W, Pukrittayakamee S, ter Kuile F, Tawfiq KM, Holloway PA, White NJ. Thiamine deficiency and malaria in adults from southeast Asia. Lancet. 1999 Feb 13;353(9152):546-9.”12 (52%) of 23 patients with severe malaria and ten (19%) of 54 patients with uncomplicated malaria had alpha values above the normal range (p<0.0001 and p=0.0014, respectively, compared with controls), which indicated severe thiamine deficiency” Pietrzak I, Baczyk K, Mlynarczyk M, Kaczmarek M. [Content of thiamin in plasma and erythrocytes in patients with end stage renal disease] Przegl Lek. 1996;53(5):423-6. Polish.”We suggest the need of thiamine supplementation in ESRD patients especially in those treated by dialysis. The supplementation of thiamine is needed particularly in patients on peritoneal dialysis”Relation of thiamine to other dataHung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. 2001 Nov;38(5):941-7.“We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency”Huang S, Ren G. [Thiamine status of university teacher families in Changsha] Hunan Yi Ke Da Xue Xue Bao. 1998;23(1):27-30. Chinese.“We conclude that those people who take the refined cereals and its products as a staple food, is in the risk of thiamine deficiency”Suzuki M, Itokawa Y. Effects of thiamine supplementation on exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106.“High-dose thiamine (vitamin B1) supplementation (100 mg/day) may be helpful in preventing or accelerating recovery from exercise-induced fatigue… Thiamine supplementation significantly suppressed the increase in blood glucose in the normal thiamine group and significantly decreased the number of complaints shortly after exercise in the subjective fatigue assessment of 30 items”Kimura M, Itokawa Y, Fujiwara M. Cooking losses of thiamin in food and its nutritional significance. J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl 1:S17-24.”The thiamin contents in cooked daily meals were 50-60 percent of the calculated values on an average”Cruickshank AM, Telfer AB, Shenkin A. Thiamine deficiency in the critically ill. Intensive Care Med. 1988;14(4):384-7.“We performed a retrospective study on 158 patients admitted to the Intensive Care Unit who required nutritional support. Patients who survived had significantly higher body thiamine status than those who died”Onodera K, Kisara K, Okabe H, Ogura Y. [studies on the effects of thiamine deficiency on rat testes (author's transl)] Nippon Yakurigaku Zasshi. 1980 Mar;76(2):143-52. Japanese.“In the thiamine deficient group, the seminiferous tubuli of rats having erections had atrophied”Labadarios D, Rossouw JE, McConnell JB, M, R. Thiamine deficiency in fulminant hepatic failure and effects of supplementation. Int J Vitam Nutr Res. 1977;47(1):17-22.“Nine out of 24 patients with acute hepatocellular necrosis leading to fulminant hepatic failure showed biochemical evidence of thiamine deficiency early in the course of their illness”Why haven’t we heard of benfo before? The patent on the manufacture of benfo expired decades ago. Pharmaceutical companies pursue drugs that can be patented so they can have a monopoly and charge 100 times what the drug is worth. They have spent a lot of money on AGE inhibitors that don’t work as well as benfo. Ingestion of benfo may result in the elimination of AGE-protein crosslinks, which are a major constituent of arterial plaque. I am intrigued by the idea that benfo may cause the removal of plaque from the blood vessels, but I am concerned about the rapid manner in which it may cause the removal of plaque from the blood vessels. If the plaque is being removed, a large chunk might break off and cause a stroke or heart attack. If I was older than 60 or if I had a serious problem with high blood pressure I would probably start out by taking very low doses of benfo and gradually increase my dosage. Of course, there are no reports of strokes or heart attacks from benfo in the medical literature, but it’s a thought to consider. My PhD research will mostly consist of double-blind controlled studies on the administration of benfo in normal individuals, diabetics, individuals with high blood pressure, Alzheimer patients etc. I believe the researchers who have investigated benfo to date have been extremely short sighted by not discovering they full potential of benfo in the clinical studies that have already been performed on humans.It is illegal to make claims about benfo and sell it as a dietary supplement unless the claims are based on substantial scientific evidence. The three case studies outlined in this document are not from a double-blind controlled study and FDA regulations would not allow for them to be referred to as substantial scientific evidence. Claims should not be made based on these preliminary findings. For questions or comments email robholladay99@...Since I am not a physician, it would be inappropriate for me to answer emails asking for medical advice.

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I started on this B1 night before last. I've been whining about this long drawn out virus I've been fighting, and either the B1 is helping mucho over the last two days, or I'm suddenly getting stronger anyway. I feel lots more energy, and my legs are finally getting some strength back. It's so hard to tell if it is the Benfotiamine or just my body finally winning. Who knows. I do know I've seen no side effects even though I've been taking 600mg twice a day. After a few days more I'll cut that in half... No digestive upsets, no headaches, just a positive feeling about life in general.

(MS)

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Sent: Tuesday, March 23, 2004 7:26 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

Tom, thanks for the great article. I will be starting this form of B1 when I finish my bottle of thiamine. Will keep everyone posted on any benefits I receive. Are you taking this form of B1 and did you find out about it through the Brewer Science Library? White is the educatuional cordinater at the library and publishes a quarterly newslettet. She is a wonderful source of info about ms and other dis-eases in the body. Best Wishes, Kathy

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msalternatives ; MSersLife ; MS-Christians ; MSfriends ; MSViews_Multiple_Sclerosis ; low dose naltrexone ; JJUK ; mscured

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Sent: Saturday, March 20, 2004 11:01 PM

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Research on Benfotiamine Clinton Holladay, M.S.Copyright 2003 Clinton HolladayJune 5, 2003A short while ago a group of individuals I know purchased a large amount of benfotiamine and began ingesting it orally. I was urged by these individuals to place some of the research I have been conducting on benfo (benfotiamine) online along with the results of their benfo use. I was asked to do this in a manner that would allow individuals that do not have a background in the health sciences to comprehend it. I will be pursuing a PhD shortly and benfo will be central to my research. I am not a physician and the following information is not intended to be used as medical advice. Advanced glycation endproducts or AGEs are produced by the processing of sugars within the cell. They are one of the primary causes of aging and general wear and tear on your cells. Diabetics age the same way as normal people, but because they often have abnormal levels of sugars in their cells, they age faster. When blood sugar levels are high, certain cells in the body are flooded with glucose, particularly neurons and cells in the eyes and kidneys. Diabetics often suffer from nerve damage, kidney failure, and premature blindness. Numerous researchers have concentrated their efforts on AGE-blocking mechanisms because they would limit the wear and tear on the body’s cells and allow individuals to live longer and healthier, particularly diabetics. Benfo has emerged as the premier AGE inhibitor.Case StudiesIt is important to note that the following case studies are not double-blind controlled studies. Case study #1. Female, early fifties, non-diabetic, suffers from chronic fatigue, depression, and the normal aches and pains that accompany middle age. Her diet is average. She is able to do about two hours of physical labor a day, and she has suffered from depression for years. She has tried numerous treatments for depression including Prozac, and some of them have helped, but none have completely eliminated the depression. Sometimes she aches all over. She was addicted to caffeine for several years, but only consumes it about once a week now. She has high blood pressure, and treats it with Vasotec and also takes Maxide (a diuretic).She ingested 650 mg of benfo once a day for five days and did not notice any difference. On day 6 she doubled the dose to 1300 mg and started to notice a change a few hours later. There was a dramatic increase in stamina and energy. She is now able to do eight hours of physical work each day. She has an extremely heightened sense of well-being and all aspects of the depression have left. She has better clarity of thought, and sleeps better. Previously she would usually wake up two or three times a night. Now she sleeps through the whole night and has said she is in a deeper sleep at night. She has reported being able to control her appetite more. She has reported less shortness of breath. On day 13 she has had no weight change. On day 13 she experienced what felt exactly like a caffeine withdrawal headache. She immediately consumed two cans of mountain dew and the headache did not leave. Previous to this, caffeine had always relieved a headache of this sort for her. At day 14 she still had a headache and the tips of her toes started tingling. She reduced her dose to 650 mg per day once a day on day 14. On day 15 she still had a headache. On day 16 her toes started tingling and the headache left. On day 17 her pinkie started tingling. Her blood pressure has always fluctuated between 120/80 and 150/90. Throughout the treatment her blood pressure has fluctuated like it normally does. She says she feels like she did when she was thirty years old. Comment: The tingling is likely the cause of blood circulating to parts of her body that have not had a great deal of circulation in recent years.Case study #2. Male, mid fifties, non-diabetic. Average diet. Overall health is better than average for his age. He gets indigestion at night and takes Prilosec. He has the normal aches and pains that accompany middle age. When he wakes up in the morning his feet are inflexible, but that would go away after walking on them for about two minutes. After driving for two hours he is stiff when he gets out of his car. Most of the aches and pains and the foot inflexibility appeared in the last five to fifteen years. He began taking 650 mg of benfo once a day. On day 3 nothing hurt when he woke up. By day five all his aches and pains had disappeared. He is no longer stiff when he gets out of his car after driving for two hours. He feels more flexible. He says it has fixed everything that has gone wrong with him in the past fifteen years. He says he feels more cheerful but is not sure if it is because of repair to neurological damage or because his aches and pains are gone. He has reported a greater clarity of thought. He says he feels like he did when he was age 25-40 (he says he felt the same during those years). Up until twelve months ago his blood pressure has been 120/90. For the past twelve months it has averaged 130/120. On day 5 his blood pressure was 120/85 and it has remained consistent every day since then. Now he can only take a fifteen minute nap during the day whereas before he could fall asleep for hours. At night he sleeps better, probably because the aches and pains are gone. His appetite is only about 80% of what it used to be. He has reported increased stamina and energy. Before taking benfo it was getting hard for him to do ten hours of work per day. Now he can do fourteen hours of work per day. He still requires the same amount of sleep at night, but if he does not get his full requirement he doesn’t notice it nearly as much.Comment: The decrease in caloric intake may be because he was lacking an essential nutrient- not enough thiamine? The stiffening of the joints brought on by old age is partly a symptom poor blood circulation. The fact that this individual has become much more flexible is a possible indication of increased circulation.Case study #3. Male, late forties. He has been a type 1 diabetic for twenty years. Average diet. Over the last five years his health has declined more rapidly. He has more aches and pains than the average person because he is diabetic. He aches so much at night that he usually can’t get to sleep unless he takes Ibuprofen. He began taking 650 mg benfo once a day. On day 2 he noticed a decline in the severity of his aches and pains. He still needs the same amount of sleep, but if he doesn’t get his full requirement he doesn’t notice nearly as much. He has had an increase in stamina and energy. He says his stamina has doubled. On day 14 he felt like he did ten years ago, and it keeps improving each day. He is more cheerful, but like #2 he can’t tell if it’s because his aches and pains are gone or if benfo has a neurological effect on him. I will not disclose the brand of benfo which was used because I do not wish to be seen as promoting any particular brand. These case studies will be updated on July 5, 2003 and new ones will be added. The updates will be posted on www.geocities.com/robholladay99/updates.html The following exerpts are from medical journals. The abstracts (summaries) for most of them can be viewed online through the pubmed database, which is a free database most biomedical scientists use. To find pubmed, go to google.com and type in pubmed. Once you’re in pubmed, type in part of the title and you should be able to find the abstract. When typing in the title use "benfotiamine" not "benfo". As an anti-spamming measure, many search engines will not index web pages that list the key search words more than seven times throughout the document, hence this document was modified after it was created . Several things are important to note in the following literature. First of all, not only does benfo stop some effects of aging, it reverses them. Gradually over time people’s neurons quit working because of normal wear and tear. However, when benfo was ingested, not only did the nerve damage stop, some of the damage done through aging was repaired. A strong point is made that benfo is the most bioavailable source of thiamine. This means benfo is better absorbed than other sources of thiamine. Also, high levels of thiamine have analgesic (pain-relieving) effects on animals. In the Russian study the pain level of the patients decreased from 8.2 to 2.3, a decrease of about four hundred percent. Research articles on benfoWada T, Tagaki H, Minakami H, Hamanka W, Okamoto K, Ito, A, Sahashi Y. 1961. A new thiamine derivative, S-benzoylthiamine O-monophosphate. Science 134: 195-196.Benfo “is more easily absorbed in the body than thiamine hydrochloride, and administration results in higher thiamine and cocarboxylase levels in organs; moreover, these levels last for a longer period of time…It does not cause any unfavorable symptom in animals such as thiamine hydrochloride does…The LD50 by oral administration in mice, dd-strain hybrid, weighing 14 to 16g was 15g/kg of body weight”Bitsch R, Wolf M, Moller J, Heuzeroth L, Gruneklee D. Bioavailability assessment of the lipophilic benfo as compared to a water-soluble thiamin derivative. Ann Nutr Metab. 1991;35(5):292-6. “in presence of allicin, the active principle of garlic, the water-soluble thiamin hydrochloride is transformed into a lipid-soluble compound being identified as allithiamine…Ten healthy young men…The volunteers ingested a single dose of 40 mg benfo…Thus, the measured values reveal, when compared with mononitrate, a clearly improved thiamin bioavailability from benfo, due to the more lipophilic properties of this substance or possibly its dephosphorylated metabolite and a more rapid transformation into the physiologically active derivative. This may be of great advantage in the treatment of neurological disorders responding to high thiamin doses and further on in situations when the active intestinal absorbtion mechanisms are impaired”Stracke H, Lindemann A, Federlin K. A benfo-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.“Benfo…was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold...Therapy-specific adverse effects were not seen”Loew D. Pharmacokinetics of thiamine derivatives especially of benfo. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.“The effective form of thiamine, thiamine diphosphate, is an organic compound needed by the organism for vital functions…Due to this peculiarity the conditions for absorbtion of lipid-soluble vitamins differ from those for water-soluble thiamine derivatives. Unlike the latter, allithiamines are absorbed passively, they traverse the intestinal absorption barrier faster and more readily, leading to higher blood and tissue concentrations even when comparatively low doses are given…It therefore fulfills important pharmacodynamic conditions for rational therapy. Due to their greater biovailability and better tissue passage lipid-soluble thiamine analogues like benfo are preferable to water-soluble thiamine derivatives for treatment of various pathological conditions, e.g. cardiomyopathy, Werincke-Korsakow syndrome, and alcoholic or diabetic polyneuropathies…Due to its excellent pharmacokinetic profile and to its excellent tolerability benfo should be preferred in treatment of relevant conditions like neuropathies”Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter CH. Comparative bioavailability of two vitamin B1 preparations: benfo and thiamine mononitrate. Eur J Clin Pharmacol. 1997;52(4):319-20.“a study using equimolar quantities of the two preparations for exact comparison of the bioavailability of benfo and thiamine mononitrate has never been performed. Therfore, the present trial was undertaken…the higher thiamine content in the erythrocytes and the higher thiamine excretion in urine after oral benfo administration are proof of the considerably higher relative bioavailability of benfo than thiamine mononitrate”Simeonov S, Pavlova M, Mitkov M, Mincheva L, Troev D. Therapeutic efficacy of "Milgamma" in patients with painful diabetic neuropathy. Folia Med (Plovdiv). 1997;39(4):5-10.“Forty-Five diabetes patients with painful peripheral polyneuropathy were enrolled in a 3-month observational study comparing the therapeutic efficiacy of Milgamma tablets (benfo)…Statistically significant relief of both background and peak neuropathic pain was achieved in all of the Milgamma-treated patients…No adverse reactions were observed…Our results underscore the importance of Milgamma tablets as an indispensable element in the therapeutic regimen of patients with painful diabetic polyneuropathy”Greb A, Bitsch R. Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther. 1998 Apr;36(4):216-21.“Seven healthy volunteers…a single oral dose of either benfo…fursultiamin…thiaminedisulfide…In this study the allithiamine derivative benfo proved the best bioavailability. Owing to its excellent absorption properties it can be concluded that oral administration of benfo is suitable for therapeutical purposes”Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfo in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.Good review, full-text is available free online. “In bioavailability studies on healthy human subjects, it was shown that absorption of benfo was several times better than that of water-soluble vitamin B1 and that there was a 120-fold higher increase of metabolically active thiamine diphosphate in erythrocytes (Heinrich, 1990)…In animals given dosages that exceeded basic requirements by 100- or 1000-fold thiamine has analgesic and neuroprotective effects(woelk and peeler-Ichakawa, 1985; Jurna, 1988; Reeh, 1988, 1991; Wild, 1988). However, if high levels are to be achieved with oral vitamin B1 treatment, lipid soluble thiamine derivatives or pro-drugs with high bioavailability, such as benfo, are required…320 mg/day during weeks 1 to 4 and 120 mg benfo/day during weeks 5 to 8…Within the 8-week study period, benfo led to a significant improvement of the threshold of vibration perception at the great toe, motor function, and the overall symptom score. Marked improvement occurred in both pain and co-ordination”Sadekov RA, Danilov AB, Vein AM. [Diabetic polyneuropathy treatment by milgamma-100 preparation] Zh Nevrol Psikhiatr Im S S Korsakova. 1998;98(9):30-2. Russian.“benfo…was studied in treatment of diabetic polyneuropathy in 14 patients…After the course of treatment the intensity of pains was decreased according to visual analogous scale on the average from 8.2 to 2.3 scores, the indices of vibratory sensitivity improved significantly as well as the data of cardiovascular tests…The treatment resulted in the improvement of the condition in 93% of the cases” T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine pharmacokinetics by end-stage renal disease (ESRD). Int J Clin Pharmacol Ther. 1999 Sep;37(9):449-55.“20 end-stage renal disease(ESRD) patients…After a single oral dose of 100 mg benfo…ESRD patients may benefit from high-dose thiamine derivatives notwithstanding their chemical form. However, the better absorption and high transfer rate of debenzoylated BTMP (benfo) to TDP (thiamine diphosphate) even at much lower doses compensates for reduced renal excretion and may protect, therefore, against numerous adverse effects of uremia”Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different benfo dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.320, 120, and 150 mg benfo/day was administered to “diabetic patients suffering from painful peripheral diabetic neuropathy. In a 6-week open clinical trial, 36 patients…An overall beneficial therapeutic effect on the neuropathy status was observed in all three groups during the study…The greatest change occurred in the group of patients receiving the high dose of benfo…Metabolic control did not change over the study...Extremely interesting is the result of recent in vitro experiences that thiamine pyrophosphate and pyroxidine inhibit the formation of glycation end products" T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfo. Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.“20 end-stage renal disease (ESRD) patients…After benfo administration, the peak plasma concentration of TDP exceeded that in healthy subjects by 51%...Compared with thiamine nitrate, the oral administration of benfo leads to higher TDP concentrations in erythrocytes accompanied with a significant improvement of the erythrocyte transkelotase activity in ESRD patients”Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M. Benfo is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.“We investigated the hypothesis that benfo, a lipophilic derivative of thiamine, affects replication delay and generation of advanced glycosylation endproducts (AGE) in human umbilical vein endothelial cells cultured in the presence of high glucose…Benfo, a derivative of thiamine with better bioavailability, corrects defective replication and increased AGE generation in endothelial cells cultured in high glucose, to a similar extent as thiamine. These effects may result from normalization of accelerated glycolysis and the consequent decrease in metabolites that are extremely active in generating nonenzymatic protein glycation. The potential role of thiamine administration in the prevention or treatment of vascular complications of diabetes deserves further investigation”Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M, Geyer J, Kopcke W, Sauerland C, Bretzel RG, Federlin KF. Efficacy of benfo versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.“After three months preventative administration of both vitamin B1 preparations NCV (nerve conduction velocity) had increased substantially…It was nearly normal after six months with benfo, while the administration of thiamine nitrate resulted in no further amelioration. NCV was nearly normalized after six months of benfo application but not with thiamine. Furthermore, benfo induced a major inhibition of neural imidazole-type AGE formation and completely prevented diabetes induced glycoxidation products”Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M. Benfo blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.“Our results in both endothelial cells cultured for several days and retinas from rats with nine months of diabetes showed that benfo, a lipid-soluble thiamine derivative, prevents activation of three major pathways involved in hyperglycemia-induced vascular damage: the hexosamine pathway, the intracellular AGE formation pathway and the DAG-PKC pathway…We showed that benfo blocks these pathways of hyperglycemic damage by increasing the activity of transketolase…Administration of benfo for nine months also completely prevented the development of experimental diabetic retinopathy in rats...Thus we conclude that augmentation of transketolase activity is solely responsible for the observed effects of benfo”Comment: This study is very significant because it demonstrates how benfo blocks several other aging mechanisms besides AGE formation. However, I am not yet convinced of the statement that transketolase activity is solely responsible for the observed effects of benfo. The following four studies are located on the Internet but are not yet listed on Medline. To find them, go to google.com and type in part of the titleBergfeld R, Matsumara X. Du, Brownlee M. Benfo prevents the consequences of hyperglycemia-induced mitochondrial overproduction of reactive oxygen species, and experimental diabetic retinopathy.“diabetic rats were treated with benfo (80 mg/kg weight) for 36 weeks…Benfo decreases AGE formation by 60%...These data suggest that treatment with benfo may be an effective approach to prevent the development of diabetic complications”Lin J, Alt A, Liersch J, Bretzel R, Brownlee M, Hammes H. Benfo inhibits intracellular formation of advanced glycation end products in vivo“Here, we studied the effect of benfo, a lipid-soluble thiamine derivative with known AGE-inhibiting properties in vitro on the intracellular formation of (CML) and methylgloxal-derived AGE in red blood cells. Blood was collected from 6 type 1 diabetic patients before and after treatment with 600 mg/day benfo for 28 days…Thiamine derivatives, in particular the lipid-soluble prodrug benfo, are effective inhibitors of intracellular formation of AGE and CML”Stracke H, Werkmann D, Mavrakis K, Federlin K, Kopke W, Sauerland C, Hammes H, Bretzel RG. Influence of vitamin B1 on diabetic neuropathy-studies in streptozotocin-diabetic rats.“we investigated the effects of oral administration of thiamine and benfo on the development of glucose oxidation products in the nerve and on nerve conduction velocity in streptozotocin-diabetic rats…Conclusion: Early treatment with benfo normalizes increased cellular oxidative stress and the reduced nerve conduction velocity”Hammes H, Bretzel, R.G., Federlin, K, Horiuchi S, Niwa T, Stracke H. Benfo inhibits the formation of advanced glycation end products in diabetic rats.“benfo (100 mg/kg x day) and thiamin (70.18 mg/kg x day) administered orally for 6 months…neither benfo nor thiamin treatment affected metabolic control…Benfo administration in diabetic rats induced a major inhibition of neutral imidazolone-type AGE formation and completely prevented diabetes-induced glycoxidation formation. Treatment with thiamin did not affect AGE or CML levels”ThiamineAllithiamines are lipid-soluble sources of thiamine. Benfo is an allithiamine. Thiamine is water-soluble and is also known as vitamin B1.After reviewing the relevant medical literature on thiamine, I have come to conclude that large portions of the population may be thiamine deficient. In addition, many individuals that are not technically thiamine deficient would likely receive benefit from thiamine supplementation. Thiamine deficiency is associated with numerous undesirable medical conditions.Relation of thiamine to heart diseaseShamir R, Dagan O, Abramovitch D, Abramovitch T, Vidne BA, Dinari G. Thiamine deficiency in children with congenital heart disease before and after corrective surgery. JPEN J Parenter Enteral Nutr. 2000 May-Jun;24(3):154-8.Thiamine deficiency “is common in children with congenital heart disease (CHD) referred for corrective surgery both before and after surgery. Our results suggest that neither diuretic treatment nor malnutrition can fully explain the development of TD in these children”Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E, Levy R. [Right heart failure caused by thiamine deficiency (cardiac beriberi)] Presse Med. 2000 Feb 12;29(5):240-1. French.Beaud C, Fuhrman C, Perchet H, Monnet I, Chouaid C, Housset B. [Thiamine deficiency. A cause of cardiac insufficiency not to be ignored] Rev Mal Respir. 1998 Jun;15(3):303-4. French.“Thiamine deficiency is one of the classical causes of high output for heart failure”Okura H, Gohma I, Hatta K, Imanaka T. Thiamine deficiency and pulmonary hypertension in Crow-Fukase syndrome. Intern Med. 1995 Jul;34(7):674-5. “After oral administration of prednisolone and thiamine, echocardiogram showed marked improvement of the pulmonary hypertension”Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc. 1995 May;95(5):541-4. “Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk”Shimon I, Almog S, Vered Z, Seligmann H, Shefi M, Peleg E, Rosenthal T, Motro M, Halkin H, Ezra D. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med. 1995 May;98(5):485-90.“Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy”Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered Z, Ezra D. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med. 1991 Aug;91(2):151-5.”These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements”Relation of thiamine to neurological disordersLonsdale D, Shamberger RJ, Audhya T. Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: a pilot study. Neuroendocrinol Lett. 2002 Aug;23(4):303-8.“Thiamine tetrahydrofurfuryl disulfide appears to have a beneficial clinical effect on some autistic children, since 8 of the 10 children improved clinically”Nakagawasai O, Tadano T, Hozumi S, Taniguchi R, Tan-No K, Esashi A, Niijima F, Kisara K. Characteristics of depressive behavior induced by feeding thiamine-deficient diet in mice.Life Sci. 2001 Jul 27;69(10):1181-91.Ambrose ML, Bowden SC, Whelan G. Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings. Alcohol Clin Exp Res. 2001 Jan;25(1):112-6.“A therapeutic relationship between dose and working memory performance was indicated”Older MW, Dickerson JW. Thiamine and the elderly orthopaedic patient. Age Ageing. 1982 May;11(2):101-7.“In both groups those patients who were noticeably confused after operation were found to have a considerable fall in their thiamine status suggesting this may be a contributory factor to postoperative confusion”Winston AP, son CP, Madira W, Gatward NM, Palmer RL. Prevalence of thiamin deficiency in anorexia nervosa. Int J Eat Disord. 2000 Dec;28(4):451-4.“Fourteen patients (38%) had results in the deficient range; 7 (19%) met the most stringent published criterion for deficiency. Deficiency was not related to duration of eating restraint, frequency of vomiting, or alcohol consumption”Terasawa M, Nakahara T, Tsukada N, Sugawara A, Itokawa Y. The relationship between thiamine deficiency and performance of a learning task in rats. Metab Brain Dis. 1999 Sep;14(3):137-48.“We taught rats to press a lever to escape from the pain of electrical stimulation by learning to turn a switch off… The rats that were fed the thiamine-deficient diet showed a slower response time and a longer running time than the rats fed the normal diet… We found that the thiamine concentration in the blood of the rats in the trained group was significantly higher than that in the group without training”Jimenez-Jimenez FJ, Molina JA, Hernanz A, Fernandez-Vivancos E, de Bustos F, Barcenilla B, Gomez-Escalonilla C, Zurdo M, Berbel A, Villanueva C. Cerebrospinal fluid levels of thiamine in patients with Parkinson's disease. Neurosci Lett. 1999 Aug 13;271(1):33-6.“These results suggest that low CSF free thiamine levels could be related with the risk for PD”Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J. 1997 Dec;74(12):803-8.“Diabetic peripheral neuropathy in Dar es Salaam is associated with thiamine deficiency”Langlais PJ, G, Guo SX, Bondy SC. Increased cerebral free radical production during thiamine deficiency. Metab Brain Dis. 1997 Jun;12(2):137-43.“These findings suggest that increased formation of free radicals occurs during the more acute symptomatic stage of thiamine deficiency and may contribute to the structural damage described in this model of Wernicke's encephalopathy”Easton CJ, Bauer LO. Beneficial effects of thiamine on recognition memory and P300 in abstinent cocaine-dependent patients. Psychiatry Res. 1997 May 30;70(3):165-74. “Thiamine was found to significantly improve recognition accuracy and P300 amplitude, at the midline parietal (Pz) electrode. The improvement was most reliable under conditions of increased memory load”Benton D, Griffiths R, Haller J. Thiamine supplementation mood and cognitive functioning. Psychopharmacology (Berl). 1997 Jan;129(1):66-71. ”An improvement in thiamine status was associated with reports of being more clearheaded, composed and energetic. The taking of thiamine had no influence on memory but reaction times were faster following supplementation”Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's disease. Metab Brain Dis. 1996 Mar;11(1):89-94.”Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100 mg/day had a mild beneficial effect in patients with Alzheimer's disease in a 12-week open trial. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function”Gold M, Chen MF, K. Plasma and red blood cell thiamine deficiency in patients with dementia of the Alzheimer's type. Arch Neurol. 1995 Nov;52(11):1081-6.“A significant proportion of patients with SDAT may have a thiamine deficiency, which may have an impact on cognitive function. Currently used assays may not be adequate to assess thiamine status”Adamolekun B, Eniola A. Thiamine-responsive acute cerebellar ataxia following febrile illness. Cent Afr J Med. 1993 Feb;39(2):40-1. Review.“acute thiamine depletion may be the pathogenetic mechanism for post-pyrexial acute cerebellar ataxia”Ben-Hur T, Wolff E, River Y. [Thiamin deficiency is common in Israel] Harefuah. 1992 Nov 15;123(10):382-4, 436, 435. Hebrew.“Thiamin levels should be determined not only in alcoholics and those with classic B1 deficiency syndromes, but in the routine workup of patients with sensory-motor neuropathy, dementia, gait disorders, cerebellar syndromes and confusional states”Sacks W, Esser AH, Feitel B, Abbott K. Acetazolamide and thiamine: an ancillary therapy for chronic mental illness. Psychiatry Res. 1989 Jun;28(3):279-88.“Overall, 50% of the patients showed improvement on all assessment scales. No untoward effects occurred in these patients…”Relation of thiamine and geriatric patientsSmidt LJ, Cremin FM, Grivetti LE, Clifford AJ. Influence of thiamin supplementation on the health and general well-being of an elderly Irish population with marginal thiamin deficiency. J Gerontol. 1991 Jan;46(1):M16-22.”thiamin-supplemented women experienced significantly increased appetite, energy intake, body weight and general well-being, and decreased fatigue. Thiamin supplementation also tended to reduce daytime sleep time, improve sleep patterns, and increase activity. These data suggest that evaluation of thiamin status is indicated when nonspecific conditions such as anorexia, weight loss, fatigue, depression, and sleep disorders are present in elderly persons”Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels in elder patients admitted through the emergency department. Acad Emerg Med. 2000 Oct;7(10):1156-9.“CONCLUSIONS: Elder nursing home patients seen in the ED and admitted to the hospital are frequently thiamine-deficient”Wilkinson TJ, Hanger HC, Elmslie J, PM, Sainsbury R. The response to treatment of subclinical thiamine deficiency in the elderly. Am J Clin Nutr. 1997 Oct;66(4):925-8.“Only the subjects with persistently low TPP concentrations showed subjective benefits from treatment with improvements in quality of life… There was a trend toward benefits in sleep and energy… Quality of life was enhanced by providing thiamine supplements. Blood pressure and weight were lower after thiamine supplementation”Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte thiamin concentrations in geriatric outpatients. J Am Coll Nutr. 1996 Jun;15(3):231-6.“CONCLUSION: About 50% of geriatric outpatients in this study had low plasma thiamin levels”Nichols HK, Basu TK. Thiamin status of the elderly: dietary intake and thiamin pyrophosphate response. J Am Coll Nutr. 1994 Feb;13(1):57-61.“Average daily thiamin intake was above the recommended requirement… however, almost half of the total study population had TPP effect > 14%, suggesting thiamin deficiency… CONCLUSION: These findings raise questions about the reliability of dietary intake in assessing metabolic availability of thiamin in the elderly”O'Keeffe ST, Tormey WP, Glasgow R, Lavan JN. Thiamine deficiency in hospitalized elderly patients. Gerontology. 1994;40(1):18-24.“Necropsy studies suggest that thiamine deficiency is underdiagnosed in life… There was no difference in anthropometric indices or in the prevalence of other nutrient deficiencies between the two groups. Thiamine deficiency is common in elderly patients admitted to hospital and may contribute to the development of delirium”Iber FL, Blass JP, Brin M, Leevy CM. Thiamin in the elderly--relation to alcoholism and to neurological degenerative disease. Am J Clin Nutr. 1982 Nov;36(5 Suppl):1067-82. Review.“There is no known toxicity for thiamin”Relation of thiamine to diabetesAvena R, Arora S, Carmody BJ, Cosby K, Sidawy AN. Thiamine (Vitamin B1) protects against glucose- and insulin-mediated proliferation of human infragenicular arterial smooth muscle cells. Ann Vasc Surg. 2000 Jan;14(1):37-43.“Vitamin B1 intake may prove important in delaying the atherosclerotic complications of diabetes”La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA, Molinatti GM, Porta M. Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions. Diabetologia. 1996 Nov;39(11):1263-8.Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S, Scheinman M, T. Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells. Surgery. 2001 Nov;130(5):851-8.“The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes”Hassan R, Qureshi H, Zuberi SJ. Effect of thiamine on glucose utilization in hepatic cirrhosis. J Gastroenterol Hepatol. 1991 Jan-Feb;6(1):59-60.“It is therefore suggested that thiamine supplements be given to cirrhotics with hyperglycaemia, to improve glucose utilization”Rindi G, Laforenza U. Thiamine intestinal transport and related issues: recent aspects.Proc Soc Exp Biol Med. 2000 Sep;224(4):246-55. Review.“Thiamine uptake is enhanced by thiamine deficiency, and reduced by thyroid hormone and diabetes”Saito N, Kimura M, Kuchiba A, Itokawa Y. Blood thiamine levels in outpatients with diabetes mellitus. J Nutr Sci Vitaminol (Tokyo). 1987 Dec;33(6):421-30.“From the above findings it was concluded that diabetic outpatients tend to have a low blood thiamine level, with low erythrocyte transketolase activity and high erythrocyte TPP effect, and showed marginal thiamine deficiency” Relation of thiamine to diseaseWallace AE, Weeks WB. Thiamine treatment of chronic hepatitis B infection. Am J Gastroenterol. 2001 Mar;96(3):864-8.”In each case study, thiamine administration was associated with reduction in aminotransferase levels and the fall of HBV DNA to undetectable levels… The relationship between thiamine administration and chronic hepatitis B infection warrants further study. If proven effective in reducing liver damage or inducing remission of the hepatitis B virus in larger trials, thiamine will offer obvious advantages over the current treatments for chronic viral hepatitis B infection”Rossouw JE, Labadarios D, Krasner N, M, R. Red blood cell transketolase activity and the effect of thiamine supplementation in patients with chronic liver disease. Scand J Gastroenterol. 1978;13(2):133-8.“Biochemical evidence of thiamine deficiency was found in 58% of patients with chronic liver disease… high doses of thiamine should be included in the routine nutritional management of patients with severe chronic liver disease”Shoji S, Furuishi K, Misumi S, Miyazaki T, Kino M, Yamataka K. Thiamine disulfide as a potent inhibitor of human immunodeficiency virus (type-1) production. Biochem Biophys Res Commun. 1994 Nov 30;205(1):967-75.” The results suggest that thiamine disulfide may be important for AIDS chemotherapy”Shoji S, Furuishi K, Ogata A, Yamataka K, Tachibana K, Mukai R, Uda A, Harano K, Matsushita S, Misumi S. An allosteric drug, o,o'-bismyristoyl thiamine disulfide, suppresses HIV-1 replication through prevention of nuclear translocation of both HIV-1 Tat and NF-kappa B. Biochem Biophys Res Commun. 1998 Aug 28;249(3):745-53.Butterworth RF, Gaudreau C, Vincelette J, Bourgault AM, Lamothe F, Nutini AM. Thiamine deficiency and Wernicke's encephalopathy in AIDS. Metab Brain Dis. 1991 Dec;6(4):207-12.“we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse… it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex”Haisraeli-Shalish M, Livneh A, Katz J, Doolman R, Sela BA. Recurrent aphthous stomatitis and thiamine deficiency. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Dec;82(6):634-6.” 70 patients with recurrent aphthous stomatitis and in 50 members of a control group… Low levels of vitamin B1 were detected in 49 patients but in only two members of the control group… Our finding suggests an association between thiamine deficiency and recurrent aphthous stomatitis”Engel D. Tropical pyomyositis, a thiamine-deficiency disease. Med Hypotheses. 1981 Mar;7(3):345-52.“it is suggested that thiamine deficiency is an essential contributary factor in producing tropical pyomyositis… Thiamine deficiency induces a biochemical lesion (s) in the pyruvate oxidase system of the muscle, which breaks down its normal resistance to infection and opens the gate to bacterial agents”Krishna S, AM, Supanaranond W, Pukrittayakamee S, ter Kuile F, Tawfiq KM, Holloway PA, White NJ. Thiamine deficiency and malaria in adults from southeast Asia. Lancet. 1999 Feb 13;353(9152):546-9.”12 (52%) of 23 patients with severe malaria and ten (19%) of 54 patients with uncomplicated malaria had alpha values above the normal range (p<0.0001 and p=0.0014, respectively, compared with controls), which indicated severe thiamine deficiency” Pietrzak I, Baczyk K, Mlynarczyk M, Kaczmarek M. [Content of thiamin in plasma and erythrocytes in patients with end stage renal disease] Przegl Lek. 1996;53(5):423-6. Polish.”We suggest the need of thiamine supplementation in ESRD patients especially in those treated by dialysis. The supplementation of thiamine is needed particularly in patients on peritoneal dialysis”Relation of thiamine to other dataHung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. 2001 Nov;38(5):941-7.“We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency”Huang S, Ren G. [Thiamine status of university teacher families in Changsha] Hunan Yi Ke Da Xue Xue Bao. 1998;23(1):27-30. Chinese.“We conclude that those people who take the refined cereals and its products as a staple food, is in the risk of thiamine deficiency”Suzuki M, Itokawa Y. Effects of thiamine supplementation on exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106.“High-dose thiamine (vitamin B1) supplementation (100 mg/day) may be helpful in preventing or accelerating recovery from exercise-induced fatigue… Thiamine supplementation significantly suppressed the increase in blood glucose in the normal thiamine group and significantly decreased the number of complaints shortly after exercise in the subjective fatigue assessment of 30 items”Kimura M, Itokawa Y, Fujiwara M. Cooking losses of thiamin in food and its nutritional significance. J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl 1:S17-24.”The thiamin contents in cooked daily meals were 50-60 percent of the calculated values on an average”Cruickshank AM, Telfer AB, Shenkin A. Thiamine deficiency in the critically ill. Intensive Care Med. 1988;14(4):384-7.“We performed a retrospective study on 158 patients admitted to the Intensive Care Unit who required nutritional support. Patients who survived had significantly higher body thiamine status than those who died”Onodera K, Kisara K, Okabe H, Ogura Y. [studies on the effects of thiamine deficiency on rat testes (author's transl)] Nippon Yakurigaku Zasshi. 1980 Mar;76(2):143-52. Japanese.“In the thiamine deficient group, the seminiferous tubuli of rats having erections had atrophied”Labadarios D, Rossouw JE, McConnell JB, M, R. Thiamine deficiency in fulminant hepatic failure and effects of supplementation. Int J Vitam Nutr Res. 1977;47(1):17-22.“Nine out of 24 patients with acute hepatocellular necrosis leading to fulminant hepatic failure showed biochemical evidence of thiamine deficiency early in the course of their illness”Why haven’t we heard of benfo before? The patent on the manufacture of benfo expired decades ago. Pharmaceutical companies pursue drugs that can be patented so they can have a monopoly and charge 100 times what the drug is worth. They have spent a lot of money on AGE inhibitors that don’t work as well as benfo. Ingestion of benfo may result in the elimination of AGE-protein crosslinks, which are a major constituent of arterial plaque. I am intrigued by the idea that benfo may cause the removal of plaque from the blood vessels, but I am concerned about the rapid manner in which it may cause the removal of plaque from the blood vessels. If the plaque is being removed, a large chunk might break off and cause a stroke or heart attack. If I was older than 60 or if I had a serious problem with high blood pressure I would probably start out by taking very low doses of benfo and gradually increase my dosage. Of course, there are no reports of strokes or heart attacks from benfo in the medical literature, but it’s a thought to consider. My PhD research will mostly consist of double-blind controlled studies on the administration of benfo in normal individuals, diabetics, individuals with high blood pressure, Alzheimer patients etc. I believe the researchers who have investigated benfo to date have been extremely short sighted by not discovering they full potential of benfo in the clinical studies that have already been performed on humans.It is illegal to make claims about benfo and sell it as a dietary supplement unless the claims are based on substantial scientific evidence. The three case studies outlined in this document are not from a double-blind controlled study and FDA regulations would not allow for them to be referred to as substantial scientific evidence. Claims should not be made based on these preliminary findings. For questions or comments email robholladay99@...Since I am not a physician, it would be inappropriate for me to answer emails asking for medical advice.

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Just a note...We dispense a LOT of Vitamin B1 injection (some people just don't absorb the B vitamins well through the gut, so they use an injection). People are using 200mg and more each day and report significant improvements. I hold firm to the belief that many (if not most) chronic conditions (like MS and CFS) have their roots deeply buried in nutrition problems. It seems that B1 is a vital nutrient for proper nerve and muscle function.

Here's a link to an updated protocol. Dale Humpherys has used this approach for over 25 years - and he has encouraged hundreds (if not thousands) of others to use this approach. http://www.thecompounder.com/HumpherysNewProtocol.html

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Any health related information on our web pages or in our newsletters is for educational purposes only. None of the information we provide is to be construed as medical advice. Before applying any therapy or use of herbs, you may want to seek advice from your health care professional. Our information should not be a substitute for physician evaluation or treatment by a health care professional and is not intended to provide or confirm a diagnosis.

----- Original Message -----

From:

low dose naltrexone

Sent: Wednesday, March 24, 2004 7:47 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

I started on this B1 night before last. I've been whining about this long drawn out virus I've been fighting, and either the B1 is helping mucho over the last two days, or I'm suddenly getting stronger anyway. I feel lots more energy, and my legs are finally getting some strength back. It's so hard to tell if it is the Benfotiamine or just my body finally winning. Who knows. I do know I've seen no side effects even though I've been taking 600mg twice a day. After a few days more I'll cut that in half... No digestive upsets, no headaches, just a positive feeling about life in general.

(MS)

----- Original Message -----

From: ruben/kathy lintzenich

low dose naltrexone

Sent: Tuesday, March 23, 2004 7:26 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

Tom, thanks for the great article. I will be starting this form of B1 when I finish my bottle of thiamine. Will keep everyone posted on any benefits I receive. Are you taking this form of B1 and did you find out about it through the Brewer Science Library? White is the educatuional cordinater at the library and publishes a quarterly newslettet. She is a wonderful source of info about ms and other dis-eases in the body. Best Wishes, Kathy

----- Original Message -----

From: tmbayuk

msalternatives ; MSersLife ; MS-Christians ; MSfriends ; MSViews_Multiple_Sclerosis ; low dose naltrexone ; JJUK ; mscured

Sent: Monday, March 22, 2004 10:50 AM

Subject: [low dose naltrexone] Fw: check this out!

----- Original Message ----- From:

tmbayuk

Sent: Saturday, March 20, 2004 11:01 PM

Subject: check this out!

Research on Benfotiamine Clinton Holladay, M.S.Copyright 2003 Clinton HolladayJune 5, 2003A short while ago a group of individuals I know purchased a large amount of benfotiamine and began ingesting it orally. I was urged by these individuals to place some of the research I have been conducting on benfo (benfotiamine) online along with the results of their benfo use. I was asked to do this in a manner that would allow individuals that do not have a background in the health sciences to comprehend it. I will be pursuing a PhD shortly and benfo will be central to my research. I am not a physician and the following information is not intended to be used as medical advice. Advanced glycation endproducts or AGEs are produced by the processing of sugars within the cell. They are one of the primary causes of aging and general wear and tear on your cells. Diabetics age the same way as normal people, but because they often have abnormal levels of sugars in their cells, they age faster. When blood sugar levels are high, certain cells in the body are flooded with glucose, particularly neurons and cells in the eyes and kidneys. Diabetics often suffer from nerve damage, kidney failure, and premature blindness. Numerous researchers have concentrated their efforts on AGE-blocking mechanisms because they would limit the wear and tear on the body’s cells and allow individuals to live longer and healthier, particularly diabetics. Benfo has emerged as the premier AGE inhibitor.Case StudiesIt is important to note that the following case studies are not double-blind controlled studies. Case study #1. Female, early fifties, non-diabetic, suffers from chronic fatigue, depression, and the normal aches and pains that accompany middle age. Her diet is average. She is able to do about two hours of physical labor a day, and she has suffered from depression for years. She has tried numerous treatments for depression including Prozac, and some of them have helped, but none have completely eliminated the depression. Sometimes she aches all over. She was addicted to caffeine for several years, but only consumes it about once a week now. She has high blood pressure, and treats it with Vasotec and also takes Maxide (a diuretic).She ingested 650 mg of benfo once a day for five days and did not notice any difference. On day 6 she doubled the dose to 1300 mg and started to notice a change a few hours later. There was a dramatic increase in stamina and energy. She is now able to do eight hours of physical work each day. She has an extremely heightened sense of well-being and all aspects of the depression have left. She has better clarity of thought, and sleeps better. Previously she would usually wake up two or three times a night. Now she sleeps through the whole night and has said she is in a deeper sleep at night. She has reported being able to control her appetite more. She has reported less shortness of breath. On day 13 she has had no weight change. On day 13 she experienced what felt exactly like a caffeine withdrawal headache. She immediately consumed two cans of mountain dew and the headache did not leave. Previous to this, caffeine had always relieved a headache of this sort for her. At day 14 she still had a headache and the tips of her toes started tingling. She reduced her dose to 650 mg per day once a day on day 14. On day 15 she still had a headache. On day 16 her toes started tingling and the headache left. On day 17 her pinkie started tingling. Her blood pressure has always fluctuated between 120/80 and 150/90. Throughout the treatment her blood pressure has fluctuated like it normally does. She says she feels like she did when she was thirty years old. Comment: The tingling is likely the cause of blood circulating to parts of her body that have not had a great deal of circulation in recent years.Case study #2. Male, mid fifties, non-diabetic. Average diet. Overall health is better than average for his age. He gets indigestion at night and takes Prilosec. He has the normal aches and pains that accompany middle age. When he wakes up in the morning his feet are inflexible, but that would go away after walking on them for about two minutes. After driving for two hours he is stiff when he gets out of his car. Most of the aches and pains and the foot inflexibility appeared in the last five to fifteen years. He began taking 650 mg of benfo once a day. On day 3 nothing hurt when he woke up. By day five all his aches and pains had disappeared. He is no longer stiff when he gets out of his car after driving for two hours. He feels more flexible. He says it has fixed everything that has gone wrong with him in the past fifteen years. He says he feels more cheerful but is not sure if it is because of repair to neurological damage or because his aches and pains are gone. He has reported a greater clarity of thought. He says he feels like he did when he was age 25-40 (he says he felt the same during those years). Up until twelve months ago his blood pressure has been 120/90. For the past twelve months it has averaged 130/120. On day 5 his blood pressure was 120/85 and it has remained consistent every day since then. Now he can only take a fifteen minute nap during the day whereas before he could fall asleep for hours. At night he sleeps better, probably because the aches and pains are gone. His appetite is only about 80% of what it used to be. He has reported increased stamina and energy. Before taking benfo it was getting hard for him to do ten hours of work per day. Now he can do fourteen hours of work per day. He still requires the same amount of sleep at night, but if he does not get his full requirement he doesn’t notice it nearly as much.Comment: The decrease in caloric intake may be because he was lacking an essential nutrient- not enough thiamine? The stiffening of the joints brought on by old age is partly a symptom poor blood circulation. The fact that this individual has become much more flexible is a possible indication of increased circulation.Case study #3. Male, late forties. He has been a type 1 diabetic for twenty years. Average diet. Over the last five years his health has declined more rapidly. He has more aches and pains than the average person because he is diabetic. He aches so much at night that he usually can’t get to sleep unless he takes Ibuprofen. He began taking 650 mg benfo once a day. On day 2 he noticed a decline in the severity of his aches and pains. He still needs the same amount of sleep, but if he doesn’t get his full requirement he doesn’t notice nearly as much. He has had an increase in stamina and energy. He says his stamina has doubled. On day 14 he felt like he did ten years ago, and it keeps improving each day. He is more cheerful, but like #2 he can’t tell if it’s because his aches and pains are gone or if benfo has a neurological effect on him. I will not disclose the brand of benfo which was used because I do not wish to be seen as promoting any particular brand. These case studies will be updated on July 5, 2003 and new ones will be added. The updates will be posted on www.geocities.com/robholladay99/updates.html The following exerpts are from medical journals. The abstracts (summaries) for most of them can be viewed online through the pubmed database, which is a free database most biomedical scientists use. To find pubmed, go to google.com and type in pubmed. Once you’re in pubmed, type in part of the title and you should be able to find the abstract. When typing in the title use "benfotiamine" not "benfo". As an anti-spamming measure, many search engines will not index web pages that list the key search words more than seven times throughout the document, hence this document was modified after it was created . Several things are important to note in the following literature. First of all, not only does benfo stop some effects of aging, it reverses them. Gradually over time people’s neurons quit working because of normal wear and tear. However, when benfo was ingested, not only did the nerve damage stop, some of the damage done through aging was repaired. A strong point is made that benfo is the most bioavailable source of thiamine. This means benfo is better absorbed than other sources of thiamine. Also, high levels of thiamine have analgesic (pain-relieving) effects on animals. In the Russian study the pain level of the patients decreased from 8.2 to 2.3, a decrease of about four hundred percent. Research articles on benfoWada T, Tagaki H, Minakami H, Hamanka W, Okamoto K, Ito, A, Sahashi Y. 1961. A new thiamine derivative, S-benzoylthiamine O-monophosphate. Science 134: 195-196.Benfo “is more easily absorbed in the body than thiamine hydrochloride, and administration results in higher thiamine and cocarboxylase levels in organs; moreover, these levels last for a longer period of time…It does not cause any unfavorable symptom in animals such as thiamine hydrochloride does…The LD50 by oral administration in mice, dd-strain hybrid, weighing 14 to 16g was 15g/kg of body weight”Bitsch R, Wolf M, Moller J, Heuzeroth L, Gruneklee D. Bioavailability assessment of the lipophilic benfo as compared to a water-soluble thiamin derivative. Ann Nutr Metab. 1991;35(5):292-6. “in presence of allicin, the active principle of garlic, the water-soluble thiamin hydrochloride is transformed into a lipid-soluble compound being identified as allithiamine…Ten healthy young men…The volunteers ingested a single dose of 40 mg benfo…Thus, the measured values reveal, when compared with mononitrate, a clearly improved thiamin bioavailability from benfo, due to the more lipophilic properties of this substance or possibly its dephosphorylated metabolite and a more rapid transformation into the physiologically active derivative. This may be of great advantage in the treatment of neurological disorders responding to high thiamin doses and further on in situations when the active intestinal absorbtion mechanisms are impaired”Stracke H, Lindemann A, Federlin K. A benfo-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.“Benfo…was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold...Therapy-specific adverse effects were not seen”Loew D. Pharmacokinetics of thiamine derivatives especially of benfo. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.“The effective form of thiamine, thiamine diphosphate, is an organic compound needed by the organism for vital functions…Due to this peculiarity the conditions for absorbtion of lipid-soluble vitamins differ from those for water-soluble thiamine derivatives. Unlike the latter, allithiamines are absorbed passively, they traverse the intestinal absorption barrier faster and more readily, leading to higher blood and tissue concentrations even when comparatively low doses are given…It therefore fulfills important pharmacodynamic conditions for rational therapy. Due to their greater biovailability and better tissue passage lipid-soluble thiamine analogues like benfo are preferable to water-soluble thiamine derivatives for treatment of various pathological conditions, e.g. cardiomyopathy, Werincke-Korsakow syndrome, and alcoholic or diabetic polyneuropathies…Due to its excellent pharmacokinetic profile and to its excellent tolerability benfo should be preferred in treatment of relevant conditions like neuropathies”Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter CH. Comparative bioavailability of two vitamin B1 preparations: benfo and thiamine mononitrate. Eur J Clin Pharmacol. 1997;52(4):319-20.“a study using equimolar quantities of the two preparations for exact comparison of the bioavailability of benfo and thiamine mononitrate has never been performed. Therfore, the present trial was undertaken…the higher thiamine content in the erythrocytes and the higher thiamine excretion in urine after oral benfo administration are proof of the considerably higher relative bioavailability of benfo than thiamine mononitrate”Simeonov S, Pavlova M, Mitkov M, Mincheva L, Troev D. Therapeutic efficacy of "Milgamma" in patients with painful diabetic neuropathy. Folia Med (Plovdiv). 1997;39(4):5-10.“Forty-Five diabetes patients with painful peripheral polyneuropathy were enrolled in a 3-month observational study comparing the therapeutic efficiacy of Milgamma tablets (benfo)…Statistically significant relief of both background and peak neuropathic pain was achieved in all of the Milgamma-treated patients…No adverse reactions were observed…Our results underscore the importance of Milgamma tablets as an indispensable element in the therapeutic regimen of patients with painful diabetic polyneuropathy”Greb A, Bitsch R. Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther. 1998 Apr;36(4):216-21.“Seven healthy volunteers…a single oral dose of either benfo…fursultiamin…thiaminedisulfide…In this study the allithiamine derivative benfo proved the best bioavailability. Owing to its excellent absorption properties it can be concluded that oral administration of benfo is suitable for therapeutical purposes”Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfo in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.Good review, full-text is available free online. “In bioavailability studies on healthy human subjects, it was shown that absorption of benfo was several times better than that of water-soluble vitamin B1 and that there was a 120-fold higher increase of metabolically active thiamine diphosphate in erythrocytes (Heinrich, 1990)…In animals given dosages that exceeded basic requirements by 100- or 1000-fold thiamine has analgesic and neuroprotective effects(woelk and peeler-Ichakawa, 1985; Jurna, 1988; Reeh, 1988, 1991; Wild, 1988). However, if high levels are to be achieved with oral vitamin B1 treatment, lipid soluble thiamine derivatives or pro-drugs with high bioavailability, such as benfo, are required…320 mg/day during weeks 1 to 4 and 120 mg benfo/day during weeks 5 to 8…Within the 8-week study period, benfo led to a significant improvement of the threshold of vibration perception at the great toe, motor function, and the overall symptom score. Marked improvement occurred in both pain and co-ordination”Sadekov RA, Danilov AB, Vein AM. [Diabetic polyneuropathy treatment by milgamma-100 preparation] Zh Nevrol Psikhiatr Im S S Korsakova. 1998;98(9):30-2. Russian.“benfo…was studied in treatment of diabetic polyneuropathy in 14 patients…After the course of treatment the intensity of pains was decreased according to visual analogous scale on the average from 8.2 to 2.3 scores, the indices of vibratory sensitivity improved significantly as well as the data of cardiovascular tests…The treatment resulted in the improvement of the condition in 93% of the cases” T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine pharmacokinetics by end-stage renal disease (ESRD). Int J Clin Pharmacol Ther. 1999 Sep;37(9):449-55.“20 end-stage renal disease(ESRD) patients…After a single oral dose of 100 mg benfo…ESRD patients may benefit from high-dose thiamine derivatives notwithstanding their chemical form. However, the better absorption and high transfer rate of debenzoylated BTMP (benfo) to TDP (thiamine diphosphate) even at much lower doses compensates for reduced renal excretion and may protect, therefore, against numerous adverse effects of uremia”Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different benfo dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.320, 120, and 150 mg benfo/day was administered to “diabetic patients suffering from painful peripheral diabetic neuropathy. In a 6-week open clinical trial, 36 patients…An overall beneficial therapeutic effect on the neuropathy status was observed in all three groups during the study…The greatest change occurred in the group of patients receiving the high dose of benfo…Metabolic control did not change over the study...Extremely interesting is the result of recent in vitro experiences that thiamine pyrophosphate and pyroxidine inhibit the formation of glycation end products" T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfo. Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.“20 end-stage renal disease (ESRD) patients…After benfo administration, the peak plasma concentration of TDP exceeded that in healthy subjects by 51%...Compared with thiamine nitrate, the oral administration of benfo leads to higher TDP concentrations in erythrocytes accompanied with a significant improvement of the erythrocyte transkelotase activity in ESRD patients”Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M. Benfo is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.“We investigated the hypothesis that benfo, a lipophilic derivative of thiamine, affects replication delay and generation of advanced glycosylation endproducts (AGE) in human umbilical vein endothelial cells cultured in the presence of high glucose…Benfo, a derivative of thiamine with better bioavailability, corrects defective replication and increased AGE generation in endothelial cells cultured in high glucose, to a similar extent as thiamine. These effects may result from normalization of accelerated glycolysis and the consequent decrease in metabolites that are extremely active in generating nonenzymatic protein glycation. The potential role of thiamine administration in the prevention or treatment of vascular complications of diabetes deserves further investigation”Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M, Geyer J, Kopcke W, Sauerland C, Bretzel RG, Federlin KF. Efficacy of benfo versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.“After three months preventative administration of both vitamin B1 preparations NCV (nerve conduction velocity) had increased substantially…It was nearly normal after six months with benfo, while the administration of thiamine nitrate resulted in no further amelioration. NCV was nearly normalized after six months of benfo application but not with thiamine. Furthermore, benfo induced a major inhibition of neural imidazole-type AGE formation and completely prevented diabetes induced glycoxidation products”Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M. Benfo blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.“Our results in both endothelial cells cultured for several days and retinas from rats with nine months of diabetes showed that benfo, a lipid-soluble thiamine derivative, prevents activation of three major pathways involved in hyperglycemia-induced vascular damage: the hexosamine pathway, the intracellular AGE formation pathway and the DAG-PKC pathway…We showed that benfo blocks these pathways of hyperglycemic damage by increasing the activity of transketolase…Administration of benfo for nine months also completely prevented the development of experimental diabetic retinopathy in rats...Thus we conclude that augmentation of transketolase activity is solely responsible for the observed effects of benfo”Comment: This study is very significant because it demonstrates how benfo blocks several other aging mechanisms besides AGE formation. However, I am not yet convinced of the statement that transketolase activity is solely responsible for the observed effects of benfo. The following four studies are located on the Internet but are not yet listed on Medline. To find them, go to google.com and type in part of the titleBergfeld R, Matsumara X. Du, Brownlee M. Benfo prevents the consequences of hyperglycemia-induced mitochondrial overproduction of reactive oxygen species, and experimental diabetic retinopathy.“diabetic rats were treated with benfo (80 mg/kg weight) for 36 weeks…Benfo decreases AGE formation by 60%...These data suggest that treatment with benfo may be an effective approach to prevent the development of diabetic complications”Lin J, Alt A, Liersch J, Bretzel R, Brownlee M, Hammes H. Benfo inhibits intracellular formation of advanced glycation end products in vivo“Here, we studied the effect of benfo, a lipid-soluble thiamine derivative with known AGE-inhibiting properties in vitro on the intracellular formation of (CML) and methylgloxal-derived AGE in red blood cells. Blood was collected from 6 type 1 diabetic patients before and after treatment with 600 mg/day benfo for 28 days…Thiamine derivatives, in particular the lipid-soluble prodrug benfo, are effective inhibitors of intracellular formation of AGE and CML”Stracke H, Werkmann D, Mavrakis K, Federlin K, Kopke W, Sauerland C, Hammes H, Bretzel RG. Influence of vitamin B1 on diabetic neuropathy-studies in streptozotocin-diabetic rats.“we investigated the effects of oral administration of thiamine and benfo on the development of glucose oxidation products in the nerve and on nerve conduction velocity in streptozotocin-diabetic rats…Conclusion: Early treatment with benfo normalizes increased cellular oxidative stress and the reduced nerve conduction velocity”Hammes H, Bretzel, R.G., Federlin, K, Horiuchi S, Niwa T, Stracke H. Benfo inhibits the formation of advanced glycation end products in diabetic rats.“benfo (100 mg/kg x day) and thiamin (70.18 mg/kg x day) administered orally for 6 months…neither benfo nor thiamin treatment affected metabolic control…Benfo administration in diabetic rats induced a major inhibition of neutral imidazolone-type AGE formation and completely prevented diabetes-induced glycoxidation formation. Treatment with thiamin did not affect AGE or CML levels”ThiamineAllithiamines are lipid-soluble sources of thiamine. Benfo is an allithiamine. Thiamine is water-soluble and is also known as vitamin B1.After reviewing the relevant medical literature on thiamine, I have come to conclude that large portions of the population may be thiamine deficient. In addition, many individuals that are not technically thiamine deficient would likely receive benefit from thiamine supplementation. Thiamine deficiency is associated with numerous undesirable medical conditions.Relation of thiamine to heart diseaseShamir R, Dagan O, Abramovitch D, Abramovitch T, Vidne BA, Dinari G. Thiamine deficiency in children with congenital heart disease before and after corrective surgery. JPEN J Parenter Enteral Nutr. 2000 May-Jun;24(3):154-8.Thiamine deficiency “is common in children with congenital heart disease (CHD) referred for corrective surgery both before and after surgery. Our results suggest that neither diuretic treatment nor malnutrition can fully explain the development of TD in these children”Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E, Levy R. [Right heart failure caused by thiamine deficiency (cardiac beriberi)] Presse Med. 2000 Feb 12;29(5):240-1. French.Beaud C, Fuhrman C, Perchet H, Monnet I, Chouaid C, Housset B. [Thiamine deficiency. A cause of cardiac insufficiency not to be ignored] Rev Mal Respir. 1998 Jun;15(3):303-4. French.“Thiamine deficiency is one of the classical causes of high output for heart failure”Okura H, Gohma I, Hatta K, Imanaka T. Thiamine deficiency and pulmonary hypertension in Crow-Fukase syndrome. Intern Med. 1995 Jul;34(7):674-5. “After oral administration of prednisolone and thiamine, echocardiogram showed marked improvement of the pulmonary hypertension”Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc. 1995 May;95(5):541-4. “Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk”Shimon I, Almog S, Vered Z, Seligmann H, Shefi M, Peleg E, Rosenthal T, Motro M, Halkin H, Ezra D. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med. 1995 May;98(5):485-90.“Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy”Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered Z, Ezra D. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med. 1991 Aug;91(2):151-5.”These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements”Relation of thiamine to neurological disordersLonsdale D, Shamberger RJ, Audhya T. Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: a pilot study. Neuroendocrinol Lett. 2002 Aug;23(4):303-8.“Thiamine tetrahydrofurfuryl disulfide appears to have a beneficial clinical effect on some autistic children, since 8 of the 10 children improved clinically”Nakagawasai O, Tadano T, Hozumi S, Taniguchi R, Tan-No K, Esashi A, Niijima F, Kisara K. Characteristics of depressive behavior induced by feeding thiamine-deficient diet in mice.Life Sci. 2001 Jul 27;69(10):1181-91.Ambrose ML, Bowden SC, Whelan G. Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings. Alcohol Clin Exp Res. 2001 Jan;25(1):112-6.“A therapeutic relationship between dose and working memory performance was indicated”Older MW, Dickerson JW. Thiamine and the elderly orthopaedic patient. Age Ageing. 1982 May;11(2):101-7.“In both groups those patients who were noticeably confused after operation were found to have a considerable fall in their thiamine status suggesting this may be a contributory factor to postoperative confusion”Winston AP, son CP, Madira W, Gatward NM, Palmer RL. Prevalence of thiamin deficiency in anorexia nervosa. Int J Eat Disord. 2000 Dec;28(4):451-4.“Fourteen patients (38%) had results in the deficient range; 7 (19%) met the most stringent published criterion for deficiency. Deficiency was not related to duration of eating restraint, frequency of vomiting, or alcohol consumption”Terasawa M, Nakahara T, Tsukada N, Sugawara A, Itokawa Y. The relationship between thiamine deficiency and performance of a learning task in rats. Metab Brain Dis. 1999 Sep;14(3):137-48.“We taught rats to press a lever to escape from the pain of electrical stimulation by learning to turn a switch off… The rats that were fed the thiamine-deficient diet showed a slower response time and a longer running time than the rats fed the normal diet… We found that the thiamine concentration in the blood of the rats in the trained group was significantly higher than that in the group without training”Jimenez-Jimenez FJ, Molina JA, Hernanz A, Fernandez-Vivancos E, de Bustos F, Barcenilla B, Gomez-Escalonilla C, Zurdo M, Berbel A, Villanueva C. Cerebrospinal fluid levels of thiamine in patients with Parkinson's disease. Neurosci Lett. 1999 Aug 13;271(1):33-6.“These results suggest that low CSF free thiamine levels could be related with the risk for PD”Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J. 1997 Dec;74(12):803-8.“Diabetic peripheral neuropathy in Dar es Salaam is associated with thiamine deficiency”Langlais PJ, G, Guo SX, Bondy SC. Increased cerebral free radical production during thiamine deficiency. Metab Brain Dis. 1997 Jun;12(2):137-43.“These findings suggest that increased formation of free radicals occurs during the more acute symptomatic stage of thiamine deficiency and may contribute to the structural damage described in this model of Wernicke's encephalopathy”Easton CJ, Bauer LO. Beneficial effects of thiamine on recognition memory and P300 in abstinent cocaine-dependent patients. Psychiatry Res. 1997 May 30;70(3):165-74. “Thiamine was found to significantly improve recognition accuracy and P300 amplitude, at the midline parietal (Pz) electrode. The improvement was most reliable under conditions of increased memory load”Benton D, Griffiths R, Haller J. Thiamine supplementation mood and cognitive functioning. Psychopharmacology (Berl). 1997 Jan;129(1):66-71. ”An improvement in thiamine status was associated with reports of being more clearheaded, composed and energetic. The taking of thiamine had no influence on memory but reaction times were faster following supplementation”Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's disease. Metab Brain Dis. 1996 Mar;11(1):89-94.”Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100 mg/day had a mild beneficial effect in patients with Alzheimer's disease in a 12-week open trial. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function”Gold M, Chen MF, K. Plasma and red blood cell thiamine deficiency in patients with dementia of the Alzheimer's type. Arch Neurol. 1995 Nov;52(11):1081-6.“A significant proportion of patients with SDAT may have a thiamine deficiency, which may have an impact on cognitive function. Currently used assays may not be adequate to assess thiamine status”Adamolekun B, Eniola A. Thiamine-responsive acute cerebellar ataxia following febrile illness. Cent Afr J Med. 1993 Feb;39(2):40-1. Review.“acute thiamine depletion may be the pathogenetic mechanism for post-pyrexial acute cerebellar ataxia”Ben-Hur T, Wolff E, River Y. [Thiamin deficiency is common in Israel] Harefuah. 1992 Nov 15;123(10):382-4, 436, 435. Hebrew.“Thiamin levels should be determined not only in alcoholics and those with classic B1 deficiency syndromes, but in the routine workup of patients with sensory-motor neuropathy, dementia, gait disorders, cerebellar syndromes and confusional states”Sacks W, Esser AH, Feitel B, Abbott K. Acetazolamide and thiamine: an ancillary therapy for chronic mental illness. Psychiatry Res. 1989 Jun;28(3):279-88.“Overall, 50% of the patients showed improvement on all assessment scales. No untoward effects occurred in these patients…”Relation of thiamine and geriatric patientsSmidt LJ, Cremin FM, Grivetti LE, Clifford AJ. Influence of thiamin supplementation on the health and general well-being of an elderly Irish population with marginal thiamin deficiency. J Gerontol. 1991 Jan;46(1):M16-22.”thiamin-supplemented women experienced significantly increased appetite, energy intake, body weight and general well-being, and decreased fatigue. Thiamin supplementation also tended to reduce daytime sleep time, improve sleep patterns, and increase activity. These data suggest that evaluation of thiamin status is indicated when nonspecific conditions such as anorexia, weight loss, fatigue, depression, and sleep disorders are present in elderly persons”Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels in elder patients admitted through the emergency department. Acad Emerg Med. 2000 Oct;7(10):1156-9.“CONCLUSIONS: Elder nursing home patients seen in the ED and admitted to the hospital are frequently thiamine-deficient”Wilkinson TJ, Hanger HC, Elmslie J, PM, Sainsbury R. The response to treatment of subclinical thiamine deficiency in the elderly. Am J Clin Nutr. 1997 Oct;66(4):925-8.“Only the subjects with persistently low TPP concentrations showed subjective benefits from treatment with improvements in quality of life… There was a trend toward benefits in sleep and energy… Quality of life was enhanced by providing thiamine supplements. Blood pressure and weight were lower after thiamine supplementation”Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte thiamin concentrations in geriatric outpatients. J Am Coll Nutr. 1996 Jun;15(3):231-6.“CONCLUSION: About 50% of geriatric outpatients in this study had low plasma thiamin levels”Nichols HK, Basu TK. Thiamin status of the elderly: dietary intake and thiamin pyrophosphate response. J Am Coll Nutr. 1994 Feb;13(1):57-61.“Average daily thiamin intake was above the recommended requirement… however, almost half of the total study population had TPP effect > 14%, suggesting thiamin deficiency… CONCLUSION: These findings raise questions about the reliability of dietary intake in assessing metabolic availability of thiamin in the elderly”O'Keeffe ST, Tormey WP, Glasgow R, Lavan JN. Thiamine deficiency in hospitalized elderly patients. Gerontology. 1994;40(1):18-24.“Necropsy studies suggest that thiamine deficiency is underdiagnosed in life… There was no difference in anthropometric indices or in the prevalence of other nutrient deficiencies between the two groups. Thiamine deficiency is common in elderly patients admitted to hospital and may contribute to the development of delirium”Iber FL, Blass JP, Brin M, Leevy CM. Thiamin in the elderly--relation to alcoholism and to neurological degenerative disease. Am J Clin Nutr. 1982 Nov;36(5 Suppl):1067-82. Review.“There is no known toxicity for thiamin”Relation of thiamine to diabetesAvena R, Arora S, Carmody BJ, Cosby K, Sidawy AN. Thiamine (Vitamin B1) protects against glucose- and insulin-mediated proliferation of human infragenicular arterial smooth muscle cells. Ann Vasc Surg. 2000 Jan;14(1):37-43.“Vitamin B1 intake may prove important in delaying the atherosclerotic complications of diabetes”La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA, Molinatti GM, Porta M. Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions. Diabetologia. 1996 Nov;39(11):1263-8.Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S, Scheinman M, T. Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells. Surgery. 2001 Nov;130(5):851-8.“The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes”Hassan R, Qureshi H, Zuberi SJ. Effect of thiamine on glucose utilization in hepatic cirrhosis. J Gastroenterol Hepatol. 1991 Jan-Feb;6(1):59-60.“It is therefore suggested that thiamine supplements be given to cirrhotics with hyperglycaemia, to improve glucose utilization”Rindi G, Laforenza U. Thiamine intestinal transport and related issues: recent aspects.Proc Soc Exp Biol Med. 2000 Sep;224(4):246-55. Review.“Thiamine uptake is enhanced by thiamine deficiency, and reduced by thyroid hormone and diabetes”Saito N, Kimura M, Kuchiba A, Itokawa Y. Blood thiamine levels in outpatients with diabetes mellitus. J Nutr Sci Vitaminol (Tokyo). 1987 Dec;33(6):421-30.“From the above findings it was concluded that diabetic outpatients tend to have a low blood thiamine level, with low erythrocyte transketolase activity and high erythrocyte TPP effect, and showed marginal thiamine deficiency” Relation of thiamine to diseaseWallace AE, Weeks WB. Thiamine treatment of chronic hepatitis B infection. Am J Gastroenterol. 2001 Mar;96(3):864-8.”In each case study, thiamine administration was associated with reduction in aminotransferase levels and the fall of HBV DNA to undetectable levels… The relationship between thiamine administration and chronic hepatitis B infection warrants further study. If proven effective in reducing liver damage or inducing remission of the hepatitis B virus in larger trials, thiamine will offer obvious advantages over the current treatments for chronic viral hepatitis B infection”Rossouw JE, Labadarios D, Krasner N, M, R. Red blood cell transketolase activity and the effect of thiamine supplementation in patients with chronic liver disease. Scand J Gastroenterol. 1978;13(2):133-8.“Biochemical evidence of thiamine deficiency was found in 58% of patients with chronic liver disease… high doses of thiamine should be included in the routine nutritional management of patients with severe chronic liver disease”Shoji S, Furuishi K, Misumi S, Miyazaki T, Kino M, Yamataka K. Thiamine disulfide as a potent inhibitor of human immunodeficiency virus (type-1) production. Biochem Biophys Res Commun. 1994 Nov 30;205(1):967-75.” The results suggest that thiamine disulfide may be important for AIDS chemotherapy”Shoji S, Furuishi K, Ogata A, Yamataka K, Tachibana K, Mukai R, Uda A, Harano K, Matsushita S, Misumi S. An allosteric drug, o,o'-bismyristoyl thiamine disulfide, suppresses HIV-1 replication through prevention of nuclear translocation of both HIV-1 Tat and NF-kappa B. Biochem Biophys Res Commun. 1998 Aug 28;249(3):745-53.Butterworth RF, Gaudreau C, Vincelette J, Bourgault AM, Lamothe F, Nutini AM. Thiamine deficiency and Wernicke's encephalopathy in AIDS. Metab Brain Dis. 1991 Dec;6(4):207-12.“we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse… it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex”Haisraeli-Shalish M, Livneh A, Katz J, Doolman R, Sela BA. Recurrent aphthous stomatitis and thiamine deficiency. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Dec;82(6):634-6.” 70 patients with recurrent aphthous stomatitis and in 50 members of a control group… Low levels of vitamin B1 were detected in 49 patients but in only two members of the control group… Our finding suggests an association between thiamine deficiency and recurrent aphthous stomatitis”Engel D. Tropical pyomyositis, a thiamine-deficiency disease. Med Hypotheses. 1981 Mar;7(3):345-52.“it is suggested that thiamine deficiency is an essential contributary factor in producing tropical pyomyositis… Thiamine deficiency induces a biochemical lesion (s) in the pyruvate oxidase system of the muscle, which breaks down its normal resistance to infection and opens the gate to bacterial agents”Krishna S, AM, Supanaranond W, Pukrittayakamee S, ter Kuile F, Tawfiq KM, Holloway PA, White NJ. Thiamine deficiency and malaria in adults from southeast Asia. Lancet. 1999 Feb 13;353(9152):546-9.”12 (52%) of 23 patients with severe malaria and ten (19%) of 54 patients with uncomplicated malaria had alpha values above the normal range (p<0.0001 and p=0.0014, respectively, compared with controls), which indicated severe thiamine deficiency” Pietrzak I, Baczyk K, Mlynarczyk M, Kaczmarek M. [Content of thiamin in plasma and erythrocytes in patients with end stage renal disease] Przegl Lek. 1996;53(5):423-6. Polish.”We suggest the need of thiamine supplementation in ESRD patients especially in those treated by dialysis. The supplementation of thiamine is needed particularly in patients on peritoneal dialysis”Relation of thiamine to other dataHung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. 2001 Nov;38(5):941-7.“We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency”Huang S, Ren G. [Thiamine status of university teacher families in Changsha] Hunan Yi Ke Da Xue Xue Bao. 1998;23(1):27-30. Chinese.“We conclude that those people who take the refined cereals and its products as a staple food, is in the risk of thiamine deficiency”Suzuki M, Itokawa Y. Effects of thiamine supplementation on exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106.“High-dose thiamine (vitamin B1) supplementation (100 mg/day) may be helpful in preventing or accelerating recovery from exercise-induced fatigue… Thiamine supplementation significantly suppressed the increase in blood glucose in the normal thiamine group and significantly decreased the number of complaints shortly after exercise in the subjective fatigue assessment of 30 items”Kimura M, Itokawa Y, Fujiwara M. Cooking losses of thiamin in food and its nutritional significance. J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl 1:S17-24.”The thiamin contents in cooked daily meals were 50-60 percent of the calculated values on an average”Cruickshank AM, Telfer AB, Shenkin A. Thiamine deficiency in the critically ill. Intensive Care Med. 1988;14(4):384-7.“We performed a retrospective study on 158 patients admitted to the Intensive Care Unit who required nutritional support. Patients who survived had significantly higher body thiamine status than those who died”Onodera K, Kisara K, Okabe H, Ogura Y. [studies on the effects of thiamine deficiency on rat testes (author's transl)] Nippon Yakurigaku Zasshi. 1980 Mar;76(2):143-52. Japanese.“In the thiamine deficient group, the seminiferous tubuli of rats having erections had atrophied”Labadarios D, Rossouw JE, McConnell JB, M, R. Thiamine deficiency in fulminant hepatic failure and effects of supplementation. Int J Vitam Nutr Res. 1977;47(1):17-22.“Nine out of 24 patients with acute hepatocellular necrosis leading to fulminant hepatic failure showed biochemical evidence of thiamine deficiency early in the course of their illness”Why haven’t we heard of benfo before? The patent on the manufacture of benfo expired decades ago. Pharmaceutical companies pursue drugs that can be patented so they can have a monopoly and charge 100 times what the drug is worth. They have spent a lot of money on AGE inhibitors that don’t work as well as benfo. Ingestion of benfo may result in the elimination of AGE-protein crosslinks, which are a major constituent of arterial plaque. I am intrigued by the idea that benfo may cause the removal of plaque from the blood vessels, but I am concerned about the rapid manner in which it may cause the removal of plaque from the blood vessels. If the plaque is being removed, a large chunk might break off and cause a stroke or heart attack. If I was older than 60 or if I had a serious problem with high blood pressure I would probably start out by taking very low doses of benfo and gradually increase my dosage. Of course, there are no reports of strokes or heart attacks from benfo in the medical literature, but it’s a thought to consider. My PhD research will mostly consist of double-blind controlled studies on the administration of benfo in normal individuals, diabetics, individuals with high blood pressure, Alzheimer patients etc. I believe the researchers who have investigated benfo to date have been extremely short sighted by not discovering they full potential of benfo in the clinical studies that have already been performed on humans.It is illegal to make claims about benfo and sell it as a dietary supplement unless the claims are based on substantial scientific evidence. The three case studies outlined in this document are not from a double-blind controlled study and FDA regulations would not allow for them to be referred to as substantial scientific evidence. Claims should not be made based on these preliminary findings. For questions or comments email robholladay99@...Since I am not a physician, it would be inappropriate for me to answer emails asking for medical advice.

SECURALL, INC.

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[Guest guest]

Hi Kathy,

Yes and I completely agree.

Regards,

Tom

[Guest guest]

Larry, I agree with a lot of th etheories, but your opinion from Pharmacist to Pharmacist: Vitamin C at high (over 4gm per day) dose is associated with crystals in the urine, stones, and pain, and vitamin B6 a component of the B100 vitamins is linked with DE-MYELINATION! in doses of (allegedly) over 150 mg per day. what's your read on this?

n

----- Original Message -----

From: Larry J. Frieders

low dose naltrexone

Sent: Thursday, March 25, 2004 2:44 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

Just a note...We dispense a LOT of Vitamin B1 injection (some people just don't absorb the B vitamins well through the gut, so they use an injection). People are using 200mg and more each day and report significant improvements. I hold firm to the belief that many (if not most) chronic conditions (like MS and CFS) have their roots deeply buried in nutrition problems. It seems that B1 is a vital nutrient for proper nerve and muscle function.

Here's a link to an updated protocol. Dale Humpherys has used this approach for over 25 years - and he has encouraged hundreds (if not thousands) of others to use this approach. http://www.thecompounder.com/HumpherysNewProtocol.html

Larry J. Frieders,RPh |The Compounder575 W. Illinois Ave ~ Aurora, IL 60506 630-859-0333 FAX 630-859-0114 Sample newsletter http://www.theCompounder.com/NL-Sample.html

Any health related information on our web pages or in our newsletters is for educational purposes only. None of the information we provide is to be construed as medical advice. Before applying any therapy or use of herbs, you may want to seek advice from your health care professional. Our information should not be a substitute for physician evaluation or treatment by a health care professional and is not intended to provide or confirm a diagnosis.

----- Original Message -----

From:

low dose naltrexone

Sent: Wednesday, March 24, 2004 7:47 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

I started on this B1 night before last. I've been whining about this long drawn out virus I've been fighting, and either the B1 is helping mucho over the last two days, or I'm suddenly getting stronger anyway. I feel lots more energy, and my legs are finally getting some strength back. It's so hard to tell if it is the Benfotiamine or just my body finally winning. Who knows. I do know I've seen no side effects even though I've been taking 600mg twice a day. After a few days more I'll cut that in half... No digestive upsets, no headaches, just a positive feeling about life in general.

(MS)

----- Original Message -----

From: ruben/kathy lintzenich

low dose naltrexone

Sent: Tuesday, March 23, 2004 7:26 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

Tom, thanks for the great article. I will be starting this form of B1 when I finish my bottle of thiamine. Will keep everyone posted on any benefits I receive. Are you taking this form of B1 and did you find out about it through the Brewer Science Library? White is the educatuional cordinater at the library and publishes a quarterly newslettet. She is a wonderful source of info about ms and other dis-eases in the body. Best Wishes, Kathy

----- Original Message -----

From: tmbayuk

msalternatives ; MSersLife ; MS-Christians ; MSfriends ; MSViews_Multiple_Sclerosis ; low dose naltrexone ; JJUK ; mscured

Sent: Monday, March 22, 2004 10:50 AM

Subject: [low dose naltrexone] Fw: check this out!

----- Original Message ----- From:

tmbayuk

Sent: Saturday, March 20, 2004 11:01 PM

Subject: check this out!

Research on Benfotiamine Clinton Holladay, M.S.Copyright 2003 Clinton HolladayJune 5, 2003A short while ago a group of individuals I know purchased a large amount of benfotiamine and began ingesting it orally. I was urged by these individuals to place some of the research I have been conducting on benfo (benfotiamine) online along with the results of their benfo use. I was asked to do this in a manner that would allow individuals that do not have a background in the health sciences to comprehend it. I will be pursuing a PhD shortly and benfo will be central to my research. I am not a physician and the following information is not intended to be used as medical advice. Advanced glycation endproducts or AGEs are produced by the processing of sugars within the cell. They are one of the primary causes of aging and general wear and tear on your cells. Diabetics age the same way as normal people, but because they often have abnormal levels of sugars in their cells, they age faster. When blood sugar levels are high, certain cells in the body are flooded with glucose, particularly neurons and cells in the eyes and kidneys. Diabetics often suffer from nerve damage, kidney failure, and premature blindness. Numerous researchers have concentrated their efforts on AGE-blocking mechanisms because they would limit the wear and tear on the body’s cells and allow individuals to live longer and healthier, particularly diabetics. Benfo has emerged as the premier AGE inhibitor.Case StudiesIt is important to note that the following case studies are not double-blind controlled studies. Case study #1. Female, early fifties, non-diabetic, suffers from chronic fatigue, depression, and the normal aches and pains that accompany middle age. Her diet is average. She is able to do about two hours of physical labor a day, and she has suffered from depression for years. She has tried numerous treatments for depression including Prozac, and some of them have helped, but none have completely eliminated the depression. Sometimes she aches all over. She was addicted to caffeine for several years, but only consumes it about once a week now. She has high blood pressure, and treats it with Vasotec and also takes Maxide (a diuretic).She ingested 650 mg of benfo once a day for five days and did not notice any difference. On day 6 she doubled the dose to 1300 mg and started to notice a change a few hours later. There was a dramatic increase in stamina and energy. She is now able to do eight hours of physical work each day. She has an extremely heightened sense of well-being and all aspects of the depression have left. She has better clarity of thought, and sleeps better. Previously she would usually wake up two or three times a night. Now she sleeps through the whole night and has said she is in a deeper sleep at night. She has reported being able to control her appetite more. She has reported less shortness of breath. On day 13 she has had no weight change. On day 13 she experienced what felt exactly like a caffeine withdrawal headache. She immediately consumed two cans of mountain dew and the headache did not leave. Previous to this, caffeine had always relieved a headache of this sort for her. At day 14 she still had a headache and the tips of her toes started tingling. She reduced her dose to 650 mg per day once a day on day 14. On day 15 she still had a headache. On day 16 her toes started tingling and the headache left. On day 17 her pinkie started tingling. Her blood pressure has always fluctuated between 120/80 and 150/90. Throughout the treatment her blood pressure has fluctuated like it normally does. She says she feels like she did when she was thirty years old. Comment: The tingling is likely the cause of blood circulating to parts of her body that have not had a great deal of circulation in recent years.Case study #2. Male, mid fifties, non-diabetic. Average diet. Overall health is better than average for his age. He gets indigestion at night and takes Prilosec. He has the normal aches and pains that accompany middle age. When he wakes up in the morning his feet are inflexible, but that would go away after walking on them for about two minutes. After driving for two hours he is stiff when he gets out of his car. Most of the aches and pains and the foot inflexibility appeared in the last five to fifteen years. He began taking 650 mg of benfo once a day. On day 3 nothing hurt when he woke up. By day five all his aches and pains had disappeared. He is no longer stiff when he gets out of his car after driving for two hours. He feels more flexible. He says it has fixed everything that has gone wrong with him in the past fifteen years. He says he feels more cheerful but is not sure if it is because of repair to neurological damage or because his aches and pains are gone. He has reported a greater clarity of thought. He says he feels like he did when he was age 25-40 (he says he felt the same during those years). Up until twelve months ago his blood pressure has been 120/90. For the past twelve months it has averaged 130/120. On day 5 his blood pressure was 120/85 and it has remained consistent every day since then. Now he can only take a fifteen minute nap during the day whereas before he could fall asleep for hours. At night he sleeps better, probably because the aches and pains are gone. His appetite is only about 80% of what it used to be. He has reported increased stamina and energy. Before taking benfo it was getting hard for him to do ten hours of work per day. Now he can do fourteen hours of work per day. He still requires the same amount of sleep at night, but if he does not get his full requirement he doesn’t notice it nearly as much.Comment: The decrease in caloric intake may be because he was lacking an essential nutrient- not enough thiamine? The stiffening of the joints brought on by old age is partly a symptom poor blood circulation. The fact that this individual has become much more flexible is a possible indication of increased circulation.Case study #3. Male, late forties. He has been a type 1 diabetic for twenty years. Average diet. Over the last five years his health has declined more rapidly. He has more aches and pains than the average person because he is diabetic. He aches so much at night that he usually can’t get to sleep unless he takes Ibuprofen. He began taking 650 mg benfo once a day. On day 2 he noticed a decline in the severity of his aches and pains. He still needs the same amount of sleep, but if he doesn’t get his full requirement he doesn’t notice nearly as much. He has had an increase in stamina and energy. He says his stamina has doubled. On day 14 he felt like he did ten years ago, and it keeps improving each day. He is more cheerful, but like #2 he can’t tell if it’s because his aches and pains are gone or if benfo has a neurological effect on him. I will not disclose the brand of benfo which was used because I do not wish to be seen as promoting any particular brand. These case studies will be updated on July 5, 2003 and new ones will be added. The updates will be posted on www.geocities.com/robholladay99/updates.html The following exerpts are from medical journals. The abstracts (summaries) for most of them can be viewed online through the pubmed database, which is a free database most biomedical scientists use. To find pubmed, go to google.com and type in pubmed. Once you’re in pubmed, type in part of the title and you should be able to find the abstract. When typing in the title use "benfotiamine" not "benfo". As an anti-spamming measure, many search engines will not index web pages that list the key search words more than seven times throughout the document, hence this document was modified after it was created . Several things are important to note in the following literature. First of all, not only does benfo stop some effects of aging, it reverses them. Gradually over time people’s neurons quit working because of normal wear and tear. However, when benfo was ingested, not only did the nerve damage stop, some of the damage done through aging was repaired. A strong point is made that benfo is the most bioavailable source of thiamine. This means benfo is better absorbed than other sources of thiamine. Also, high levels of thiamine have analgesic (pain-relieving) effects on animals. In the Russian study the pain level of the patients decreased from 8.2 to 2.3, a decrease of about four hundred percent. Research articles on benfoWada T, Tagaki H, Minakami H, Hamanka W, Okamoto K, Ito, A, Sahashi Y. 1961. A new thiamine derivative, S-benzoylthiamine O-monophosphate. Science 134: 195-196.Benfo “is more easily absorbed in the body than thiamine hydrochloride, and administration results in higher thiamine and cocarboxylase levels in organs; moreover, these levels last for a longer period of time…It does not cause any unfavorable symptom in animals such as thiamine hydrochloride does…The LD50 by oral administration in mice, dd-strain hybrid, weighing 14 to 16g was 15g/kg of body weight”Bitsch R, Wolf M, Moller J, Heuzeroth L, Gruneklee D. Bioavailability assessment of the lipophilic benfo as compared to a water-soluble thiamin derivative. Ann Nutr Metab. 1991;35(5):292-6. “in presence of allicin, the active principle of garlic, the water-soluble thiamin hydrochloride is transformed into a lipid-soluble compound being identified as allithiamine…Ten healthy young men…The volunteers ingested a single dose of 40 mg benfo…Thus, the measured values reveal, when compared with mononitrate, a clearly improved thiamin bioavailability from benfo, due to the more lipophilic properties of this substance or possibly its dephosphorylated metabolite and a more rapid transformation into the physiologically active derivative. This may be of great advantage in the treatment of neurological disorders responding to high thiamin doses and further on in situations when the active intestinal absorbtion mechanisms are impaired”Stracke H, Lindemann A, Federlin K. A benfo-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.“Benfo…was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold...Therapy-specific adverse effects were not seen”Loew D. Pharmacokinetics of thiamine derivatives especially of benfo. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.“The effective form of thiamine, thiamine diphosphate, is an organic compound needed by the organism for vital functions…Due to this peculiarity the conditions for absorbtion of lipid-soluble vitamins differ from those for water-soluble thiamine derivatives. Unlike the latter, allithiamines are absorbed passively, they traverse the intestinal absorption barrier faster and more readily, leading to higher blood and tissue concentrations even when comparatively low doses are given…It therefore fulfills important pharmacodynamic conditions for rational therapy. Due to their greater biovailability and better tissue passage lipid-soluble thiamine analogues like benfo are preferable to water-soluble thiamine derivatives for treatment of various pathological conditions, e.g. cardiomyopathy, Werincke-Korsakow syndrome, and alcoholic or diabetic polyneuropathies…Due to its excellent pharmacokinetic profile and to its excellent tolerability benfo should be preferred in treatment of relevant conditions like neuropathies”Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter CH. Comparative bioavailability of two vitamin B1 preparations: benfo and thiamine mononitrate. Eur J Clin Pharmacol. 1997;52(4):319-20.“a study using equimolar quantities of the two preparations for exact comparison of the bioavailability of benfo and thiamine mononitrate has never been performed. Therfore, the present trial was undertaken…the higher thiamine content in the erythrocytes and the higher thiamine excretion in urine after oral benfo administration are proof of the considerably higher relative bioavailability of benfo than thiamine mononitrate”Simeonov S, Pavlova M, Mitkov M, Mincheva L, Troev D. Therapeutic efficacy of "Milgamma" in patients with painful diabetic neuropathy. Folia Med (Plovdiv). 1997;39(4):5-10.“Forty-Five diabetes patients with painful peripheral polyneuropathy were enrolled in a 3-month observational study comparing the therapeutic efficiacy of Milgamma tablets (benfo)…Statistically significant relief of both background and peak neuropathic pain was achieved in all of the Milgamma-treated patients…No adverse reactions were observed…Our results underscore the importance of Milgamma tablets as an indispensable element in the therapeutic regimen of patients with painful diabetic polyneuropathy”Greb A, Bitsch R. Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther. 1998 Apr;36(4):216-21.“Seven healthy volunteers…a single oral dose of either benfo…fursultiamin…thiaminedisulfide…In this study the allithiamine derivative benfo proved the best bioavailability. Owing to its excellent absorption properties it can be concluded that oral administration of benfo is suitable for therapeutical purposes”Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfo in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.Good review, full-text is available free online. “In bioavailability studies on healthy human subjects, it was shown that absorption of benfo was several times better than that of water-soluble vitamin B1 and that there was a 120-fold higher increase of metabolically active thiamine diphosphate in erythrocytes (Heinrich, 1990)…In animals given dosages that exceeded basic requirements by 100- or 1000-fold thiamine has analgesic and neuroprotective effects(woelk and peeler-Ichakawa, 1985; Jurna, 1988; Reeh, 1988, 1991; Wild, 1988). However, if high levels are to be achieved with oral vitamin B1 treatment, lipid soluble thiamine derivatives or pro-drugs with high bioavailability, such as benfo, are required…320 mg/day during weeks 1 to 4 and 120 mg benfo/day during weeks 5 to 8…Within the 8-week study period, benfo led to a significant improvement of the threshold of vibration perception at the great toe, motor function, and the overall symptom score. Marked improvement occurred in both pain and co-ordination”Sadekov RA, Danilov AB, Vein AM. [Diabetic polyneuropathy treatment by milgamma-100 preparation] Zh Nevrol Psikhiatr Im S S Korsakova. 1998;98(9):30-2. Russian.“benfo…was studied in treatment of diabetic polyneuropathy in 14 patients…After the course of treatment the intensity of pains was decreased according to visual analogous scale on the average from 8.2 to 2.3 scores, the indices of vibratory sensitivity improved significantly as well as the data of cardiovascular tests…The treatment resulted in the improvement of the condition in 93% of the cases” T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine pharmacokinetics by end-stage renal disease (ESRD). Int J Clin Pharmacol Ther. 1999 Sep;37(9):449-55.“20 end-stage renal disease(ESRD) patients…After a single oral dose of 100 mg benfo…ESRD patients may benefit from high-dose thiamine derivatives notwithstanding their chemical form. However, the better absorption and high transfer rate of debenzoylated BTMP (benfo) to TDP (thiamine diphosphate) even at much lower doses compensates for reduced renal excretion and may protect, therefore, against numerous adverse effects of uremia”Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different benfo dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.320, 120, and 150 mg benfo/day was administered to “diabetic patients suffering from painful peripheral diabetic neuropathy. In a 6-week open clinical trial, 36 patients…An overall beneficial therapeutic effect on the neuropathy status was observed in all three groups during the study…The greatest change occurred in the group of patients receiving the high dose of benfo…Metabolic control did not change over the study...Extremely interesting is the result of recent in vitro experiences that thiamine pyrophosphate and pyroxidine inhibit the formation of glycation end products" T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfo. Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.“20 end-stage renal disease (ESRD) patients…After benfo administration, the peak plasma concentration of TDP exceeded that in healthy subjects by 51%...Compared with thiamine nitrate, the oral administration of benfo leads to higher TDP concentrations in erythrocytes accompanied with a significant improvement of the erythrocyte transkelotase activity in ESRD patients”Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M. Benfo is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.“We investigated the hypothesis that benfo, a lipophilic derivative of thiamine, affects replication delay and generation of advanced glycosylation endproducts (AGE) in human umbilical vein endothelial cells cultured in the presence of high glucose…Benfo, a derivative of thiamine with better bioavailability, corrects defective replication and increased AGE generation in endothelial cells cultured in high glucose, to a similar extent as thiamine. These effects may result from normalization of accelerated glycolysis and the consequent decrease in metabolites that are extremely active in generating nonenzymatic protein glycation. The potential role of thiamine administration in the prevention or treatment of vascular complications of diabetes deserves further investigation”Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M, Geyer J, Kopcke W, Sauerland C, Bretzel RG, Federlin KF. Efficacy of benfo versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.“After three months preventative administration of both vitamin B1 preparations NCV (nerve conduction velocity) had increased substantially…It was nearly normal after six months with benfo, while the administration of thiamine nitrate resulted in no further amelioration. NCV was nearly normalized after six months of benfo application but not with thiamine. Furthermore, benfo induced a major inhibition of neural imidazole-type AGE formation and completely prevented diabetes induced glycoxidation products”Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M. Benfo blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.“Our results in both endothelial cells cultured for several days and retinas from rats with nine months of diabetes showed that benfo, a lipid-soluble thiamine derivative, prevents activation of three major pathways involved in hyperglycemia-induced vascular damage: the hexosamine pathway, the intracellular AGE formation pathway and the DAG-PKC pathway…We showed that benfo blocks these pathways of hyperglycemic damage by increasing the activity of transketolase…Administration of benfo for nine months also completely prevented the development of experimental diabetic retinopathy in rats...Thus we conclude that augmentation of transketolase activity is solely responsible for the observed effects of benfo”Comment: This study is very significant because it demonstrates how benfo blocks several other aging mechanisms besides AGE formation. However, I am not yet convinced of the statement that transketolase activity is solely responsible for the observed effects of benfo. The following four studies are located on the Internet but are not yet listed on Medline. To find them, go to google.com and type in part of the titleBergfeld R, Matsumara X. Du, Brownlee M. Benfo prevents the consequences of hyperglycemia-induced mitochondrial overproduction of reactive oxygen species, and experimental diabetic retinopathy.“diabetic rats were treated with benfo (80 mg/kg weight) for 36 weeks…Benfo decreases AGE formation by 60%...These data suggest that treatment with benfo may be an effective approach to prevent the development of diabetic complications”Lin J, Alt A, Liersch J, Bretzel R, Brownlee M, Hammes H. Benfo inhibits intracellular formation of advanced glycation end products in vivo“Here, we studied the effect of benfo, a lipid-soluble thiamine derivative with known AGE-inhibiting properties in vitro on the intracellular formation of (CML) and methylgloxal-derived AGE in red blood cells. Blood was collected from 6 type 1 diabetic patients before and after treatment with 600 mg/day benfo for 28 days…Thiamine derivatives, in particular the lipid-soluble prodrug benfo, are effective inhibitors of intracellular formation of AGE and CML”Stracke H, Werkmann D, Mavrakis K, Federlin K, Kopke W, Sauerland C, Hammes H, Bretzel RG. Influence of vitamin B1 on diabetic neuropathy-studies in streptozotocin-diabetic rats.“we investigated the effects of oral administration of thiamine and benfo on the development of glucose oxidation products in the nerve and on nerve conduction velocity in streptozotocin-diabetic rats…Conclusion: Early treatment with benfo normalizes increased cellular oxidative stress and the reduced nerve conduction velocity”Hammes H, Bretzel, R.G., Federlin, K, Horiuchi S, Niwa T, Stracke H. Benfo inhibits the formation of advanced glycation end products in diabetic rats.“benfo (100 mg/kg x day) and thiamin (70.18 mg/kg x day) administered orally for 6 months…neither benfo nor thiamin treatment affected metabolic control…Benfo administration in diabetic rats induced a major inhibition of neutral imidazolone-type AGE formation and completely prevented diabetes-induced glycoxidation formation. Treatment with thiamin did not affect AGE or CML levels”ThiamineAllithiamines are lipid-soluble sources of thiamine. Benfo is an allithiamine. Thiamine is water-soluble and is also known as vitamin B1.After reviewing the relevant medical literature on thiamine, I have come to conclude that large portions of the population may be thiamine deficient. In addition, many individuals that are not technically thiamine deficient would likely receive benefit from thiamine supplementation. Thiamine deficiency is associated with numerous undesirable medical conditions.Relation of thiamine to heart diseaseShamir R, Dagan O, Abramovitch D, Abramovitch T, Vidne BA, Dinari G. Thiamine deficiency in children with congenital heart disease before and after corrective surgery. JPEN J Parenter Enteral Nutr. 2000 May-Jun;24(3):154-8.Thiamine deficiency “is common in children with congenital heart disease (CHD) referred for corrective surgery both before and after surgery. Our results suggest that neither diuretic treatment nor malnutrition can fully explain the development of TD in these children”Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E, Levy R. [Right heart failure caused by thiamine deficiency (cardiac beriberi)] Presse Med. 2000 Feb 12;29(5):240-1. French.Beaud C, Fuhrman C, Perchet H, Monnet I, Chouaid C, Housset B. [Thiamine deficiency. A cause of cardiac insufficiency not to be ignored] Rev Mal Respir. 1998 Jun;15(3):303-4. French.“Thiamine deficiency is one of the classical causes of high output for heart failure”Okura H, Gohma I, Hatta K, Imanaka T. Thiamine deficiency and pulmonary hypertension in Crow-Fukase syndrome. Intern Med. 1995 Jul;34(7):674-5. “After oral administration of prednisolone and thiamine, echocardiogram showed marked improvement of the pulmonary hypertension”Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc. 1995 May;95(5):541-4. “Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk”Shimon I, Almog S, Vered Z, Seligmann H, Shefi M, Peleg E, Rosenthal T, Motro M, Halkin H, Ezra D. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med. 1995 May;98(5):485-90.“Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy”Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered Z, Ezra D. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med. 1991 Aug;91(2):151-5.”These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements”Relation of thiamine to neurological disordersLonsdale D, Shamberger RJ, Audhya T. Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: a pilot study. Neuroendocrinol Lett. 2002 Aug;23(4):303-8.“Thiamine tetrahydrofurfuryl disulfide appears to have a beneficial clinical effect on some autistic children, since 8 of the 10 children improved clinically”Nakagawasai O, Tadano T, Hozumi S, Taniguchi R, Tan-No K, Esashi A, Niijima F, Kisara K. Characteristics of depressive behavior induced by feeding thiamine-deficient diet in mice.Life Sci. 2001 Jul 27;69(10):1181-91.Ambrose ML, Bowden SC, Whelan G. Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings. Alcohol Clin Exp Res. 2001 Jan;25(1):112-6.“A therapeutic relationship between dose and working memory performance was indicated”Older MW, Dickerson JW. Thiamine and the elderly orthopaedic patient. Age Ageing. 1982 May;11(2):101-7.“In both groups those patients who were noticeably confused after operation were found to have a considerable fall in their thiamine status suggesting this may be a contributory factor to postoperative confusion”Winston AP, son CP, Madira W, Gatward NM, Palmer RL. Prevalence of thiamin deficiency in anorexia nervosa. Int J Eat Disord. 2000 Dec;28(4):451-4.“Fourteen patients (38%) had results in the deficient range; 7 (19%) met the most stringent published criterion for deficiency. Deficiency was not related to duration of eating restraint, frequency of vomiting, or alcohol consumption”Terasawa M, Nakahara T, Tsukada N, Sugawara A, Itokawa Y. The relationship between thiamine deficiency and performance of a learning task in rats. Metab Brain Dis. 1999 Sep;14(3):137-48.“We taught rats to press a lever to escape from the pain of electrical stimulation by learning to turn a switch off… The rats that were fed the thiamine-deficient diet showed a slower response time and a longer running time than the rats fed the normal diet… We found that the thiamine concentration in the blood of the rats in the trained group was significantly higher than that in the group without training”Jimenez-Jimenez FJ, Molina JA, Hernanz A, Fernandez-Vivancos E, de Bustos F, Barcenilla B, Gomez-Escalonilla C, Zurdo M, Berbel A, Villanueva C. Cerebrospinal fluid levels of thiamine in patients with Parkinson's disease. Neurosci Lett. 1999 Aug 13;271(1):33-6.“These results suggest that low CSF free thiamine levels could be related with the risk for PD”Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J. 1997 Dec;74(12):803-8.“Diabetic peripheral neuropathy in Dar es Salaam is associated with thiamine deficiency”Langlais PJ, G, Guo SX, Bondy SC. Increased cerebral free radical production during thiamine deficiency. Metab Brain Dis. 1997 Jun;12(2):137-43.“These findings suggest that increased formation of free radicals occurs during the more acute symptomatic stage of thiamine deficiency and may contribute to the structural damage described in this model of Wernicke's encephalopathy”Easton CJ, Bauer LO. Beneficial effects of thiamine on recognition memory and P300 in abstinent cocaine-dependent patients. Psychiatry Res. 1997 May 30;70(3):165-74. “Thiamine was found to significantly improve recognition accuracy and P300 amplitude, at the midline parietal (Pz) electrode. The improvement was most reliable under conditions of increased memory load”Benton D, Griffiths R, Haller J. Thiamine supplementation mood and cognitive functioning. Psychopharmacology (Berl). 1997 Jan;129(1):66-71. ”An improvement in thiamine status was associated with reports of being more clearheaded, composed and energetic. The taking of thiamine had no influence on memory but reaction times were faster following supplementation”Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's disease. Metab Brain Dis. 1996 Mar;11(1):89-94.”Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100 mg/day had a mild beneficial effect in patients with Alzheimer's disease in a 12-week open trial. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function”Gold M, Chen MF, K. Plasma and red blood cell thiamine deficiency in patients with dementia of the Alzheimer's type. Arch Neurol. 1995 Nov;52(11):1081-6.“A significant proportion of patients with SDAT may have a thiamine deficiency, which may have an impact on cognitive function. Currently used assays may not be adequate to assess thiamine status”Adamolekun B, Eniola A. Thiamine-responsive acute cerebellar ataxia following febrile illness. Cent Afr J Med. 1993 Feb;39(2):40-1. Review.“acute thiamine depletion may be the pathogenetic mechanism for post-pyrexial acute cerebellar ataxia”Ben-Hur T, Wolff E, River Y. [Thiamin deficiency is common in Israel] Harefuah. 1992 Nov 15;123(10):382-4, 436, 435. Hebrew.“Thiamin levels should be determined not only in alcoholics and those with classic B1 deficiency syndromes, but in the routine workup of patients with sensory-motor neuropathy, dementia, gait disorders, cerebellar syndromes and confusional states”Sacks W, Esser AH, Feitel B, Abbott K. Acetazolamide and thiamine: an ancillary therapy for chronic mental illness. Psychiatry Res. 1989 Jun;28(3):279-88.“Overall, 50% of the patients showed improvement on all assessment scales. No untoward effects occurred in these patients…”Relation of thiamine and geriatric patientsSmidt LJ, Cremin FM, Grivetti LE, Clifford AJ. Influence of thiamin supplementation on the health and general well-being of an elderly Irish population with marginal thiamin deficiency. J Gerontol. 1991 Jan;46(1):M16-22.”thiamin-supplemented women experienced significantly increased appetite, energy intake, body weight and general well-being, and decreased fatigue. Thiamin supplementation also tended to reduce daytime sleep time, improve sleep patterns, and increase activity. These data suggest that evaluation of thiamin status is indicated when nonspecific conditions such as anorexia, weight loss, fatigue, depression, and sleep disorders are present in elderly persons”Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels in elder patients admitted through the emergency department. Acad Emerg Med. 2000 Oct;7(10):1156-9.“CONCLUSIONS: Elder nursing home patients seen in the ED and admitted to the hospital are frequently thiamine-deficient”Wilkinson TJ, Hanger HC, Elmslie J, PM, Sainsbury R. The response to treatment of subclinical thiamine deficiency in the elderly. Am J Clin Nutr. 1997 Oct;66(4):925-8.“Only the subjects with persistently low TPP concentrations showed subjective benefits from treatment with improvements in quality of life… There was a trend toward benefits in sleep and energy… Quality of life was enhanced by providing thiamine supplements. Blood pressure and weight were lower after thiamine supplementation”Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte thiamin concentrations in geriatric outpatients. J Am Coll Nutr. 1996 Jun;15(3):231-6.“CONCLUSION: About 50% of geriatric outpatients in this study had low plasma thiamin levels”Nichols HK, Basu TK. Thiamin status of the elderly: dietary intake and thiamin pyrophosphate response. J Am Coll Nutr. 1994 Feb;13(1):57-61.“Average daily thiamin intake was above the recommended requirement… however, almost half of the total study population had TPP effect > 14%, suggesting thiamin deficiency… CONCLUSION: These findings raise questions about the reliability of dietary intake in assessing metabolic availability of thiamin in the elderly”O'Keeffe ST, Tormey WP, Glasgow R, Lavan JN. Thiamine deficiency in hospitalized elderly patients. Gerontology. 1994;40(1):18-24.“Necropsy studies suggest that thiamine deficiency is underdiagnosed in life… There was no difference in anthropometric indices or in the prevalence of other nutrient deficiencies between the two groups. Thiamine deficiency is common in elderly patients admitted to hospital and may contribute to the development of delirium”Iber FL, Blass JP, Brin M, Leevy CM. Thiamin in the elderly--relation to alcoholism and to neurological degenerative disease. Am J Clin Nutr. 1982 Nov;36(5 Suppl):1067-82. Review.“There is no known toxicity for thiamin”Relation of thiamine to diabetesAvena R, Arora S, Carmody BJ, Cosby K, Sidawy AN. Thiamine (Vitamin B1) protects against glucose- and insulin-mediated proliferation of human infragenicular arterial smooth muscle cells. Ann Vasc Surg. 2000 Jan;14(1):37-43.“Vitamin B1 intake may prove important in delaying the atherosclerotic complications of diabetes”La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA, Molinatti GM, Porta M. Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions. Diabetologia. 1996 Nov;39(11):1263-8.Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S, Scheinman M, T. Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells. Surgery. 2001 Nov;130(5):851-8.“The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes”Hassan R, Qureshi H, Zuberi SJ. Effect of thiamine on glucose utilization in hepatic cirrhosis. J Gastroenterol Hepatol. 1991 Jan-Feb;6(1):59-60.“It is therefore suggested that thiamine supplements be given to cirrhotics with hyperglycaemia, to improve glucose utilization”Rindi G, Laforenza U. Thiamine intestinal transport and related issues: recent aspects.Proc Soc Exp Biol Med. 2000 Sep;224(4):246-55. Review.“Thiamine uptake is enhanced by thiamine deficiency, and reduced by thyroid hormone and diabetes”Saito N, Kimura M, Kuchiba A, Itokawa Y. Blood thiamine levels in outpatients with diabetes mellitus. J Nutr Sci Vitaminol (Tokyo). 1987 Dec;33(6):421-30.“From the above findings it was concluded that diabetic outpatients tend to have a low blood thiamine level, with low erythrocyte transketolase activity and high erythrocyte TPP effect, and showed marginal thiamine deficiency” Relation of thiamine to diseaseWallace AE, Weeks WB. Thiamine treatment of chronic hepatitis B infection. Am J Gastroenterol. 2001 Mar;96(3):864-8.”In each case study, thiamine administration was associated with reduction in aminotransferase levels and the fall of HBV DNA to undetectable levels… The relationship between thiamine administration and chronic hepatitis B infection warrants further study. If proven effective in reducing liver damage or inducing remission of the hepatitis B virus in larger trials, thiamine will offer obvious advantages over the current treatments for chronic viral hepatitis B infection”Rossouw JE, Labadarios D, Krasner N, M, R. Red blood cell transketolase activity and the effect of thiamine supplementation in patients with chronic liver disease. Scand J Gastroenterol. 1978;13(2):133-8.“Biochemical evidence of thiamine deficiency was found in 58% of patients with chronic liver disease… high doses of thiamine should be included in the routine nutritional management of patients with severe chronic liver disease”Shoji S, Furuishi K, Misumi S, Miyazaki T, Kino M, Yamataka K. Thiamine disulfide as a potent inhibitor of human immunodeficiency virus (type-1) production. Biochem Biophys Res Commun. 1994 Nov 30;205(1):967-75.” The results suggest that thiamine disulfide may be important for AIDS chemotherapy”Shoji S, Furuishi K, Ogata A, Yamataka K, Tachibana K, Mukai R, Uda A, Harano K, Matsushita S, Misumi S. An allosteric drug, o,o'-bismyristoyl thiamine disulfide, suppresses HIV-1 replication through prevention of nuclear translocation of both HIV-1 Tat and NF-kappa B. Biochem Biophys Res Commun. 1998 Aug 28;249(3):745-53.Butterworth RF, Gaudreau C, Vincelette J, Bourgault AM, Lamothe F, Nutini AM. Thiamine deficiency and Wernicke's encephalopathy in AIDS. Metab Brain Dis. 1991 Dec;6(4):207-12.“we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse… it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex”Haisraeli-Shalish M, Livneh A, Katz J, Doolman R, Sela BA. Recurrent aphthous stomatitis and thiamine deficiency. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Dec;82(6):634-6.” 70 patients with recurrent aphthous stomatitis and in 50 members of a control group… Low levels of vitamin B1 were detected in 49 patients but in only two members of the control group… Our finding suggests an association between thiamine deficiency and recurrent aphthous stomatitis”Engel D. Tropical pyomyositis, a thiamine-deficiency disease. Med Hypotheses. 1981 Mar;7(3):345-52.“it is suggested that thiamine deficiency is an essential contributary factor in producing tropical pyomyositis… Thiamine deficiency induces a biochemical lesion (s) in the pyruvate oxidase system of the muscle, which breaks down its normal resistance to infection and opens the gate to bacterial agents”Krishna S, AM, Supanaranond W, Pukrittayakamee S, ter Kuile F, Tawfiq KM, Holloway PA, White NJ. Thiamine deficiency and malaria in adults from southeast Asia. Lancet. 1999 Feb 13;353(9152):546-9.”12 (52%) of 23 patients with severe malaria and ten (19%) of 54 patients with uncomplicated malaria had alpha values above the normal range (p<0.0001 and p=0.0014, respectively, compared with controls), which indicated severe thiamine deficiency” Pietrzak I, Baczyk K, Mlynarczyk M, Kaczmarek M. [Content of thiamin in plasma and erythrocytes in patients with end stage renal disease] Przegl Lek. 1996;53(5):423-6. Polish.”We suggest the need of thiamine supplementation in ESRD patients especially in those treated by dialysis. The supplementation of thiamine is needed particularly in patients on peritoneal dialysis”Relation of thiamine to other dataHung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. 2001 Nov;38(5):941-7.“We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency”Huang S, Ren G. [Thiamine status of university teacher families in Changsha] Hunan Yi Ke Da Xue Xue Bao. 1998;23(1):27-30. Chinese.“We conclude that those people who take the refined cereals and its products as a staple food, is in the risk of thiamine deficiency”Suzuki M, Itokawa Y. Effects of thiamine supplementation on exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106.“High-dose thiamine (vitamin B1) supplementation (100 mg/day) may be helpful in preventing or accelerating recovery from exercise-induced fatigue… Thiamine supplementation significantly suppressed the increase in blood glucose in the normal thiamine group and significantly decreased the number of complaints shortly after exercise in the subjective fatigue assessment of 30 items”Kimura M, Itokawa Y, Fujiwara M. Cooking losses of thiamin in food and its nutritional significance. J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl 1:S17-24.”The thiamin contents in cooked daily meals were 50-60 percent of the calculated values on an average”Cruickshank AM, Telfer AB, Shenkin A. Thiamine deficiency in the critically ill. Intensive Care Med. 1988;14(4):384-7.“We performed a retrospective study on 158 patients admitted to the Intensive Care Unit who required nutritional support. Patients who survived had significantly higher body thiamine status than those who died”Onodera K, Kisara K, Okabe H, Ogura Y. [studies on the effects of thiamine deficiency on rat testes (author's transl)] Nippon Yakurigaku Zasshi. 1980 Mar;76(2):143-52. Japanese.“In the thiamine deficient group, the seminiferous tubuli of rats having erections had atrophied”Labadarios D, Rossouw JE, McConnell JB, M, R. Thiamine deficiency in fulminant hepatic failure and effects of supplementation. Int J Vitam Nutr Res. 1977;47(1):17-22.“Nine out of 24 patients with acute hepatocellular necrosis leading to fulminant hepatic failure showed biochemical evidence of thiamine deficiency early in the course of their illness”Why haven’t we heard of benfo before? The patent on the manufacture of benfo expired decades ago. Pharmaceutical companies pursue drugs that can be patented so they can have a monopoly and charge 100 times what the drug is worth. They have spent a lot of money on AGE inhibitors that don’t work as well as benfo. Ingestion of benfo may result in the elimination of AGE-protein crosslinks, which are a major constituent of arterial plaque. I am intrigued by the idea that benfo may cause the removal of plaque from the blood vessels, but I am concerned about the rapid manner in which it may cause the removal of plaque from the blood vessels. If the plaque is being removed, a large chunk might break off and cause a stroke or heart attack. If I was older than 60 or if I had a serious problem with high blood pressure I would probably start out by taking very low doses of benfo and gradually increase my dosage. Of course, there are no reports of strokes or heart attacks from benfo in the medical literature, but it’s a thought to consider. My PhD research will mostly consist of double-blind controlled studies on the administration of benfo in normal individuals, diabetics, individuals with high blood pressure, Alzheimer patients etc. I believe the researchers who have investigated benfo to date have been extremely short sighted by not discovering they full potential of benfo in the clinical studies that have already been performed on humans.It is illegal to make claims about benfo and sell it as a dietary supplement unless the claims are based on substantial scientific evidence. The three case studies outlined in this document are not from a double-blind controlled study and FDA regulations would not allow for them to be referred to as substantial scientific evidence. Claims should not be made based on these preliminary findings. For questions or comments email robholladay99@...Since I am not a physician, it would be inappropriate for me to answer emails asking for medical advice.

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I think a single 4Gm dose of ascorbic acid might change pH and maybe even crystallize. If spaced out through the day and combined with sufficient water (one ounce for every 2 pounds of body weight) I'd wager there's be not problem.

The B1 issue is a strange one, but nobody has reported any forms of negative reaction. I have heard that some people use 400mg or more IM each day. They feel better and so on and there's seemingly no complications. A person in BC has been using these doses for over 25 years. He's not alone. This is based on work by Dr. F Klenner back in the 1960's.

WHO made the connection between B1 and DEmyelination and when was it made? Fifty years ago most of us got enough B vitamins in our food. Today, we're practically starving for nutrition - yet we're fat as hogs (I really can explain this). It is similar to the saying "if you eat a good balanced diet then you don't need to take vitamins." I agree 100% but I ask who in the US is able to eat a good balanced diet? Where would a person find good, non-contaminated produce, or meat without hormones, or clean (non-pasteurized) milk, or clean water - and so on? Fields are not tilled and crops are not rotated. Instead they add potassium, nitrogen and phosphorous to the fields and call it fertilizing (plus a good dose of estrogen-like pesticides for fun and profit). What about all the other vitamins and minerals that are leached from the soil - and not replaced?

Larry J. Frieders,RPh |The Compounder575 W. Illinois Ave ~ Aurora, IL 60506 630-859-0333 FAX 630-859-0114 Sample newsletter http://www.theCompounder.com/NL-Sample.html

Any health related information on our web pages or in our newsletters is for educational purposes only. None of the information we provide is to be construed as medical advice. Before applying any therapy or use of herbs, you may want to seek advice from your health care professional. Our information should not be a substitute for physician evaluation or treatment by a health care professional and is not intended to provide or confirm a diagnosis.

----- Original Message -----

From: n Quinn

low dose naltrexone

Sent: Thursday, March 25, 2004 10:57 AM

Subject: Re: [low dose naltrexone] Fw: check this out!

Larry, I agree with a lot of th etheories, but your opinion from Pharmacist to Pharmacist: Vitamin C at high (over 4gm per day) dose is associated with crystals in the urine, stones, and pain, and vitamin B6 a component of the B100 vitamins is linked with DE-MYELINATION! in doses of (allegedly) over 150 mg per day. what's your read on this?

n

----- Original Message -----

From: Larry J. Frieders

low dose naltrexone

Sent: Thursday, March 25, 2004 2:44 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

Just a note...We dispense a LOT of Vitamin B1 injection (some people just don't absorb the B vitamins well through the gut, so they use an injection). People are using 200mg and more each day and report significant improvements. I hold firm to the belief that many (if not most) chronic conditions (like MS and CFS) have their roots deeply buried in nutrition problems. It seems that B1 is a vital nutrient for proper nerve and muscle function.

Here's a link to an updated protocol. Dale Humpherys has used this approach for over 25 years - and he has encouraged hundreds (if not thousands) of others to use this approach. http://www.thecompounder.com/HumpherysNewProtocol.html

Larry J. Frieders,RPh |The Compounder575 W. Illinois Ave ~ Aurora, IL 60506 630-859-0333 FAX 630-859-0114 Sample newsletter http://www.theCompounder.com/NL-Sample.html

Any health related information on our web pages or in our newsletters is for educational purposes only. None of the information we provide is to be construed as medical advice. Before applying any therapy or use of herbs, you may want to seek advice from your health care professional. Our information should not be a substitute for physician evaluation or treatment by a health care professional and is not intended to provide or confirm a diagnosis.

----- Original Message -----

From:

low dose naltrexone

Sent: Wednesday, March 24, 2004 7:47 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

I started on this B1 night before last. I've been whining about this long drawn out virus I've been fighting, and either the B1 is helping mucho over the last two days, or I'm suddenly getting stronger anyway. I feel lots more energy, and my legs are finally getting some strength back. It's so hard to tell if it is the Benfotiamine or just my body finally winning. Who knows. I do know I've seen no side effects even though I've been taking 600mg twice a day. After a few days more I'll cut that in half... No digestive upsets, no headaches, just a positive feeling about life in general.

(MS)

----- Original Message -----

From: ruben/kathy lintzenich

low dose naltrexone

Sent: Tuesday, March 23, 2004 7:26 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

Tom, thanks for the great article. I will be starting this form of B1 when I finish my bottle of thiamine. Will keep everyone posted on any benefits I receive. Are you taking this form of B1 and did you find out about it through the Brewer Science Library? White is the educatuional cordinater at the library and publishes a quarterly newslettet. She is a wonderful source of info about ms and other dis-eases in the body. Best Wishes, Kathy

----- Original Message -----

From: tmbayuk

msalternatives ; MSersLife ; MS-Christians ; MSfriends ; MSViews_Multiple_Sclerosis ; low dose naltrexone ; JJUK ; mscured

Sent: Monday, March 22, 2004 10:50 AM

Subject: [low dose naltrexone] Fw: check this out!

----- Original Message ----- From:

tmbayuk

Sent: Saturday, March 20, 2004 11:01 PM

Subject: check this out!

Research on Benfotiamine Clinton Holladay, M.S.Copyright 2003 Clinton HolladayJune 5, 2003A short while ago a group of individuals I know purchased a large amount of benfotiamine and began ingesting it orally. I was urged by these individuals to place some of the research I have been conducting on benfo (benfotiamine) online along with the results of their benfo use. I was asked to do this in a manner that would allow individuals that do not have a background in the health sciences to comprehend it. I will be pursuing a PhD shortly and benfo will be central to my research. I am not a physician and the following information is not intended to be used as medical advice. Advanced glycation endproducts or AGEs are produced by the processing of sugars within the cell. They are one of the primary causes of aging and general wear and tear on your cells. Diabetics age the same way as normal people, but because they often have abnormal levels of sugars in their cells, they age faster. When blood sugar levels are high, certain cells in the body are flooded with glucose, particularly neurons and cells in the eyes and kidneys. Diabetics often suffer from nerve damage, kidney failure, and premature blindness. Numerous researchers have concentrated their efforts on AGE-blocking mechanisms because they would limit the wear and tear on the body’s cells and allow individuals to live longer and healthier, particularly diabetics. Benfo has emerged as the premier AGE inhibitor.Case StudiesIt is important to note that the following case studies are not double-blind controlled studies. Case study #1. Female, early fifties, non-diabetic, suffers from chronic fatigue, depression, and the normal aches and pains that accompany middle age. Her diet is average. She is able to do about two hours of physical labor a day, and she has suffered from depression for years. She has tried numerous treatments for depression including Prozac, and some of them have helped, but none have completely eliminated the depression. Sometimes she aches all over. She was addicted to caffeine for several years, but only consumes it about once a week now. She has high blood pressure, and treats it with Vasotec and also takes Maxide (a diuretic).She ingested 650 mg of benfo once a day for five days and did not notice any difference. On day 6 she doubled the dose to 1300 mg and started to notice a change a few hours later. There was a dramatic increase in stamina and energy. She is now able to do eight hours of physical work each day. She has an extremely heightened sense of well-being and all aspects of the depression have left. She has better clarity of thought, and sleeps better. Previously she would usually wake up two or three times a night. Now she sleeps through the whole night and has said she is in a deeper sleep at night. She has reported being able to control her appetite more. She has reported less shortness of breath. On day 13 she has had no weight change. On day 13 she experienced what felt exactly like a caffeine withdrawal headache. She immediately consumed two cans of mountain dew and the headache did not leave. Previous to this, caffeine had always relieved a headache of this sort for her. At day 14 she still had a headache and the tips of her toes started tingling. She reduced her dose to 650 mg per day once a day on day 14. On day 15 she still had a headache. On day 16 her toes started tingling and the headache left. On day 17 her pinkie started tingling. Her blood pressure has always fluctuated between 120/80 and 150/90. Throughout the treatment her blood pressure has fluctuated like it normally does. She says she feels like she did when she was thirty years old. Comment: The tingling is likely the cause of blood circulating to parts of her body that have not had a great deal of circulation in recent years.Case study #2. Male, mid fifties, non-diabetic. Average diet. Overall health is better than average for his age. He gets indigestion at night and takes Prilosec. He has the normal aches and pains that accompany middle age. When he wakes up in the morning his feet are inflexible, but that would go away after walking on them for about two minutes. After driving for two hours he is stiff when he gets out of his car. Most of the aches and pains and the foot inflexibility appeared in the last five to fifteen years. He began taking 650 mg of benfo once a day. On day 3 nothing hurt when he woke up. By day five all his aches and pains had disappeared. He is no longer stiff when he gets out of his car after driving for two hours. He feels more flexible. He says it has fixed everything that has gone wrong with him in the past fifteen years. He says he feels more cheerful but is not sure if it is because of repair to neurological damage or because his aches and pains are gone. He has reported a greater clarity of thought. He says he feels like he did when he was age 25-40 (he says he felt the same during those years). Up until twelve months ago his blood pressure has been 120/90. For the past twelve months it has averaged 130/120. On day 5 his blood pressure was 120/85 and it has remained consistent every day since then. Now he can only take a fifteen minute nap during the day whereas before he could fall asleep for hours. At night he sleeps better, probably because the aches and pains are gone. His appetite is only about 80% of what it used to be. He has reported increased stamina and energy. Before taking benfo it was getting hard for him to do ten hours of work per day. Now he can do fourteen hours of work per day. He still requires the same amount of sleep at night, but if he does not get his full requirement he doesn’t notice it nearly as much.Comment: The decrease in caloric intake may be because he was lacking an essential nutrient- not enough thiamine? The stiffening of the joints brought on by old age is partly a symptom poor blood circulation. The fact that this individual has become much more flexible is a possible indication of increased circulation.Case study #3. Male, late forties. He has been a type 1 diabetic for twenty years. Average diet. Over the last five years his health has declined more rapidly. He has more aches and pains than the average person because he is diabetic. He aches so much at night that he usually can’t get to sleep unless he takes Ibuprofen. He began taking 650 mg benfo once a day. On day 2 he noticed a decline in the severity of his aches and pains. He still needs the same amount of sleep, but if he doesn’t get his full requirement he doesn’t notice nearly as much. He has had an increase in stamina and energy. He says his stamina has doubled. On day 14 he felt like he did ten years ago, and it keeps improving each day. He is more cheerful, but like #2 he can’t tell if it’s because his aches and pains are gone or if benfo has a neurological effect on him. I will not disclose the brand of benfo which was used because I do not wish to be seen as promoting any particular brand. These case studies will be updated on July 5, 2003 and new ones will be added. The updates will be posted on www.geocities.com/robholladay99/updates.html The following exerpts are from medical journals. The abstracts (summaries) for most of them can be viewed online through the pubmed database, which is a free database most biomedical scientists use. To find pubmed, go to google.com and type in pubmed. Once you’re in pubmed, type in part of the title and you should be able to find the abstract. When typing in the title use "benfotiamine" not "benfo". As an anti-spamming measure, many search engines will not index web pages that list the key search words more than seven times throughout the document, hence this document was modified after it was created . Several things are important to note in the following literature. First of all, not only does benfo stop some effects of aging, it reverses them. Gradually over time people’s neurons quit working because of normal wear and tear. However, when benfo was ingested, not only did the nerve damage stop, some of the damage done through aging was repaired. A strong point is made that benfo is the most bioavailable source of thiamine. This means benfo is better absorbed than other sources of thiamine. Also, high levels of thiamine have analgesic (pain-relieving) effects on animals. In the Russian study the pain level of the patients decreased from 8.2 to 2.3, a decrease of about four hundred percent. Research articles on benfoWada T, Tagaki H, Minakami H, Hamanka W, Okamoto K, Ito, A, Sahashi Y. 1961. A new thiamine derivative, S-benzoylthiamine O-monophosphate. Science 134: 195-196.Benfo “is more easily absorbed in the body than thiamine hydrochloride, and administration results in higher thiamine and cocarboxylase levels in organs; moreover, these levels last for a longer period of time…It does not cause any unfavorable symptom in animals such as thiamine hydrochloride does…The LD50 by oral administration in mice, dd-strain hybrid, weighing 14 to 16g was 15g/kg of body weight”Bitsch R, Wolf M, Moller J, Heuzeroth L, Gruneklee D. Bioavailability assessment of the lipophilic benfo as compared to a water-soluble thiamin derivative. Ann Nutr Metab. 1991;35(5):292-6. “in presence of allicin, the active principle of garlic, the water-soluble thiamin hydrochloride is transformed into a lipid-soluble compound being identified as allithiamine…Ten healthy young men…The volunteers ingested a single dose of 40 mg benfo…Thus, the measured values reveal, when compared with mononitrate, a clearly improved thiamin bioavailability from benfo, due to the more lipophilic properties of this substance or possibly its dephosphorylated metabolite and a more rapid transformation into the physiologically active derivative. This may be of great advantage in the treatment of neurological disorders responding to high thiamin doses and further on in situations when the active intestinal absorbtion mechanisms are impaired”Stracke H, Lindemann A, Federlin K. A benfo-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.“Benfo…was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold...Therapy-specific adverse effects were not seen”Loew D. Pharmacokinetics of thiamine derivatives especially of benfo. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.“The effective form of thiamine, thiamine diphosphate, is an organic compound needed by the organism for vital functions…Due to this peculiarity the conditions for absorbtion of lipid-soluble vitamins differ from those for water-soluble thiamine derivatives. Unlike the latter, allithiamines are absorbed passively, they traverse the intestinal absorption barrier faster and more readily, leading to higher blood and tissue concentrations even when comparatively low doses are given…It therefore fulfills important pharmacodynamic conditions for rational therapy. Due to their greater biovailability and better tissue passage lipid-soluble thiamine analogues like benfo are preferable to water-soluble thiamine derivatives for treatment of various pathological conditions, e.g. cardiomyopathy, Werincke-Korsakow syndrome, and alcoholic or diabetic polyneuropathies…Due to its excellent pharmacokinetic profile and to its excellent tolerability benfo should be preferred in treatment of relevant conditions like neuropathies”Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter CH. Comparative bioavailability of two vitamin B1 preparations: benfo and thiamine mononitrate. Eur J Clin Pharmacol. 1997;52(4):319-20.“a study using equimolar quantities of the two preparations for exact comparison of the bioavailability of benfo and thiamine mononitrate has never been performed. Therfore, the present trial was undertaken…the higher thiamine content in the erythrocytes and the higher thiamine excretion in urine after oral benfo administration are proof of the considerably higher relative bioavailability of benfo than thiamine mononitrate”Simeonov S, Pavlova M, Mitkov M, Mincheva L, Troev D. Therapeutic efficacy of "Milgamma" in patients with painful diabetic neuropathy. Folia Med (Plovdiv). 1997;39(4):5-10.“Forty-Five diabetes patients with painful peripheral polyneuropathy were enrolled in a 3-month observational study comparing the therapeutic efficiacy of Milgamma tablets (benfo)…Statistically significant relief of both background and peak neuropathic pain was achieved in all of the Milgamma-treated patients…No adverse reactions were observed…Our results underscore the importance of Milgamma tablets as an indispensable element in the therapeutic regimen of patients with painful diabetic polyneuropathy”Greb A, Bitsch R. Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther. 1998 Apr;36(4):216-21.“Seven healthy volunteers…a single oral dose of either benfo…fursultiamin…thiaminedisulfide…In this study the allithiamine derivative benfo proved the best bioavailability. Owing to its excellent absorption properties it can be concluded that oral administration of benfo is suitable for therapeutical purposes”Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfo in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.Good review, full-text is available free online. “In bioavailability studies on healthy human subjects, it was shown that absorption of benfo was several times better than that of water-soluble vitamin B1 and that there was a 120-fold higher increase of metabolically active thiamine diphosphate in erythrocytes (Heinrich, 1990)…In animals given dosages that exceeded basic requirements by 100- or 1000-fold thiamine has analgesic and neuroprotective effects(woelk and peeler-Ichakawa, 1985; Jurna, 1988; Reeh, 1988, 1991; Wild, 1988). However, if high levels are to be achieved with oral vitamin B1 treatment, lipid soluble thiamine derivatives or pro-drugs with high bioavailability, such as benfo, are required…320 mg/day during weeks 1 to 4 and 120 mg benfo/day during weeks 5 to 8…Within the 8-week study period, benfo led to a significant improvement of the threshold of vibration perception at the great toe, motor function, and the overall symptom score. Marked improvement occurred in both pain and co-ordination”Sadekov RA, Danilov AB, Vein AM. [Diabetic polyneuropathy treatment by milgamma-100 preparation] Zh Nevrol Psikhiatr Im S S Korsakova. 1998;98(9):30-2. Russian.“benfo…was studied in treatment of diabetic polyneuropathy in 14 patients…After the course of treatment the intensity of pains was decreased according to visual analogous scale on the average from 8.2 to 2.3 scores, the indices of vibratory sensitivity improved significantly as well as the data of cardiovascular tests…The treatment resulted in the improvement of the condition in 93% of the cases” T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine pharmacokinetics by end-stage renal disease (ESRD). Int J Clin Pharmacol Ther. 1999 Sep;37(9):449-55.“20 end-stage renal disease(ESRD) patients…After a single oral dose of 100 mg benfo…ESRD patients may benefit from high-dose thiamine derivatives notwithstanding their chemical form. However, the better absorption and high transfer rate of debenzoylated BTMP (benfo) to TDP (thiamine diphosphate) even at much lower doses compensates for reduced renal excretion and may protect, therefore, against numerous adverse effects of uremia”Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different benfo dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.320, 120, and 150 mg benfo/day was administered to “diabetic patients suffering from painful peripheral diabetic neuropathy. In a 6-week open clinical trial, 36 patients…An overall beneficial therapeutic effect on the neuropathy status was observed in all three groups during the study…The greatest change occurred in the group of patients receiving the high dose of benfo…Metabolic control did not change over the study...Extremely interesting is the result of recent in vitro experiences that thiamine pyrophosphate and pyroxidine inhibit the formation of glycation end products" T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfo. Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.“20 end-stage renal disease (ESRD) patients…After benfo administration, the peak plasma concentration of TDP exceeded that in healthy subjects by 51%...Compared with thiamine nitrate, the oral administration of benfo leads to higher TDP concentrations in erythrocytes accompanied with a significant improvement of the erythrocyte transkelotase activity in ESRD patients”Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M. Benfo is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.“We investigated the hypothesis that benfo, a lipophilic derivative of thiamine, affects replication delay and generation of advanced glycosylation endproducts (AGE) in human umbilical vein endothelial cells cultured in the presence of high glucose…Benfo, a derivative of thiamine with better bioavailability, corrects defective replication and increased AGE generation in endothelial cells cultured in high glucose, to a similar extent as thiamine. These effects may result from normalization of accelerated glycolysis and the consequent decrease in metabolites that are extremely active in generating nonenzymatic protein glycation. The potential role of thiamine administration in the prevention or treatment of vascular complications of diabetes deserves further investigation”Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M, Geyer J, Kopcke W, Sauerland C, Bretzel RG, Federlin KF. Efficacy of benfo versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.“After three months preventative administration of both vitamin B1 preparations NCV (nerve conduction velocity) had increased substantially…It was nearly normal after six months with benfo, while the administration of thiamine nitrate resulted in no further amelioration. NCV was nearly normalized after six months of benfo application but not with thiamine. Furthermore, benfo induced a major inhibition of neural imidazole-type AGE formation and completely prevented diabetes induced glycoxidation products”Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M. Benfo blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.“Our results in both endothelial cells cultured for several days and retinas from rats with nine months of diabetes showed that benfo, a lipid-soluble thiamine derivative, prevents activation of three major pathways involved in hyperglycemia-induced vascular damage: the hexosamine pathway, the intracellular AGE formation pathway and the DAG-PKC pathway…We showed that benfo blocks these pathways of hyperglycemic damage by increasing the activity of transketolase…Administration of benfo for nine months also completely prevented the development of experimental diabetic retinopathy in rats...Thus we conclude that augmentation of transketolase activity is solely responsible for the observed effects of benfo”Comment: This study is very significant because it demonstrates how benfo blocks several other aging mechanisms besides AGE formation. However, I am not yet convinced of the statement that transketolase activity is solely responsible for the observed effects of benfo. The following four studies are located on the Internet but are not yet listed on Medline. To find them, go to google.com and type in part of the titleBergfeld R, Matsumara X. Du, Brownlee M. Benfo prevents the consequences of hyperglycemia-induced mitochondrial overproduction of reactive oxygen species, and experimental diabetic retinopathy.“diabetic rats were treated with benfo (80 mg/kg weight) for 36 weeks…Benfo decreases AGE formation by 60%...These data suggest that treatment with benfo may be an effective approach to prevent the development of diabetic complications”Lin J, Alt A, Liersch J, Bretzel R, Brownlee M, Hammes H. Benfo inhibits intracellular formation of advanced glycation end products in vivo“Here, we studied the effect of benfo, a lipid-soluble thiamine derivative with known AGE-inhibiting properties in vitro on the intracellular formation of (CML) and methylgloxal-derived AGE in red blood cells. Blood was collected from 6 type 1 diabetic patients before and after treatment with 600 mg/day benfo for 28 days…Thiamine derivatives, in particular the lipid-soluble prodrug benfo, are effective inhibitors of intracellular formation of AGE and CML”Stracke H, Werkmann D, Mavrakis K, Federlin K, Kopke W, Sauerland C, Hammes H, Bretzel RG. Influence of vitamin B1 on diabetic neuropathy-studies in streptozotocin-diabetic rats.“we investigated the effects of oral administration of thiamine and benfo on the development of glucose oxidation products in the nerve and on nerve conduction velocity in streptozotocin-diabetic rats…Conclusion: Early treatment with benfo normalizes increased cellular oxidative stress and the reduced nerve conduction velocity”Hammes H, Bretzel, R.G., Federlin, K, Horiuchi S, Niwa T, Stracke H. Benfo inhibits the formation of advanced glycation end products in diabetic rats.“benfo (100 mg/kg x day) and thiamin (70.18 mg/kg x day) administered orally for 6 months…neither benfo nor thiamin treatment affected metabolic control…Benfo administration in diabetic rats induced a major inhibition of neutral imidazolone-type AGE formation and completely prevented diabetes-induced glycoxidation formation. Treatment with thiamin did not affect AGE or CML levels”ThiamineAllithiamines are lipid-soluble sources of thiamine. Benfo is an allithiamine. Thiamine is water-soluble and is also known as vitamin B1.After reviewing the relevant medical literature on thiamine, I have come to conclude that large portions of the population may be thiamine deficient. In addition, many individuals that are not technically thiamine deficient would likely receive benefit from thiamine supplementation. Thiamine deficiency is associated with numerous undesirable medical conditions.Relation of thiamine to heart diseaseShamir R, Dagan O, Abramovitch D, Abramovitch T, Vidne BA, Dinari G. Thiamine deficiency in children with congenital heart disease before and after corrective surgery. JPEN J Parenter Enteral Nutr. 2000 May-Jun;24(3):154-8.Thiamine deficiency “is common in children with congenital heart disease (CHD) referred for corrective surgery both before and after surgery. Our results suggest that neither diuretic treatment nor malnutrition can fully explain the development of TD in these children”Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E, Levy R. [Right heart failure caused by thiamine deficiency (cardiac beriberi)] Presse Med. 2000 Feb 12;29(5):240-1. French.Beaud C, Fuhrman C, Perchet H, Monnet I, Chouaid C, Housset B. [Thiamine deficiency. A cause of cardiac insufficiency not to be ignored] Rev Mal Respir. 1998 Jun;15(3):303-4. French.“Thiamine deficiency is one of the classical causes of high output for heart failure”Okura H, Gohma I, Hatta K, Imanaka T. Thiamine deficiency and pulmonary hypertension in Crow-Fukase syndrome. Intern Med. 1995 Jul;34(7):674-5. “After oral administration of prednisolone and thiamine, echocardiogram showed marked improvement of the pulmonary hypertension”Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc. 1995 May;95(5):541-4. “Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk”Shimon I, Almog S, Vered Z, Seligmann H, Shefi M, Peleg E, Rosenthal T, Motro M, Halkin H, Ezra D. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med. 1995 May;98(5):485-90.“Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy”Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered Z, Ezra D. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med. 1991 Aug;91(2):151-5.”These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements”Relation of thiamine to neurological disordersLonsdale D, Shamberger RJ, Audhya T. Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: a pilot study. Neuroendocrinol Lett. 2002 Aug;23(4):303-8.“Thiamine tetrahydrofurfuryl disulfide appears to have a beneficial clinical effect on some autistic children, since 8 of the 10 children improved clinically”Nakagawasai O, Tadano T, Hozumi S, Taniguchi R, Tan-No K, Esashi A, Niijima F, Kisara K. Characteristics of depressive behavior induced by feeding thiamine-deficient diet in mice.Life Sci. 2001 Jul 27;69(10):1181-91.Ambrose ML, Bowden SC, Whelan G. Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings. Alcohol Clin Exp Res. 2001 Jan;25(1):112-6.“A therapeutic relationship between dose and working memory performance was indicated”Older MW, Dickerson JW. Thiamine and the elderly orthopaedic patient. Age Ageing. 1982 May;11(2):101-7.“In both groups those patients who were noticeably confused after operation were found to have a considerable fall in their thiamine status suggesting this may be a contributory factor to postoperative confusion”Winston AP, son CP, Madira W, Gatward NM, Palmer RL. Prevalence of thiamin deficiency in anorexia nervosa. Int J Eat Disord. 2000 Dec;28(4):451-4.“Fourteen patients (38%) had results in the deficient range; 7 (19%) met the most stringent published criterion for deficiency. Deficiency was not related to duration of eating restraint, frequency of vomiting, or alcohol consumption”Terasawa M, Nakahara T, Tsukada N, Sugawara A, Itokawa Y. The relationship between thiamine deficiency and performance of a learning task in rats. Metab Brain Dis. 1999 Sep;14(3):137-48.“We taught rats to press a lever to escape from the pain of electrical stimulation by learning to turn a switch off… The rats that were fed the thiamine-deficient diet showed a slower response time and a longer running time than the rats fed the normal diet… We found that the thiamine concentration in the blood of the rats in the trained group was significantly higher than that in the group without training”Jimenez-Jimenez FJ, Molina JA, Hernanz A, Fernandez-Vivancos E, de Bustos F, Barcenilla B, Gomez-Escalonilla C, Zurdo M, Berbel A, Villanueva C. Cerebrospinal fluid levels of thiamine in patients with Parkinson's disease. Neurosci Lett. 1999 Aug 13;271(1):33-6.“These results suggest that low CSF free thiamine levels could be related with the risk for PD”Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J. 1997 Dec;74(12):803-8.“Diabetic peripheral neuropathy in Dar es Salaam is associated with thiamine deficiency”Langlais PJ, G, Guo SX, Bondy SC. Increased cerebral free radical production during thiamine deficiency. Metab Brain Dis. 1997 Jun;12(2):137-43.“These findings suggest that increased formation of free radicals occurs during the more acute symptomatic stage of thiamine deficiency and may contribute to the structural damage described in this model of Wernicke's encephalopathy”Easton CJ, Bauer LO. Beneficial effects of thiamine on recognition memory and P300 in abstinent cocaine-dependent patients. Psychiatry Res. 1997 May 30;70(3):165-74. “Thiamine was found to significantly improve recognition accuracy and P300 amplitude, at the midline parietal (Pz) electrode. The improvement was most reliable under conditions of increased memory load”Benton D, Griffiths R, Haller J. Thiamine supplementation mood and cognitive functioning. Psychopharmacology (Berl). 1997 Jan;129(1):66-71. ”An improvement in thiamine status was associated with reports of being more clearheaded, composed and energetic. The taking of thiamine had no influence on memory but reaction times were faster following supplementation”Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's disease. Metab Brain Dis. 1996 Mar;11(1):89-94.”Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100 mg/day had a mild beneficial effect in patients with Alzheimer's disease in a 12-week open trial. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function”Gold M, Chen MF, K. Plasma and red blood cell thiamine deficiency in patients with dementia of the Alzheimer's type. Arch Neurol. 1995 Nov;52(11):1081-6.“A significant proportion of patients with SDAT may have a thiamine deficiency, which may have an impact on cognitive function. Currently used assays may not be adequate to assess thiamine status”Adamolekun B, Eniola A. Thiamine-responsive acute cerebellar ataxia following febrile illness. Cent Afr J Med. 1993 Feb;39(2):40-1. Review.“acute thiamine depletion may be the pathogenetic mechanism for post-pyrexial acute cerebellar ataxia”Ben-Hur T, Wolff E, River Y. [Thiamin deficiency is common in Israel] Harefuah. 1992 Nov 15;123(10):382-4, 436, 435. Hebrew.“Thiamin levels should be determined not only in alcoholics and those with classic B1 deficiency syndromes, but in the routine workup of patients with sensory-motor neuropathy, dementia, gait disorders, cerebellar syndromes and confusional states”Sacks W, Esser AH, Feitel B, Abbott K. Acetazolamide and thiamine: an ancillary therapy for chronic mental illness. Psychiatry Res. 1989 Jun;28(3):279-88.“Overall, 50% of the patients showed improvement on all assessment scales. No untoward effects occurred in these patients…”Relation of thiamine and geriatric patientsSmidt LJ, Cremin FM, Grivetti LE, Clifford AJ. Influence of thiamin supplementation on the health and general well-being of an elderly Irish population with marginal thiamin deficiency. J Gerontol. 1991 Jan;46(1):M16-22.”thiamin-supplemented women experienced significantly increased appetite, energy intake, body weight and general well-being, and decreased fatigue. Thiamin supplementation also tended to reduce daytime sleep time, improve sleep patterns, and increase activity. These data suggest that evaluation of thiamin status is indicated when nonspecific conditions such as anorexia, weight loss, fatigue, depression, and sleep disorders are present in elderly persons”Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels in elder patients admitted through the emergency department. Acad Emerg Med. 2000 Oct;7(10):1156-9.“CONCLUSIONS: Elder nursing home patients seen in the ED and admitted to the hospital are frequently thiamine-deficient”Wilkinson TJ, Hanger HC, Elmslie J, PM, Sainsbury R. The response to treatment of subclinical thiamine deficiency in the elderly. Am J Clin Nutr. 1997 Oct;66(4):925-8.“Only the subjects with persistently low TPP concentrations showed subjective benefits from treatment with improvements in quality of life… There was a trend toward benefits in sleep and energy… Quality of life was enhanced by providing thiamine supplements. Blood pressure and weight were lower after thiamine supplementation”Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte thiamin concentrations in geriatric outpatients. J Am Coll Nutr. 1996 Jun;15(3):231-6.“CONCLUSION: About 50% of geriatric outpatients in this study had low plasma thiamin levels”Nichols HK, Basu TK. Thiamin status of the elderly: dietary intake and thiamin pyrophosphate response. J Am Coll Nutr. 1994 Feb;13(1):57-61.“Average daily thiamin intake was above the recommended requirement… however, almost half of the total study population had TPP effect > 14%, suggesting thiamin deficiency… CONCLUSION: These findings raise questions about the reliability of dietary intake in assessing metabolic availability of thiamin in the elderly”O'Keeffe ST, Tormey WP, Glasgow R, Lavan JN. Thiamine deficiency in hospitalized elderly patients. Gerontology. 1994;40(1):18-24.“Necropsy studies suggest that thiamine deficiency is underdiagnosed in life… There was no difference in anthropometric indices or in the prevalence of other nutrient deficiencies between the two groups. Thiamine deficiency is common in elderly patients admitted to hospital and may contribute to the development of delirium”Iber FL, Blass JP, Brin M, Leevy CM. Thiamin in the elderly--relation to alcoholism and to neurological degenerative disease. Am J Clin Nutr. 1982 Nov;36(5 Suppl):1067-82. Review.“There is no known toxicity for thiamin”Relation of thiamine to diabetesAvena R, Arora S, Carmody BJ, Cosby K, Sidawy AN. Thiamine (Vitamin B1) protects against glucose- and insulin-mediated proliferation of human infragenicular arterial smooth muscle cells. Ann Vasc Surg. 2000 Jan;14(1):37-43.“Vitamin B1 intake may prove important in delaying the atherosclerotic complications of diabetes”La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA, Molinatti GM, Porta M. Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions. Diabetologia. 1996 Nov;39(11):1263-8.Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S, Scheinman M, T. Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells. Surgery. 2001 Nov;130(5):851-8.“The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes”Hassan R, Qureshi H, Zuberi SJ. Effect of thiamine on glucose utilization in hepatic cirrhosis. J Gastroenterol Hepatol. 1991 Jan-Feb;6(1):59-60.“It is therefore suggested that thiamine supplements be given to cirrhotics with hyperglycaemia, to improve glucose utilization”Rindi G, Laforenza U. Thiamine intestinal transport and related issues: recent aspects.Proc Soc Exp Biol Med. 2000 Sep;224(4):246-55. Review.“Thiamine uptake is enhanced by thiamine deficiency, and reduced by thyroid hormone and diabetes”Saito N, Kimura M, Kuchiba A, Itokawa Y. Blood thiamine levels in outpatients with diabetes mellitus. J Nutr Sci Vitaminol (Tokyo). 1987 Dec;33(6):421-30.“From the above findings it was concluded that diabetic outpatients tend to have a low blood thiamine level, with low erythrocyte transketolase activity and high erythrocyte TPP effect, and showed marginal thiamine deficiency” Relation of thiamine to diseaseWallace AE, Weeks WB. Thiamine treatment of chronic hepatitis B infection. Am J Gastroenterol. 2001 Mar;96(3):864-8.”In each case study, thiamine administration was associated with reduction in aminotransferase levels and the fall of HBV DNA to undetectable levels… The relationship between thiamine administration and chronic hepatitis B infection warrants further study. If proven effective in reducing liver damage or inducing remission of the hepatitis B virus in larger trials, thiamine will offer obvious advantages over the current treatments for chronic viral hepatitis B infection”Rossouw JE, Labadarios D, Krasner N, M, R. Red blood cell transketolase activity and the effect of thiamine supplementation in patients with chronic liver disease. Scand J Gastroenterol. 1978;13(2):133-8.“Biochemical evidence of thiamine deficiency was found in 58% of patients with chronic liver disease… high doses of thiamine should be included in the routine nutritional management of patients with severe chronic liver disease”Shoji S, Furuishi K, Misumi S, Miyazaki T, Kino M, Yamataka K. Thiamine disulfide as a potent inhibitor of human immunodeficiency virus (type-1) production. Biochem Biophys Res Commun. 1994 Nov 30;205(1):967-75.” The results suggest that thiamine disulfide may be important for AIDS chemotherapy”Shoji S, Furuishi K, Ogata A, Yamataka K, Tachibana K, Mukai R, Uda A, Harano K, Matsushita S, Misumi S. An allosteric drug, o,o'-bismyristoyl thiamine disulfide, suppresses HIV-1 replication through prevention of nuclear translocation of both HIV-1 Tat and NF-kappa B. Biochem Biophys Res Commun. 1998 Aug 28;249(3):745-53.Butterworth RF, Gaudreau C, Vincelette J, Bourgault AM, Lamothe F, Nutini AM. Thiamine deficiency and Wernicke's encephalopathy in AIDS. Metab Brain Dis. 1991 Dec;6(4):207-12.“we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse… it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex”Haisraeli-Shalish M, Livneh A, Katz J, Doolman R, Sela BA. Recurrent aphthous stomatitis and thiamine deficiency. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Dec;82(6):634-6.” 70 patients with recurrent aphthous stomatitis and in 50 members of a control group… Low levels of vitamin B1 were detected in 49 patients but in only two members of the control group… Our finding suggests an association between thiamine deficiency and recurrent aphthous stomatitis”Engel D. Tropical pyomyositis, a thiamine-deficiency disease. Med Hypotheses. 1981 Mar;7(3):345-52.“it is suggested that thiamine deficiency is an essential contributary factor in producing tropical pyomyositis… Thiamine deficiency induces a biochemical lesion (s) in the pyruvate oxidase system of the muscle, which breaks down its normal resistance to infection and opens the gate to bacterial agents”Krishna S, AM, Supanaranond W, Pukrittayakamee S, ter Kuile F, Tawfiq KM, Holloway PA, White NJ. Thiamine deficiency and malaria in adults from southeast Asia. Lancet. 1999 Feb 13;353(9152):546-9.”12 (52%) of 23 patients with severe malaria and ten (19%) of 54 patients with uncomplicated malaria had alpha values above the normal range (p<0.0001 and p=0.0014, respectively, compared with controls), which indicated severe thiamine deficiency” Pietrzak I, Baczyk K, Mlynarczyk M, Kaczmarek M. [Content of thiamin in plasma and erythrocytes in patients with end stage renal disease] Przegl Lek. 1996;53(5):423-6. Polish.”We suggest the need of thiamine supplementation in ESRD patients especially in those treated by dialysis. The supplementation of thiamine is needed particularly in patients on peritoneal dialysis”Relation of thiamine to other dataHung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. 2001 Nov;38(5):941-7.“We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency”Huang S, Ren G. [Thiamine status of university teacher families in Changsha] Hunan Yi Ke Da Xue Xue Bao. 1998;23(1):27-30. Chinese.“We conclude that those people who take the refined cereals and its products as a staple food, is in the risk of thiamine deficiency”Suzuki M, Itokawa Y. Effects of thiamine supplementation on exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106.“High-dose thiamine (vitamin B1) supplementation (100 mg/day) may be helpful in preventing or accelerating recovery from exercise-induced fatigue… Thiamine supplementation significantly suppressed the increase in blood glucose in the normal thiamine group and significantly decreased the number of complaints shortly after exercise in the subjective fatigue assessment of 30 items”Kimura M, Itokawa Y, Fujiwara M. Cooking losses of thiamin in food and its nutritional significance. J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl 1:S17-24.”The thiamin contents in cooked daily meals were 50-60 percent of the calculated values on an average”Cruickshank AM, Telfer AB, Shenkin A. Thiamine deficiency in the critically ill. Intensive Care Med. 1988;14(4):384-7.“We performed a retrospective study on 158 patients admitted to the Intensive Care Unit who required nutritional support. Patients who survived had significantly higher body thiamine status than those who died”Onodera K, Kisara K, Okabe H, Ogura Y. [studies on the effects of thiamine deficiency on rat testes (author's transl)] Nippon Yakurigaku Zasshi. 1980 Mar;76(2):143-52. Japanese.“In the thiamine deficient group, the seminiferous tubuli of rats having erections had atrophied”Labadarios D, Rossouw JE, McConnell JB, M, R. Thiamine deficiency in fulminant hepatic failure and effects of supplementation. Int J Vitam Nutr Res. 1977;47(1):17-22.“Nine out of 24 patients with acute hepatocellular necrosis leading to fulminant hepatic failure showed biochemical evidence of thiamine deficiency early in the course of their illness”Why haven’t we heard of benfo before? The patent on the manufacture of benfo expired decades ago. Pharmaceutical companies pursue drugs that can be patented so they can have a monopoly and charge 100 times what the drug is worth. They have spent a lot of money on AGE inhibitors that don’t work as well as benfo. Ingestion of benfo may result in the elimination of AGE-protein crosslinks, which are a major constituent of arterial plaque. I am intrigued by the idea that benfo may cause the removal of plaque from the blood vessels, but I am concerned about the rapid manner in which it may cause the removal of plaque from the blood vessels. If the plaque is being removed, a large chunk might break off and cause a stroke or heart attack. If I was older than 60 or if I had a serious problem with high blood pressure I would probably start out by taking very low doses of benfo and gradually increase my dosage. Of course, there are no reports of strokes or heart attacks from benfo in the medical literature, but it’s a thought to consider. My PhD research will mostly consist of double-blind controlled studies on the administration of benfo in normal individuals, diabetics, individuals with high blood pressure, Alzheimer patients etc. I believe the researchers who have investigated benfo to date have been extremely short sighted by not discovering they full potential of benfo in the clinical studies that have already been performed on humans.It is illegal to make claims about benfo and sell it as a dietary supplement unless the claims are based on substantial scientific evidence. The three case studies outlined in this document are not from a double-blind controlled study and FDA regulations would not allow for them to be referred to as substantial scientific evidence. Claims should not be made based on these preliminary findings. For questions or comments email robholladay99@...Since I am not a physician, it would be inappropriate for me to answer emails asking for medical advice.

SECURALL, INC.

The Difference is 'ALARMING'

602-7582283

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[Guest guest]

,

I’m thrilled to read your taking

600mg twice a day and it’s helping. When I read the article, he suggests

that oral cannot be ingested properly. That an injection in the muscle is the

way to go. . . . oooch. I’m going to try oral B1 at those

levels to see what happens.

(MS)

-----Original

Message-----

From:

[mailto:jatrac1@...]

Sent: Wednesday, March 24, 2004

8:48 PM

low dose naltrexone

Subject: Re: [low dose naltrexone]

Fw: check this out!

I started on this B1 night before last. I've been whining

about this long drawn out virus I've been fighting, and either the B1 is

helping mucho over the last two days, or I'm suddenly getting stronger

anyway. I feel lots more energy, and my legs are finally getting some

strength back. It's so hard to tell if it is the Benfotiamine or just my

body finally winning. Who knows. I do know I've seen no side

effects even though I've been taking 600mg twice a day. After a few days

more I'll cut that in half... No digestive upsets, no headaches, just a

positive feeling about life in general.

(MS)

----- Original

Message -----

From: ruben/kathy

lintzenich

low dose naltrexone

Sent: Tuesday,

March 23, 2004 7:26 PM

Subject: Re:

[low dose naltrexone] Fw: check this out!

Tom,

thanks for the great article. I will be starting this form of B1 when I finish

my bottle of thiamine. Will keep everyone posted on any benefits I receive. Are

you taking this form of B1 and did you find out about it through the

Brewer Science Library? White is the educatuional cordinater at the

library and publishes a quarterly newslettet. She is a wonderful source of info

about ms and other dis-eases in the body. Best Wishes, Kathy

----- Original

Message -----

From: tmbayuk

msalternatives ; MSersLife

; MS-Christians ; MSfriends

; MSViews_Multiple_Sclerosis

; low dose naltrexone

; JJUK ;

mscured

Sent: Monday,

March 22, 2004 10:50 AM

Subject: [low dose naltrexone]

Fw: check this out!

----- Original

Message -----

From:

tmbayuk

Sent: Saturday,

March 20, 2004 11:01 PM

Subject: check this

out!

Research on Benfotiamine

Clinton Holladay, M.S.

Copyright 2003 Clinton Holladay

June 5, 2003

A short while ago a group of individuals I know

purchased a large amount of benfotiamine and began ingesting it orally. I

was urged by these individuals to place some of the research I have been

conducting on benfo (benfotiamine) online along with the results of their benfo

use. I was asked to do this in a manner that would allow individuals that

do not have a background in the health sciences to comprehend it. I will

be pursuing a PhD shortly and benfo will be central to my research. I am

not a physician and the following information is not intended to be used as

medical advice.

Advanced glycation endproducts or AGEs are produced by the processing of sugars

within the cell. They are one of the primary causes of aging and general

wear and tear on your cells. Diabetics age the same way as normal people,

but because they often have abnormal levels of sugars in their cells, they age

faster. When blood sugar levels are high, certain cells in the body are

flooded with glucose, particularly neurons and cells in the eyes and

kidneys. Diabetics often suffer from nerve damage, kidney failure, and premature

blindness. Numerous researchers have concentrated their efforts on

AGE-blocking mechanisms because they would limit the wear and tear on the

body’s cells and allow individuals to live longer and healthier,

particularly diabetics. Benfo has emerged as the premier AGE inhibitor.

Case Studies

It is important to note that the following case studies are not double-blind

controlled studies.

Case study #1. Female, early fifties, non-diabetic, suffers from chronic

fatigue, depression, and the normal aches and pains that accompany middle

age. Her diet is average. She is able to do about two hours of

physical labor a day, and she has suffered from depression for years. She

has tried numerous treatments for depression including Prozac, and some of them

have helped, but none have completely eliminated the depression.

Sometimes she aches all over. She was addicted to caffeine for several

years, but only consumes it about once a week now. She has high

blood pressure, and treats it with Vasotec and also takes Maxide (a

diuretic).

She ingested 650 mg of benfo once a day for five days and did not notice any

difference. On day 6 she doubled the dose to 1300 mg and started to

notice a change a few hours later. There was a dramatic increase in

stamina and energy. She is now able to do eight hours of physical work

each day. She has an extremely heightened sense of well-being and all

aspects of the depression have left. She has better clarity of thought,

and sleeps better. Previously she would usually wake up two or three

times a night. Now she sleeps through the whole night and has said she is

in a deeper sleep at night. She has reported being able to control her

appetite more. She has reported less shortness of breath. On day 13

she has had no weight change. On day 13 she experienced what felt exactly

like a caffeine withdrawal headache. She immediately consumed two cans of

mountain dew and the headache did not leave. Previous to this, caffeine

had always relieved a headache of this sort for her. At day 14 she still had a

headache and the tips of her toes started tingling. She reduced her dose

to 650 mg per day once a day on day 14. On day 15 she still had a

headache. On day 16 her toes started tingling and the headache

left. On day 17 her pinkie started tingling. Her blood pressure has

always fluctuated between 120/80 and 150/90. Throughout the treatment her

blood pressure has fluctuated like it normally does. She says she feels

like she did when she was thirty years old.

Comment: The tingling is likely the cause of blood circulating to parts of her

body that have not had a great deal of circulation in recent years.

Case study #2. Male, mid fifties, non-diabetic. Average diet.

Overall health is better than average for his age. He gets indigestion at

night and takes Prilosec. He has the normal aches and pains that

accompany middle age. When he wakes up in the morning his feet are

inflexible, but that would go away after walking on them for about two

minutes. After driving for two hours he is stiff when he gets out of his

car. Most of the aches and pains and the foot inflexibility

appeared in the last five to fifteen years.

He began taking 650 mg of benfo once a day. On day 3 nothing hurt when he

woke up. By day five all his aches and pains had disappeared. He is

no longer stiff when he gets out of his car after driving for two hours.

He feels more flexible. He says it has fixed everything that has gone

wrong with him in the past fifteen years. He says he feels more cheerful

but is not sure if it is because of repair to neurological damage or because

his aches and pains are gone. He has reported a greater clarity of

thought. He says he feels like he did when he was age 25-40 (he says he

felt the same during those years). Up until twelve months ago his blood

pressure has been 120/90. For the past twelve months it has averaged

130/120. On day 5 his blood pressure was 120/85 and it has remained

consistent every day since then. Now he can only take a fifteen minute

nap during the day whereas before he could fall asleep for hours. At

night he sleeps better, probably because the aches and pains are gone.

His appetite is only about 80% of what it used to be. He has reported

increased stamina and energy. Before taking benfo it was getting hard for

him to do ten hours of work per day. Now he can do fourteen hours of work

per day. He still requires the same amount of sleep at night, but if he

does not get his full requirement he doesn’t notice it nearly as much.

Comment: The decrease in caloric intake may be because he was lacking an

essential nutrient- not enough thiamine? The stiffening of the joints brought

on by old age is partly a symptom poor blood circulation. The fact that this

individual has become much more flexible is a possible indication of increased

circulation.

Case study #3. Male, late forties. He has been a type 1 diabetic

for twenty years. Average diet. Over the last five years his health

has declined more rapidly. He has more aches and pains than the average

person because he is diabetic. He aches so much at night that he usually

can’t get to sleep unless he takes Ibuprofen.

He began taking 650 mg benfo once a day. On day 2 he noticed a decline in

the severity of his aches and pains. He still needs the same amount of

sleep, but if he doesn’t get his full requirement he doesn’t notice

nearly as much. He has had an increase in stamina and energy. He

says his stamina has doubled. On day 14 he felt like he did ten years

ago, and it keeps improving each day. He is more cheerful, but like #2 he

can’t tell if it’s because his aches and pains are gone or if benfo

has a neurological effect on him.

I will not disclose the brand of benfo which was used because I do not wish to

be seen as promoting any particular brand. These case studies will be

updated on July 5, 2003 and new ones will be added. The updates will be posted

on www.geocities.com/robholladay99/updates.html

The following exerpts are from medical journals. The abstracts

(summaries) for most of them can be viewed online through the pubmed database,

which is a free database most biomedical scientists use. To find pubmed,

go to google.com and type in pubmed. Once you’re in pubmed, type in

part of the title and you should be able to find the abstract. When typing

in the title use " benfotiamine " not " benfo " . As an

anti-spamming measure, many search engines will not index web pages that list

the key search words more than seven times throughout the document, hence this

document was modified after it was created .

Several things are important to note in the following literature. First

of all, not only does benfo stop some effects of aging, it reverses them.

Gradually over time people’s neurons quit working because of normal wear

and tear. However, when benfo was ingested, not only did the nerve damage

stop, some of the damage done through aging was repaired. A strong point

is made that benfo is the most bioavailable source of thiamine. This

means benfo is better absorbed than other sources of thiamine. Also, high

levels of thiamine have analgesic (pain-relieving) effects on animals. In

the Russian study the pain level of the patients decreased from 8.2 to 2.3, a

decrease of about four hundred percent.

Research articles on benfo

Wada T, Tagaki H, Minakami H, Hamanka W, Okamoto K, Ito, A, Sahashi Y.

1961. A new thiamine derivative, S-benzoylthiamine O-monophosphate.

Science 134: 195-196.

Benfo “is more easily absorbed in the body than thiamine hydrochloride,

and administration results in higher thiamine and cocarboxylase levels in

organs; moreover, these levels last for a longer period of time…It does

not cause any unfavorable symptom in animals such as thiamine hydrochloride

does…The LD50 by oral administration in mice, dd-strain hybrid, weighing

14 to 16g was 15g/kg of body weight”

Bitsch R, Wolf M, Moller J, Heuzeroth L, Gruneklee D. Bioavailability

assessment of the lipophilic benfo as compared to a water-soluble thiamin

derivative. Ann Nutr Metab. 1991;35(5):292-6.

“in presence of allicin, the active principle of garlic, the

water-soluble thiamin hydrochloride is transformed into a lipid-soluble

compound being identified as allithiamine…Ten healthy young men…The

volunteers ingested a single dose of 40 mg benfo…Thus, the measured

values reveal, when compared with mononitrate, a clearly improved thiamin

bioavailability from benfo, due to the more lipophilic properties of this

substance or possibly its dephosphorylated metabolite and a more rapid

transformation into the physiologically active derivative. This may be of

great advantage in the treatment of neurological disorders responding to high

thiamin doses and further on in situations when the active intestinal

absorbtion mechanisms are impaired”

Stracke H, Lindemann A, Federlin K. A benfo-vitamin B combination in

treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes.

1996;104(4):311-6.

“Benfo…was studied over a period of 12 weeks on 24 diabetic

patients with diabetic polyneuropathy. The results showed a significant

improvement of nerve conduction velocity in the peroneal nerve and a

statistical trend toward improvement of the vibration perception

threshold...Therapy-specific adverse effects were not seen”

Loew D. Pharmacokinetics of thiamine derivatives especially of

benfo. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.

“The effective form of thiamine, thiamine diphosphate, is an organic

compound needed by the organism for vital functions…Due to this

peculiarity the conditions for absorbtion of lipid-soluble vitamins differ from

those for water-soluble thiamine derivatives. Unlike the latter,

allithiamines are absorbed passively, they traverse the intestinal absorption

barrier faster and more readily, leading to higher blood and tissue

concentrations even when comparatively low doses are given…It therefore

fulfills important pharmacodynamic conditions for rational therapy. Due

to their greater biovailability and better tissue passage lipid-soluble

thiamine analogues like benfo are preferable to water-soluble thiamine

derivatives for treatment of various pathological conditions, e.g.

cardiomyopathy, Werincke-Korsakow syndrome, and alcoholic or diabetic

polyneuropathies…Due to its excellent pharmacokinetic profile and to its

excellent tolerability benfo should be preferred in treatment of relevant

conditions like neuropathies”

Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter CH.

Comparative bioavailability of two vitamin B1 preparations: benfo and thiamine

mononitrate. Eur J Clin Pharmacol. 1997;52(4):319-20.

“a study using equimolar quantities of the two preparations for exact

comparison of the bioavailability of benfo and thiamine mononitrate has never

been performed. Therfore, the present trial was undertaken…the

higher thiamine content in the erythrocytes and the higher thiamine excretion

in urine after oral benfo administration are proof of the considerably higher

relative bioavailability of benfo than thiamine mononitrate”

Simeonov S, Pavlova M, Mitkov M, Mincheva L, Troev D. Therapeutic

efficacy of " Milgamma " in patients with painful diabetic

neuropathy. Folia Med (Plovdiv). 1997;39(4):5-10.

“Forty-Five diabetes patients with painful peripheral polyneuropathy were

enrolled in a 3-month observational study comparing the therapeutic efficiacy

of Milgamma tablets (benfo)…Statistically significant relief of both

background and peak neuropathic pain was achieved in all of the

Milgamma-treated patients…No adverse reactions were observed…Our

results underscore the importance of Milgamma tablets as an indispensable

element in the therapeutic regimen of patients with painful diabetic

polyneuropathy”

Greb A, Bitsch R. Comparative bioavailability of various thiamine

derivatives after oral administration. Int J Clin Pharmacol Ther. 1998

Apr;36(4):216-21.

“Seven healthy volunteers…a single oral dose of either

benfo…fursultiamin…thiaminedisulfide…In this study the

allithiamine derivative benfo proved the best bioavailability. Owing to

its excellent absorption properties it can be concluded that oral

administration of benfo is suitable for therapeutical purposes”

Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfo in treatment of alcoholic

polyneuropathy: an 8-week randomized controlled study (BAP I Study).

Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.

Good review, full-text is available free online. “In

bioavailability studies on healthy human subjects, it was shown that absorption

of benfo was several times better than that of water-soluble vitamin B1 and

that there was a 120-fold higher increase of metabolically active thiamine

diphosphate in erythrocytes (Heinrich, 1990)…In animals given dosages

that exceeded basic requirements by 100- or 1000-fold thiamine has analgesic

and neuroprotective effects(woelk and peeler-Ichakawa, 1985; Jurna, 1988; Reeh,

1988, 1991; Wild, 1988). However, if high levels are to be achieved with

oral vitamin B1 treatment, lipid soluble thiamine derivatives or pro-drugs with

high bioavailability, such as benfo, are required…320 mg/day during weeks

1 to 4 and 120 mg benfo/day during weeks 5 to 8…Within the 8-week study

period, benfo led to a significant improvement of the threshold of vibration

perception at the great toe, motor function, and the overall symptom

score. Marked improvement occurred in both pain and co-ordination”

Sadekov RA, Danilov AB, Vein AM. [Diabetic polyneuropathy treatment

by milgamma-100 preparation] Zh Nevrol Psikhiatr Im S S Korsakova.

1998;98(9):30-2. Russian.

“benfo…was studied in treatment of diabetic polyneuropathy in 14

patients…After the course of treatment the intensity of pains was

decreased according to visual analogous scale on the average from 8.2 to 2.3

scores, the indices of vibratory sensitivity improved significantly as well as

the data of cardiovascular tests…The treatment resulted in the improvement

of the condition in 93% of the cases”

T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine

pharmacokinetics by end-stage renal disease (ESRD). Int J Clin Pharmacol

Ther. 1999 Sep;37(9):449-55.

“20 end-stage renal disease(ESRD) patients…After a single oral dose

of 100 mg benfo…ESRD patients may benefit from high-dose thiamine

derivatives notwithstanding their chemical form. However, the better

absorption and high transfer rate of debenzoylated BTMP (benfo) to TDP

(thiamine diphosphate) even at much lower doses compensates for reduced renal

excretion and may protect, therefore, against numerous adverse effects of

uremia”

Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P.

Effectiveness of different benfo dosage regimens in the treatment of painful

diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.

320, 120, and 150 mg benfo/day was administered to “diabetic

patients suffering from painful peripheral diabetic neuropathy. In a

6-week open clinical trial, 36 patients…An overall beneficial therapeutic

effect on the neuropathy status was observed in all three groups during the

study…The greatest change occurred in the group of patients receiving the

high dose of benfo…Metabolic control did not change over the study...Extremely

interesting is the result of recent in vitro experiences that thiamine

pyrophosphate and pyroxidine inhibit the formation of glycation end

products "

T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate

concentrations in erythrocytes can be achieved in dialysis patients by oral

administration of benfo. Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.

“20 end-stage renal disease (ESRD) patients…After benfo

administration, the peak plasma concentration of TDP exceeded that in healthy

subjects by 51%...Compared with thiamine nitrate, the oral administration of

benfo leads to higher TDP concentrations in erythrocytes accompanied with a

significant improvement of the erythrocyte transkelotase activity in ESRD

patients”

Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M.

Benfo is similar to thiamine in correcting endothelial cell defects induced by

high glucose. Acta Diabetol. 2001;38(3):135-8.

“We investigated the hypothesis that benfo, a lipophilic derivative of

thiamine, affects replication delay and generation of advanced glycosylation

endproducts (AGE) in human umbilical vein endothelial cells cultured in the

presence of high glucose…Benfo, a derivative of thiamine with better

bioavailability, corrects defective replication and increased AGE generation in

endothelial cells cultured in high glucose, to a similar extent as

thiamine. These effects may result from normalization of accelerated

glycolysis and the consequent decrease in metabolites that are extremely active

in generating nonenzymatic protein glycation. The potential role of

thiamine administration in the prevention or treatment of vascular

complications of diabetes deserves further investigation”

Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M, Geyer J,

Kopcke W, Sauerland C, Bretzel RG, Federlin KF. Efficacy of benfo versus

thiamine on function and glycation products of peripheral nerves in diabetic

rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.

“After three months preventative administration of both vitamin B1

preparations NCV (nerve conduction velocity) had increased

substantially…It was nearly normal after six months with benfo, while the

administration of thiamine nitrate resulted in no further amelioration.

NCV was nearly normalized after six months of benfo application but not with

thiamine. Furthermore, benfo induced a major inhibition of neural

imidazole-type AGE formation and completely prevented diabetes induced

glycoxidation products”

Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A,

Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M.

Benfo blocks three major pathways of hyperglycemic damage and prevents

experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.

“Our results in both endothelial cells cultured for several days and

retinas from rats with nine months of diabetes showed that benfo, a

lipid-soluble thiamine derivative, prevents activation of three major pathways

involved in hyperglycemia-induced vascular damage: the hexosamine pathway, the

intracellular AGE formation pathway and the DAG-PKC pathway…We showed

that benfo blocks these pathways of hyperglycemic damage by increasing the

activity of transketolase…Administration of benfo for nine months also completely

prevented the development of experimental diabetic retinopathy in rats...Thus

we conclude that augmentation of transketolase activity is solely responsible

for the observed effects of benfo”

Comment: This study is very significant because it demonstrates how benfo

blocks several other aging mechanisms besides AGE formation. However, I

am not yet convinced of the statement that transketolase activity is solely

responsible for the observed effects of benfo.

The following four studies are located on the

Internet but are not yet listed on Medline. To find them, go to

google.com and type in part of the title

Bergfeld R, Matsumara X. Du, Brownlee M. Benfo prevents the consequences

of hyperglycemia-induced mitochondrial overproduction of reactive oxygen

species, and experimental diabetic retinopathy.

“diabetic rats were treated with benfo (80 mg/kg weight) for 36

weeks…Benfo decreases AGE formation by 60%...These data suggest that

treatment with benfo may be an effective approach to prevent the development of

diabetic complications”

Lin J, Alt A, Liersch J, Bretzel R, Brownlee M, Hammes H. Benfo inhibits

intracellular formation of advanced glycation end products in vivo

“Here, we studied the effect of benfo, a lipid-soluble thiamine

derivative with known AGE-inhibiting properties in vitro on the intracellular

formation of (CML) and methylgloxal-derived AGE in red blood cells. Blood

was collected from 6 type 1 diabetic patients before and after treatment with

600 mg/day benfo for 28 days…Thiamine derivatives, in particular the

lipid-soluble prodrug benfo, are effective inhibitors of intracellular

formation of AGE and CML”

Stracke H, Werkmann D, Mavrakis K, Federlin K, Kopke W, Sauerland C, Hammes H,

Bretzel RG. Influence of vitamin B1 on diabetic neuropathy-studies in

streptozotocin-diabetic rats.

“we investigated the effects of oral administration of thiamine and benfo

on the development of glucose oxidation products in the nerve and on nerve

conduction velocity in streptozotocin-diabetic rats…Conclusion: Early treatment

with benfo normalizes increased cellular oxidative stress and the reduced nerve

conduction velocity”

Hammes H, Bretzel, R.G., Federlin, K, Horiuchi S, Niwa T, Stracke H.

Benfo inhibits the formation of advanced glycation end products in diabetic

rats.

“benfo (100 mg/kg x day) and thiamin (70.18 mg/kg x day) administered

orally for 6 months…neither benfo nor thiamin treatment affected

metabolic control…Benfo administration in diabetic rats induced a major

inhibition of neutral imidazolone-type AGE formation and completely prevented

diabetes-induced glycoxidation formation. Treatment with thiamin did not

affect AGE or CML levels”

Thiamine

Allithiamines are lipid-soluble sources of thiamine. Benfo is an

allithiamine. Thiamine is water-soluble and is also known as vitamin B1.

After reviewing the relevant medical literature on thiamine, I have come to

conclude that large portions of the population may be thiamine deficient.

In addition, many individuals that are not technically thiamine deficient would

likely receive benefit from thiamine supplementation. Thiamine deficiency

is associated with numerous undesirable medical conditions.

Relation of thiamine to heart disease

Shamir R, Dagan O, Abramovitch D, Abramovitch T, Vidne BA, Dinari G. Thiamine

deficiency in children with congenital heart disease before and after

corrective surgery. JPEN J Parenter Enteral Nutr. 2000

May-Jun;24(3):154-8.

Thiamine deficiency “is common in children with congenital heart disease

(CHD) referred for corrective surgery both before and after surgery. Our

results suggest that neither diuretic treatment nor malnutrition can fully

explain the development of TD in these children”

Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E, Levy

R. [Right heart failure caused by thiamine deficiency (cardiac

beriberi)] Presse Med. 2000 Feb 12;29(5):240-1. French.

Beaud C, Fuhrman C, Perchet H, Monnet I, Chouaid C, Housset B.

[Thiamine deficiency. A cause of cardiac insufficiency not to be ignored]

Rev Mal Respir. 1998 Jun;15(3):303-4. French.

“Thiamine deficiency is one of the classical causes of high output for

heart failure”

Okura H, Gohma I, Hatta K, Imanaka T. Thiamine deficiency and pulmonary

hypertension in Crow-Fukase syndrome. Intern Med. 1995 Jul;34(7):674-5.

“After oral administration of prednisolone and thiamine,

echocardiogram showed marked improvement of the pulmonary hypertension”

Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications,

and the management of congestive heart failure. J Am Diet Assoc. 1995

May;95(5):541-4.

“Thiamin deficiency may occur in a substantial proportion of

patients with congestive heart failure, and dietary inadequacy may contribute

to increased risk”

Shimon I, Almog S, Vered Z, Seligmann H, Shefi M, Peleg E, Rosenthal T, Motro

M, Halkin H, Ezra D. Improved left ventricular function after thiamine

supplementation in patients with congestive heart failure receiving long-term

furosemide therapy. Am J Med. 1995 May;98(5):485-90.

“Thiamine repletion can improve left ventricular function and biochemical

evidence of thiamine deficiency in some patients with moderate-to-severe CHF

who are receiving longterm furosemide therapy”

Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered Z, Ezra

D. Thiamine deficiency in patients with congestive heart failure

receiving long-term furosemide therapy: a pilot study. Am J Med. 1991

Aug;91(2):151-5.

”These preliminary findings suggest that long-term furosemide therapy may

be associated with clinically significant thiamine deficiency due to urinary

loss and contribute to impaired cardiac performance in patients with CHF.

This deficit may be prevented or corrected by appropriate thiamine

supplements”

Relation of thiamine to neurological

disorders

Lonsdale D, Shamberger RJ, Audhya T. Treatment of autism spectrum

children with thiamine tetrahydrofurfuryl disulfide: a pilot study.

Neuroendocrinol Lett. 2002 Aug;23(4):303-8.

“Thiamine tetrahydrofurfuryl disulfide appears to have a beneficial

clinical effect on some autistic children, since 8 of the 10 children improved

clinically”

Nakagawasai O, Tadano T, Hozumi S, Taniguchi R, Tan-No K, Esashi A, Niijima F,

Kisara K. Characteristics of depressive behavior induced by feeding

thiamine-deficient diet in mice.

Life Sci. 2001 Jul 27;69(10):1181-91.

Ambrose ML, Bowden SC, Whelan G. Thiamin treatment and working memory

function of alcohol-dependent people: preliminary findings. Alcohol Clin

Exp Res. 2001 Jan;25(1):112-6.

“A therapeutic relationship between dose and working memory performance

was indicated”

Older MW, Dickerson JW. Thiamine and the elderly orthopaedic

patient. Age Ageing. 1982 May;11(2):101-7.

“In both groups those patients who were noticeably confused after

operation were found to have a considerable fall in their thiamine status

suggesting this may be a contributory factor to postoperative confusion”

Winston AP, son CP, Madira W, Gatward NM, Palmer RL. Prevalence of

thiamin deficiency in anorexia nervosa. Int J Eat Disord. 2000 Dec;28(4):451-4.

“Fourteen patients (38%) had results in the deficient range; 7 (19%) met

the most stringent published criterion for deficiency. Deficiency was not

related to duration of eating restraint, frequency of vomiting, or alcohol

consumption”

Terasawa M, Nakahara T, Tsukada N, Sugawara A, Itokawa Y. The

relationship between thiamine deficiency and performance of a learning task in

rats. Metab Brain Dis. 1999 Sep;14(3):137-48.

“We taught rats to press a lever to escape from the pain of electrical

stimulation by learning to turn a switch off… The rats that were fed the

thiamine-deficient diet showed a slower response time and a longer running time

than the rats fed the normal diet… We found that the thiamine

concentration in the blood of the rats in the trained group was significantly

higher than that in the group without training”

Jimenez-Jimenez FJ, Molina JA, Hernanz A, Fernandez-Vivancos E, de Bustos F,

Barcenilla B, Gomez-Escalonilla C, Zurdo M, Berbel A, Villanueva C.

Cerebrospinal fluid levels of thiamine in patients with Parkinson's

disease. Neurosci Lett. 1999 Aug 13;271(1):33-6.

“These results suggest that low CSF free thiamine levels could be related

with the risk for PD”

Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in

the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med

J. 1997 Dec;74(12):803-8.

“Diabetic peripheral neuropathy in Dar es Salaam is associated with

thiamine deficiency”

Langlais PJ, G, Guo SX, Bondy SC. Increased cerebral free

radical production during thiamine deficiency. Metab Brain Dis. 1997

Jun;12(2):137-43.

“These findings suggest that increased formation of free radicals occurs

during the more acute symptomatic stage of thiamine deficiency and may

contribute to the structural damage described in this model of Wernicke's

encephalopathy”

Easton CJ, Bauer LO. Beneficial effects of thiamine on recognition memory

and P300 in abstinent cocaine-dependent patients. Psychiatry Res. 1997

May 30;70(3):165-74.

“Thiamine was found to significantly improve recognition accuracy

and P300 amplitude, at the midline parietal (Pz) electrode. The improvement was

most reliable under conditions of increased memory load”

Benton D, Griffiths R, Haller J. Thiamine supplementation mood and

cognitive functioning. Psychopharmacology (Berl). 1997 Jan;129(1):66-71.

”An improvement in thiamine status was associated with reports of

being more clearheaded, composed and energetic. The taking of thiamine had no

influence on memory but reaction times were faster following

supplementation”

Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's

disease. Metab Brain Dis. 1996 Mar;11(1):89-94.

”Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100

mg/day had a mild beneficial effect in patients with Alzheimer's disease in a

12-week open trial. The improvement could be observed not only in their

emotional or other mental symptoms but also in intellectual function”

Gold M, Chen MF, K. Plasma and red blood cell thiamine deficiency

in patients with dementia of the Alzheimer's type. Arch Neurol. 1995

Nov;52(11):1081-6.

“A significant proportion of patients with SDAT may have a thiamine

deficiency, which may have an impact on cognitive function. Currently used

assays may not be adequate to assess thiamine status”

Adamolekun B, Eniola A. Thiamine-responsive acute cerebellar ataxia

following febrile illness. Cent Afr J Med. 1993 Feb;39(2):40-1. Review.

“acute thiamine depletion may be the pathogenetic mechanism for post-pyrexial

acute cerebellar ataxia”

Ben-Hur T, Wolff E, River Y. [Thiamin deficiency is common in

Israel] Harefuah. 1992 Nov 15;123(10):382-4, 436, 435. Hebrew.

“Thiamin levels should be determined not only in alcoholics and those

with classic B1 deficiency syndromes, but in the routine workup of patients

with sensory-motor neuropathy, dementia, gait disorders, cerebellar syndromes

and confusional states”

Sacks W, Esser AH, Feitel B, Abbott K. Acetazolamide and thiamine: an

ancillary therapy for chronic mental illness. Psychiatry Res. 1989

Jun;28(3):279-88.

“Overall, 50% of the patients showed improvement on all assessment

scales. No untoward effects occurred in these patients…”

Relation of thiamine and geriatric patients

Smidt LJ, Cremin FM, Grivetti LE, Clifford AJ. Influence of thiamin

supplementation on the health and general well-being of an elderly Irish

population with marginal thiamin deficiency. J Gerontol. 1991

Jan;46(1):M16-22.

”thiamin-supplemented women experienced significantly increased appetite,

energy intake, body weight and general well-being, and decreased fatigue.

Thiamin supplementation also tended to reduce daytime sleep time, improve sleep

patterns, and increase activity. These data suggest that evaluation of thiamin

status is indicated when nonspecific conditions such as anorexia, weight loss,

fatigue, depression, and sleep disorders are present in elderly persons”

Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels in elder

patients admitted through the emergency department. Acad Emerg Med. 2000

Oct;7(10):1156-9.

“CONCLUSIONS: Elder nursing home patients seen in the ED and admitted to

the hospital are frequently thiamine-deficient”

Wilkinson TJ, Hanger HC, Elmslie J, PM, Sainsbury R. The response

to treatment of subclinical thiamine deficiency in the elderly. Am J Clin

Nutr. 1997 Oct;66(4):925-8.

“Only the subjects with persistently low TPP concentrations showed

subjective benefits from treatment with improvements in quality of life…

There was a trend toward benefits in sleep and energy… Quality of life

was enhanced by providing thiamine supplements. Blood pressure and weight were

lower after thiamine supplementation”

Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte thiamin

concentrations in geriatric outpatients. J Am Coll Nutr. 1996

Jun;15(3):231-6.

“CONCLUSION: About 50% of geriatric outpatients in this study had low

plasma thiamin levels”

Nichols HK, Basu TK. Thiamin status of the elderly: dietary intake and

thiamin pyrophosphate response. J Am Coll Nutr. 1994 Feb;13(1):57-61.

“Average daily thiamin intake was above the recommended

requirement… however, almost half of the total study population had TPP

effect > 14%, suggesting thiamin deficiency… CONCLUSION: These

findings raise questions about the reliability of dietary intake in assessing

metabolic availability of thiamin in the elderly”

O'Keeffe ST, Tormey WP, Glasgow R, Lavan JN. Thiamine deficiency in

hospitalized elderly patients. Gerontology. 1994;40(1):18-24.

“Necropsy studies suggest that thiamine deficiency is underdiagnosed in

life… There was no difference in anthropometric indices or in the

prevalence of other nutrient deficiencies between the two groups. Thiamine

deficiency is common in elderly patients admitted to hospital and may

contribute to the development of delirium”

Iber FL, Blass JP, Brin M, Leevy CM. Thiamin in the elderly--relation to

alcoholism and to neurological degenerative disease. Am J Clin Nutr. 1982

Nov;36(5 Suppl):1067-82. Review.

“There is no known toxicity for thiamin”

Relation of thiamine to diabetes

Avena R, Arora S, Carmody BJ, Cosby K, Sidawy AN. Thiamine (Vitamin B1)

protects against glucose- and insulin-mediated proliferation of human

infragenicular arterial smooth muscle cells. Ann Vasc Surg. 2000

Jan;14(1):37-43.

“Vitamin B1 intake may prove important in delaying the atherosclerotic

complications of diabetes”

La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA, Molinatti GM, Porta

M. Thiamine corrects delayed replication and decreases production of

lactate and advanced glycation end-products in bovine retinal and human

umbilical vein endothelial cells cultured under high glucose conditions.

Diabetologia. 1996 Nov;39(11):1263-8.

Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S, Scheinman M,

T. Thiamine reverses hyperglycemia-induced dysfunction in cultured

endothelial cells. Surgery. 2001 Nov;130(5):851-8.

“The data from this study lead to the speculation that thiamine intake

may mitigate or delay vascular complications of diabetes”

Hassan R, Qureshi H, Zuberi SJ. Effect of thiamine on glucose utilization

in hepatic cirrhosis. J Gastroenterol Hepatol. 1991 Jan-Feb;6(1):59-60.

“It is therefore suggested that thiamine supplements be given to

cirrhotics with hyperglycaemia, to improve glucose utilization”

Rindi G, Laforenza U. Thiamine intestinal transport and related issues:

recent aspects.

Proc Soc Exp Biol Med. 2000 Sep;224(4):246-55. Review.

“Thiamine uptake is enhanced by thiamine deficiency, and reduced by

thyroid hormone and diabetes”

Saito N, Kimura M, Kuchiba A, Itokawa Y. Blood thiamine levels in

outpatients with diabetes mellitus. J Nutr Sci Vitaminol (Tokyo). 1987

Dec;33(6):421-30.

“From the above findings it was concluded that diabetic outpatients tend

to have a low blood thiamine level, with low erythrocyte transketolase activity

and high erythrocyte TPP effect, and showed marginal thiamine deficiency”

Relation of thiamine to disease

Wallace AE, Weeks WB. Thiamine treatment of chronic hepatitis B

infection. Am J Gastroenterol. 2001 Mar;96(3):864-8.

”In each case study, thiamine administration was associated with

reduction in aminotransferase levels and the fall of HBV DNA to undetectable

levels… The relationship between thiamine administration and chronic

hepatitis B infection warrants further study. If proven effective in reducing

liver damage or inducing remission of the hepatitis B virus in larger trials,

thiamine will offer obvious advantages over the current treatments for chronic

viral hepatitis B infection”

Rossouw JE, Labadarios D, Krasner N, M, R. Red blood cell

transketolase activity and the effect of thiamine supplementation in patients

with chronic liver disease. Scand J Gastroenterol. 1978;13(2):133-8.

“Biochemical evidence of thiamine deficiency was found in 58% of patients

with chronic liver disease… high doses of thiamine should be included in

the routine nutritional management of patients with severe chronic liver

disease”

Shoji S, Furuishi K, Misumi S, Miyazaki T, Kino M, Yamataka K. Thiamine

disulfide as a potent inhibitor of human immunodeficiency virus (type-1)

production. Biochem Biophys Res Commun. 1994 Nov 30;205(1):967-75.

” The results suggest that thiamine disulfide may be important for AIDS

chemotherapy”

Shoji S, Furuishi K, Ogata A, Yamataka K, Tachibana K, Mukai R, Uda A, Harano

K, Matsushita S, Misumi S. An allosteric drug, o,o'-bismyristoyl thiamine

disulfide, suppresses HIV-1 replication through prevention of nuclear

translocation of both HIV-1 Tat and NF-kappa B. Biochem Biophys Res

Commun. 1998 Aug 28;249(3):745-53.

Butterworth RF, Gaudreau C, Vincelette J, Bourgault AM, Lamothe F, Nutini

AM. Thiamine deficiency and Wernicke's encephalopathy in AIDS.

Metab Brain Dis. 1991 Dec;6(4):207-12.

“we now report biochemical evidence of thiamine deficiency in 9/39 (23%)

of patients with AIDS or AIDS-related complex. In no cases was there history of

alcohol abuse… it is recommended that dietary thiamine supplementation be

initiated in all newly diagnosed cases of AIDS or AIDS-related complex”

Haisraeli-Shalish M, Livneh A, Katz J, Doolman R, Sela BA. Recurrent

aphthous stomatitis and thiamine deficiency. Oral Surg Oral Med Oral

Pathol Oral Radiol Endod. 1996 Dec;82(6):634-6.

” 70 patients with recurrent aphthous stomatitis and in 50 members of a

control group… Low levels of vitamin B1 were detected in 49 patients but

in only two members of the control group… Our finding suggests an

association between thiamine deficiency and recurrent aphthous stomatitis”

Engel D. Tropical pyomyositis, a thiamine-deficiency disease. Med

Hypotheses. 1981 Mar;7(3):345-52.

“it is suggested that thiamine deficiency is an essential contributary

factor in producing tropical pyomyositis… Thiamine deficiency induces a biochemical

lesion (s) in the pyruvate oxidase system of the muscle, which breaks down

its normal resistance to infection and opens the gate to bacterial

agents”

Krishna S, AM, Supanaranond W, Pukrittayakamee S, ter Kuile F, Tawfiq

KM, Holloway PA, White NJ. Thiamine deficiency and malaria in adults from

southeast Asia. Lancet. 1999 Feb 13;353(9152):546-9.

”12 (52%) of 23 patients with severe malaria and ten (19%) of 54 patients

with uncomplicated malaria had alpha values above the normal range (p<0.0001

and p=0.0014, respectively, compared with controls), which indicated severe

thiamine deficiency”

Pietrzak I, Baczyk K, Mlynarczyk M, Kaczmarek M. [Content of

thiamin in plasma and erythrocytes in patients with end stage renal

disease] Przegl Lek. 1996;53(5):423-6. Polish.

”We suggest the need of thiamine supplementation in ESRD patients

especially in those treated by dialysis. The supplementation of thiamine is

needed particularly in patients on peritoneal dialysis”

Relation of thiamine to other data

Hung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine

deficiency and unexplained encephalopathy in hemodialysis and peritoneal

dialysis patients. Am J Kidney Dis. 2001 Nov;38(5):941-7.

“We conclude that in regular dialysis patients, unexplained

encephalopathy can be mainly attributed to thiamine deficiency”

Huang S, Ren G. [Thiamine status of university teacher families in

Changsha] Hunan Yi Ke Da Xue Xue Bao. 1998;23(1):27-30. Chinese.

“We conclude that those people who take the refined cereals and its

products as a staple food, is in the risk of thiamine deficiency”

Suzuki M, Itokawa Y. Effects of thiamine supplementation on

exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106.

“High-dose thiamine (vitamin B1) supplementation (100 mg/day) may be

helpful in preventing or accelerating recovery from exercise-induced

fatigue… Thiamine supplementation significantly suppressed the increase

in blood glucose in the normal thiamine group and significantly decreased the

number of complaints shortly after exercise in the subjective fatigue

assessment of 30 items”

Kimura M, Itokawa Y, Fujiwara M. Cooking losses of thiamin in food and

its nutritional significance. J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl

1:S17-24.

”The thiamin contents in cooked daily meals were 50-60 percent of the

calculated values on an average”

Cruickshank AM, Telfer AB, Shenkin A. Thiamine deficiency in the

critically ill. Intensive Care Med. 1988;14(4):384-7.

“We performed a retrospective study on 158 patients admitted to the

Intensive Care Unit who required nutritional support. Patients who survived had

significantly higher body thiamine status than those who died”

Onodera K, Kisara K, Okabe H, Ogura Y. [studies on the effects of

thiamine deficiency on rat testes (author's transl)] Nippon Yakurigaku

Zasshi. 1980 Mar;76(2):143-52. Japanese.

“In the thiamine deficient group, the seminiferous tubuli of rats having

erections had atrophied”

Labadarios D, Rossouw JE, McConnell JB, M, R. Thiamine

deficiency in fulminant hepatic failure and effects of supplementation.

Int J Vitam Nutr Res. 1977;47(1):17-22.

“Nine out of 24 patients with acute hepatocellular necrosis leading to

fulminant hepatic failure showed biochemical evidence of thiamine deficiency

early in the course of their illness”

Why haven’t we heard of benfo before? The patent on the manufacture

of benfo expired decades ago. Pharmaceutical companies pursue drugs that

can be patented so they can have a monopoly and charge 100 times what the drug

is worth. They have spent a lot of money on AGE inhibitors that

don’t work as well as benfo. Ingestion of benfo may result in the

elimination of AGE-protein crosslinks, which are a major constituent of

arterial plaque. I am intrigued by the idea that benfo may cause the removal of

plaque from the blood vessels, but I am concerned about the rapid manner in

which it may cause the removal of plaque from the blood vessels. If the

plaque is being removed, a large chunk might break off and cause a stroke or

heart attack. If I was older than 60 or if I had a serious problem with high

blood pressure I would probably start out by taking very low doses of benfo and

gradually increase my dosage. Of course, there are no reports of strokes

or heart attacks from benfo in the medical literature, but it’s a thought

to consider.

My PhD research will mostly consist of double-blind controlled studies on the

administration of benfo in normal individuals, diabetics, individuals with high

blood pressure, Alzheimer patients etc. I believe the researchers who

have investigated benfo to date have been extremely short sighted by not

discovering they full potential of benfo in the clinical studies that have

already been performed on humans.

It is illegal to make claims about benfo and sell it as a dietary supplement

unless the claims are based on substantial scientific evidence. The three

case studies outlined in this document are not from a double-blind controlled

study and FDA regulations would not allow for them to be referred to as

substantial scientific evidence. Claims should not be made based on these

preliminary findings.

For questions or comments email robholladay99@...

Since I am not a physician, it would be inappropriate for me to answer emails

asking for medical advice.

SECURALL, INC.

The Difference is

'ALARMING'

602-7582283

602-2965003 fax

[Guest guest]

, it is the Benfotiamine form that I'm taking.

----- Original Message -----

From: Baden

low dose naltrexone

Sent: Thursday, March 25, 2004 2:48 PM

Subject: RE: [low dose naltrexone] Fw: check this out!

,

I’m thrilled to read your taking 600mg twice a day and it’s helping. When I read the article, he suggests that oral cannot be ingested properly. That an injection in the muscle is the way to go. . . . oooch. I’m going to try oral B1 at those levels to see what happens.

(MS)

-----Original Message-----From: [mailto:jatrac1@...] Sent: Wednesday, March 24, 2004 8:48 PMlow dose naltrexone Subject: Re: [low dose naltrexone] Fw: check this out!

I started on this B1 night before last. I've been whining about this long drawn out virus I've been fighting, and either the B1 is helping mucho over the last two days, or I'm suddenly getting stronger anyway. I feel lots more energy, and my legs are finally getting some strength back. It's so hard to tell if it is the Benfotiamine or just my body finally winning. Who knows. I do know I've seen no side effects even though I've been taking 600mg twice a day. After a few days more I'll cut that in half... No digestive upsets, no headaches, just a positive feeling about life in general.

(MS)

----- Original Message -----

From: ruben/kathy lintzenich

low dose naltrexone

Sent: Tuesday, March 23, 2004 7:26 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

Tom, thanks for the great article. I will be starting this form of B1 when I finish my bottle of thiamine. Will keep everyone posted on any benefits I receive. Are you taking this form of B1 and did you find out about it through the Brewer Science Library? White is the educatuional cordinater at the library and publishes a quarterly newslettet. She is a wonderful source of info about ms and other dis-eases in the body. Best Wishes, Kathy

----- Original Message -----

From: tmbayuk

msalternatives ; MSersLife ; MS-Christians ; MSfriends ; MSViews_Multiple_Sclerosis ; low dose naltrexone ; JJUK ; mscured

Sent: Monday, March 22, 2004 10:50 AM

Subject: [low dose naltrexone] Fw: check this out!

----- Original Message -----

From:

tmbayuk

Sent: Saturday, March 20, 2004 11:01 PM

Subject: check this out!

Research on Benfotiamine Clinton Holladay, M.S.Copyright 2003 Clinton HolladayJune 5, 2003

A short while ago a group of individuals I know purchased a large amount of benfotiamine and began ingesting it orally. I was urged by these individuals to place some of the research I have been conducting on benfo (benfotiamine) online along with the results of their benfo use. I was asked to do this in a manner that would allow individuals that do not have a background in the health sciences to comprehend it. I will be pursuing a PhD shortly and benfo will be central to my research. I am not a physician and the following information is not intended to be used as medical advice. Advanced glycation endproducts or AGEs are produced by the processing of sugars within the cell. They are one of the primary causes of aging and general wear and tear on your cells. Diabetics age the same way as normal people, but because they often have abnormal levels of sugars in their cells, they age faster. When blood sugar levels are high, certain cells in the body are flooded with glucose, particularly neurons and cells in the eyes and kidneys. Diabetics often suffer from nerve damage, kidney failure, and premature blindness. Numerous researchers have concentrated their efforts on AGE-blocking mechanisms because they would limit the wear and tear on the body’s cells and allow individuals to live longer and healthier, particularly diabetics. Benfo has emerged as the premier AGE inhibitor.Case StudiesIt is important to note that the following case studies are not double-blind controlled studies. Case study #1. Female, early fifties, non-diabetic, suffers from chronic fatigue, depression, and the normal aches and pains that accompany middle age. Her diet is average. She is able to do about two hours of physical labor a day, and she has suffered from depression for years. She has tried numerous treatments for depression including Prozac, and some of them have helped, but none have completely eliminated the depression. Sometimes she aches all over. She was addicted to caffeine for several years, but only consumes it about once a week now. She has high blood pressure, and treats it with Vasotec and also takes Maxide (a diuretic).She ingested 650 mg of benfo once a day for five days and did not notice any difference. On day 6 she doubled the dose to 1300 mg and started to notice a change a few hours later. There was a dramatic increase in stamina and energy. She is now able to do eight hours of physical work each day. She has an extremely heightened sense of well-being and all aspects of the depression have left. She has better clarity of thought, and sleeps better. Previously she would usually wake up two or three times a night. Now she sleeps through the whole night and has said she is in a deeper sleep at night. She has reported being able to control her appetite more. She has reported less shortness of breath. On day 13 she has had no weight change. On day 13 she experienced what felt exactly like a caffeine withdrawal headache. She immediately consumed two cans of mountain dew and the headache did not leave. Previous to this, caffeine had always relieved a headache of this sort for her. At day 14 she still had a headache and the tips of her toes started tingling. She reduced her dose to 650 mg per day once a day on day 14. On day 15 she still had a headache. On day 16 her toes started tingling and the headache left. On day 17 her pinkie started tingling. Her blood pressure has always fluctuated between 120/80 and 150/90. Throughout the treatment her blood pressure has fluctuated like it normally does. She says she feels like she did when she was thirty years old. Comment: The tingling is likely the cause of blood circulating to parts of her body that have not had a great deal of circulation in recent years.Case study #2. Male, mid fifties, non-diabetic. Average diet. Overall health is better than average for his age. He gets indigestion at night and takes Prilosec. He has the normal aches and pains that accompany middle age. When he wakes up in the morning his feet are inflexible, but that would go away after walking on them for about two minutes. After driving for two hours he is stiff when he gets out of his car. Most of the aches and pains and the foot inflexibility appeared in the last five to fifteen years. He began taking 650 mg of benfo once a day. On day 3 nothing hurt when he woke up. By day five all his aches and pains had disappeared. He is no longer stiff when he gets out of his car after driving for two hours. He feels more flexible. He says it has fixed everything that has gone wrong with him in the past fifteen years. He says he feels more cheerful but is not sure if it is because of repair to neurological damage or because his aches and pains are gone. He has reported a greater clarity of thought. He says he feels like he did when he was age 25-40 (he says he felt the same during those years). Up until twelve months ago his blood pressure has been 120/90. For the past twelve months it has averaged 130/120. On day 5 his blood pressure was 120/85 and it has remained consistent every day since then. Now he can only take a fifteen minute nap during the day whereas before he could fall asleep for hours. At night he sleeps better, probably because the aches and pains are gone. His appetite is only about 80% of what it used to be. He has reported increased stamina and energy. Before taking benfo it was getting hard for him to do ten hours of work per day. Now he can do fourteen hours of work per day. He still requires the same amount of sleep at night, but if he does not get his full requirement he doesn’t notice it nearly as much.Comment: The decrease in caloric intake may be because he was lacking an essential nutrient- not enough thiamine? The stiffening of the joints brought on by old age is partly a symptom poor blood circulation. The fact that this individual has become much more flexible is a possible indication of increased circulation.Case study #3. Male, late forties. He has been a type 1 diabetic for twenty years. Average diet. Over the last five years his health has declined more rapidly. He has more aches and pains than the average person because he is diabetic. He aches so much at night that he usually can’t get to sleep unless he takes Ibuprofen. He began taking 650 mg benfo once a day. On day 2 he noticed a decline in the severity of his aches and pains. He still needs the same amount of sleep, but if he doesn’t get his full requirement he doesn’t notice nearly as much. He has had an increase in stamina and energy. He says his stamina has doubled. On day 14 he felt like he did ten years ago, and it keeps improving each day. He is more cheerful, but like #2 he can’t tell if it’s because his aches and pains are gone or if benfo has a neurological effect on him. I will not disclose the brand of benfo which was used because I do not wish to be seen as promoting any particular brand. These case studies will be updated on July 5, 2003 and new ones will be added. The updates will be posted on www.geocities.com/robholladay99/updates.html The following exerpts are from medical journals. The abstracts (summaries) for most of them can be viewed online through the pubmed database, which is a free database most biomedical scientists use. To find pubmed, go to google.com and type in pubmed. Once you’re in pubmed, type in part of the title and you should be able to find the abstract. When typing in the title use "benfotiamine" not "benfo". As an anti-spamming measure, many search engines will not index web pages that list the key search words more than seven times throughout the document, hence this document was modified after it was created . Several things are important to note in the following literature. First of all, not only does benfo stop some effects of aging, it reverses them. Gradually over time people’s neurons quit working because of normal wear and tear. However, when benfo was ingested, not only did the nerve damage stop, some of the damage done through aging was repaired. A strong point is made that benfo is the most bioavailable source of thiamine. This means benfo is better absorbed than other sources of thiamine. Also, high levels of thiamine have analgesic (pain-relieving) effects on animals. In the Russian study the pain level of the patients decreased from 8.2 to 2.3, a decrease of about four hundred percent. Research articles on benfoWada T, Tagaki H, Minakami H, Hamanka W, Okamoto K, Ito, A, Sahashi Y. 1961. A new thiamine derivative, S-benzoylthiamine O-monophosphate. Science 134: 195-196.Benfo “is more easily absorbed in the body than thiamine hydrochloride, and administration results in higher thiamine and cocarboxylase levels in organs; moreover, these levels last for a longer period of time…It does not cause any unfavorable symptom in animals such as thiamine hydrochloride does…The LD50 by oral administration in mice, dd-strain hybrid, weighing 14 to 16g was 15g/kg of body weight”Bitsch R, Wolf M, Moller J, Heuzeroth L, Gruneklee D. Bioavailability assessment of the lipophilic benfo as compared to a water-soluble thiamin derivative. Ann Nutr Metab. 1991;35(5):292-6. “in presence of allicin, the active principle of garlic, the water-soluble thiamin hydrochloride is transformed into a lipid-soluble compound being identified as allithiamine…Ten healthy young men…The volunteers ingested a single dose of 40 mg benfo…Thus, the measured values reveal, when compared with mononitrate, a clearly improved thiamin bioavailability from benfo, due to the more lipophilic properties of this substance or possibly its dephosphorylated metabolite and a more rapid transformation into the physiologically active derivative. This may be of great advantage in the treatment of neurological disorders responding to high thiamin doses and further on in situations when the active intestinal absorbtion mechanisms are impaired”Stracke H, Lindemann A, Federlin K. A benfo-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.“Benfo…was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold...Therapy-specific adverse effects were not seen”Loew D. Pharmacokinetics of thiamine derivatives especially of benfo. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.“The effective form of thiamine, thiamine diphosphate, is an organic compound needed by the organism for vital functions…Due to this peculiarity the conditions for absorbtion of lipid-soluble vitamins differ from those for water-soluble thiamine derivatives. Unlike the latter, allithiamines are absorbed passively, they traverse the intestinal absorption barrier faster and more readily, leading to higher blood and tissue concentrations even when comparatively low doses are given…It therefore fulfills important pharmacodynamic conditions for rational therapy. Due to their greater biovailability and better tissue passage lipid-soluble thiamine analogues like benfo are preferable to water-soluble thiamine derivatives for treatment of various pathological conditions, e.g. cardiomyopathy, Werincke-Korsakow syndrome, and alcoholic or diabetic polyneuropathies…Due to its excellent pharmacokinetic profile and to its excellent tolerability benfo should be preferred in treatment of relevant conditions like neuropathies”Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter CH. Comparative bioavailability of two vitamin B1 preparations: benfo and thiamine mononitrate. Eur J Clin Pharmacol. 1997;52(4):319-20.“a study using equimolar quantities of the two preparations for exact comparison of the bioavailability of benfo and thiamine mononitrate has never been performed. Therfore, the present trial was undertaken…the higher thiamine content in the erythrocytes and the higher thiamine excretion in urine after oral benfo administration are proof of the considerably higher relative bioavailability of benfo than thiamine mononitrate”Simeonov S, Pavlova M, Mitkov M, Mincheva L, Troev D. Therapeutic efficacy of "Milgamma" in patients with painful diabetic neuropathy. Folia Med (Plovdiv). 1997;39(4):5-10.“Forty-Five diabetes patients with painful peripheral polyneuropathy were enrolled in a 3-month observational study comparing the therapeutic efficiacy of Milgamma tablets (benfo)…Statistically significant relief of both background and peak neuropathic pain was achieved in all of the Milgamma-treated patients…No adverse reactions were observed…Our results underscore the importance of Milgamma tablets as an indispensable element in the therapeutic regimen of patients with painful diabetic polyneuropathy”Greb A, Bitsch R. Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther. 1998 Apr;36(4):216-21.“Seven healthy volunteers…a single oral dose of either benfo…fursultiamin…thiaminedisulfide…In this study the allithiamine derivative benfo proved the best bioavailability. Owing to its excellent absorption properties it can be concluded that oral administration of benfo is suitable for therapeutical purposes”Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfo in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.Good review, full-text is available free online. “In bioavailability studies on healthy human subjects, it was shown that absorption of benfo was several times better than that of water-soluble vitamin B1 and that there was a 120-fold higher increase of metabolically active thiamine diphosphate in erythrocytes (Heinrich, 1990)…In animals given dosages that exceeded basic requirements by 100- or 1000-fold thiamine has analgesic and neuroprotective effects(woelk and peeler-Ichakawa, 1985; Jurna, 1988; Reeh, 1988, 1991; Wild, 1988). However, if high levels are to be achieved with oral vitamin B1 treatment, lipid soluble thiamine derivatives or pro-drugs with high bioavailability, such as benfo, are required…320 mg/day during weeks 1 to 4 and 120 mg benfo/day during weeks 5 to 8…Within the 8-week study period, benfo led to a significant improvement of the threshold of vibration perception at the great toe, motor function, and the overall symptom score. Marked improvement occurred in both pain and co-ordination”Sadekov RA, Danilov AB, Vein AM. [Diabetic polyneuropathy treatment by milgamma-100 preparation] Zh Nevrol Psikhiatr Im S S Korsakova. 1998;98(9):30-2. Russian.“benfo…was studied in treatment of diabetic polyneuropathy in 14 patients…After the course of treatment the intensity of pains was decreased according to visual analogous scale on the average from 8.2 to 2.3 scores, the indices of vibratory sensitivity improved significantly as well as the data of cardiovascular tests…The treatment resulted in the improvement of the condition in 93% of the cases” T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine pharmacokinetics by end-stage renal disease (ESRD). Int J Clin Pharmacol Ther. 1999 Sep;37(9):449-55.“20 end-stage renal disease(ESRD) patients…After a single oral dose of 100 mg benfo…ESRD patients may benefit from high-dose thiamine derivatives notwithstanding their chemical form. However, the better absorption and high transfer rate of debenzoylated BTMP (benfo) to TDP (thiamine diphosphate) even at much lower doses compensates for reduced renal excretion and may protect, therefore, against numerous adverse effects of uremia”Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different benfo dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.320, 120, and 150 mg benfo/day was administered to “diabetic patients suffering from painful peripheral diabetic neuropathy. In a 6-week open clinical trial, 36 patients…An overall beneficial therapeutic effect on the neuropathy status was observed in all three groups during the study…The greatest change occurred in the group of patients receiving the high dose of benfo…Metabolic control did not change over the study...Extremely interesting is the result of recent in vitro experiences that thiamine pyrophosphate and pyroxidine inhibit the formation of glycation end products" T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfo. Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.“20 end-stage renal disease (ESRD) patients…After benfo administration, the peak plasma concentration of TDP exceeded that in healthy subjects by 51%...Compared with thiamine nitrate, the oral administration of benfo leads to higher TDP concentrations in erythrocytes accompanied with a significant improvement of the erythrocyte transkelotase activity in ESRD patients”Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M. Benfo is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.“We investigated the hypothesis that benfo, a lipophilic derivative of thiamine, affects replication delay and generation of advanced glycosylation endproducts (AGE) in human umbilical vein endothelial cells cultured in the presence of high glucose…Benfo, a derivative of thiamine with better bioavailability, corrects defective replication and increased AGE generation in endothelial cells cultured in high glucose, to a similar extent as thiamine. These effects may result from normalization of accelerated glycolysis and the consequent decrease in metabolites that are extremely active in generating nonenzymatic protein glycation. The potential role of thiamine administration in the prevention or treatment of vascular complications of diabetes deserves further investigation”Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M, Geyer J, Kopcke W, Sauerland C, Bretzel RG, Federlin KF. Efficacy of benfo versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.“After three months preventative administration of both vitamin B1 preparations NCV (nerve conduction velocity) had increased substantially…It was nearly normal after six months with benfo, while the administration of thiamine nitrate resulted in no further amelioration. NCV was nearly normalized after six months of benfo application but not with thiamine. Furthermore, benfo induced a major inhibition of neural imidazole-type AGE formation and completely prevented diabetes induced glycoxidation products”Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M. Benfo blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.“Our results in both endothelial cells cultured for several days and retinas from rats with nine months of diabetes showed that benfo, a lipid-soluble thiamine derivative, prevents activation of three major pathways involved in hyperglycemia-induced vascular damage: the hexosamine pathway, the intracellular AGE formation pathway and the DAG-PKC pathway…We showed that benfo blocks these pathways of hyperglycemic damage by increasing the activity of transketolase…Administration of benfo for nine months also completely prevented the development of experimental diabetic retinopathy in rats...Thus we conclude that augmentation of transketolase activity is solely responsible for the observed effects of benfo”Comment: This study is very significant because it demonstrates how benfo blocks several other aging mechanisms besides AGE formation. However, I am not yet convinced of the statement that transketolase activity is solely responsible for the observed effects of benfo. The following four studies are located on the Internet but are not yet listed on Medline. To find them, go to google.com and type in part of the titleBergfeld R, Matsumara X. Du, Brownlee M. Benfo prevents the consequences of hyperglycemia-induced mitochondrial overproduction of reactive oxygen species, and experimental diabetic retinopathy.“diabetic rats were treated with benfo (80 mg/kg weight) for 36 weeks…Benfo decreases AGE formation by 60%...These data suggest that treatment with benfo may be an effective approach to prevent the development of diabetic complications”Lin J, Alt A, Liersch J, Bretzel R, Brownlee M, Hammes H. Benfo inhibits intracellular formation of advanced glycation end products in vivo“Here, we studied the effect of benfo, a lipid-soluble thiamine derivative with known AGE-inhibiting properties in vitro on the intracellular formation of (CML) and methylgloxal-derived AGE in red blood cells. Blood was collected from 6 type 1 diabetic patients before and after treatment with 600 mg/day benfo for 28 days…Thiamine derivatives, in particular the lipid-soluble prodrug benfo, are effective inhibitors of intracellular formation of AGE and CML”Stracke H, Werkmann D, Mavrakis K, Federlin K, Kopke W, Sauerland C, Hammes H, Bretzel RG. Influence of vitamin B1 on diabetic neuropathy-studies in streptozotocin-diabetic rats.“we investigated the effects of oral administration of thiamine and benfo on the development of glucose oxidation products in the nerve and on nerve conduction velocity in streptozotocin-diabetic rats…Conclusion: Early treatment with benfo normalizes increased cellular oxidative stress and the reduced nerve conduction velocity”Hammes H, Bretzel, R.G., Federlin, K, Horiuchi S, Niwa T, Stracke H. Benfo inhibits the formation of advanced glycation end products in diabetic rats.“benfo (100 mg/kg x day) and thiamin (70.18 mg/kg x day) administered orally for 6 months…neither benfo nor thiamin treatment affected metabolic control…Benfo administration in diabetic rats induced a major inhibition of neutral imidazolone-type AGE formation and completely prevented diabetes-induced glycoxidation formation. Treatment with thiamin did not affect AGE or CML levels”ThiamineAllithiamines are lipid-soluble sources of thiamine. Benfo is an allithiamine. Thiamine is water-soluble and is also known as vitamin B1.After reviewing the relevant medical literature on thiamine, I have come to conclude that large portions of the population may be thiamine deficient. In addition, many individuals that are not technically thiamine deficient would likely receive benefit from thiamine supplementation. Thiamine deficiency is associated with numerous undesirable medical conditions.Relation of thiamine to heart diseaseShamir R, Dagan O, Abramovitch D, Abramovitch T, Vidne BA, Dinari G. Thiamine deficiency in children with congenital heart disease before and after corrective surgery. JPEN J Parenter Enteral Nutr. 2000 May-Jun;24(3):154-8.Thiamine deficiency “is common in children with congenital heart disease (CHD) referred for corrective surgery both before and after surgery. Our results suggest that neither diuretic treatment nor malnutrition can fully explain the development of TD in these children”Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E, Levy R. [Right heart failure caused by thiamine deficiency (cardiac beriberi)] Presse Med. 2000 Feb 12;29(5):240-1. French.Beaud C, Fuhrman C, Perchet H, Monnet I, Chouaid C, Housset B. [Thiamine deficiency. A cause of cardiac insufficiency not to be ignored] Rev Mal Respir. 1998 Jun;15(3):303-4. French.“Thiamine deficiency is one of the classical causes of high output for heart failure”Okura H, Gohma I, Hatta K, Imanaka T. Thiamine deficiency and pulmonary hypertension in Crow-Fukase syndrome. Intern Med. 1995 Jul;34(7):674-5. “After oral administration of prednisolone and thiamine, echocardiogram showed marked improvement of the pulmonary hypertension”Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc. 1995 May;95(5):541-4. “Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk”Shimon I, Almog S, Vered Z, Seligmann H, Shefi M, Peleg E, Rosenthal T, Motro M, Halkin H, Ezra D. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med. 1995 May;98(5):485-90.“Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy”Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered Z, Ezra D. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med. 1991 Aug;91(2):151-5.”These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements”Relation of thiamine to neurological disordersLonsdale D, Shamberger RJ, Audhya T. Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: a pilot study. Neuroendocrinol Lett. 2002 Aug;23(4):303-8.“Thiamine tetrahydrofurfuryl disulfide appears to have a beneficial clinical effect on some autistic children, since 8 of the 10 children improved clinically”Nakagawasai O, Tadano T, Hozumi S, Taniguchi R, Tan-No K, Esashi A, Niijima F, Kisara K. Characteristics of depressive behavior induced by feeding thiamine-deficient diet in mice.Life Sci. 2001 Jul 27;69(10):1181-91.Ambrose ML, Bowden SC, Whelan G. Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings. Alcohol Clin Exp Res. 2001 Jan;25(1):112-6.“A therapeutic relationship between dose and working memory performance was indicated”Older MW, Dickerson JW. Thiamine and the elderly orthopaedic patient. Age Ageing. 1982 May;11(2):101-7.“In both groups those patients who were noticeably confused after operation were found to have a considerable fall in their thiamine status suggesting this may be a contributory factor to postoperative confusion”Winston AP, son CP, Madira W, Gatward NM, Palmer RL. Prevalence of thiamin deficiency in anorexia nervosa. Int J Eat Disord. 2000 Dec;28(4):451-4.“Fourteen patients (38%) had results in the deficient range; 7 (19%) met the most stringent published criterion for deficiency. Deficiency was not related to duration of eating restraint, frequency of vomiting, or alcohol consumption”Terasawa M, Nakahara T, Tsukada N, Sugawara A, Itokawa Y. The relationship between thiamine deficiency and performance of a learning task in rats. Metab Brain Dis. 1999 Sep;14(3):137-48.“We taught rats to press a lever to escape from the pain of electrical stimulation by learning to turn a switch off… The rats that were fed the thiamine-deficient diet showed a slower response time and a longer running time than the rats fed the normal diet… We found that the thiamine concentration in the blood of the rats in the trained group was significantly higher than that in the group without training”Jimenez-Jimenez FJ, Molina JA, Hernanz A, Fernandez-Vivancos E, de Bustos F, Barcenilla B, Gomez-Escalonilla C, Zurdo M, Berbel A, Villanueva C. Cerebrospinal fluid levels of thiamine in patients with Parkinson's disease. Neurosci Lett. 1999 Aug 13;271(1):33-6.“These results suggest that low CSF free thiamine levels could be related with the risk for PD”Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J. 1997 Dec;74(12):803-8.“Diabetic peripheral neuropathy in Dar es Salaam is associated with thiamine deficiency”Langlais PJ, G, Guo SX, Bondy SC. Increased cerebral free radical production during thiamine deficiency. Metab Brain Dis. 1997 Jun;12(2):137-43.“These findings suggest that increased formation of free radicals occurs during the more acute symptomatic stage of thiamine deficiency and may contribute to the structural damage described in this model of Wernicke's encephalopathy”Easton CJ, Bauer LO. Beneficial effects of thiamine on recognition memory and P300 in abstinent cocaine-dependent patients. Psychiatry Res. 1997 May 30;70(3):165-74. “Thiamine was found to significantly improve recognition accuracy and P300 amplitude, at the midline parietal (Pz) electrode. The improvement was most reliable under conditions of increased memory load”Benton D, Griffiths R, Haller J. Thiamine supplementation mood and cognitive functioning. Psychopharmacology (Berl). 1997 Jan;129(1):66-71. ”An improvement in thiamine status was associated with reports of being more clearheaded, composed and energetic. The taking of thiamine had no influence on memory but reaction times were faster following supplementation”Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's disease. Metab Brain Dis. 1996 Mar;11(1):89-94.”Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100 mg/day had a mild beneficial effect in patients with Alzheimer's disease in a 12-week open trial. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function”Gold M, Chen MF, K. Plasma and red blood cell thiamine deficiency in patients with dementia of the Alzheimer's type. Arch Neurol. 1995 Nov;52(11):1081-6.“A significant proportion of patients with SDAT may have a thiamine deficiency, which may have an impact on cognitive function. Currently used assays may not be adequate to assess thiamine status”Adamolekun B, Eniola A. Thiamine-responsive acute cerebellar ataxia following febrile illness. Cent Afr J Med. 1993 Feb;39(2):40-1. Review.“acute thiamine depletion may be the pathogenetic mechanism for post-pyrexial acute cerebellar ataxia”Ben-Hur T, Wolff E, River Y. [Thiamin deficiency is common in Israel] Harefuah. 1992 Nov 15;123(10):382-4, 436, 435. Hebrew.“Thiamin levels should be determined not only in alcoholics and those with classic B1 deficiency syndromes, but in the routine workup of patients with sensory-motor neuropathy, dementia, gait disorders, cerebellar syndromes and confusional states”Sacks W, Esser AH, Feitel B, Abbott K. Acetazolamide and thiamine: an ancillary therapy for chronic mental illness. Psychiatry Res. 1989 Jun;28(3):279-88.“Overall, 50% of the patients showed improvement on all assessment scales. No untoward effects occurred in these patients…”Relation of thiamine and geriatric patientsSmidt LJ, Cremin FM, Grivetti LE, Clifford AJ. Influence of thiamin supplementation on the health and general well-being of an elderly Irish population with marginal thiamin deficiency. J Gerontol. 1991 Jan;46(1):M16-22.”thiamin-supplemented women experienced significantly increased appetite, energy intake, body weight and general well-being, and decreased fatigue. Thiamin supplementation also tended to reduce daytime sleep time, improve sleep patterns, and increase activity. These data suggest that evaluation of thiamin status is indicated when nonspecific conditions such as anorexia, weight loss, fatigue, depression, and sleep disorders are present in elderly persons”Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels in elder patients admitted through the emergency department. Acad Emerg Med. 2000 Oct;7(10):1156-9.“CONCLUSIONS: Elder nursing home patients seen in the ED and admitted to the hospital are frequently thiamine-deficient”Wilkinson TJ, Hanger HC, Elmslie J, PM, Sainsbury R. The response to treatment of subclinical thiamine deficiency in the elderly. Am J Clin Nutr. 1997 Oct;66(4):925-8.“Only the subjects with persistently low TPP concentrations showed subjective benefits from treatment with improvements in quality of life… There was a trend toward benefits in sleep and energy… Quality of life was enhanced by providing thiamine supplements. Blood pressure and weight were lower after thiamine supplementation”Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte thiamin concentrations in geriatric outpatients. J Am Coll Nutr. 1996 Jun;15(3):231-6.“CONCLUSION: About 50% of geriatric outpatients in this study had low plasma thiamin levels”Nichols HK, Basu TK. Thiamin status of the elderly: dietary intake and thiamin pyrophosphate response. J Am Coll Nutr. 1994 Feb;13(1):57-61.“Average daily thiamin intake was above the recommended requirement… however, almost half of the total study population had TPP effect > 14%, suggesting thiamin deficiency… CONCLUSION: These findings raise questions about the reliability of dietary intake in assessing metabolic availability of thiamin in the elderly”O'Keeffe ST, Tormey WP, Glasgow R, Lavan JN. Thiamine deficiency in hospitalized elderly patients. Gerontology. 1994;40(1):18-24.“Necropsy studies suggest that thiamine deficiency is underdiagnosed in life… There was no difference in anthropometric indices or in the prevalence of other nutrient deficiencies between the two groups. Thiamine deficiency is common in elderly patients admitted to hospital and may contribute to the development of delirium”Iber FL, Blass JP, Brin M, Leevy CM. Thiamin in the elderly--relation to alcoholism and to neurological degenerative disease. Am J Clin Nutr. 1982 Nov;36(5 Suppl):1067-82. Review.“There is no known toxicity for thiamin”Relation of thiamine to diabetesAvena R, Arora S, Carmody BJ, Cosby K, Sidawy AN. Thiamine (Vitamin B1) protects against glucose- and insulin-mediated proliferation of human infragenicular arterial smooth muscle cells. Ann Vasc Surg. 2000 Jan;14(1):37-43.“Vitamin B1 intake may prove important in delaying the atherosclerotic complications of diabetes”La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA, Molinatti GM, Porta M. Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions. Diabetologia. 1996 Nov;39(11):1263-8.Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S, Scheinman M, T. Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells. Surgery. 2001 Nov;130(5):851-8.“The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes”Hassan R, Qureshi H, Zuberi SJ. Effect of thiamine on glucose utilization in hepatic cirrhosis. J Gastroenterol Hepatol. 1991 Jan-Feb;6(1):59-60.“It is therefore suggested that thiamine supplements be given to cirrhotics with hyperglycaemia, to improve glucose utilization”Rindi G, Laforenza U. Thiamine intestinal transport and related issues: recent aspects.Proc Soc Exp Biol Med. 2000 Sep;224(4):246-55. Review.“Thiamine uptake is enhanced by thiamine deficiency, and reduced by thyroid hormone and diabetes”Saito N, Kimura M, Kuchiba A, Itokawa Y. Blood thiamine levels in outpatients with diabetes mellitus. J Nutr Sci Vitaminol (Tokyo). 1987 Dec;33(6):421-30.“From the above findings it was concluded that diabetic outpatients tend to have a low blood thiamine level, with low erythrocyte transketolase activity and high erythrocyte TPP effect, and showed marginal thiamine deficiency” Relation of thiamine to diseaseWallace AE, Weeks WB. Thiamine treatment of chronic hepatitis B infection. Am J Gastroenterol. 2001 Mar;96(3):864-8.”In each case study, thiamine administration was associated with reduction in aminotransferase levels and the fall of HBV DNA to undetectable levels… The relationship between thiamine administration and chronic hepatitis B infection warrants further study. If proven effective in reducing liver damage or inducing remission of the hepatitis B virus in larger trials, thiamine will offer obvious advantages over the current treatments for chronic viral hepatitis B infection”Rossouw JE, Labadarios D, Krasner N, M, R. Red blood cell transketolase activity and the effect of thiamine supplementation in patients with chronic liver disease. Scand J Gastroenterol. 1978;13(2):133-8.“Biochemical evidence of thiamine deficiency was found in 58% of patients with chronic liver disease… high doses of thiamine should be included in the routine nutritional management of patients with severe chronic liver disease”Shoji S, Furuishi K, Misumi S, Miyazaki T, Kino M, Yamataka K. Thiamine disulfide as a potent inhibitor of human immunodeficiency virus (type-1) production. Biochem Biophys Res Commun. 1994 Nov 30;205(1):967-75.” The results suggest that thiamine disulfide may be important for AIDS chemotherapy”Shoji S, Furuishi K, Ogata A, Yamataka K, Tachibana K, Mukai R, Uda A, Harano K, Matsushita S, Misumi S. An allosteric drug, o,o'-bismyristoyl thiamine disulfide, suppresses HIV-1 replication through prevention of nuclear translocation of both HIV-1 Tat and NF-kappa B. Biochem Biophys Res Commun. 1998 Aug 28;249(3):745-53.Butterworth RF, Gaudreau C, Vincelette J, Bourgault AM, Lamothe F, Nutini AM. Thiamine deficiency and Wernicke's encephalopathy in AIDS. Metab Brain Dis. 1991 Dec;6(4):207-12.“we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse… it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex”Haisraeli-Shalish M, Livneh A, Katz J, Doolman R, Sela BA. Recurrent aphthous stomatitis and thiamine deficiency. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Dec;82(6):634-6.” 70 patients with recurrent aphthous stomatitis and in 50 members of a control group… Low levels of vitamin B1 were detected in 49 patients but in only two members of the control group… Our finding suggests an association between thiamine deficiency and recurrent aphthous stomatitis”Engel D. Tropical pyomyositis, a thiamine-deficiency disease. Med Hypotheses. 1981 Mar;7(3):345-52.“it is suggested that thiamine deficiency is an essential contributary factor in producing tropical pyomyositis… Thiamine deficiency induces a biochemical lesion (s) in the pyruvate oxidase system of the muscle, which breaks down its normal resistance to infection and opens the gate to bacterial agents”Krishna S, AM, Supanaranond W, Pukrittayakamee S, ter Kuile F, Tawfiq KM, Holloway PA, White NJ. Thiamine deficiency and malaria in adults from southeast Asia. Lancet. 1999 Feb 13;353(9152):546-9.”12 (52%) of 23 patients with severe malaria and ten (19%) of 54 patients with uncomplicated malaria had alpha values above the normal range (p<0.0001 and p=0.0014, respectively, compared with controls), which indicated severe thiamine deficiency” Pietrzak I, Baczyk K, Mlynarczyk M, Kaczmarek M. [Content of thiamin in plasma and erythrocytes in patients with end stage renal disease] Przegl Lek. 1996;53(5):423-6. Polish.”We suggest the need of thiamine supplementation in ESRD patients especially in those treated by dialysis. The supplementation of thiamine is needed particularly in patients on peritoneal dialysis”Relation of thiamine to other dataHung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. 2001 Nov;38(5):941-7.“We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency”Huang S, Ren G. [Thiamine status of university teacher families in Changsha] Hunan Yi Ke Da Xue Xue Bao. 1998;23(1):27-30. Chinese.“We conclude that those people who take the refined cereals and its products as a staple food, is in the risk of thiamine deficiency”Suzuki M, Itokawa Y. Effects of thiamine supplementation on exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106.“High-dose thiamine (vitamin B1) supplementation (100 mg/day) may be helpful in preventing or accelerating recovery from exercise-induced fatigue… Thiamine supplementation significantly suppressed the increase in blood glucose in the normal thiamine group and significantly decreased the number of complaints shortly after exercise in the subjective fatigue assessment of 30 items”Kimura M, Itokawa Y, Fujiwara M. Cooking losses of thiamin in food and its nutritional significance. J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl 1:S17-24.”The thiamin contents in cooked daily meals were 50-60 percent of the calculated values on an average”Cruickshank AM, Telfer AB, Shenkin A. Thiamine deficiency in the critically ill. Intensive Care Med. 1988;14(4):384-7.“We performed a retrospective study on 158 patients admitted to the Intensive Care Unit who required nutritional support. Patients who survived had significantly higher body thiamine status than those who died”Onodera K, Kisara K, Okabe H, Ogura Y. [studies on the effects of thiamine deficiency on rat testes (author's transl)] Nippon Yakurigaku Zasshi. 1980 Mar;76(2):143-52. Japanese.“In the thiamine deficient group, the seminiferous tubuli of rats having erections had atrophied”Labadarios D, Rossouw JE, McConnell JB, M, R. Thiamine deficiency in fulminant hepatic failure and effects of supplementation. Int J Vitam Nutr Res. 1977;47(1):17-22.“Nine out of 24 patients with acute hepatocellular necrosis leading to fulminant hepatic failure showed biochemical evidence of thiamine deficiency early in the course of their illness”Why haven’t we heard of benfo before? The patent on the manufacture of benfo expired decades ago. Pharmaceutical companies pursue drugs that can be patented so they can have a monopoly and charge 100 times what the drug is worth. They have spent a lot of money on AGE inhibitors that don’t work as well as benfo. Ingestion of benfo may result in the elimination of AGE-protein crosslinks, which are a major constituent of arterial plaque. I am intrigued by the idea that benfo may cause the removal of plaque from the blood vessels, but I am concerned about the rapid manner in which it may cause the removal of plaque from the blood vessels. If the plaque is being removed, a large chunk might break off and cause a stroke or heart attack. If I was older than 60 or if I had a serious problem with high blood pressure I would probably start out by taking very low doses of benfo and gradually increase my dosage. Of course, there are no reports of strokes or heart attacks from benfo in the medical literature, but it’s a thought to consider. My PhD research will mostly consist of double-blind controlled studies on the administration of benfo in normal individuals, diabetics, individuals with high blood pressure, Alzheimer patients etc. I believe the researchers who have investigated benfo to date have been extremely short sighted by not discovering they full potential of benfo in the clinical studies that have already been performed on humans.It is illegal to make claims about benfo and sell it as a dietary supplement unless the claims are based on substantial scientific evidence. The three case studies outlined in this document are not from a double-blind controlled study and FDA regulations would not allow for them to be referred to as substantial scientific evidence. Claims should not be made based on these preliminary findings. For questions or comments email robholladay99@...Since I am not a physician, it would be inappropriate for me to answer emails asking for medical advice.

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[Guest guest]

Sorry Larry, the de Myelination was B6 (Pyridoxine, not B1) I mentioned the B6 in the context of one of the multi-B preparations (B100 it was called) mentioned on that website.. I do think they have a point about B6 but I'm not sure at what level side-effects start. The British food safety organisation (search under food standards UK) warn that the risk factors are 1. taking over 150mg per day and 2 extended or continuous usage of this particular B vitamin.

Your advice as always is excellent, and logical.

----- Original Message -----

From: Larry J. Frieders

low dose naltrexone

Sent: Thursday, March 25, 2004 8:34 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

I think a single 4Gm dose of ascorbic acid might change pH and maybe even crystallize. If spaced out through the day and combined with sufficient water (one ounce for every 2 pounds of body weight) I'd wager there's be not problem.

The B1 issue is a strange one, but nobody has reported any forms of negative reaction. I have heard that some people use 400mg or more IM each day. They feel better and so on and there's seemingly no complications. A person in BC has been using these doses for over 25 years. He's not alone. This is based on work by Dr. F Klenner back in the 1960's.

WHO made the connection between B1 and DEmyelination and when was it made? Fifty years ago most of us got enough B vitamins in our food. Today, we're practically starving for nutrition - yet we're fat as hogs (I really can explain this). It is similar to the saying "if you eat a good balanced diet then you don't need to take vitamins." I agree 100% but I ask who in the US is able to eat a good balanced diet? Where would a person find good, non-contaminated produce, or meat without hormones, or clean (non-pasteurized) milk, or clean water - and so on? Fields are not tilled and crops are not rotated. Instead they add potassium, nitrogen and phosphorous to the fields and call it fertilizing (plus a good dose of estrogen-like pesticides for fun and profit). What about all the other vitamins and minerals that are leached from the soil - and not replaced?

Larry J. Frieders,RPh |The Compounder575 W. Illinois Ave ~ Aurora, IL 60506 630-859-0333 FAX 630-859-0114 Sample newsletter http://www.theCompounder.com/NL-Sample.html

Any health related information on our web pages or in our newsletters is for educational purposes only. None of the information we provide is to be construed as medical advice. Before applying any therapy or use of herbs, you may want to seek advice from your health care professional. Our information should not be a substitute for physician evaluation or treatment by a health care professional and is not intended to provide or confirm a diagnosis.

----- Original Message -----

From: n Quinn

low dose naltrexone

Sent: Thursday, March 25, 2004 10:57 AM

Subject: Re: [low dose naltrexone] Fw: check this out!

Larry, I agree with a lot of th etheories, but your opinion from Pharmacist to Pharmacist: Vitamin C at high (over 4gm per day) dose is associated with crystals in the urine, stones, and pain, and vitamin B6 a component of the B100 vitamins is linked with DE-MYELINATION! in doses of (allegedly) over 150 mg per day. what's your read on this?

n

----- Original Message -----

From: Larry J. Frieders

low dose naltrexone

Sent: Thursday, March 25, 2004 2:44 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

Just a note...We dispense a LOT of Vitamin B1 injection (some people just don't absorb the B vitamins well through the gut, so they use an injection). People are using 200mg and more each day and report significant improvements. I hold firm to the belief that many (if not most) chronic conditions (like MS and CFS) have their roots deeply buried in nutrition problems. It seems that B1 is a vital nutrient for proper nerve and muscle function.

Here's a link to an updated protocol. Dale Humpherys has used this approach for over 25 years - and he has encouraged hundreds (if not thousands) of others to use this approach. http://www.thecompounder.com/HumpherysNewProtocol.html

Larry J. Frieders,RPh |The Compounder575 W. Illinois Ave ~ Aurora, IL 60506 630-859-0333 FAX 630-859-0114 Sample newsletter http://www.theCompounder.com/NL-Sample.html

Any health related information on our web pages or in our newsletters is for educational purposes only. None of the information we provide is to be construed as medical advice. Before applying any therapy or use of herbs, you may want to seek advice from your health care professional. Our information should not be a substitute for physician evaluation or treatment by a health care professional and is not intended to provide or confirm a diagnosis.

----- Original Message -----

From:

low dose naltrexone

Sent: Wednesday, March 24, 2004 7:47 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

I started on this B1 night before last. I've been whining about this long drawn out virus I've been fighting, and either the B1 is helping mucho over the last two days, or I'm suddenly getting stronger anyway. I feel lots more energy, and my legs are finally getting some strength back. It's so hard to tell if it is the Benfotiamine or just my body finally winning. Who knows. I do know I've seen no side effects even though I've been taking 600mg twice a day. After a few days more I'll cut that in half... No digestive upsets, no headaches, just a positive feeling about life in general.

(MS)

----- Original Message -----

From: ruben/kathy lintzenich

low dose naltrexone

Sent: Tuesday, March 23, 2004 7:26 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

Tom, thanks for the great article. I will be starting this form of B1 when I finish my bottle of thiamine. Will keep everyone posted on any benefits I receive. Are you taking this form of B1 and did you find out about it through the Brewer Science Library? White is the educatuional cordinater at the library and publishes a quarterly newslettet. She is a wonderful source of info about ms and other dis-eases in the body. Best Wishes, Kathy

----- Original Message -----

From: tmbayuk

msalternatives ; MSersLife ; MS-Christians ; MSfriends ; MSViews_Multiple_Sclerosis ; low dose naltrexone ; JJUK ; mscured

Sent: Monday, March 22, 2004 10:50 AM

Subject: [low dose naltrexone] Fw: check this out!

----- Original Message ----- From:

tmbayuk

Sent: Saturday, March 20, 2004 11:01 PM

Subject: check this out!

Research on Benfotiamine Clinton Holladay, M.S.Copyright 2003 Clinton HolladayJune 5, 2003A short while ago a group of individuals I know purchased a large amount of benfotiamine and began ingesting it orally. I was urged by these individuals to place some of the research I have been conducting on benfo (benfotiamine) online along with the results of their benfo use. I was asked to do this in a manner that would allow individuals that do not have a background in the health sciences to comprehend it. I will be pursuing a PhD shortly and benfo will be central to my research. I am not a physician and the following information is not intended to be used as medical advice. Advanced glycation endproducts or AGEs are produced by the processing of sugars within the cell. They are one of the primary causes of aging and general wear and tear on your cells. Diabetics age the same way as normal people, but because they often have abnormal levels of sugars in their cells, they age faster. When blood sugar levels are high, certain cells in the body are flooded with glucose, particularly neurons and cells in the eyes and kidneys. Diabetics often suffer from nerve damage, kidney failure, and premature blindness. Numerous researchers have concentrated their efforts on AGE-blocking mechanisms because they would limit the wear and tear on the body’s cells and allow individuals to live longer and healthier, particularly diabetics. Benfo has emerged as the premier AGE inhibitor.Case StudiesIt is important to note that the following case studies are not double-blind controlled studies. Case study #1. Female, early fifties, non-diabetic, suffers from chronic fatigue, depression, and the normal aches and pains that accompany middle age. Her diet is average. She is able to do about two hours of physical labor a day, and she has suffered from depression for years. She has tried numerous treatments for depression including Prozac, and some of them have helped, but none have completely eliminated the depression. Sometimes she aches all over. She was addicted to caffeine for several years, but only consumes it about once a week now. She has high blood pressure, and treats it with Vasotec and also takes Maxide (a diuretic).She ingested 650 mg of benfo once a day for five days and did not notice any difference. On day 6 she doubled the dose to 1300 mg and started to notice a change a few hours later. There was a dramatic increase in stamina and energy. She is now able to do eight hours of physical work each day. She has an extremely heightened sense of well-being and all aspects of the depression have left. She has better clarity of thought, and sleeps better. Previously she would usually wake up two or three times a night. Now she sleeps through the whole night and has said she is in a deeper sleep at night. She has reported being able to control her appetite more. She has reported less shortness of breath. On day 13 she has had no weight change. On day 13 she experienced what felt exactly like a caffeine withdrawal headache. She immediately consumed two cans of mountain dew and the headache did not leave. Previous to this, caffeine had always relieved a headache of this sort for her. At day 14 she still had a headache and the tips of her toes started tingling. She reduced her dose to 650 mg per day once a day on day 14. On day 15 she still had a headache. On day 16 her toes started tingling and the headache left. On day 17 her pinkie started tingling. Her blood pressure has always fluctuated between 120/80 and 150/90. Throughout the treatment her blood pressure has fluctuated like it normally does. She says she feels like she did when she was thirty years old. Comment: The tingling is likely the cause of blood circulating to parts of her body that have not had a great deal of circulation in recent years.Case study #2. Male, mid fifties, non-diabetic. Average diet. Overall health is better than average for his age. He gets indigestion at night and takes Prilosec. He has the normal aches and pains that accompany middle age. When he wakes up in the morning his feet are inflexible, but that would go away after walking on them for about two minutes. After driving for two hours he is stiff when he gets out of his car. Most of the aches and pains and the foot inflexibility appeared in the last five to fifteen years. He began taking 650 mg of benfo once a day. On day 3 nothing hurt when he woke up. By day five all his aches and pains had disappeared. He is no longer stiff when he gets out of his car after driving for two hours. He feels more flexible. He says it has fixed everything that has gone wrong with him in the past fifteen years. He says he feels more cheerful but is not sure if it is because of repair to neurological damage or because his aches and pains are gone. He has reported a greater clarity of thought. He says he feels like he did when he was age 25-40 (he says he felt the same during those years). Up until twelve months ago his blood pressure has been 120/90. For the past twelve months it has averaged 130/120. On day 5 his blood pressure was 120/85 and it has remained consistent every day since then. Now he can only take a fifteen minute nap during the day whereas before he could fall asleep for hours. At night he sleeps better, probably because the aches and pains are gone. His appetite is only about 80% of what it used to be. He has reported increased stamina and energy. Before taking benfo it was getting hard for him to do ten hours of work per day. Now he can do fourteen hours of work per day. He still requires the same amount of sleep at night, but if he does not get his full requirement he doesn’t notice it nearly as much.Comment: The decrease in caloric intake may be because he was lacking an essential nutrient- not enough thiamine? The stiffening of the joints brought on by old age is partly a symptom poor blood circulation. The fact that this individual has become much more flexible is a possible indication of increased circulation.Case study #3. Male, late forties. He has been a type 1 diabetic for twenty years. Average diet. Over the last five years his health has declined more rapidly. He has more aches and pains than the average person because he is diabetic. He aches so much at night that he usually can’t get to sleep unless he takes Ibuprofen. He began taking 650 mg benfo once a day. On day 2 he noticed a decline in the severity of his aches and pains. He still needs the same amount of sleep, but if he doesn’t get his full requirement he doesn’t notice nearly as much. He has had an increase in stamina and energy. He says his stamina has doubled. On day 14 he felt like he did ten years ago, and it keeps improving each day. He is more cheerful, but like #2 he can’t tell if it’s because his aches and pains are gone or if benfo has a neurological effect on him. I will not disclose the brand of benfo which was used because I do not wish to be seen as promoting any particular brand. These case studies will be updated on July 5, 2003 and new ones will be added. The updates will be posted on www.geocities.com/robholladay99/updates.html The following exerpts are from medical journals. The abstracts (summaries) for most of them can be viewed online through the pubmed database, which is a free database most biomedical scientists use. To find pubmed, go to google.com and type in pubmed. Once you’re in pubmed, type in part of the title and you should be able to find the abstract. When typing in the title use "benfotiamine" not "benfo". As an anti-spamming measure, many search engines will not index web pages that list the key search words more than seven times throughout the document, hence this document was modified after it was created . Several things are important to note in the following literature. First of all, not only does benfo stop some effects of aging, it reverses them. Gradually over time people’s neurons quit working because of normal wear and tear. However, when benfo was ingested, not only did the nerve damage stop, some of the damage done through aging was repaired. A strong point is made that benfo is the most bioavailable source of thiamine. This means benfo is better absorbed than other sources of thiamine. Also, high levels of thiamine have analgesic (pain-relieving) effects on animals. In the Russian study the pain level of the patients decreased from 8.2 to 2.3, a decrease of about four hundred percent. Research articles on benfoWada T, Tagaki H, Minakami H, Hamanka W, Okamoto K, Ito, A, Sahashi Y. 1961. A new thiamine derivative, S-benzoylthiamine O-monophosphate. Science 134: 195-196.Benfo “is more easily absorbed in the body than thiamine hydrochloride, and administration results in higher thiamine and cocarboxylase levels in organs; moreover, these levels last for a longer period of time…It does not cause any unfavorable symptom in animals such as thiamine hydrochloride does…The LD50 by oral administration in mice, dd-strain hybrid, weighing 14 to 16g was 15g/kg of body weight”Bitsch R, Wolf M, Moller J, Heuzeroth L, Gruneklee D. Bioavailability assessment of the lipophilic benfo as compared to a water-soluble thiamin derivative. Ann Nutr Metab. 1991;35(5):292-6. “in presence of allicin, the active principle of garlic, the water-soluble thiamin hydrochloride is transformed into a lipid-soluble compound being identified as allithiamine…Ten healthy young men…The volunteers ingested a single dose of 40 mg benfo…Thus, the measured values reveal, when compared with mononitrate, a clearly improved thiamin bioavailability from benfo, due to the more lipophilic properties of this substance or possibly its dephosphorylated metabolite and a more rapid transformation into the physiologically active derivative. This may be of great advantage in the treatment of neurological disorders responding to high thiamin doses and further on in situations when the active intestinal absorbtion mechanisms are impaired”Stracke H, Lindemann A, Federlin K. A benfo-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.“Benfo…was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold...Therapy-specific adverse effects were not seen”Loew D. Pharmacokinetics of thiamine derivatives especially of benfo. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.“The effective form of thiamine, thiamine diphosphate, is an organic compound needed by the organism for vital functions…Due to this peculiarity the conditions for absorbtion of lipid-soluble vitamins differ from those for water-soluble thiamine derivatives. Unlike the latter, allithiamines are absorbed passively, they traverse the intestinal absorption barrier faster and more readily, leading to higher blood and tissue concentrations even when comparatively low doses are given…It therefore fulfills important pharmacodynamic conditions for rational therapy. Due to their greater biovailability and better tissue passage lipid-soluble thiamine analogues like benfo are preferable to water-soluble thiamine derivatives for treatment of various pathological conditions, e.g. cardiomyopathy, Werincke-Korsakow syndrome, and alcoholic or diabetic polyneuropathies…Due to its excellent pharmacokinetic profile and to its excellent tolerability benfo should be preferred in treatment of relevant conditions like neuropathies”Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter CH. Comparative bioavailability of two vitamin B1 preparations: benfo and thiamine mononitrate. Eur J Clin Pharmacol. 1997;52(4):319-20.“a study using equimolar quantities of the two preparations for exact comparison of the bioavailability of benfo and thiamine mononitrate has never been performed. Therfore, the present trial was undertaken…the higher thiamine content in the erythrocytes and the higher thiamine excretion in urine after oral benfo administration are proof of the considerably higher relative bioavailability of benfo than thiamine mononitrate”Simeonov S, Pavlova M, Mitkov M, Mincheva L, Troev D. Therapeutic efficacy of "Milgamma" in patients with painful diabetic neuropathy. Folia Med (Plovdiv). 1997;39(4):5-10.“Forty-Five diabetes patients with painful peripheral polyneuropathy were enrolled in a 3-month observational study comparing the therapeutic efficiacy of Milgamma tablets (benfo)…Statistically significant relief of both background and peak neuropathic pain was achieved in all of the Milgamma-treated patients…No adverse reactions were observed…Our results underscore the importance of Milgamma tablets as an indispensable element in the therapeutic regimen of patients with painful diabetic polyneuropathy”Greb A, Bitsch R. Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther. 1998 Apr;36(4):216-21.“Seven healthy volunteers…a single oral dose of either benfo…fursultiamin…thiaminedisulfide…In this study the allithiamine derivative benfo proved the best bioavailability. Owing to its excellent absorption properties it can be concluded that oral administration of benfo is suitable for therapeutical purposes”Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfo in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.Good review, full-text is available free online. “In bioavailability studies on healthy human subjects, it was shown that absorption of benfo was several times better than that of water-soluble vitamin B1 and that there was a 120-fold higher increase of metabolically active thiamine diphosphate in erythrocytes (Heinrich, 1990)…In animals given dosages that exceeded basic requirements by 100- or 1000-fold thiamine has analgesic and neuroprotective effects(woelk and peeler-Ichakawa, 1985; Jurna, 1988; Reeh, 1988, 1991; Wild, 1988). However, if high levels are to be achieved with oral vitamin B1 treatment, lipid soluble thiamine derivatives or pro-drugs with high bioavailability, such as benfo, are required…320 mg/day during weeks 1 to 4 and 120 mg benfo/day during weeks 5 to 8…Within the 8-week study period, benfo led to a significant improvement of the threshold of vibration perception at the great toe, motor function, and the overall symptom score. Marked improvement occurred in both pain and co-ordination”Sadekov RA, Danilov AB, Vein AM. [Diabetic polyneuropathy treatment by milgamma-100 preparation] Zh Nevrol Psikhiatr Im S S Korsakova. 1998;98(9):30-2. Russian.“benfo…was studied in treatment of diabetic polyneuropathy in 14 patients…After the course of treatment the intensity of pains was decreased according to visual analogous scale on the average from 8.2 to 2.3 scores, the indices of vibratory sensitivity improved significantly as well as the data of cardiovascular tests…The treatment resulted in the improvement of the condition in 93% of the cases” T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine pharmacokinetics by end-stage renal disease (ESRD). Int J Clin Pharmacol Ther. 1999 Sep;37(9):449-55.“20 end-stage renal disease(ESRD) patients…After a single oral dose of 100 mg benfo…ESRD patients may benefit from high-dose thiamine derivatives notwithstanding their chemical form. However, the better absorption and high transfer rate of debenzoylated BTMP (benfo) to TDP (thiamine diphosphate) even at much lower doses compensates for reduced renal excretion and may protect, therefore, against numerous adverse effects of uremia”Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different benfo dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.320, 120, and 150 mg benfo/day was administered to “diabetic patients suffering from painful peripheral diabetic neuropathy. In a 6-week open clinical trial, 36 patients…An overall beneficial therapeutic effect on the neuropathy status was observed in all three groups during the study…The greatest change occurred in the group of patients receiving the high dose of benfo…Metabolic control did not change over the study...Extremely interesting is the result of recent in vitro experiences that thiamine pyrophosphate and pyroxidine inhibit the formation of glycation end products" T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfo. Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.“20 end-stage renal disease (ESRD) patients…After benfo administration, the peak plasma concentration of TDP exceeded that in healthy subjects by 51%...Compared with thiamine nitrate, the oral administration of benfo leads to higher TDP concentrations in erythrocytes accompanied with a significant improvement of the erythrocyte transkelotase activity in ESRD patients”Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M. Benfo is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.“We investigated the hypothesis that benfo, a lipophilic derivative of thiamine, affects replication delay and generation of advanced glycosylation endproducts (AGE) in human umbilical vein endothelial cells cultured in the presence of high glucose…Benfo, a derivative of thiamine with better bioavailability, corrects defective replication and increased AGE generation in endothelial cells cultured in high glucose, to a similar extent as thiamine. These effects may result from normalization of accelerated glycolysis and the consequent decrease in metabolites that are extremely active in generating nonenzymatic protein glycation. The potential role of thiamine administration in the prevention or treatment of vascular complications of diabetes deserves further investigation”Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M, Geyer J, Kopcke W, Sauerland C, Bretzel RG, Federlin KF. Efficacy of benfo versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.“After three months preventative administration of both vitamin B1 preparations NCV (nerve conduction velocity) had increased substantially…It was nearly normal after six months with benfo, while the administration of thiamine nitrate resulted in no further amelioration. NCV was nearly normalized after six months of benfo application but not with thiamine. Furthermore, benfo induced a major inhibition of neural imidazole-type AGE formation and completely prevented diabetes induced glycoxidation products”Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M. Benfo blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.“Our results in both endothelial cells cultured for several days and retinas from rats with nine months of diabetes showed that benfo, a lipid-soluble thiamine derivative, prevents activation of three major pathways involved in hyperglycemia-induced vascular damage: the hexosamine pathway, the intracellular AGE formation pathway and the DAG-PKC pathway…We showed that benfo blocks these pathways of hyperglycemic damage by increasing the activity of transketolase…Administration of benfo for nine months also completely prevented the development of experimental diabetic retinopathy in rats...Thus we conclude that augmentation of transketolase activity is solely responsible for the observed effects of benfo”Comment: This study is very significant because it demonstrates how benfo blocks several other aging mechanisms besides AGE formation. However, I am not yet convinced of the statement that transketolase activity is solely responsible for the observed effects of benfo. The following four studies are located on the Internet but are not yet listed on Medline. To find them, go to google.com and type in part of the titleBergfeld R, Matsumara X. Du, Brownlee M. Benfo prevents the consequences of hyperglycemia-induced mitochondrial overproduction of reactive oxygen species, and experimental diabetic retinopathy.“diabetic rats were treated with benfo (80 mg/kg weight) for 36 weeks…Benfo decreases AGE formation by 60%...These data suggest that treatment with benfo may be an effective approach to prevent the development of diabetic complications”Lin J, Alt A, Liersch J, Bretzel R, Brownlee M, Hammes H. Benfo inhibits intracellular formation of advanced glycation end products in vivo“Here, we studied the effect of benfo, a lipid-soluble thiamine derivative with known AGE-inhibiting properties in vitro on the intracellular formation of (CML) and methylgloxal-derived AGE in red blood cells. Blood was collected from 6 type 1 diabetic patients before and after treatment with 600 mg/day benfo for 28 days…Thiamine derivatives, in particular the lipid-soluble prodrug benfo, are effective inhibitors of intracellular formation of AGE and CML”Stracke H, Werkmann D, Mavrakis K, Federlin K, Kopke W, Sauerland C, Hammes H, Bretzel RG. Influence of vitamin B1 on diabetic neuropathy-studies in streptozotocin-diabetic rats.“we investigated the effects of oral administration of thiamine and benfo on the development of glucose oxidation products in the nerve and on nerve conduction velocity in streptozotocin-diabetic rats…Conclusion: Early treatment with benfo normalizes increased cellular oxidative stress and the reduced nerve conduction velocity”Hammes H, Bretzel, R.G., Federlin, K, Horiuchi S, Niwa T, Stracke H. Benfo inhibits the formation of advanced glycation end products in diabetic rats.“benfo (100 mg/kg x day) and thiamin (70.18 mg/kg x day) administered orally for 6 months…neither benfo nor thiamin treatment affected metabolic control…Benfo administration in diabetic rats induced a major inhibition of neutral imidazolone-type AGE formation and completely prevented diabetes-induced glycoxidation formation. Treatment with thiamin did not affect AGE or CML levels”ThiamineAllithiamines are lipid-soluble sources of thiamine. Benfo is an allithiamine. Thiamine is water-soluble and is also known as vitamin B1.After reviewing the relevant medical literature on thiamine, I have come to conclude that large portions of the population may be thiamine deficient. In addition, many individuals that are not technically thiamine deficient would likely receive benefit from thiamine supplementation. Thiamine deficiency is associated with numerous undesirable medical conditions.Relation of thiamine to heart diseaseShamir R, Dagan O, Abramovitch D, Abramovitch T, Vidne BA, Dinari G. Thiamine deficiency in children with congenital heart disease before and after corrective surgery. JPEN J Parenter Enteral Nutr. 2000 May-Jun;24(3):154-8.Thiamine deficiency “is common in children with congenital heart disease (CHD) referred for corrective surgery both before and after surgery. Our results suggest that neither diuretic treatment nor malnutrition can fully explain the development of TD in these children”Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E, Levy R. [Right heart failure caused by thiamine deficiency (cardiac beriberi)] Presse Med. 2000 Feb 12;29(5):240-1. French.Beaud C, Fuhrman C, Perchet H, Monnet I, Chouaid C, Housset B. [Thiamine deficiency. A cause of cardiac insufficiency not to be ignored] Rev Mal Respir. 1998 Jun;15(3):303-4. French.“Thiamine deficiency is one of the classical causes of high output for heart failure”Okura H, Gohma I, Hatta K, Imanaka T. Thiamine deficiency and pulmonary hypertension in Crow-Fukase syndrome. Intern Med. 1995 Jul;34(7):674-5. “After oral administration of prednisolone and thiamine, echocardiogram showed marked improvement of the pulmonary hypertension”Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc. 1995 May;95(5):541-4. “Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk”Shimon I, Almog S, Vered Z, Seligmann H, Shefi M, Peleg E, Rosenthal T, Motro M, Halkin H, Ezra D. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med. 1995 May;98(5):485-90.“Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy”Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered Z, Ezra D. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med. 1991 Aug;91(2):151-5.”These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements”Relation of thiamine to neurological disordersLonsdale D, Shamberger RJ, Audhya T. Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: a pilot study. Neuroendocrinol Lett. 2002 Aug;23(4):303-8.“Thiamine tetrahydrofurfuryl disulfide appears to have a beneficial clinical effect on some autistic children, since 8 of the 10 children improved clinically”Nakagawasai O, Tadano T, Hozumi S, Taniguchi R, Tan-No K, Esashi A, Niijima F, Kisara K. Characteristics of depressive behavior induced by feeding thiamine-deficient diet in mice.Life Sci. 2001 Jul 27;69(10):1181-91.Ambrose ML, Bowden SC, Whelan G. Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings. Alcohol Clin Exp Res. 2001 Jan;25(1):112-6.“A therapeutic relationship between dose and working memory performance was indicated”Older MW, Dickerson JW. Thiamine and the elderly orthopaedic patient. Age Ageing. 1982 May;11(2):101-7.“In both groups those patients who were noticeably confused after operation were found to have a considerable fall in their thiamine status suggesting this may be a contributory factor to postoperative confusion”Winston AP, son CP, Madira W, Gatward NM, Palmer RL. Prevalence of thiamin deficiency in anorexia nervosa. Int J Eat Disord. 2000 Dec;28(4):451-4.“Fourteen patients (38%) had results in the deficient range; 7 (19%) met the most stringent published criterion for deficiency. Deficiency was not related to duration of eating restraint, frequency of vomiting, or alcohol consumption”Terasawa M, Nakahara T, Tsukada N, Sugawara A, Itokawa Y. The relationship between thiamine deficiency and performance of a learning task in rats. Metab Brain Dis. 1999 Sep;14(3):137-48.“We taught rats to press a lever to escape from the pain of electrical stimulation by learning to turn a switch off… The rats that were fed the thiamine-deficient diet showed a slower response time and a longer running time than the rats fed the normal diet… We found that the thiamine concentration in the blood of the rats in the trained group was significantly higher than that in the group without training”Jimenez-Jimenez FJ, Molina JA, Hernanz A, Fernandez-Vivancos E, de Bustos F, Barcenilla B, Gomez-Escalonilla C, Zurdo M, Berbel A, Villanueva C. Cerebrospinal fluid levels of thiamine in patients with Parkinson's disease. Neurosci Lett. 1999 Aug 13;271(1):33-6.“These results suggest that low CSF free thiamine levels could be related with the risk for PD”Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J. 1997 Dec;74(12):803-8.“Diabetic peripheral neuropathy in Dar es Salaam is associated with thiamine deficiency”Langlais PJ, G, Guo SX, Bondy SC. Increased cerebral free radical production during thiamine deficiency. Metab Brain Dis. 1997 Jun;12(2):137-43.“These findings suggest that increased formation of free radicals occurs during the more acute symptomatic stage of thiamine deficiency and may contribute to the structural damage described in this model of Wernicke's encephalopathy”Easton CJ, Bauer LO. Beneficial effects of thiamine on recognition memory and P300 in abstinent cocaine-dependent patients. Psychiatry Res. 1997 May 30;70(3):165-74. “Thiamine was found to significantly improve recognition accuracy and P300 amplitude, at the midline parietal (Pz) electrode. The improvement was most reliable under conditions of increased memory load”Benton D, Griffiths R, Haller J. Thiamine supplementation mood and cognitive functioning. Psychopharmacology (Berl). 1997 Jan;129(1):66-71. ”An improvement in thiamine status was associated with reports of being more clearheaded, composed and energetic. The taking of thiamine had no influence on memory but reaction times were faster following supplementation”Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's disease. Metab Brain Dis. 1996 Mar;11(1):89-94.”Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100 mg/day had a mild beneficial effect in patients with Alzheimer's disease in a 12-week open trial. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function”Gold M, Chen MF, K. Plasma and red blood cell thiamine deficiency in patients with dementia of the Alzheimer's type. Arch Neurol. 1995 Nov;52(11):1081-6.“A significant proportion of patients with SDAT may have a thiamine deficiency, which may have an impact on cognitive function. Currently used assays may not be adequate to assess thiamine status”Adamolekun B, Eniola A. Thiamine-responsive acute cerebellar ataxia following febrile illness. Cent Afr J Med. 1993 Feb;39(2):40-1. Review.“acute thiamine depletion may be the pathogenetic mechanism for post-pyrexial acute cerebellar ataxia”Ben-Hur T, Wolff E, River Y. [Thiamin deficiency is common in Israel] Harefuah. 1992 Nov 15;123(10):382-4, 436, 435. Hebrew.“Thiamin levels should be determined not only in alcoholics and those with classic B1 deficiency syndromes, but in the routine workup of patients with sensory-motor neuropathy, dementia, gait disorders, cerebellar syndromes and confusional states”Sacks W, Esser AH, Feitel B, Abbott K. Acetazolamide and thiamine: an ancillary therapy for chronic mental illness. Psychiatry Res. 1989 Jun;28(3):279-88.“Overall, 50% of the patients showed improvement on all assessment scales. No untoward effects occurred in these patients…”Relation of thiamine and geriatric patientsSmidt LJ, Cremin FM, Grivetti LE, Clifford AJ. Influence of thiamin supplementation on the health and general well-being of an elderly Irish population with marginal thiamin deficiency. J Gerontol. 1991 Jan;46(1):M16-22.”thiamin-supplemented women experienced significantly increased appetite, energy intake, body weight and general well-being, and decreased fatigue. Thiamin supplementation also tended to reduce daytime sleep time, improve sleep patterns, and increase activity. These data suggest that evaluation of thiamin status is indicated when nonspecific conditions such as anorexia, weight loss, fatigue, depression, and sleep disorders are present in elderly persons”Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels in elder patients admitted through the emergency department. Acad Emerg Med. 2000 Oct;7(10):1156-9.“CONCLUSIONS: Elder nursing home patients seen in the ED and admitted to the hospital are frequently thiamine-deficient”Wilkinson TJ, Hanger HC, Elmslie J, PM, Sainsbury R. The response to treatment of subclinical thiamine deficiency in the elderly. Am J Clin Nutr. 1997 Oct;66(4):925-8.“Only the subjects with persistently low TPP concentrations showed subjective benefits from treatment with improvements in quality of life… There was a trend toward benefits in sleep and energy… Quality of life was enhanced by providing thiamine supplements. Blood pressure and weight were lower after thiamine supplementation”Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte thiamin concentrations in geriatric outpatients. J Am Coll Nutr. 1996 Jun;15(3):231-6.“CONCLUSION: About 50% of geriatric outpatients in this study had low plasma thiamin levels”Nichols HK, Basu TK. Thiamin status of the elderly: dietary intake and thiamin pyrophosphate response. J Am Coll Nutr. 1994 Feb;13(1):57-61.“Average daily thiamin intake was above the recommended requirement… however, almost half of the total study population had TPP effect > 14%, suggesting thiamin deficiency… CONCLUSION: These findings raise questions about the reliability of dietary intake in assessing metabolic availability of thiamin in the elderly”O'Keeffe ST, Tormey WP, Glasgow R, Lavan JN. Thiamine deficiency in hospitalized elderly patients. Gerontology. 1994;40(1):18-24.“Necropsy studies suggest that thiamine deficiency is underdiagnosed in life… There was no difference in anthropometric indices or in the prevalence of other nutrient deficiencies between the two groups. Thiamine deficiency is common in elderly patients admitted to hospital and may contribute to the development of delirium”Iber FL, Blass JP, Brin M, Leevy CM. Thiamin in the elderly--relation to alcoholism and to neurological degenerative disease. Am J Clin Nutr. 1982 Nov;36(5 Suppl):1067-82. Review.“There is no known toxicity for thiamin”Relation of thiamine to diabetesAvena R, Arora S, Carmody BJ, Cosby K, Sidawy AN. Thiamine (Vitamin B1) protects against glucose- and insulin-mediated proliferation of human infragenicular arterial smooth muscle cells. Ann Vasc Surg. 2000 Jan;14(1):37-43.“Vitamin B1 intake may prove important in delaying the atherosclerotic complications of diabetes”La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA, Molinatti GM, Porta M. Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions. Diabetologia. 1996 Nov;39(11):1263-8.Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S, Scheinman M, T. Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells. Surgery. 2001 Nov;130(5):851-8.“The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes”Hassan R, Qureshi H, Zuberi SJ. Effect of thiamine on glucose utilization in hepatic cirrhosis. J Gastroenterol Hepatol. 1991 Jan-Feb;6(1):59-60.“It is therefore suggested that thiamine supplements be given to cirrhotics with hyperglycaemia, to improve glucose utilization”Rindi G, Laforenza U. Thiamine intestinal transport and related issues: recent aspects.Proc Soc Exp Biol Med. 2000 Sep;224(4):246-55. Review.“Thiamine uptake is enhanced by thiamine deficiency, and reduced by thyroid hormone and diabetes”Saito N, Kimura M, Kuchiba A, Itokawa Y. Blood thiamine levels in outpatients with diabetes mellitus. J Nutr Sci Vitaminol (Tokyo). 1987 Dec;33(6):421-30.“From the above findings it was concluded that diabetic outpatients tend to have a low blood thiamine level, with low erythrocyte transketolase activity and high erythrocyte TPP effect, and showed marginal thiamine deficiency” Relation of thiamine to diseaseWallace AE, Weeks WB. Thiamine treatment of chronic hepatitis B infection. Am J Gastroenterol. 2001 Mar;96(3):864-8.”In each case study, thiamine administration was associated with reduction in aminotransferase levels and the fall of HBV DNA to undetectable levels… The relationship between thiamine administration and chronic hepatitis B infection warrants further study. If proven effective in reducing liver damage or inducing remission of the hepatitis B virus in larger trials, thiamine will offer obvious advantages over the current treatments for chronic viral hepatitis B infection”Rossouw JE, Labadarios D, Krasner N, M, R. Red blood cell transketolase activity and the effect of thiamine supplementation in patients with chronic liver disease. Scand J Gastroenterol. 1978;13(2):133-8.“Biochemical evidence of thiamine deficiency was found in 58% of patients with chronic liver disease… high doses of thiamine should be included in the routine nutritional management of patients with severe chronic liver disease”Shoji S, Furuishi K, Misumi S, Miyazaki T, Kino M, Yamataka K. Thiamine disulfide as a potent inhibitor of human immunodeficiency virus (type-1) production. Biochem Biophys Res Commun. 1994 Nov 30;205(1):967-75.” The results suggest that thiamine disulfide may be important for AIDS chemotherapy”Shoji S, Furuishi K, Ogata A, Yamataka K, Tachibana K, Mukai R, Uda A, Harano K, Matsushita S, Misumi S. An allosteric drug, o,o'-bismyristoyl thiamine disulfide, suppresses HIV-1 replication through prevention of nuclear translocation of both HIV-1 Tat and NF-kappa B. Biochem Biophys Res Commun. 1998 Aug 28;249(3):745-53.Butterworth RF, Gaudreau C, Vincelette J, Bourgault AM, Lamothe F, Nutini AM. Thiamine deficiency and Wernicke's encephalopathy in AIDS. Metab Brain Dis. 1991 Dec;6(4):207-12.“we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse… it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex”Haisraeli-Shalish M, Livneh A, Katz J, Doolman R, Sela BA. Recurrent aphthous stomatitis and thiamine deficiency. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Dec;82(6):634-6.” 70 patients with recurrent aphthous stomatitis and in 50 members of a control group… Low levels of vitamin B1 were detected in 49 patients but in only two members of the control group… Our finding suggests an association between thiamine deficiency and recurrent aphthous stomatitis”Engel D. Tropical pyomyositis, a thiamine-deficiency disease. Med Hypotheses. 1981 Mar;7(3):345-52.“it is suggested that thiamine deficiency is an essential contributary factor in producing tropical pyomyositis… Thiamine deficiency induces a biochemical lesion (s) in the pyruvate oxidase system of the muscle, which breaks down its normal resistance to infection and opens the gate to bacterial agents”Krishna S, AM, Supanaranond W, Pukrittayakamee S, ter Kuile F, Tawfiq KM, Holloway PA, White NJ. Thiamine deficiency and malaria in adults from southeast Asia. Lancet. 1999 Feb 13;353(9152):546-9.”12 (52%) of 23 patients with severe malaria and ten (19%) of 54 patients with uncomplicated malaria had alpha values above the normal range (p<0.0001 and p=0.0014, respectively, compared with controls), which indicated severe thiamine deficiency” Pietrzak I, Baczyk K, Mlynarczyk M, Kaczmarek M. [Content of thiamin in plasma and erythrocytes in patients with end stage renal disease] Przegl Lek. 1996;53(5):423-6. Polish.”We suggest the need of thiamine supplementation in ESRD patients especially in those treated by dialysis. The supplementation of thiamine is needed particularly in patients on peritoneal dialysis”Relation of thiamine to other dataHung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. 2001 Nov;38(5):941-7.“We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency”Huang S, Ren G. [Thiamine status of university teacher families in Changsha] Hunan Yi Ke Da Xue Xue Bao. 1998;23(1):27-30. Chinese.“We conclude that those people who take the refined cereals and its products as a staple food, is in the risk of thiamine deficiency”Suzuki M, Itokawa Y. Effects of thiamine supplementation on exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106.“High-dose thiamine (vitamin B1) supplementation (100 mg/day) may be helpful in preventing or accelerating recovery from exercise-induced fatigue… Thiamine supplementation significantly suppressed the increase in blood glucose in the normal thiamine group and significantly decreased the number of complaints shortly after exercise in the subjective fatigue assessment of 30 items”Kimura M, Itokawa Y, Fujiwara M. Cooking losses of thiamin in food and its nutritional significance. J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl 1:S17-24.”The thiamin contents in cooked daily meals were 50-60 percent of the calculated values on an average”Cruickshank AM, Telfer AB, Shenkin A. Thiamine deficiency in the critically ill. Intensive Care Med. 1988;14(4):384-7.“We performed a retrospective study on 158 patients admitted to the Intensive Care Unit who required nutritional support. Patients who survived had significantly higher body thiamine status than those who died”Onodera K, Kisara K, Okabe H, Ogura Y. [studies on the effects of thiamine deficiency on rat testes (author's transl)] Nippon Yakurigaku Zasshi. 1980 Mar;76(2):143-52. Japanese.“In the thiamine deficient group, the seminiferous tubuli of rats having erections had atrophied”Labadarios D, Rossouw JE, McConnell JB, M, R. Thiamine deficiency in fulminant hepatic failure and effects of supplementation. Int J Vitam Nutr Res. 1977;47(1):17-22.“Nine out of 24 patients with acute hepatocellular necrosis leading to fulminant hepatic failure showed biochemical evidence of thiamine deficiency early in the course of their illness”Why haven’t we heard of benfo before? The patent on the manufacture of benfo expired decades ago. Pharmaceutical companies pursue drugs that can be patented so they can have a monopoly and charge 100 times what the drug is worth. They have spent a lot of money on AGE inhibitors that don’t work as well as benfo. Ingestion of benfo may result in the elimination of AGE-protein crosslinks, which are a major constituent of arterial plaque. I am intrigued by the idea that benfo may cause the removal of plaque from the blood vessels, but I am concerned about the rapid manner in which it may cause the removal of plaque from the blood vessels. If the plaque is being removed, a large chunk might break off and cause a stroke or heart attack. If I was older than 60 or if I had a serious problem with high blood pressure I would probably start out by taking very low doses of benfo and gradually increase my dosage. Of course, there are no reports of strokes or heart attacks from benfo in the medical literature, but it’s a thought to consider. My PhD research will mostly consist of double-blind controlled studies on the administration of benfo in normal individuals, diabetics, individuals with high blood pressure, Alzheimer patients etc. I believe the researchers who have investigated benfo to date have been extremely short sighted by not discovering they full potential of benfo in the clinical studies that have already been performed on humans.It is illegal to make claims about benfo and sell it as a dietary supplement unless the claims are based on substantial scientific evidence. The three case studies outlined in this document are not from a double-blind controlled study and FDA regulations would not allow for them to be referred to as substantial scientific evidence. Claims should not be made based on these preliminary findings. For questions or comments email robholladay99@...Since I am not a physician, it would be inappropriate for me to answer emails asking for medical advice.

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As far as I know the liver extract was removed for fears of BSE an almost epidemic disease in some countries, but not the USA..the risk occurs when the source of the liver cannot be verified..back to the clean food theory!

By the way injections, even water! are all Prescription only in Ireland, and very few patients are encouraged to self-administer.Dr Humphreys article is interesting, but if it works, why use LDN?

n

----- Original Message -----

From: Larry J. Frieders

low dose naltrexone

Sent: Thursday, March 25, 2004 8:34 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

I think a single 4Gm dose of ascorbic acid might change pH and maybe even crystallize. If spaced out through the day and combined with sufficient water (one ounce for every 2 pounds of body weight) I'd wager there's be not problem.

The B1 issue is a strange one, but nobody has reported any forms of negative reaction. I have heard that some people use 400mg or more IM each day. They feel better and so on and there's seemingly no complications. A person in BC has been using these doses for over 25 years. He's not alone. This is based on work by Dr. F Klenner back in the 1960's.

WHO made the connection between B1 and DEmyelination and when was it made? Fifty years ago most of us got enough B vitamins in our food. Today, we're practically starving for nutrition - yet we're fat as hogs (I really can explain this). It is similar to the saying "if you eat a good balanced diet then you don't need to take vitamins." I agree 100% but I ask who in the US is able to eat a good balanced diet? Where would a person find good, non-contaminated produce, or meat without hormones, or clean (non-pasteurized) milk, or clean water - and so on? Fields are not tilled and crops are not rotated. Instead they add potassium, nitrogen and phosphorous to the fields and call it fertilizing (plus a good dose of estrogen-like pesticides for fun and profit). What about all the other vitamins and minerals that are leached from the soil - and not replaced?

Larry J. Frieders,RPh |The Compounder575 W. Illinois Ave ~ Aurora, IL 60506 630-859-0333 FAX 630-859-0114 Sample newsletter http://www.theCompounder.com/NL-Sample.html

Any health related information on our web pages or in our newsletters is for educational purposes only. None of the information we provide is to be construed as medical advice. Before applying any therapy or use of herbs, you may want to seek advice from your health care professional. Our information should not be a substitute for physician evaluation or treatment by a health care professional and is not intended to provide or confirm a diagnosis.

----- Original Message -----

From: n Quinn

low dose naltrexone

Sent: Thursday, March 25, 2004 10:57 AM

Subject: Re: [low dose naltrexone] Fw: check this out!

Larry, I agree with a lot of th etheories, but your opinion from Pharmacist to Pharmacist: Vitamin C at high (over 4gm per day) dose is associated with crystals in the urine, stones, and pain, and vitamin B6 a component of the B100 vitamins is linked with DE-MYELINATION! in doses of (allegedly) over 150 mg per day. what's your read on this?

n

----- Original Message -----

From: Larry J. Frieders

low dose naltrexone

Sent: Thursday, March 25, 2004 2:44 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

Just a note...We dispense a LOT of Vitamin B1 injection (some people just don't absorb the B vitamins well through the gut, so they use an injection). People are using 200mg and more each day and report significant improvements. I hold firm to the belief that many (if not most) chronic conditions (like MS and CFS) have their roots deeply buried in nutrition problems. It seems that B1 is a vital nutrient for proper nerve and muscle function.

Here's a link to an updated protocol. Dale Humpherys has used this approach for over 25 years - and he has encouraged hundreds (if not thousands) of others to use this approach. http://www.thecompounder.com/HumpherysNewProtocol.html

Larry J. Frieders,RPh |The Compounder575 W. Illinois Ave ~ Aurora, IL 60506 630-859-0333 FAX 630-859-0114 Sample newsletter http://www.theCompounder.com/NL-Sample.html

Any health related information on our web pages or in our newsletters is for educational purposes only. None of the information we provide is to be construed as medical advice. Before applying any therapy or use of herbs, you may want to seek advice from your health care professional. Our information should not be a substitute for physician evaluation or treatment by a health care professional and is not intended to provide or confirm a diagnosis.

----- Original Message -----

From:

low dose naltrexone

Sent: Wednesday, March 24, 2004 7:47 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

I started on this B1 night before last. I've been whining about this long drawn out virus I've been fighting, and either the B1 is helping mucho over the last two days, or I'm suddenly getting stronger anyway. I feel lots more energy, and my legs are finally getting some strength back. It's so hard to tell if it is the Benfotiamine or just my body finally winning. Who knows. I do know I've seen no side effects even though I've been taking 600mg twice a day. After a few days more I'll cut that in half... No digestive upsets, no headaches, just a positive feeling about life in general.

(MS)

----- Original Message -----

From: ruben/kathy lintzenich

low dose naltrexone

Sent: Tuesday, March 23, 2004 7:26 PM

Subject: Re: [low dose naltrexone] Fw: check this out!

Tom, thanks for the great article. I will be starting this form of B1 when I finish my bottle of thiamine. Will keep everyone posted on any benefits I receive. Are you taking this form of B1 and did you find out about it through the Brewer Science Library? White is the educatuional cordinater at the library and publishes a quarterly newslettet. She is a wonderful source of info about ms and other dis-eases in the body. Best Wishes, Kathy

----- Original Message -----

From: tmbayuk

msalternatives ; MSersLife ; MS-Christians ; MSfriends ; MSViews_Multiple_Sclerosis ; low dose naltrexone ; JJUK ; mscured

Sent: Monday, March 22, 2004 10:50 AM

Subject: [low dose naltrexone] Fw: check this out!

----- Original Message ----- From:

tmbayuk

Sent: Saturday, March 20, 2004 11:01 PM

Subject: check this out!

Research on Benfotiamine Clinton Holladay, M.S.Copyright 2003 Clinton HolladayJune 5, 2003A short while ago a group of individuals I know purchased a large amount of benfotiamine and began ingesting it orally. I was urged by these individuals to place some of the research I have been conducting on benfo (benfotiamine) online along with the results of their benfo use. I was asked to do this in a manner that would allow individuals that do not have a background in the health sciences to comprehend it. I will be pursuing a PhD shortly and benfo will be central to my research. I am not a physician and the following information is not intended to be used as medical advice. Advanced glycation endproducts or AGEs are produced by the processing of sugars within the cell. They are one of the primary causes of aging and general wear and tear on your cells. Diabetics age the same way as normal people, but because they often have abnormal levels of sugars in their cells, they age faster. When blood sugar levels are high, certain cells in the body are flooded with glucose, particularly neurons and cells in the eyes and kidneys. Diabetics often suffer from nerve damage, kidney failure, and premature blindness. Numerous researchers have concentrated their efforts on AGE-blocking mechanisms because they would limit the wear and tear on the body’s cells and allow individuals to live longer and healthier, particularly diabetics. Benfo has emerged as the premier AGE inhibitor.Case StudiesIt is important to note that the following case studies are not double-blind controlled studies. Case study #1. Female, early fifties, non-diabetic, suffers from chronic fatigue, depression, and the normal aches and pains that accompany middle age. Her diet is average. She is able to do about two hours of physical labor a day, and she has suffered from depression for years. She has tried numerous treatments for depression including Prozac, and some of them have helped, but none have completely eliminated the depression. Sometimes she aches all over. She was addicted to caffeine for several years, but only consumes it about once a week now. She has high blood pressure, and treats it with Vasotec and also takes Maxide (a diuretic).She ingested 650 mg of benfo once a day for five days and did not notice any difference. On day 6 she doubled the dose to 1300 mg and started to notice a change a few hours later. There was a dramatic increase in stamina and energy. She is now able to do eight hours of physical work each day. She has an extremely heightened sense of well-being and all aspects of the depression have left. She has better clarity of thought, and sleeps better. Previously she would usually wake up two or three times a night. Now she sleeps through the whole night and has said she is in a deeper sleep at night. She has reported being able to control her appetite more. She has reported less shortness of breath. On day 13 she has had no weight change. On day 13 she experienced what felt exactly like a caffeine withdrawal headache. She immediately consumed two cans of mountain dew and the headache did not leave. Previous to this, caffeine had always relieved a headache of this sort for her. At day 14 she still had a headache and the tips of her toes started tingling. She reduced her dose to 650 mg per day once a day on day 14. On day 15 she still had a headache. On day 16 her toes started tingling and the headache left. On day 17 her pinkie started tingling. Her blood pressure has always fluctuated between 120/80 and 150/90. Throughout the treatment her blood pressure has fluctuated like it normally does. She says she feels like she did when she was thirty years old. Comment: The tingling is likely the cause of blood circulating to parts of her body that have not had a great deal of circulation in recent years.Case study #2. Male, mid fifties, non-diabetic. Average diet. Overall health is better than average for his age. He gets indigestion at night and takes Prilosec. He has the normal aches and pains that accompany middle age. When he wakes up in the morning his feet are inflexible, but that would go away after walking on them for about two minutes. After driving for two hours he is stiff when he gets out of his car. Most of the aches and pains and the foot inflexibility appeared in the last five to fifteen years. He began taking 650 mg of benfo once a day. On day 3 nothing hurt when he woke up. By day five all his aches and pains had disappeared. He is no longer stiff when he gets out of his car after driving for two hours. He feels more flexible. He says it has fixed everything that has gone wrong with him in the past fifteen years. He says he feels more cheerful but is not sure if it is because of repair to neurological damage or because his aches and pains are gone. He has reported a greater clarity of thought. He says he feels like he did when he was age 25-40 (he says he felt the same during those years). Up until twelve months ago his blood pressure has been 120/90. For the past twelve months it has averaged 130/120. On day 5 his blood pressure was 120/85 and it has remained consistent every day since then. Now he can only take a fifteen minute nap during the day whereas before he could fall asleep for hours. At night he sleeps better, probably because the aches and pains are gone. His appetite is only about 80% of what it used to be. He has reported increased stamina and energy. Before taking benfo it was getting hard for him to do ten hours of work per day. Now he can do fourteen hours of work per day. He still requires the same amount of sleep at night, but if he does not get his full requirement he doesn’t notice it nearly as much.Comment: The decrease in caloric intake may be because he was lacking an essential nutrient- not enough thiamine? The stiffening of the joints brought on by old age is partly a symptom poor blood circulation. The fact that this individual has become much more flexible is a possible indication of increased circulation.Case study #3. Male, late forties. He has been a type 1 diabetic for twenty years. Average diet. Over the last five years his health has declined more rapidly. He has more aches and pains than the average person because he is diabetic. He aches so much at night that he usually can’t get to sleep unless he takes Ibuprofen. He began taking 650 mg benfo once a day. On day 2 he noticed a decline in the severity of his aches and pains. He still needs the same amount of sleep, but if he doesn’t get his full requirement he doesn’t notice nearly as much. He has had an increase in stamina and energy. He says his stamina has doubled. On day 14 he felt like he did ten years ago, and it keeps improving each day. He is more cheerful, but like #2 he can’t tell if it’s because his aches and pains are gone or if benfo has a neurological effect on him. I will not disclose the brand of benfo which was used because I do not wish to be seen as promoting any particular brand. These case studies will be updated on July 5, 2003 and new ones will be added. The updates will be posted on www.geocities.com/robholladay99/updates.html The following exerpts are from medical journals. The abstracts (summaries) for most of them can be viewed online through the pubmed database, which is a free database most biomedical scientists use. To find pubmed, go to google.com and type in pubmed. Once you’re in pubmed, type in part of the title and you should be able to find the abstract. When typing in the title use "benfotiamine" not "benfo". As an anti-spamming measure, many search engines will not index web pages that list the key search words more than seven times throughout the document, hence this document was modified after it was created . Several things are important to note in the following literature. First of all, not only does benfo stop some effects of aging, it reverses them. Gradually over time people’s neurons quit working because of normal wear and tear. However, when benfo was ingested, not only did the nerve damage stop, some of the damage done through aging was repaired. A strong point is made that benfo is the most bioavailable source of thiamine. This means benfo is better absorbed than other sources of thiamine. Also, high levels of thiamine have analgesic (pain-relieving) effects on animals. In the Russian study the pain level of the patients decreased from 8.2 to 2.3, a decrease of about four hundred percent. Research articles on benfoWada T, Tagaki H, Minakami H, Hamanka W, Okamoto K, Ito, A, Sahashi Y. 1961. A new thiamine derivative, S-benzoylthiamine O-monophosphate. Science 134: 195-196.Benfo “is more easily absorbed in the body than thiamine hydrochloride, and administration results in higher thiamine and cocarboxylase levels in organs; moreover, these levels last for a longer period of time…It does not cause any unfavorable symptom in animals such as thiamine hydrochloride does…The LD50 by oral administration in mice, dd-strain hybrid, weighing 14 to 16g was 15g/kg of body weight”Bitsch R, Wolf M, Moller J, Heuzeroth L, Gruneklee D. Bioavailability assessment of the lipophilic benfo as compared to a water-soluble thiamin derivative. Ann Nutr Metab. 1991;35(5):292-6. “in presence of allicin, the active principle of garlic, the water-soluble thiamin hydrochloride is transformed into a lipid-soluble compound being identified as allithiamine…Ten healthy young men…The volunteers ingested a single dose of 40 mg benfo…Thus, the measured values reveal, when compared with mononitrate, a clearly improved thiamin bioavailability from benfo, due to the more lipophilic properties of this substance or possibly its dephosphorylated metabolite and a more rapid transformation into the physiologically active derivative. This may be of great advantage in the treatment of neurological disorders responding to high thiamin doses and further on in situations when the active intestinal absorbtion mechanisms are impaired”Stracke H, Lindemann A, Federlin K. A benfo-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.“Benfo…was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold...Therapy-specific adverse effects were not seen”Loew D. Pharmacokinetics of thiamine derivatives especially of benfo. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.“The effective form of thiamine, thiamine diphosphate, is an organic compound needed by the organism for vital functions…Due to this peculiarity the conditions for absorbtion of lipid-soluble vitamins differ from those for water-soluble thiamine derivatives. Unlike the latter, allithiamines are absorbed passively, they traverse the intestinal absorption barrier faster and more readily, leading to higher blood and tissue concentrations even when comparatively low doses are given…It therefore fulfills important pharmacodynamic conditions for rational therapy. Due to their greater biovailability and better tissue passage lipid-soluble thiamine analogues like benfo are preferable to water-soluble thiamine derivatives for treatment of various pathological conditions, e.g. cardiomyopathy, Werincke-Korsakow syndrome, and alcoholic or diabetic polyneuropathies…Due to its excellent pharmacokinetic profile and to its excellent tolerability benfo should be preferred in treatment of relevant conditions like neuropathies”Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter CH. Comparative bioavailability of two vitamin B1 preparations: benfo and thiamine mononitrate. Eur J Clin Pharmacol. 1997;52(4):319-20.“a study using equimolar quantities of the two preparations for exact comparison of the bioavailability of benfo and thiamine mononitrate has never been performed. Therfore, the present trial was undertaken…the higher thiamine content in the erythrocytes and the higher thiamine excretion in urine after oral benfo administration are proof of the considerably higher relative bioavailability of benfo than thiamine mononitrate”Simeonov S, Pavlova M, Mitkov M, Mincheva L, Troev D. Therapeutic efficacy of "Milgamma" in patients with painful diabetic neuropathy. Folia Med (Plovdiv). 1997;39(4):5-10.“Forty-Five diabetes patients with painful peripheral polyneuropathy were enrolled in a 3-month observational study comparing the therapeutic efficiacy of Milgamma tablets (benfo)…Statistically significant relief of both background and peak neuropathic pain was achieved in all of the Milgamma-treated patients…No adverse reactions were observed…Our results underscore the importance of Milgamma tablets as an indispensable element in the therapeutic regimen of patients with painful diabetic polyneuropathy”Greb A, Bitsch R. Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther. 1998 Apr;36(4):216-21.“Seven healthy volunteers…a single oral dose of either benfo…fursultiamin…thiaminedisulfide…In this study the allithiamine derivative benfo proved the best bioavailability. Owing to its excellent absorption properties it can be concluded that oral administration of benfo is suitable for therapeutical purposes”Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfo in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.Good review, full-text is available free online. “In bioavailability studies on healthy human subjects, it was shown that absorption of benfo was several times better than that of water-soluble vitamin B1 and that there was a 120-fold higher increase of metabolically active thiamine diphosphate in erythrocytes (Heinrich, 1990)…In animals given dosages that exceeded basic requirements by 100- or 1000-fold thiamine has analgesic and neuroprotective effects(woelk and peeler-Ichakawa, 1985; Jurna, 1988; Reeh, 1988, 1991; Wild, 1988). However, if high levels are to be achieved with oral vitamin B1 treatment, lipid soluble thiamine derivatives or pro-drugs with high bioavailability, such as benfo, are required…320 mg/day during weeks 1 to 4 and 120 mg benfo/day during weeks 5 to 8…Within the 8-week study period, benfo led to a significant improvement of the threshold of vibration perception at the great toe, motor function, and the overall symptom score. Marked improvement occurred in both pain and co-ordination”Sadekov RA, Danilov AB, Vein AM. [Diabetic polyneuropathy treatment by milgamma-100 preparation] Zh Nevrol Psikhiatr Im S S Korsakova. 1998;98(9):30-2. Russian.“benfo…was studied in treatment of diabetic polyneuropathy in 14 patients…After the course of treatment the intensity of pains was decreased according to visual analogous scale on the average from 8.2 to 2.3 scores, the indices of vibratory sensitivity improved significantly as well as the data of cardiovascular tests…The treatment resulted in the improvement of the condition in 93% of the cases” T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine pharmacokinetics by end-stage renal disease (ESRD). Int J Clin Pharmacol Ther. 1999 Sep;37(9):449-55.“20 end-stage renal disease(ESRD) patients…After a single oral dose of 100 mg benfo…ESRD patients may benefit from high-dose thiamine derivatives notwithstanding their chemical form. However, the better absorption and high transfer rate of debenzoylated BTMP (benfo) to TDP (thiamine diphosphate) even at much lower doses compensates for reduced renal excretion and may protect, therefore, against numerous adverse effects of uremia”Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different benfo dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.320, 120, and 150 mg benfo/day was administered to “diabetic patients suffering from painful peripheral diabetic neuropathy. In a 6-week open clinical trial, 36 patients…An overall beneficial therapeutic effect on the neuropathy status was observed in all three groups during the study…The greatest change occurred in the group of patients receiving the high dose of benfo…Metabolic control did not change over the study...Extremely interesting is the result of recent in vitro experiences that thiamine pyrophosphate and pyroxidine inhibit the formation of glycation end products" T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfo. Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.“20 end-stage renal disease (ESRD) patients…After benfo administration, the peak plasma concentration of TDP exceeded that in healthy subjects by 51%...Compared with thiamine nitrate, the oral administration of benfo leads to higher TDP concentrations in erythrocytes accompanied with a significant improvement of the erythrocyte transkelotase activity in ESRD patients”Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M. Benfo is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.“We investigated the hypothesis that benfo, a lipophilic derivative of thiamine, affects replication delay and generation of advanced glycosylation endproducts (AGE) in human umbilical vein endothelial cells cultured in the presence of high glucose…Benfo, a derivative of thiamine with better bioavailability, corrects defective replication and increased AGE generation in endothelial cells cultured in high glucose, to a similar extent as thiamine. These effects may result from normalization of accelerated glycolysis and the consequent decrease in metabolites that are extremely active in generating nonenzymatic protein glycation. The potential role of thiamine administration in the prevention or treatment of vascular complications of diabetes deserves further investigation”Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M, Geyer J, Kopcke W, Sauerland C, Bretzel RG, Federlin KF. Efficacy of benfo versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.“After three months preventative administration of both vitamin B1 preparations NCV (nerve conduction velocity) had increased substantially…It was nearly normal after six months with benfo, while the administration of thiamine nitrate resulted in no further amelioration. NCV was nearly normalized after six months of benfo application but not with thiamine. Furthermore, benfo induced a major inhibition of neural imidazole-type AGE formation and completely prevented diabetes induced glycoxidation products”Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M. Benfo blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.“Our results in both endothelial cells cultured for several days and retinas from rats with nine months of diabetes showed that benfo, a lipid-soluble thiamine derivative, prevents activation of three major pathways involved in hyperglycemia-induced vascular damage: the hexosamine pathway, the intracellular AGE formation pathway and the DAG-PKC pathway…We showed that benfo blocks these pathways of hyperglycemic damage by increasing the activity of transketolase…Administration of benfo for nine months also completely prevented the development of experimental diabetic retinopathy in rats...Thus we conclude that augmentation of transketolase activity is solely responsible for the observed effects of benfo”Comment: This study is very significant because it demonstrates how benfo blocks several other aging mechanisms besides AGE formation. However, I am not yet convinced of the statement that transketolase activity is solely responsible for the observed effects of benfo. The following four studies are located on the Internet but are not yet listed on Medline. To find them, go to google.com and type in part of the titleBergfeld R, Matsumara X. Du, Brownlee M. Benfo prevents the consequences of hyperglycemia-induced mitochondrial overproduction of reactive oxygen species, and experimental diabetic retinopathy.“diabetic rats were treated with benfo (80 mg/kg weight) for 36 weeks…Benfo decreases AGE formation by 60%...These data suggest that treatment with benfo may be an effective approach to prevent the development of diabetic complications”Lin J, Alt A, Liersch J, Bretzel R, Brownlee M, Hammes H. Benfo inhibits intracellular formation of advanced glycation end products in vivo“Here, we studied the effect of benfo, a lipid-soluble thiamine derivative with known AGE-inhibiting properties in vitro on the intracellular formation of (CML) and methylgloxal-derived AGE in red blood cells. Blood was collected from 6 type 1 diabetic patients before and after treatment with 600 mg/day benfo for 28 days…Thiamine derivatives, in particular the lipid-soluble prodrug benfo, are effective inhibitors of intracellular formation of AGE and CML”Stracke H, Werkmann D, Mavrakis K, Federlin K, Kopke W, Sauerland C, Hammes H, Bretzel RG. Influence of vitamin B1 on diabetic neuropathy-studies in streptozotocin-diabetic rats.“we investigated the effects of oral administration of thiamine and benfo on the development of glucose oxidation products in the nerve and on nerve conduction velocity in streptozotocin-diabetic rats…Conclusion: Early treatment with benfo normalizes increased cellular oxidative stress and the reduced nerve conduction velocity”Hammes H, Bretzel, R.G., Federlin, K, Horiuchi S, Niwa T, Stracke H. Benfo inhibits the formation of advanced glycation end products in diabetic rats.“benfo (100 mg/kg x day) and thiamin (70.18 mg/kg x day) administered orally for 6 months…neither benfo nor thiamin treatment affected metabolic control…Benfo administration in diabetic rats induced a major inhibition of neutral imidazolone-type AGE formation and completely prevented diabetes-induced glycoxidation formation. Treatment with thiamin did not affect AGE or CML levels”ThiamineAllithiamines are lipid-soluble sources of thiamine. Benfo is an allithiamine. Thiamine is water-soluble and is also known as vitamin B1.After reviewing the relevant medical literature on thiamine, I have come to conclude that large portions of the population may be thiamine deficient. In addition, many individuals that are not technically thiamine deficient would likely receive benefit from thiamine supplementation. Thiamine deficiency is associated with numerous undesirable medical conditions.Relation of thiamine to heart diseaseShamir R, Dagan O, Abramovitch D, Abramovitch T, Vidne BA, Dinari G. Thiamine deficiency in children with congenital heart disease before and after corrective surgery. JPEN J Parenter Enteral Nutr. 2000 May-Jun;24(3):154-8.Thiamine deficiency “is common in children with congenital heart disease (CHD) referred for corrective surgery both before and after surgery. Our results suggest that neither diuretic treatment nor malnutrition can fully explain the development of TD in these children”Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E, Levy R. [Right heart failure caused by thiamine deficiency (cardiac beriberi)] Presse Med. 2000 Feb 12;29(5):240-1. French.Beaud C, Fuhrman C, Perchet H, Monnet I, Chouaid C, Housset B. [Thiamine deficiency. A cause of cardiac insufficiency not to be ignored] Rev Mal Respir. 1998 Jun;15(3):303-4. French.“Thiamine deficiency is one of the classical causes of high output for heart failure”Okura H, Gohma I, Hatta K, Imanaka T. Thiamine deficiency and pulmonary hypertension in Crow-Fukase syndrome. Intern Med. 1995 Jul;34(7):674-5. “After oral administration of prednisolone and thiamine, echocardiogram showed marked improvement of the pulmonary hypertension”Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc. 1995 May;95(5):541-4. “Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk”Shimon I, Almog S, Vered Z, Seligmann H, Shefi M, Peleg E, Rosenthal T, Motro M, Halkin H, Ezra D. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med. 1995 May;98(5):485-90.“Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy”Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered Z, Ezra D. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med. 1991 Aug;91(2):151-5.”These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements”Relation of thiamine to neurological disordersLonsdale D, Shamberger RJ, Audhya T. Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: a pilot study. Neuroendocrinol Lett. 2002 Aug;23(4):303-8.“Thiamine tetrahydrofurfuryl disulfide appears to have a beneficial clinical effect on some autistic children, since 8 of the 10 children improved clinically”Nakagawasai O, Tadano T, Hozumi S, Taniguchi R, Tan-No K, Esashi A, Niijima F, Kisara K. Characteristics of depressive behavior induced by feeding thiamine-deficient diet in mice.Life Sci. 2001 Jul 27;69(10):1181-91.Ambrose ML, Bowden SC, Whelan G. Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings. Alcohol Clin Exp Res. 2001 Jan;25(1):112-6.“A therapeutic relationship between dose and working memory performance was indicated”Older MW, Dickerson JW. Thiamine and the elderly orthopaedic patient. Age Ageing. 1982 May;11(2):101-7.“In both groups those patients who were noticeably confused after operation were found to have a considerable fall in their thiamine status suggesting this may be a contributory factor to postoperative confusion”Winston AP, son CP, Madira W, Gatward NM, Palmer RL. Prevalence of thiamin deficiency in anorexia nervosa. Int J Eat Disord. 2000 Dec;28(4):451-4.“Fourteen patients (38%) had results in the deficient range; 7 (19%) met the most stringent published criterion for deficiency. Deficiency was not related to duration of eating restraint, frequency of vomiting, or alcohol consumption”Terasawa M, Nakahara T, Tsukada N, Sugawara A, Itokawa Y. The relationship between thiamine deficiency and performance of a learning task in rats. Metab Brain Dis. 1999 Sep;14(3):137-48.“We taught rats to press a lever to escape from the pain of electrical stimulation by learning to turn a switch off… The rats that were fed the thiamine-deficient diet showed a slower response time and a longer running time than the rats fed the normal diet… We found that the thiamine concentration in the blood of the rats in the trained group was significantly higher than that in the group without training”Jimenez-Jimenez FJ, Molina JA, Hernanz A, Fernandez-Vivancos E, de Bustos F, Barcenilla B, Gomez-Escalonilla C, Zurdo M, Berbel A, Villanueva C. Cerebrospinal fluid levels of thiamine in patients with Parkinson's disease. Neurosci Lett. 1999 Aug 13;271(1):33-6.“These results suggest that low CSF free thiamine levels could be related with the risk for PD”Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J. 1997 Dec;74(12):803-8.“Diabetic peripheral neuropathy in Dar es Salaam is associated with thiamine deficiency”Langlais PJ, G, Guo SX, Bondy SC. Increased cerebral free radical production during thiamine deficiency. Metab Brain Dis. 1997 Jun;12(2):137-43.“These findings suggest that increased formation of free radicals occurs during the more acute symptomatic stage of thiamine deficiency and may contribute to the structural damage described in this model of Wernicke's encephalopathy”Easton CJ, Bauer LO. Beneficial effects of thiamine on recognition memory and P300 in abstinent cocaine-dependent patients. Psychiatry Res. 1997 May 30;70(3):165-74. “Thiamine was found to significantly improve recognition accuracy and P300 amplitude, at the midline parietal (Pz) electrode. The improvement was most reliable under conditions of increased memory load”Benton D, Griffiths R, Haller J. Thiamine supplementation mood and cognitive functioning. Psychopharmacology (Berl). 1997 Jan;129(1):66-71. ”An improvement in thiamine status was associated with reports of being more clearheaded, composed and energetic. The taking of thiamine had no influence on memory but reaction times were faster following supplementation”Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's disease. Metab Brain Dis. 1996 Mar;11(1):89-94.”Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100 mg/day had a mild beneficial effect in patients with Alzheimer's disease in a 12-week open trial. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function”Gold M, Chen MF, K. Plasma and red blood cell thiamine deficiency in patients with dementia of the Alzheimer's type. Arch Neurol. 1995 Nov;52(11):1081-6.“A significant proportion of patients with SDAT may have a thiamine deficiency, which may have an impact on cognitive function. Currently used assays may not be adequate to assess thiamine status”Adamolekun B, Eniola A. Thiamine-responsive acute cerebellar ataxia following febrile illness. Cent Afr J Med. 1993 Feb;39(2):40-1. Review.“acute thiamine depletion may be the pathogenetic mechanism for post-pyrexial acute cerebellar ataxia”Ben-Hur T, Wolff E, River Y. [Thiamin deficiency is common in Israel] Harefuah. 1992 Nov 15;123(10):382-4, 436, 435. Hebrew.“Thiamin levels should be determined not only in alcoholics and those with classic B1 deficiency syndromes, but in the routine workup of patients with sensory-motor neuropathy, dementia, gait disorders, cerebellar syndromes and confusional states”Sacks W, Esser AH, Feitel B, Abbott K. Acetazolamide and thiamine: an ancillary therapy for chronic mental illness. Psychiatry Res. 1989 Jun;28(3):279-88.“Overall, 50% of the patients showed improvement on all assessment scales. No untoward effects occurred in these patients…”Relation of thiamine and geriatric patientsSmidt LJ, Cremin FM, Grivetti LE, Clifford AJ. Influence of thiamin supplementation on the health and general well-being of an elderly Irish population with marginal thiamin deficiency. J Gerontol. 1991 Jan;46(1):M16-22.”thiamin-supplemented women experienced significantly increased appetite, energy intake, body weight and general well-being, and decreased fatigue. Thiamin supplementation also tended to reduce daytime sleep time, improve sleep patterns, and increase activity. These data suggest that evaluation of thiamin status is indicated when nonspecific conditions such as anorexia, weight loss, fatigue, depression, and sleep disorders are present in elderly persons”Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels in elder patients admitted through the emergency department. Acad Emerg Med. 2000 Oct;7(10):1156-9.“CONCLUSIONS: Elder nursing home patients seen in the ED and admitted to the hospital are frequently thiamine-deficient”Wilkinson TJ, Hanger HC, Elmslie J, PM, Sainsbury R. The response to treatment of subclinical thiamine deficiency in the elderly. Am J Clin Nutr. 1997 Oct;66(4):925-8.“Only the subjects with persistently low TPP concentrations showed subjective benefits from treatment with improvements in quality of life… There was a trend toward benefits in sleep and energy… Quality of life was enhanced by providing thiamine supplements. Blood pressure and weight were lower after thiamine supplementation”Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte thiamin concentrations in geriatric outpatients. J Am Coll Nutr. 1996 Jun;15(3):231-6.“CONCLUSION: About 50% of geriatric outpatients in this study had low plasma thiamin levels”Nichols HK, Basu TK. Thiamin status of the elderly: dietary intake and thiamin pyrophosphate response. J Am Coll Nutr. 1994 Feb;13(1):57-61.“Average daily thiamin intake was above the recommended requirement… however, almost half of the total study population had TPP effect > 14%, suggesting thiamin deficiency… CONCLUSION: These findings raise questions about the reliability of dietary intake in assessing metabolic availability of thiamin in the elderly”O'Keeffe ST, Tormey WP, Glasgow R, Lavan JN. Thiamine deficiency in hospitalized elderly patients. Gerontology. 1994;40(1):18-24.“Necropsy studies suggest that thiamine deficiency is underdiagnosed in life… There was no difference in anthropometric indices or in the prevalence of other nutrient deficiencies between the two groups. Thiamine deficiency is common in elderly patients admitted to hospital and may contribute to the development of delirium”Iber FL, Blass JP, Brin M, Leevy CM. Thiamin in the elderly--relation to alcoholism and to neurological degenerative disease. Am J Clin Nutr. 1982 Nov;36(5 Suppl):1067-82. Review.“There is no known toxicity for thiamin”Relation of thiamine to diabetesAvena R, Arora S, Carmody BJ, Cosby K, Sidawy AN. Thiamine (Vitamin B1) protects against glucose- and insulin-mediated proliferation of human infragenicular arterial smooth muscle cells. Ann Vasc Surg. 2000 Jan;14(1):37-43.“Vitamin B1 intake may prove important in delaying the atherosclerotic complications of diabetes”La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA, Molinatti GM, Porta M. Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions. Diabetologia. 1996 Nov;39(11):1263-8.Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S, Scheinman M, T. Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells. Surgery. 2001 Nov;130(5):851-8.“The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes”Hassan R, Qureshi H, Zuberi SJ. Effect of thiamine on glucose utilization in hepatic cirrhosis. J Gastroenterol Hepatol. 1991 Jan-Feb;6(1):59-60.“It is therefore suggested that thiamine supplements be given to cirrhotics with hyperglycaemia, to improve glucose utilization”Rindi G, Laforenza U. Thiamine intestinal transport and related issues: recent aspects.Proc Soc Exp Biol Med. 2000 Sep;224(4):246-55. Review.“Thiamine uptake is enhanced by thiamine deficiency, and reduced by thyroid hormone and diabetes”Saito N, Kimura M, Kuchiba A, Itokawa Y. Blood thiamine levels in outpatients with diabetes mellitus. J Nutr Sci Vitaminol (Tokyo). 1987 Dec;33(6):421-30.“From the above findings it was concluded that diabetic outpatients tend to have a low blood thiamine level, with low erythrocyte transketolase activity and high erythrocyte TPP effect, and showed marginal thiamine deficiency” Relation of thiamine to diseaseWallace AE, Weeks WB. Thiamine treatment of chronic hepatitis B infection. Am J Gastroenterol. 2001 Mar;96(3):864-8.”In each case study, thiamine administration was associated with reduction in aminotransferase levels and the fall of HBV DNA to undetectable levels… The relationship between thiamine administration and chronic hepatitis B infection warrants further study. If proven effective in reducing liver damage or inducing remission of the hepatitis B virus in larger trials, thiamine will offer obvious advantages over the current treatments for chronic viral hepatitis B infection”Rossouw JE, Labadarios D, Krasner N, M, R. Red blood cell transketolase activity and the effect of thiamine supplementation in patients with chronic liver disease. Scand J Gastroenterol. 1978;13(2):133-8.“Biochemical evidence of thiamine deficiency was found in 58% of patients with chronic liver disease… high doses of thiamine should be included in the routine nutritional management of patients with severe chronic liver disease”Shoji S, Furuishi K, Misumi S, Miyazaki T, Kino M, Yamataka K. Thiamine disulfide as a potent inhibitor of human immunodeficiency virus (type-1) production. Biochem Biophys Res Commun. 1994 Nov 30;205(1):967-75.” The results suggest that thiamine disulfide may be important for AIDS chemotherapy”Shoji S, Furuishi K, Ogata A, Yamataka K, Tachibana K, Mukai R, Uda A, Harano K, Matsushita S, Misumi S. An allosteric drug, o,o'-bismyristoyl thiamine disulfide, suppresses HIV-1 replication through prevention of nuclear translocation of both HIV-1 Tat and NF-kappa B. Biochem Biophys Res Commun. 1998 Aug 28;249(3):745-53.Butterworth RF, Gaudreau C, Vincelette J, Bourgault AM, Lamothe F, Nutini AM. Thiamine deficiency and Wernicke's encephalopathy in AIDS. Metab Brain Dis. 1991 Dec;6(4):207-12.“we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse… it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex”Haisraeli-Shalish M, Livneh A, Katz J, Doolman R, Sela BA. Recurrent aphthous stomatitis and thiamine deficiency. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Dec;82(6):634-6.” 70 patients with recurrent aphthous stomatitis and in 50 members of a control group… Low levels of vitamin B1 were detected in 49 patients but in only two members of the control group… Our finding suggests an association between thiamine deficiency and recurrent aphthous stomatitis”Engel D. Tropical pyomyositis, a thiamine-deficiency disease. Med Hypotheses. 1981 Mar;7(3):345-52.“it is suggested that thiamine deficiency is an essential contributary factor in producing tropical pyomyositis… Thiamine deficiency induces a biochemical lesion (s) in the pyruvate oxidase system of the muscle, which breaks down its normal resistance to infection and opens the gate to bacterial agents”Krishna S, AM, Supanaranond W, Pukrittayakamee S, ter Kuile F, Tawfiq KM, Holloway PA, White NJ. Thiamine deficiency and malaria in adults from southeast Asia. Lancet. 1999 Feb 13;353(9152):546-9.”12 (52%) of 23 patients with severe malaria and ten (19%) of 54 patients with uncomplicated malaria had alpha values above the normal range (p<0.0001 and p=0.0014, respectively, compared with controls), which indicated severe thiamine deficiency” Pietrzak I, Baczyk K, Mlynarczyk M, Kaczmarek M. [Content of thiamin in plasma and erythrocytes in patients with end stage renal disease] Przegl Lek. 1996;53(5):423-6. Polish.”We suggest the need of thiamine supplementation in ESRD patients especially in those treated by dialysis. The supplementation of thiamine is needed particularly in patients on peritoneal dialysis”Relation of thiamine to other dataHung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. 2001 Nov;38(5):941-7.“We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency”Huang S, Ren G. [Thiamine status of university teacher families in Changsha] Hunan Yi Ke Da Xue Xue Bao. 1998;23(1):27-30. Chinese.“We conclude that those people who take the refined cereals and its products as a staple food, is in the risk of thiamine deficiency”Suzuki M, Itokawa Y. Effects of thiamine supplementation on exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106.“High-dose thiamine (vitamin B1) supplementation (100 mg/day) may be helpful in preventing or accelerating recovery from exercise-induced fatigue… Thiamine supplementation significantly suppressed the increase in blood glucose in the normal thiamine group and significantly decreased the number of complaints shortly after exercise in the subjective fatigue assessment of 30 items”Kimura M, Itokawa Y, Fujiwara M. Cooking losses of thiamin in food and its nutritional significance. J Nutr Sci Vitaminol (Tokyo). 1990;36 Suppl 1:S17-24.”The thiamin contents in cooked daily meals were 50-60 percent of the calculated values on an average”Cruickshank AM, Telfer AB, Shenkin A. Thiamine deficiency in the critically ill. Intensive Care Med. 1988;14(4):384-7.“We performed a retrospective study on 158 patients admitted to the Intensive Care Unit who required nutritional support. Patients who survived had significantly higher body thiamine status than those who died”Onodera K, Kisara K, Okabe H, Ogura Y. [studies on the effects of thiamine deficiency on rat testes (author's transl)] Nippon Yakurigaku Zasshi. 1980 Mar;76(2):143-52. Japanese.“In the thiamine deficient group, the seminiferous tubuli of rats having erections had atrophied”Labadarios D, Rossouw JE, McConnell JB, M, R. Thiamine deficiency in fulminant hepatic failure and effects of supplementation. Int J Vitam Nutr Res. 1977;47(1):17-22.“Nine out of 24 patients with acute hepatocellular necrosis leading to fulminant hepatic failure showed biochemical evidence of thiamine deficiency early in the course of their illness”Why haven’t we heard of benfo before? The patent on the manufacture of benfo expired decades ago. Pharmaceutical companies pursue drugs that can be patented so they can have a monopoly and charge 100 times what the drug is worth. They have spent a lot of money on AGE inhibitors that don’t work as well as benfo. Ingestion of benfo may result in the elimination of AGE-protein crosslinks, which are a major constituent of arterial plaque. I am intrigued by the idea that benfo may cause the removal of plaque from the blood vessels, but I am concerned about the rapid manner in which it may cause the removal of plaque from the blood vessels. If the plaque is being removed, a large chunk might break off and cause a stroke or heart attack. If I was older than 60 or if I had a serious problem with high blood pressure I would probably start out by taking very low doses of benfo and gradually increase my dosage. Of course, there are no reports of strokes or heart attacks from benfo in the medical literature, but it’s a thought to consider. My PhD research will mostly consist of double-blind controlled studies on the administration of benfo in normal individuals, diabetics, individuals with high blood pressure, Alzheimer patients etc. I believe the researchers who have investigated benfo to date have been extremely short sighted by not discovering they full potential of benfo in the clinical studies that have already been performed on humans.It is illegal to make claims about benfo and sell it as a dietary supplement unless the claims are based on substantial scientific evidence. The three case studies outlined in this document are not from a double-blind controlled study and FDA regulations would not allow for them to be referred to as substantial scientific evidence. Claims should not be made based on these preliminary findings. For questions or comments email robholladay99@...Since I am not a physician, it would be inappropriate for me to answer emails asking for medical advice.

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[Guest guest]

Hello -

I would like to make a suggestion. Can people perhaps place

articles such as this in the " Files " section? That way, when we

want to find it later we do not have to go digging through old

messages. It might be useful to place the pharmacy names / numbers

as well as physicians that prescribe LDN in there too. Anyone else

like to see this?

Have a great day!

--- In low dose naltrexone , " tmbayuk " <tmbayuk@v...>

wrote:

> Network Blitz

> ----- Original Message -----

> From:

> tmbayuk

> Sent: Saturday, March 20, 2004 11:01 PM

> Subject: check this out!

>

>

> Research on Benfotiamine

> Clinton Holladay, M.S.

> Copyright 2003 Clinton Holladay

> June 5, 2003

>

>

> A short while ago a group of individuals I know purchased a large

amount of benfotiamine and began ingesting it orally. I was urged

by these individuals to place some of the research I have been

conducting on benfo (benfotiamine) online along with the results of

their benfo use. I was asked to do this in a manner that would

allow individuals that do not have a background in the health

sciences to comprehend it. I will be pursuing a PhD shortly and

benfo will be central to my research. I am not a physician and the

following information is not intended to be used as medical advice.

>

> Advanced glycation endproducts or AGEs are produced by the

processing of sugars within the cell. They are one of the primary

causes of aging and general wear and tear on your cells. Diabetics

age the same way as normal people, but because they often have

abnormal levels of sugars in their cells, they age faster. When

blood sugar levels are high, certain cells in the body are flooded

with glucose, particularly neurons and cells in the eyes and

kidneys. Diabetics often suffer from nerve damage, kidney failure,

and premature blindness. Numerous researchers have concentrated

their efforts on AGE-blocking mechanisms because they would limit

the wear and tear on the body's cells and allow individuals to live

longer and healthier, particularly diabetics. Benfo has emerged as

the premier AGE inhibitor.

>

> Case Studies

> It is important to note that the following case studies are not

double-blind controlled studies.

>

> Case study #1. Female, early fifties, non-diabetic, suffers from

chronic fatigue, depression, and the normal aches and pains that

accompany middle age. Her diet is average. She is able to do about

two hours of physical labor a day, and she has suffered from

depression for years. She has tried numerous treatments for

depression including Prozac, and some of them have helped, but none

have completely eliminated the depression. Sometimes she aches all

over. She was addicted to caffeine for several years, but only

consumes it about once a week now. She has high blood pressure,

and treats it with Vasotec and also takes Maxide (a diuretic).

> She ingested 650 mg of benfo once a day for five days and did not

notice any difference. On day 6 she doubled the dose to 1300 mg and

started to notice a change a few hours later. There was a dramatic

increase in stamina and energy. She is now able to do eight hours

of physical work each day. She has an extremely heightened sense of

well-being and all aspects of the depression have left. She has

better clarity of thought, and sleeps better. Previously she would

usually wake up two or three times a night. Now she sleeps through

the whole night and has said she is in a deeper sleep at night. She

has reported being able to control her appetite more. She has

reported less shortness of breath. On day 13 she has had no weight

change. On day 13 she experienced what felt exactly like a caffeine

withdrawal headache. She immediately consumed two cans of mountain

dew and the headache did not leave. Previous to this, caffeine had

always relieved a headache of this sort for her. At day 14 she still

had a headache and the tips of her toes started tingling. She

reduced her dose to 650 mg per day once a day on day 14. On day 15

she still had a headache. On day 16 her toes started tingling and

the headache left. On day 17 her pinkie started tingling. Her

blood pressure has always fluctuated between 120/80 and 150/90.

Throughout the treatment her blood pressure has fluctuated like it

normally does. She says she feels like she did when she was thirty

years old.

> Comment: The tingling is likely the cause of blood circulating to

parts of her body that have not had a great deal of circulation in

recent years.

>

> Case study #2. Male, mid fifties, non-diabetic. Average diet.

Overall health is better than average for his age. He gets

indigestion at night and takes Prilosec. He has the normal aches

and pains that accompany middle age. When he wakes up in the

morning his feet are inflexible, but that would go away after

walking on them for about two minutes. After driving for two hours

he is stiff when he gets out of his car. Most of the aches and

pains and the foot inflexibility appeared in the last five to

fifteen years.

> He began taking 650 mg of benfo once a day. On day 3 nothing hurt

when he woke up. By day five all his aches and pains had

disappeared. He is no longer stiff when he gets out of his car

after driving for two hours. He feels more flexible. He says it

has fixed everything that has gone wrong with him in the past

fifteen years. He says he feels more cheerful but is not sure if it

is because of repair to neurological damage or because his aches and

pains are gone. He has reported a greater clarity of thought. He

says he feels like he did when he was age 25-40 (he says he felt the

same during those years). Up until twelve months ago his blood

pressure has been 120/90. For the past twelve months it has

averaged 130/120. On day 5 his blood pressure was 120/85 and it has

remained consistent every day since then. Now he can only take a

fifteen minute nap during the day whereas before he could fall

asleep for hours. At night he sleeps better, probably because the

aches and pains are gone. His appetite is only about 80% of what it

used to be. He has reported increased stamina and energy. Before

taking benfo it was getting hard for him to do ten hours of work per

day. Now he can do fourteen hours of work per day. He still

requires the same amount of sleep at night, but if he does not get

his full requirement he doesn't notice it nearly as much.

> Comment: The decrease in caloric intake may be because he was

lacking an essential nutrient- not enough thiamine? The stiffening

of the joints brought on by old age is partly a symptom poor blood

circulation. The fact that this individual has become much more

flexible is a possible indication of increased circulation.

>

> Case study #3. Male, late forties. He has been a type 1 diabetic

for twenty years. Average diet. Over the last five years his

health has declined more rapidly. He has more aches and pains than

the average person because he is diabetic. He aches so much at

night that he usually can't get to sleep unless he takes Ibuprofen.

> He began taking 650 mg benfo once a day. On day 2 he noticed a

decline in the severity of his aches and pains. He still needs the

same amount of sleep, but if he doesn't get his full requirement he

doesn't notice nearly as much. He has had an increase in stamina

and energy. He says his stamina has doubled. On day 14 he felt

like he did ten years ago, and it keeps improving each day. He is

more cheerful, but like #2 he can't tell if it's because his aches

and pains are gone or if benfo has a neurological effect on him.

>

> I will not disclose the brand of benfo which was used because I do

not wish to be seen as promoting any particular brand. These case

studies will be updated on July 5, 2003 and new ones will be added.

The updates will be posted on

www.geocities.com/robholladay99/updates.html

>

> The following exerpts are from medical journals. The abstracts

(summaries) for most of them can be viewed online through the pubmed

database, which is a free database most biomedical scientists use.

To find pubmed, go to google.com and type in pubmed. Once you're in

pubmed, type in part of the title and you should be able to find the

abstract. When typing in the title use " benfotiamine " not " benfo " .

As an anti-spamming measure, many search engines will not index web

pages that list the key search words more than seven times

throughout the document, hence this document was modified after it

was created .

> Several things are important to note in the following literature.

First of all, not only does benfo stop some effects of aging, it

reverses them. Gradually over time people's neurons quit working

because of normal wear and tear. However, when benfo was ingested,

not only did the nerve damage stop, some of the damage done through

aging was repaired. A strong point is made that benfo is the most

bioavailable source of thiamine. This means benfo is better

absorbed than other sources of thiamine. Also, high levels of

thiamine have analgesic (pain-relieving) effects on animals. In the

Russian study the pain level of the patients decreased from 8.2 to

2.3, a decrease of about four hundred percent.

>

> Research articles on benfo

>

> Wada T, Tagaki H, Minakami H, Hamanka W, Okamoto K, Ito, A,

Sahashi Y. 1961. A new thiamine derivative, S-benzoylthiamine O-

monophosphate. Science 134: 195-196.

> Benfo " is more easily absorbed in the body than thiamine

hydrochloride, and administration results in higher thiamine and

cocarboxylase levels in organs; moreover, these levels last for a

longer period of time…It does not cause any unfavorable symptom in

animals such as thiamine hydrochloride does…The LD50 by oral

administration in mice, dd-strain hybrid, weighing 14 to 16g was

15g/kg of body weight "

>

> Bitsch R, Wolf M, Moller J, Heuzeroth L, Gruneklee D.

Bioavailability assessment of the lipophilic benfo as compared to a

water-soluble thiamin derivative. Ann Nutr Metab. 1991;35(5):292-

6.

> " in presence of allicin, the active principle of garlic, the water-

soluble thiamin hydrochloride is transformed into a lipid-soluble

compound being identified as allithiamine…Ten healthy young men…The

volunteers ingested a single dose of 40 mg benfo…Thus, the measured

values reveal, when compared with mononitrate, a clearly improved

thiamin bioavailability from benfo, due to the more lipophilic

properties of this substance or possibly its dephosphorylated

metabolite and a more rapid transformation into the physiologically

active derivative. This may be of great advantage in the treatment

of neurological disorders responding to high thiamin doses and

further on in situations when the active intestinal absorbtion

mechanisms are impaired "

>

> Stracke H, Lindemann A, Federlin K. A benfo-vitamin B combination

in treatment of diabetic polyneuropathy. Exp Clin Endocrinol

Diabetes. 1996;104(4):311-6.

> " Benfo…was studied over a period of 12 weeks on 24 diabetic

patients with diabetic polyneuropathy. The results showed a

significant improvement of nerve conduction velocity in the peroneal

nerve and a statistical trend toward improvement of the vibration

perception threshold...Therapy-specific adverse effects were not

seen "

>

> Loew D. Pharmacokinetics of thiamine derivatives especially of

benfo. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.

> " The effective form of thiamine, thiamine diphosphate, is an

organic compound needed by the organism for vital functions…Due to

this peculiarity the conditions for absorbtion of lipid-soluble

vitamins differ from those for water-soluble thiamine derivatives.

Unlike the latter, allithiamines are absorbed passively, they

traverse the intestinal absorption barrier faster and more readily,

leading to higher blood and tissue concentrations even when

comparatively low doses are given…It therefore fulfills important

pharmacodynamic conditions for rational therapy. Due to their

greater biovailability and better tissue passage lipid-soluble

thiamine analogues like benfo are preferable to water-soluble

thiamine derivatives for treatment of various pathological

conditions, e.g. cardiomyopathy, Werincke-Korsakow syndrome, and

alcoholic or diabetic polyneuropathies…Due to its excellent

pharmacokinetic profile and to its excellent tolerability benfo

should be preferred in treatment of relevant conditions like

neuropathies "

>

> Schreeb KH, Freudenthaler S, Vormfelde SV, Gundert-Remy U, Gleiter

CH. Comparative bioavailability of two vitamin B1 preparations:

benfo and thiamine mononitrate. Eur J Clin Pharmacol. 1997;52

(4):319-20.

> " a study using equimolar quantities of the two preparations for

exact comparison of the bioavailability of benfo and thiamine

mononitrate has never been performed. Therfore, the present trial

was undertaken…the higher thiamine content in the erythrocytes and

the higher thiamine excretion in urine after oral benfo

administration are proof of the considerably higher relative

bioavailability of benfo than thiamine mononitrate "

>

> Simeonov S, Pavlova M, Mitkov M, Mincheva L, Troev D. Therapeutic

efficacy of " Milgamma " in patients with painful diabetic

neuropathy. Folia Med (Plovdiv). 1997;39(4):5-10.

> " Forty-Five diabetes patients with painful peripheral

polyneuropathy were enrolled in a 3-month observational study

comparing the therapeutic efficiacy of Milgamma tablets (benfo)…

Statistically significant relief of both background and peak

neuropathic pain was achieved in all of the Milgamma-treated

patients…No adverse reactions were observed…Our results underscore

the importance of Milgamma tablets as an indispensable element in

the therapeutic regimen of patients with painful diabetic

polyneuropathy "

>

> Greb A, Bitsch R. Comparative bioavailability of various thiamine

derivatives after oral administration. Int J Clin Pharmacol Ther.

1998 Apr;36(4):216-21.

> " Seven healthy volunteers…a single oral dose of either benfo…

fursultiamin…thiaminedisulfide…In this study the allithiamine

derivative benfo proved the best bioavailability. Owing to its

excellent absorption properties it can be concluded that oral

administration of benfo is suitable for therapeutical purposes "

>

> Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfo in treatment of

alcoholic polyneuropathy: an 8-week randomized controlled study (BAP

I Study). Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.

> Good review, full-text is available free online. " In

bioavailability studies on healthy human subjects, it was shown that

absorption of benfo was several times better than that of water-

soluble vitamin B1 and that there was a 120-fold higher increase of

metabolically active thiamine diphosphate in erythrocytes (Heinrich,

1990)…In animals given dosages that exceeded basic requirements by

100- or 1000-fold thiamine has analgesic and neuroprotective effects

(woelk and peeler-Ichakawa, 1985; Jurna, 1988; Reeh, 1988, 1991;

Wild, 1988). However, if high levels are to be achieved with oral

vitamin B1 treatment, lipid soluble thiamine derivatives or pro-

drugs with high bioavailability, such as benfo, are required…320

mg/day during weeks 1 to 4 and 120 mg benfo/day during weeks 5 to 8…

Within the 8-week study period, benfo led to a significant

improvement of the threshold of vibration perception at the great

toe, motor function, and the overall symptom score. Marked

improvement occurred in both pain and co-ordination "

>

> Sadekov RA, Danilov AB, Vein AM. [Diabetic polyneuropathy

treatment by milgamma-100 preparation] Zh Nevrol Psikhiatr Im S S

Korsakova. 1998;98(9):30-2. Russian.

> " benfo…was studied in treatment of diabetic polyneuropathy in 14

patients…After the course of treatment the intensity of pains was

decreased according to visual analogous scale on the average from

8.2 to 2.3 scores, the indices of vibratory sensitivity improved

significantly as well as the data of cardiovascular tests…The

treatment resulted in the improvement of the condition in 93% of the

cases "

>

> T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine

pharmacokinetics by end-stage renal disease (ESRD). Int J Clin

Pharmacol Ther. 1999 Sep;37(9):449-55.

> " 20 end-stage renal disease(ESRD) patients…After a single oral

dose of 100 mg benfo…ESRD patients may benefit from high-dose

thiamine derivatives notwithstanding their chemical form. However,

the better absorption and high transfer rate of debenzoylated BTMP

(benfo) to TDP (thiamine diphosphate) even at much lower doses

compensates for reduced renal excretion and may protect, therefore,

against numerous adverse effects of uremia "

>

> Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P.

Effectiveness of different benfo dosage regimens in the treatment of

painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49

(3):220-4.

> 320, 120, and 150 mg benfo/day was administered to " diabetic

patients suffering from painful peripheral diabetic neuropathy. In

a 6-week open clinical trial, 36 patients…An overall beneficial

therapeutic effect on the neuropathy status was observed in all

three groups during the study…The greatest change occurred in the

group of patients receiving the high dose of benfo…Metabolic control

did not change over the study...Extremely interesting is the result

of recent in vitro experiences that thiamine pyrophosphate and

pyroxidine inhibit the formation of glycation end products "

>

> T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate

concentrations in erythrocytes can be achieved in dialysis patients

by oral administration of benfo. Eur J Clin Pharmacol. 2000 Jun;56

(3):251-7.

> " 20 end-stage renal disease (ESRD) patients…After benfo

administration, the peak plasma concentration of TDP exceeded that

in healthy subjects by 51%...Compared with thiamine nitrate, the

oral administration of benfo leads to higher TDP concentrations in

erythrocytes accompanied with a significant improvement of the

erythrocyte transkelotase activity in ESRD patients "

>

> Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM,

Porta M. Benfo is similar to thiamine in correcting endothelial

cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-

8.

> " We investigated the hypothesis that benfo, a lipophilic

derivative of thiamine, affects replication delay and generation of

advanced glycosylation endproducts (AGE) in human umbilical vein

endothelial cells cultured in the presence of high glucose…Benfo, a

derivative of thiamine with better bioavailability, corrects

defective replication and increased AGE generation in endothelial

cells cultured in high glucose, to a similar extent as thiamine.

These effects may result from normalization of accelerated

glycolysis and the consequent decrease in metabolites that are

extremely active in generating nonenzymatic protein glycation. The

potential role of thiamine administration in the prevention or

treatment of vascular complications of diabetes deserves further

investigation "

>

> Stracke H, Hammes HP, Werkmann D, Mavrakis K, Bitsch I, Netzel M,

Geyer J, Kopcke W, Sauerland C, Bretzel RG, Federlin KF. Efficacy

of benfo versus thiamine on function and glycation products of

peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes.

2001;109(6):330-6.

> " After three months preventative administration of both vitamin B1

preparations NCV (nerve conduction velocity) had increased

substantially…It was nearly normal after six months with benfo,

while the administration of thiamine nitrate resulted in no further

amelioration. NCV was nearly normalized after six months of benfo

application but not with thiamine. Furthermore, benfo induced a

major inhibition of neural imidazole-type AGE formation and

completely prevented diabetes induced glycoxidation products "

>

> Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J,

Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I,

Brownlee M. Benfo blocks three major pathways of hyperglycemic

damage and prevents experimental diabetic retinopathy. Nat Med.

2003 Mar;9(3):294-9.

> " Our results in both endothelial cells cultured for several days

and retinas from rats with nine months of diabetes showed that

benfo, a lipid-soluble thiamine derivative, prevents activation of

three major pathways involved in hyperglycemia-induced vascular

damage: the hexosamine pathway, the intracellular AGE formation

pathway and the DAG-PKC pathway…We showed that benfo blocks these

pathways of hyperglycemic damage by increasing the activity of

transketolase…Administration of benfo for nine months also

completely prevented the development of experimental diabetic

retinopathy in rats...Thus we conclude that augmentation of

transketolase activity is solely responsible for the observed

effects of benfo "

> Comment: This study is very significant because it demonstrates

how benfo blocks several other aging mechanisms besides AGE

formation. However, I am not yet convinced of the statement that

transketolase activity is solely responsible for the observed

effects of benfo.

>

> The following four studies are located on the Internet but are not

yet listed on Medline. To find them, go to google.com and type in

part of the title

>

> Bergfeld R, Matsumara X. Du, Brownlee M. Benfo prevents the

consequences of hyperglycemia-induced mitochondrial overproduction

of reactive oxygen species, and experimental diabetic retinopathy.

> " diabetic rats were treated with benfo (80 mg/kg weight) for 36

weeks…Benfo decreases AGE formation by 60%...These data suggest that

treatment with benfo may be an effective approach to prevent the

development of diabetic complications "

>

> Lin J, Alt A, Liersch J, Bretzel R, Brownlee M, Hammes H. Benfo

inhibits intracellular formation of advanced glycation end products

in vivo

> " Here, we studied the effect of benfo, a lipid-soluble thiamine

derivative with known AGE-inhibiting properties in vitro on the

intracellular formation of (CML) and methylgloxal-derived AGE in red

blood cells. Blood was collected from 6 type 1 diabetic patients

before and after treatment with 600 mg/day benfo for 28 days…

Thiamine derivatives, in particular the lipid-soluble prodrug benfo,

are effective inhibitors of intracellular formation of AGE and CML "

>

> Stracke H, Werkmann D, Mavrakis K, Federlin K, Kopke W, Sauerland

C, Hammes H, Bretzel RG. Influence of vitamin B1 on diabetic

neuropathy-studies in streptozotocin-diabetic rats.

> " we investigated the effects of oral administration of thiamine

and benfo on the development of glucose oxidation products in the

nerve and on nerve conduction velocity in streptozotocin-diabetic

rats…Conclusion: Early treatment with benfo normalizes increased

cellular oxidative stress and the reduced nerve conduction velocity "

>

> Hammes H, Bretzel, R.G., Federlin, K, Horiuchi S, Niwa T, Stracke

H. Benfo inhibits the formation of advanced glycation end products

in diabetic rats.

> " benfo (100 mg/kg x day) and thiamin (70.18 mg/kg x day)

administered orally for 6 months…neither benfo nor thiamin treatment

affected metabolic control…Benfo administration in diabetic rats

induced a major inhibition of neutral imidazolone-type AGE formation

and completely prevented diabetes-induced glycoxidation formation.

Treatment with thiamin did not affect AGE or CML levels "

>

>

> Thiamine

>

> Allithiamines are lipid-soluble sources of thiamine. Benfo is an

allithiamine. Thiamine is water-soluble and is also known as

vitamin B1.

> After reviewing the relevant medical literature on thiamine, I

have come to conclude that large portions of the population may be

thiamine deficient. In addition, many individuals that are not

technically thiamine deficient would likely receive benefit from

thiamine supplementation. Thiamine deficiency is associated with

numerous undesirable medical conditions.

>

> Relation of thiamine to heart disease

>

> Shamir R, Dagan O, Abramovitch D, Abramovitch T, Vidne BA, Dinari

G. Thiamine deficiency in children with congenital heart disease

before and after corrective surgery. JPEN J Parenter Enteral Nutr.

2000 May-Jun;24(3):154-8.

> Thiamine deficiency " is common in children with congenital heart

disease (CHD) referred for corrective surgery both before and after

surgery. Our results suggest that neither diuretic treatment nor

malnutrition can fully explain the development of TD in these

children "

>

> Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E,

Levy R. [Right heart failure caused by thiamine deficiency

(cardiac beriberi)] Presse Med. 2000 Feb 12;29(5):240-1. French.

>

> Beaud C, Fuhrman C, Perchet H, Monnet I, Chouaid C, Housset B.

[Thiamine deficiency. A cause of cardiac insufficiency not to be

ignored] Rev Mal Respir. 1998 Jun;15(3):303-4. French.

> " Thiamine deficiency is one of the classical causes of high output

for heart failure "

>

> Okura H, Gohma I, Hatta K, Imanaka T. Thiamine deficiency and

pulmonary hypertension in Crow-Fukase syndrome. Intern Med. 1995

Jul;34(7):674-5.

> " After oral administration of prednisolone and thiamine,

echocardiogram showed marked improvement of the pulmonary

hypertension "

>

> Brady JA, Rock CL, Horneffer MR. Thiamin status, diuretic

medications, and the management of congestive heart failure. J Am

Diet Assoc. 1995 May;95(5):541-4.

> " Thiamin deficiency may occur in a substantial proportion of

patients with congestive heart failure, and dietary inadequacy may

contribute to increased risk "

>

> Shimon I, Almog S, Vered Z, Seligmann H, Shefi M, Peleg E,

Rosenthal T, Motro M, Halkin H, Ezra D. Improved left ventricular

function after thiamine supplementation in patients with congestive

heart failure receiving long-term furosemide therapy. Am J Med.

1995 May;98(5):485-90.

> " Thiamine repletion can improve left ventricular function and

biochemical evidence of thiamine deficiency in some patients with

moderate-to-severe CHF who are receiving longterm furosemide therapy "

>

> Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered

Z, Ezra D. Thiamine deficiency in patients with congestive heart

failure receiving long-term furosemide therapy: a pilot study. Am J

Med. 1991 Aug;91(2):151-5.

> " These preliminary findings suggest that long-term furosemide

therapy may be associated with clinically significant thiamine

deficiency due to urinary loss and contribute to impaired cardiac

performance in patients with CHF. This deficit may be prevented or

corrected by appropriate thiamine supplements "

>

> Relation of thiamine to neurological disorders

>

> Lonsdale D, Shamberger RJ, Audhya T. Treatment of autism spectrum

children with thiamine tetrahydrofurfuryl disulfide: a pilot study.

Neuroendocrinol Lett. 2002 Aug;23(4):303-8.

> " Thiamine tetrahydrofurfuryl disulfide appears to have a

beneficial clinical effect on some autistic children, since 8 of the

10 children improved clinically "

>

> Nakagawasai O, Tadano T, Hozumi S, Taniguchi R, Tan-No K, Esashi

A, Niijima F, Kisara K. Characteristics of depressive behavior

induced by feeding thiamine-deficient diet in mice.

> Life Sci. 2001 Jul 27;69(10):1181-91.

>

> Ambrose ML, Bowden SC, Whelan G. Thiamin treatment and working

memory function of alcohol-dependent people: preliminary findings.

Alcohol Clin Exp Res. 2001 Jan;25(1):112-6.

> " A therapeutic relationship between dose and working memory

performance was indicated "

>

> Older MW, Dickerson JW. Thiamine and the elderly orthopaedic

patient. Age Ageing. 1982 May;11(2):101-7.

> " In both groups those patients who were noticeably confused after

operation were found to have a considerable fall in their thiamine

status suggesting this may be a contributory factor to postoperative

confusion "

>

> Winston AP, son CP, Madira W, Gatward NM, Palmer RL.

Prevalence of thiamin deficiency in anorexia nervosa. Int J Eat

Disord. 2000 Dec;28(4):451-4.

> " Fourteen patients (38%) had results in the deficient range; 7

(19%) met the most stringent published criterion for deficiency.

Deficiency was not related to duration of eating restraint,

frequency of vomiting, or alcohol consumption "

>

> Terasawa M, Nakahara T, Tsukada N, Sugawara A, Itokawa Y. The

relationship between thiamine deficiency and performance of a

learning task in rats. Metab Brain Dis. 1999 Sep;14(3):137-48.

> " We taught rats to press a lever to escape from the pain of

electrical stimulation by learning to turn a switch off… The rats

that were fed the thiamine-deficient diet showed a slower response

time and a longer running time than the rats fed the normal diet… We

found that the thiamine concentration in the blood of the rats in

the trained group was significantly higher than that in the group

without training "

>

> Jimenez-Jimenez FJ, Molina JA, Hernanz A, Fernandez-Vivancos E, de

Bustos F, Barcenilla B, Gomez-Escalonilla C, Zurdo M, Berbel A,

Villanueva C. Cerebrospinal fluid levels of thiamine in patients

with Parkinson's disease. Neurosci Lett. 1999 Aug 13;271(1):33-6.

> " These results suggest that low CSF free thiamine levels could be

related with the risk for PD "

>

> Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and

pyridoxine in the treatment of symptomatic diabetic peripheral

neuropathy. East Afr Med J. 1997 Dec;74(12):803-8.

> " Diabetic peripheral neuropathy in Dar es Salaam is associated

with thiamine deficiency "

>

> Langlais PJ, G, Guo SX, Bondy SC. Increased cerebral

free radical production during thiamine deficiency. Metab Brain

Dis. 1997 Jun;12(2):137-43.

> " These findings suggest that increased formation of free radicals

occurs during the more acute symptomatic stage of thiamine

deficiency and may contribute to the structural damage described in

this model of Wernicke's encephalopathy "

>

> Easton CJ, Bauer LO. Beneficial effects of thiamine on

recognition memory and P300 in abstinent cocaine-dependent

patients. Psychiatry Res. 1997 May 30;70(3):165-74.

> " Thiamine was found to significantly improve recognition accuracy

and P300 amplitude, at the midline parietal (Pz) electrode. The

improvement was most reliable under conditions of increased memory

load "

>

> Benton D, Griffiths R, Haller J. Thiamine supplementation mood

and cognitive functioning. Psychopharmacology (Berl). 1997 Jan;129

(1):66-71.

> " An improvement in thiamine status was associated with reports of

being more clearheaded, composed and energetic. The taking of

thiamine had no influence on memory but reaction times were faster

following supplementation "

>

> Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer's

disease. Metab Brain Dis. 1996 Mar;11(1):89-94.

> " Fursultiamine (TTFD), a derivative of thiamine, at an oral dose

of 100 mg/day had a mild beneficial effect in patients with

Alzheimer's disease in a 12-week open trial. The improvement could

be observed not only in their emotional or other mental symptoms but

also in intellectual function "

>

> Gold M, Chen MF, K. Plasma and red blood cell thiamine

deficiency in patients with dementia of the Alzheimer's type. Arch

Neurol. 1995 Nov;52(11):1081-6.

> " A significant proportion of patients with SDAT may have a

thiamine deficiency, which may have an impact on cognitive function.

Currently used assays may not be adequate to assess thiamine status "

>

> Adamolekun B, Eniola A. Thiamine-responsive acute cerebellar

ataxia following febrile illness. Cent Afr J Med. 1993 Feb;39(2):40-

1. Review.

> " acute thiamine depletion may be the pathogenetic mechanism for

post-pyrexial acute cerebellar ataxia "

>

> Ben-Hur T, Wolff E, River Y. [Thiamin deficiency is common in

Israel] Harefuah. 1992 Nov 15;123(10):382-4, 436, 435. Hebrew.

> " Thiamin levels should be determined not only in alcoholics and

those with classic B1 deficiency syndromes, but in the routine

workup of patients with sensory-motor neuropathy, dementia, gait

disorders, cerebellar syndromes and confusional states "

>

> Sacks W, Esser AH, Feitel B, Abbott K. Acetazolamide and

thiamine: an ancillary therapy for chronic mental illness.

Psychiatry Res. 1989 Jun;28(3):279-88.

> " Overall, 50% of the patients showed improvement on all assessment

scales. No untoward effects occurred in these patients… "

>

>

> Relation of thiamine and geriatric patients

>

> Smidt LJ, Cremin FM, Grivetti LE, Clifford AJ. Influence of

thiamin supplementation on the health and general well-being of an

elderly Irish population with marginal thiamin deficiency. J

Gerontol. 1991 Jan;46(1):M16-22.

> " thiamin-supplemented women experienced significantly increased

appetite, energy intake, body weight and general well-being, and

decreased fatigue. Thiamin supplementation also tended to reduce

daytime sleep time, improve sleep patterns, and increase activity.

These data suggest that evaluation of thiamin status is indicated

when nonspecific conditions such as anorexia, weight loss, fatigue,

depression, and sleep disorders are present in elderly persons "

>

> Lee DC, Chu J, Satz W, Silbergleit R. Low plasma thiamine levels

in elder patients admitted through the emergency department. Acad

Emerg Med. 2000 Oct;7(10):1156-9.

> " CONCLUSIONS: Elder nursing home patients seen in the ED and

admitted to the hospital are frequently thiamine-deficient "

>

> Wilkinson TJ, Hanger HC, Elmslie J, PM, Sainsbury R. The

response to treatment of subclinical thiamine deficiency in the

elderly. Am J Clin Nutr. 1997 Oct;66(4):925-8.

> " Only the subjects with persistently low TPP concentrations showed

subjective benefits from treatment with improvements in quality of

life… There was a trend toward benefits in sleep and energy… Quality

of life was enhanced by providing thiamine supplements. Blood

pressure and weight were lower after thiamine supplementation "

>

> Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte

thiamin concentrations in geriatric outpatients. J Am Coll Nutr.

1996 Jun;15(3):231-6.

> " CONCLUSION: About 50% of geriatric outpatients in this study had

low plasma thiamin levels "

>

> Nichols HK, Basu TK. Thiamin status of the elderly: dietary

intake and thiamin pyrophosphate response. J Am Coll Nutr. 1994

Feb;13(1):57-61.

> " Average daily thiamin intake was above the recommended

requirement… however, almost half of the total study population had

TPP effect > 14%, suggesting thiamin deficiency… CONCLUSION: These

findings raise questions about the reliability of dietary intake in

assessing metabolic availability of thiamin in the elderly "

>

> O'Keeffe ST, Tormey WP, Glasgow R, Lavan JN. Thiamine deficiency

in hospitalized elderly patients. Gerontology. 1994;40(1):18-24.

> " Necropsy studies suggest that thiamine deficiency is

underdiagnosed in life… There was no difference in anthropometric

indices or in the prevalence of other nutrient deficiencies between

the two groups. Thiamine deficiency is common in elderly patients

admitted to hospital and may contribute to the development of

delirium "

>

> Iber FL, Blass JP, Brin M, Leevy CM. Thiamin in the elderly--

relation to alcoholism and to neurological degenerative disease. Am

J Clin Nutr. 1982 Nov;36(5 Suppl):1067-82. Review.

> " There is no known toxicity for thiamin "

>

> Relation of thiamine to diabetes

>

> Avena R, Arora S, Carmody BJ, Cosby K, Sidawy AN. Thiamine

(Vitamin B1) protects against glucose- and insulin-mediated

proliferation of human infragenicular arterial smooth muscle cells.

Ann Vasc Surg. 2000 Jan;14(1):37-43.

> " Vitamin B1 intake may prove important in delaying the

atherosclerotic complications of diabetes "

>

> La Selva M, Beltramo E, Pagnozzi F, Bena E, Molinatti PA,

Molinatti GM, Porta M. Thiamine corrects delayed replication and

decreases production of lactate and advanced glycation end-products

in bovine retinal and human umbilical vein endothelial cells

cultured under high glucose conditions. Diabetologia. 1996 Nov;39

(11):1263-8.

>

> Ascher E, Gade PV, Hingorani A, Puthukkeril S, Kallakuri S,

Scheinman M, T. Thiamine reverses hyperglycemia-induced

dysfunction in cultured endothelial cells. Surgery. 2001 Nov;130

(5):851-8.

> " The data from this study lead to the speculation that thiamine

intake may mitigate or delay vascular complications of diabetes "

>

> Hassan R, Qureshi H, Zuberi SJ. Effect of thiamine on glucose

utilization in hepatic cirrhosis. J Gastroenterol Hepatol. 1991 Jan-

Feb;6(1):59-60.

> " It is therefore suggested that thiamine supplements be given to

cirrhotics with hyperglycaemia, to improve glucose utilization "

>

> Rindi G, Laforenza U. Thiamine intestinal transport and related

issues: recent aspects.

> Proc Soc Exp Biol Med. 2000 Sep;224(4):246-55. Review.

> " Thiamine uptake is enhanced by thiamine deficiency, and reduced

by thyroid hormone and diabetes "

>

> Saito N, Kimura M, Kuchiba A, Itokawa Y. Blood thiamine levels in

outpatients with diabetes mellitus. J Nutr Sci Vitaminol (Tokyo).

1987 Dec;33(6):421-30.

> " From the above findings it was concluded that diabetic

outpatients tend to have a low blood thiamine level, with low

erythrocyte transketolase activity and high erythrocyte TPP effect,

and showed marginal thiamine deficiency "

>

>

> Relation of thiamine to disease

>

> Wallace AE, Weeks WB. Thiamine treatment of chronic hepatitis B

infection. Am J Gastroenterol. 2001 Mar;96(3):864-8.

> " In each case study, thiamine administration was associated with

reduction in aminotransferase levels and the fall of HBV DNA to

undetectable levels… The relationship between thiamine

administration and chronic hepatitis B infection warrants further

study. If proven effective in reducing liver damage or inducing

remission of the hepatitis B virus in larger trials, thiamine will

offer obvious advantages over the current treatments for chronic

viral hepatitis B infection "

>

> Rossouw JE, Labadarios D, Krasner N, M, R. Red

blood cell transketolase activity and the effect of thiamine

supplementation in patients with chronic liver disease. Scand J

Gastroenterol. 1978;13(2):133-8.

> " Biochemical evidence of thiamine deficiency was found in 58% of

patients with chronic liver disease… high doses of thiamine should

be included in the routine nutritional management of patients with

severe chronic liver disease "

>

> Shoji S, Furuishi K, Misumi S, Miyazaki T, Kino M, Yamataka K.

Thiamine disulfide as a potent inhibitor of human immunodeficiency

virus (type-1) production. Biochem Biophys Res Commun. 1994 Nov

30;205(1):967-75.

> " The results suggest that thiamine disulfide may be important for

AIDS chemotherapy "

>

> Shoji S, Furuishi K, Ogata A, Yamataka K, Tachibana K, Mukai R,

Uda A, Harano K, Matsushita S, Misumi S. An allosteric drug, o,o'-

bismyristoyl thiamine disulfide, suppresses HIV-1 replication

through prevention of nuclear translocation of both HIV-1 Tat and NF-

kappa B. Biochem Biophys Res Commun. 1998 Aug 28;249(3):745-53.

>

> Butterworth RF, Gaudreau C, Vincelette J, Bourgault AM, Lamothe F,

Nutini AM. Thiamine deficiency and Wernicke's encephalopathy in

AIDS. Metab Brain Dis. 1991 Dec;6(4):207-12.

> " we now report biochemical evidence of thiamine deficiency in 9/39

(23%) of patients with AIDS or AIDS-related complex. In no cases was

there history of alcohol abuse… it is recommended that dietary

thiamine supplementation be initiated in all newly diagnosed cases

of AIDS or AIDS-related complex "

>

> Haisraeli-Shalish M, Livneh A, Katz J, Doolman R, Sela BA.

Recurrent aphthous stomatitis and thiamine deficiency. Oral Surg

Oral Med Oral Pathol Oral Radiol Endod. 1996 Dec;82(6):634-6.

> " 70 patients with recurrent aphthous stomatitis and in 50 members

of a control group… Low levels of vitamin B1 were detected in 49

patients but in only two members of the control group… Our finding

suggests an association between thiamine deficiency and recurrent

aphthous stomatitis "

>

> Engel D. Tropical pyomyositis, a thiamine-deficiency disease.

Med Hypotheses. 1981 Mar;7(3):345-52.

> " it is suggested that thiamine deficiency is an essential

contributary factor in producing tropical pyomyositis… Thiamine

deficiency induces a biochemical lesion (s) in the pyruvate

oxidase system of the muscle, which breaks down its normal

resistance to infection and opens the gate to bacterial agents "

>

> Krishna S, AM, Supanaranond W, Pukrittayakamee S, ter Kuile

F, Tawfiq KM, Holloway PA, White NJ. Thiamine deficiency and

malaria in adults from southeast Asia. Lancet. 1999 Feb 13;353

(9152):546-9.

> " 12 (52%) of 23 patients with severe malaria and ten (19%) of 54

patients with uncomplicated malaria had alpha values above the

normal range (p<0.0001 and p=0.0014, respectively, compared with

controls), which indicated severe thiamine deficiency "

>

> Pietrzak I, Baczyk K, Mlynarczyk M, Kaczmarek M. [Content of

thiamin in plasma and erythrocytes in patients with end stage renal

disease] Przegl Lek. 1996;53(5):423-6. Polish.

> " We suggest the need of thiamine supplementation in ESRD patients

especially in those treated by dialysis. The supplementation of

thiamine is needed particularly in patients on peritoneal dialysis "

>

> Relation of thiamine to other data

>

> Hung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine

deficiency and unexplained encephalopathy in hemodialysis and

peritoneal dialysis patients. Am J Kidney Dis. 2001 Nov;38(5):941-7.

> " We conclude that in regular dialysis patients, unexplained

encephalopathy can be mainly attributed to thiamine deficiency "

>

> Huang S, Ren G. [Thiamine status of university teacher families

in Changsha] Hunan Yi Ke Da Xue Xue Bao. 1998;23(1):27-30. Chinese.

> " We conclude that those people who take the refined cereals and

its products as a staple food, is in the risk of thiamine deficiency "

>

> Suzuki M, Itokawa Y. Effects of thiamine supplementation on

exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106.

> " High-dose thiamine (vitamin B1) supplementation (100 mg/day) may

be helpful in preventing or accelerating recovery from exercise-

induced fatigue… Thiamine supplementation significantly suppressed

the increase in blood glucose in the normal thiamine group and

significantly decreased the number of complaints shortly after

exercise in the subjective fatigue assessment of 30 items "

>

> Kimura M, Itokawa Y, Fujiwara M. Cooking losses of thiamin in

food and its nutritional significance. J Nutr Sci Vitaminol

(Tokyo). 1990;36 Suppl 1:S17-24.

> " The thiamin contents in cooked daily meals were 50-60 percent of

the calculated values on an average "

>

> Cruickshank AM, Telfer AB, Shenkin A. Thiamine deficiency in the

critically ill. Intensive Care Med. 1988;14(4):384-7.

> " We performed a retrospective study on 158 patients admitted to

the Intensive Care Unit who required nutritional support. Patients

who survived had significantly higher body thiamine status than

those who died "

>

> Onodera K, Kisara K, Okabe H, Ogura Y. [studies on the effects

of thiamine deficiency on rat testes (author's transl)] Nippon

Yakurigaku Zasshi. 1980 Mar;76(2):143-52. Japanese.

> " In the thiamine deficient group, the seminiferous tubuli of rats

having erections had atrophied "

>

> Labadarios D, Rossouw JE, McConnell JB, M, R.

Thiamine deficiency in fulminant hepatic failure and effects of

supplementation. Int J Vitam Nutr Res. 1977;47(1):17-22.

> " Nine out of 24 patients with acute hepatocellular necrosis

leading to fulminant hepatic failure showed biochemical evidence of

thiamine deficiency early in the course of their illness "

>

>

> Why haven't we heard of benfo before? The patent on the

manufacture of benfo expired decades ago. Pharmaceutical companies

pursue drugs that can be patented so they can have a monopoly and

charge 100 times what the drug is worth. They have spent a lot of

money on AGE inhibitors that don't work as well as benfo. Ingestion

of benfo may result in the elimination of AGE-protein crosslinks,

which are a major constituent of arterial plaque. I am intrigued by

the idea that benfo may cause the removal of plaque from the blood

vessels, but I am concerned about the rapid manner in which it may

cause the removal of plaque from the blood vessels. If the plaque

is being removed, a large chunk might break off and cause a stroke

or heart attack. If I was older than 60 or if I had a serious

problem with high blood pressure I would probably start out by

taking very low doses of benfo and gradually increase my dosage. Of

course, there are no reports of strokes or heart attacks from benfo

in the medical literature, but it's a thought to consider.

>

> My PhD research will mostly consist of double-blind controlled

studies on the administration of benfo in normal individuals,

diabetics, individuals with high blood pressure, Alzheimer patients

etc. I believe the researchers who have investigated benfo to date

have been extremely short sighted by not discovering they full

potential of benfo in the clinical studies that have already been

performed on humans.

>

> It is illegal to make claims about benfo and sell it as a dietary

supplement unless the claims are based on substantial scientific

evidence. The three case studies outlined in this document are not

from a double-blind controlled study and FDA regulations would not

allow for them to be referred to as substantial scientific

evidence. Claims should not be made based on these preliminary

findings.

>

> For questions or comments email robholladay99@y...

> Since I am not a physician, it would be inappropriate for me to

answer emails asking for medical advice.

>

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> SECURALL, INC.

>

> The Difference is 'ALARMING'

>

> 602-7582283

>

> 602-2965003 fax