Re: Re: MB12 injections and very high Bloodwork Results

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Along with what Natasa has said, you also need to consider why you aren't able to use the b12.  High serum means you aren't using it so the next step is to find out how to get your body to use what it has and once you do that, you may no longer need the b12.  I believe DAN has some protocols for this but I don't know them.  Anyone else know?  Maybe Owens can help in this matter.  I know the possibilities of why it isn't used has been discussed before, I just can't remember the details.Cherylthere was a thread on this subject recently, I have saved a few posts that answer that question, here they are:> My pediatrician called today to tell me that not only is my son not> deficient in B12, his numbers are "through the roof" and "off the> charts"...she has been emphatic all along that this biomed stuff is all> bogus and a waste of our time and money. However, when we give the> shots and spray we see gains in language and regulating and our son has> met his 9 month to 1 year goals in under four months. She> says, "Placebo effect...the numbers don't lie.">> What's up? Is it possible that he really has no deficit in the b12> department - then why the improved language? Coincidence? As explained by our DAN! today, whom is also a MD, high serum b12 numbersindicate that perhaps the uptake of b12 is the problem and not the lack ofb12. It will be high in serum (blood) but will be low in other places in thebody where it needs to be. In other words, it is being kept in the blood butnot going to the brain or other organs. What you need to go by is what yousee as an effect of using the b12, not what the blood tests shows. If youuse something and it has a positive effect, chances are that it is somethingyou (or your child) needs and is something you should continue doing untilit is no longer helping or causing ill effects. Our pediatrician told us thesame thing as yours told you. Too much b12...., but alas, when we supplementthe b12, we get language gains...... It is such a bigger picture than most(but not all) of our pediatricians and doctors are NOT trained to look at.Go with your gut instinct and with the evidence you have. It is a watersoluble vitamin and from my understanding you cant overdose it.========.. has this doctor never heard that megadoses have been and are being used in manyneurological disorders, regardless of blood levels?... she has probably never heard of a localised b12 deficiencies (sometimes confined to parts of brain)... and she is probably blissfullyunaware of something called Hereditary partial transcobalamin IIdeficiency, where levels stay nearly normal well into adulthood... justsome examples here, quoting most interesting bits, including studies:""…While most doctors would never consider such a possibility,studies have documented local cerebral deficiencies of B12 (usingcerebrospinal fluid levels as a measure) in people with Alzheimer'sdisease, postpartum depression, and toxic neuropsychiatric disorders,including toxic depression. Cees van Tiggelen and associates suspectthis cryptic condition may also commonly afflict people with historiesof nitrous oxide or Agent Orange intoxication, alcoholics (includingthose with alcohol-related dementia), long-term users of dilantin, andpeople with brain atrophy.B12 has its mainstream advocates too. In 1975, psychiatrists K. Geageaand Jambur Ananth, then at McGill University, remarked that "astonishingresults can be obtained in some cases with B12 therapy, even if B12levels are within normal range." They had just described one such case.Their young patient's two year depression had landed him in Montreal'sJewish General Hospital after a suicide attempt. Because the man had hada total gastrectomy nine years earlier – a risk factor for B12deficiency – and because his treatment-resistant symptoms had becomeprogressively more psychotic and neurologic in quality, Geagea andAnanth took a leap of faith. The man's B12 levels were normal, but theygave him B12 shots anyway."The response to this therapeutic trial," they wrote, "was dramatic. Thepatient was discharged eight days later with complete remission." He wasstill well three years later.In 1999, in their book Stop Depression Now, Columbia Universitypsychiatrist Brown and Baylor University neuropharmacologistTeodoro Bottiglieri (a leader in vitamin/depression research) recommendthat all psychiatric patients take a daily megadose of 1 mg of oralB12…."Intern Med. 1994 Feb;33(2):82-6.Vitamin B12 metabolism and massive-dose methyl vitamin B12 therapyin Japanese patients with multiple sclerosis.Kira J, Tobimatsu S, Goto I. Department of Neurology, Faculty ofMedicine, Kyushu University, Fukuoka.Serum vitamin B12 levels and unsaturated vitamin B12 bindingcapacities were measured in 24 patients with multiple sclerosis (MS), 73patients with other neurological disorders and 21 healthy subjects.There was no decrease in the vitamin B12 levels, however, a significantdecrease in the unsaturated vitamin B12 binding capacities was observedin patients with MS when compared with other groups. A massive dose ofmethyl vitamin B12 (60 mg every day for 6 months) was administered to 6patients with chronic progressive MS, a disease which usually had amorbid prognosis and widespread demyelination in the central nervoussystem. Although the motor disability did not improve clinically, theabnormalities in both the visual and brainstem auditory evokedpotentials improved more frequently during the therapy than in thepre-treatment period. We therefore consider that a massive dose methylvitamin B12 therapy may be useful as an adjunct to immunosuppressivetreatment for chronic progressive MS.PMID: 8019047 [PubMed - indexed for MEDLINE]Isr Med Assoc J. 2003 Dec;5(12):868-72.Hereditary partial transcobalamin II deficiency with neurologic,mental and hematologic abnormalities in children and adults.Teplitsky V, Huminer D, Zoldan J, Pitlik S, Shohat M, Mittelman M.Department of Medicine C, Rabin Medical Center (Beilinson Campus),Petah Tiqva, Israel. teplitzahav (DOT) net.ilBACKGROUND: Transcobalamin II is a serum transport protein forvitamin B12. Small variations in TC-II affinity were recently linked toa high homocysteine level and increased frequency of neural tubedefects. Complete absence of TC-II or total functional abnormalitycauses tissue vitamin B12 deficiency resulting in a severe disease withmegaloblastic anemia and immunologic and intestinal abnormalities in thefirst months of life. This condition was described in hereditaryautosomal-recessive form. Low serum TC-II without any symptoms orclinical significance was noted in relatives of affected homozygotes.OBJECTIVES: To study 23 members of a four-generation family withhereditary vitamin B12 deficiency and neurologic disorders. METHODS:Thorough neurologic, hematologic and family studies were supplemented bytranscobalamin studies in 20 family members. RESULTS: Partial TC-IIdeficiency was found in 19 subjects. Apo TC-II (free TC-II unbound tovitamin B12) and total unsaturated B12 binding capacity were low in alltested individuals but one, and holo TC-II (TC-II bound by vitamin B12)was low in all family members. The presentation of the disease waschronic rather than acute. Early signs in children and young adults weredyslexia, decreased IQ, vertigo, plantar clonus and personalitydisorders. Interestingly, affected children and young adults had normalor slightly decreased serum vitamin B12 levels but were not anemic. Lowserum B12 levels were measured in early adulthood. In mid-late adulthoodmegaloblastic anemia and subacute combined degeneration of the spinalcord were diagnosed. Treatment with B12 injections resulted in asignificant improvement. The pedigree is compatible with anautosomal-dominant transmission. This family study suggests a geneticheterogeneity of TC-II deficiency. CONCLUSIONS: We report the firstfamily with a hereditary transmitted condition of low serum TC-II(partial TC-II deficiency) associated with neurologic and mentalmanifestations in childhood. Partial TC-II deficiency may decrease theamount of stored cobalamin, resulting in increased susceptibility toimpaired intestinal delivery of cobalamin and predisposing to clinicallyexpressed megaloblastic anemia at a later age. Partial TC-II deficiencyshould be suspected in families with megaloblastic anemia and inindividuals with neurologic and mental disturbances--despite normalserum vitamin B12 levels. Low serum UBBC and apo TC-II should confirmthe diagnosis. Early vitamin B12 therapy may prevent irreversibleneurologic damage.PMID: 14689755 [PubMed - indexed for MEDLINE]Rinsho Shinkeigaku. 2003 Sep;43(9):552-5.Links[A case of subacute combined degeneration with normal serum vitaminB12 level][Article in Japanese]Nagaishi A, Takashima H, Fukuda Y, Kuroda Y. Department ofInternal Medicine, Sasebo City General Hospital.A 40-year-old woman was admitted to our hospital because ofpancytopenia with megaloblastic anemia. Two months later she complainedof rapidly progressive gait disturbance and numbness in the distal partof limbs. She also told that her hair had turned totally gray in thethird decade. Neurologically, mental state, cranial nerves andcerebellar functions were normal. Superficial sensations were impairedbelow the lower thoracic level and deep sensations were completely lostin the lower limbs. Moderate weakness was found in the lower limbs,symmetrically. Deep tendon reflexes were diminished in the upper limbsand absent in the lower limbs. Babinski's reflex was positivebilaterally. MR images of the spinal cord showed hyperintensity in theposterior column below the thoracic cord. Although the serum level ofvitamin B12 was within normal range, serum homocysteine level waselevated markedly. Under the diagnosis of subacute combined degeneration(SCD) due to possible vitamin B12 deficiency, the treatment withintravenous injections of 500 micrograms/day of mecobalamin wasundertaken. Muscle strength and sensory impairment improvedprogressively and she became able to walk with a cane. The coloration ofher gray hair was also noted. After treatment, pancytopenia andmegaloblastic anemia also markedly improved. Vitamin B12 became high inserum concentration and the serum level of homocysteine became normal.These clinical and laboratory findings support the diagnosis of SCD withnormal serum level of vitamin B12 in our case, suggesting that the levelof vitamin B12 in serum does not always correlate with that in tissueand, therefore, SCD should not be excluded just only by the reason ofnormal serum vitamin B12 level.PMID: 14727562 [PubMed - indexed for MEDLINE]Brain Nerve. 2007 Oct;59(10):1141-7.Links[Clinical trials of ultra-high-dose methylcobalamin in ALS][Article in Japanese]Izumi Y, Kaji R. Department of Clinical Neuroscience, Institute ofHealth Bioscience, The University of Tokushima, Graduate School, 50-1Kuramoto-cho, Tokushima 770-8503, Japan.Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorderaffecting both upper and lower motor neurons. Weakness may begin in thelegs, hands, proximal arms, or pharynx. The course is relentless andprogressive without remissions, relapses, or even stable plateaus. Thereis no effective drug therapy for ALS, although riluzole has been shownto prolong life in sufferers, without tracheostomy. A vitamin B12analog, methylcobalamin, has a protective effect on cultured corticalneurons against glutamate-induced cytotoxicity. We have shown theultra-high-dose methylcobalamin (25 mg/day i.m.) slows down theprogressive reduction of the CMAP (compound muscle action potential)amplitudes in ALS in the short term (4 weeks). The latencies of SSR(sympathetic skin response) were shorter after treatment (50 mg/dayi.v., 2 weeks). In the long-term effect of methylcobalamin (50 mg/dayi.m., twice a week), the survival time (or the period to becomerespirator-bound) was significantly longer in the treated group than inthe untreated. Larger-scale randomized double blind trial was started inJapan in order to evaluate the long-term efficacy and the safety ofultra-high-dose methylcobalamin for sporadic or familial cases of ALS.PMID: 17969354 [PubMed - indexed for MEDLINE] B12 through the roof....are we wasting our time andmoney?>> Hello!> > Background:> In Summer 2006, I asked my Doctor if she would start me on Dr. > Neubrander's Protocol for Methyl B12 (sc shots every 3 days, 0.17 ml). > I have CFS, but learned about this Protocol through my son's ASD > Biomedical Treatment. This treatment has resulted in some improvement > in my Brainfog. > Recently, my Doctor had me do B12 Bloodwork. Results were too high to > place a number on it (i.e. beyond the highest point that the test is > able to detect). The bloodwork had been drawn 2 1/2 days after my last > shot (i.e. my next shot was due that evening).> > Question:> I am hoping that someone who has a lot of knowledge in this area could > comment on this:> > Is it normal to have extremely high serum B12 results, and therefore > not a concern, for someone who is on B12 treatment? > Is there any concern that this MB12 Protocol can cause organ damage?> > I cannot find anything about this lab result issue on Dr. Neubrander's > website, and am not not able to ask him directly as I am not a patient > of his. It is discouraging because I thought the treatment was > effective, and I know Dr. Neubrander thinks it is best to stay on the > protocol dosage for at least 2 years, to avoid set-backs. I would be > grateful for any help you can offer.>