Guest guest Posted August 2, 2008 Report Share Posted August 2, 2008 Hi folks: This is a very interesting, and extraordinarily well organized, study. Among its findings are that CR mice consuming an AGE-enhanced diet live less long than fully fed mice eating regular mouse chow. This seems to indicate the overwhelming importance of avoiding dietary AGEs, something that had gone somewhat over my head until I saw this paper. It might be argued that the benefit of a CR diet is derived from the fact that, when eating 40% less food one is consuming 40% fewer AGEs. While investigating this I came across the following quote: "... the plasma AGE content of healthy vegetarians has been reported to be higher than that of omnivores - suggesting that something about vegetarian diets may promote endogenous AGE production. Some researchers have proposed that the relatively high fructose content of vegetarian diets may explain this phenomenon ........ ", from PMID: 15607576. Uh oh. Fructose again. Fruits! Low methionine but high fructose! And while talking about AGEs, the AGE content of various foods has been discussed in PMID: 15281050. It found fats generally contain very high AGE levels. About thirty times more as a group than carbohydrates as a group. Possibly the problem with a high fat diet is not the fat, but rather the AGEs that, it seems, inevitably accompany the fat? Of course, cooking time and temperature are also critical to AGE formation, as noted in that paper. And AGEs are created 'endogenously' as well as being consumed in food. In one paper the expression "antioxidant homeostasis" was used, which was a new perspective to me. One needs, it seems, to make sure one's body's capacity to handle (eradicate) these things is not overwhelmed by excessive amounts of them. Rodney. >> Recent news on significant difference made by heat treatment of CR > diet on various health parameters.> > > Oral glycotoxins determine the effects of calorie restriction on > oxidant stress, age-related diseases, and lifespan.Cai W, He JC, Zhu > L, Chen X, Zheng F, Striker GE, Vlassara H.> Department of Geriatrics,Mount Sinai School of Medicine, One Gustave > Levy Place, New York, NY 10029, USA.> > We previously showed that the content of advanced glycation end > products (AGEs) in the diet correlates with serum AGE levels, oxidant > stress (OS), organ dysfunction, and lifespan. We now show that the > addition of a chemically defined AGE (methyl-glyoxal-BSA) to low-AGE > mouse chow increased serum levels of AGEs and OS, demonstrating that > dietary AGEs are oxidants that can induce systemic OS. OS predisposes > to the development of cardiovascular and chronic kidney diseases; > calorie restriction (CR) is the most studied means to decrease OS, > increase longevity, and reduce OS-related organ damage in mammals. > Because reduction of food intake also decreases oxidant AGE s intake, > we asked whether the beneficial effects of CR in mammals are related > to the restriction of oxidants or energy. Pair-fed mice were provided > either a CR diet or a high-AGE CR diet in which AGEs were elevated by > brief heat treatment (CR-high). Old CR-high mice developed high > levels of 8-isoprostanes, AGEs, RAGE, and p66(shc), coupled with low > AGER1 and GSH/GSSG levels, insulin resistance, marked myocardial and > renal fibrosis, and shortened lifespan. In contrast, old CR mice had > low OS, p66(shc), RAGE, and AGE levels, but high AGER1 levels, > coupled with longer lifespan. Therefore, the beneficial effects of a > CR diet may be partly related to reduced oxidant intake, a principal > determinant of oxidant status in aging mice, rather than decreased > energy intake.> > PMID: 18599606 [PubMed - in process]> PMCID: PMC2475771 [Available on 02/01/09]> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2008 Report Share Posted August 4, 2008 Useful low AGE meal plan with some cooking instructions http://www.mendosa.com/Low%20AGE%20Meal%20Plan%20Instructions.pdf On fructose consumption and its effects relative to endogenous AGE formation, this 10 year old(!) study: Long-Term Fructose Consumption Accelerates Glycation and Several Age- Related Variables in Male Rats1,2,3 Boaz Levi and Moshe J. Werman4 Department of Food Engineering and Biotechnology, TechnionIsrael Institute of Technology, Haifa, Israel Fructose intake has increased steadily during the past two decades. Fructose, like other reducing sugars, can react with proteins through the Maillard reaction (glycation), which may account for several complications of diabetes mellitus and accelerating aging. In this study, we evaluated the effect of fructose intake on some age-related variables. Rats were fed for 1 y a commercial nonpurified diet, and had free access to water or 250 g/L solutions of fructose, glucose or sucrose. Early glycation products were evaluated by blood glycated hemoglobin and fructosamine concentrations. Lipid peroxidation was estimated by urine thiobarbituric reactive substances. Skin collagen crosslinking was evaluated by solubilization in natural salt or diluted acetic acid solutions, and by the ratio between - and - collagen chains. Advanced glycation end products were evaluated by collagen-linked fluorescence in bones. The ratio between type-III and type-I collagens served as an aging variable and was measured in denatured skin collagen. The tested sugars had no effect on plasma glucose concentrations. Blood fructose, cholesterol, fructosamine and glycated hemoglobin levels, and urine lipid peroxidation products were significantly higher in fructose-fed rats compared with the other sugar-fed and control rats. Acid-soluble collagen and the type- III to type-I ratio were significantly lower, whereas insoluble collagen, the to ratio and collagen-bound fluorescence at 335/385 nm (excitation/emission) were significantly higher in fructose-fed rats than in the other groups. The data suggest that long-term fructose consumption induces adverse effects on aging; further studies are required to clarify the precise role of fructose in the aging process. http://jn.nutrition.org/cgi/content/full/128/9/1442 This study strogly suggests the significant implication of AGEs in diabetes pathology. It was a kind of milestone for the authors, for after it they became bolder in their assertions when discussing the results of an impressive series of follow up studies and papers, claiming to have established a CAUSAl relationship between high AGE consumption and various pathologies : http://diabetes.diabetesjournals.org/cgi/content/full/51/7/2082? ijkey=fcfaf2a6e8dd95606ff89944cec527f43b03dc05 Taken from the write up this very interesting and novel bit: Islet morphology. Histological examination and insulin immunostaining were performed in pancreatic sections from each group at the end of the study. Islets of HAD-fed db/db mice exhibited hyperplasia and hypertrophy combined with loss of islet structure and cellular homogeneity, changes seen only infrequently in islets from LAD-fed db/db mice. In addition, islet degeneration and insulin degranulation, including glucagon- producing cell displacement from the periphery to the center of the islets, were more evident in HAD-fed db/db mice than in LAD-fed db/db mice. Overall, LAD-fed db/ db mice presented better preserved, compact islets with intensely positive staining for insulin (Fig. 5). Comparing 10 consecutive pancreatic sections per mouse from the LAD- (n = 5) and HAD-fed (n = 5) control mice, we could not observe a discernible difference in islet structure and insulin immunostaining. Regards, Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2008 Report Share Posted August 4, 2008 Hi folks: This study finding posted by raises an interesting point: "Blood fructose, cholesterol, fructosamine and ***glycated hemoglobin*** levels, and urine lipid peroxidation productswere significantly higher in fructose-fed rats compared with theother sugar-fed and control rats." How many people here know their glycated hemoglobin (HbA1C) level? And among them how many would be prepared to make an off-the-cuff guess as to their normal fruit intake? (Rating, perhaps, from zero to 10). If we had a couple of dozen, or more, data points for these two variables we might be able to take a VERY approximate stab at determining whether, among us, it appears that high fruit intake is associated with higher HbA1C. Of course this would be nowhere even remotely close to being definitive. But it might be helpful if we cannot find any published source of this information in humans. If high fruit intake is accelerating aging it is certainly something we would want to know about. And the supposed problems with HFCS would be explained as well. I would rate my fruit intake at 3·5 on that scale (relatively low) and my most recent HbA1C was 4·7 (OK but not remarkable). Especially interesting would be the HbA1Cs of people who never eat fruit. Any takers? Please! Rodney. >> Useful low AGE meal plan with some cooking instructions> > http://www.mendosa.com/Low%20AGE%20Meal%20Plan%20Instructions.pdf> > On fructose consumption and its effects relative to endogenous AGE > formation, this 10 year old(!) study:> > Long-Term Fructose Consumption Accelerates Glycation and Several Age-> Related Variables in Male Rats1,2,3 > Boaz Levi and Moshe J. Werman4 > > Department of Food Engineering and Biotechnology, TechnionIsrael > Institute of Technology, Haifa, Israel > > Fructose intake has increased steadily during the past two decades. > Fructose, like other reducing sugars, can react with proteins through > the Maillard reaction (glycation), which may account for several > complications of diabetes mellitus and accelerating aging. In this > study, we evaluated the effect of fructose intake on some age-related > variables. Rats were fed for 1 y a commercial nonpurified diet, and > had free access to water or 250 g/L solutions of fructose, glucose or > sucrose. Early glycation products were evaluated by blood glycated > hemoglobin and fructosamine concentrations. Lipid peroxidation was > estimated by urine thiobarbituric reactive substances. Skin collagen > crosslinking was evaluated by solubilization in natural salt or > diluted acetic acid solutions, and by the ratio between - and -> collagen chains. Advanced glycation end products were evaluated by > collagen-linked fluorescence in bones. The ratio between type-III and > type-I collagens served as an aging variable and was measured in > denatured skin collagen. The tested sugars had no effect on plasma > glucose concentrations. Blood fructose, cholesterol, fructosamine and > glycated hemoglobin levels, and urine lipid peroxidation products > were significantly higher in fructose-fed rats compared with the > other sugar-fed and control rats. Acid-soluble collagen and the type-> III to type-I ratio were significantly lower, whereas insoluble > collagen, the to ratio and collagen-bound fluorescence at 335/385 > nm (excitation/emission) were significantly higher in fructose-fed > rats than in the other groups. The data suggest that long-term > fructose consumption induces adverse effects on aging; further > studies are required to clarify the precise role of fructose in the > aging process.> > http://jn.nutrition.org/cgi/content/full/128/9/1442> > This study strogly suggests the significant implication of AGEs in > diabetes pathology. It was a kind of milestone for the authors, for > after it they became bolder in their assertions when discussing the > results of an impressive series of follow up studies and papers, > claiming to have established a CAUSAl relationship between high AGE > consumption and various pathologies :> > http://diabetes.diabetesjournals.org/cgi/content/full/51/7/2082?> ijkey=fcfaf2a6e8dd95606ff89944cec527f43b03dc05> > Taken from the write up this very interesting and novel bit:> > Islet morphology.> Histological examination and insulin immunostaining were performed in > pancreatic sections from each group at the end of the study. Islets > of HAD-fed db/db mice exhibited hyperplasia and hypertrophy combined > with loss of islet structure and cellular homogeneity, changes seen > only infrequently in islets from LAD-fed db/db mice. In addition, > islet degeneration and insulin degranulation, including glucagon-> producing cell displacement from the periphery to the center of the > islets, were more evident in HAD-fed db/db mice than in LAD-fed db/db > mice. Overall, LAD-fed db/ db mice presented better preserved, > compact islets with intensely positive staining for insulin (Fig. 5). > Comparing 10 consecutive pancreatic sections per mouse from the LAD- > (n = 5) and HAD-fed (n = 5) control mice, we could not observe a > discernible difference in islet structure and insulin immunostaining. > > Regards, > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 24, 2008 Report Share Posted August 24, 2008 Would carnosine or a carnivorous diet help suppress aging and associated pathologies? Carnosine (beta-alanyl-L-histidine) is found exclusively in animal tissues. Carnosine has the potential to suppress many of the biochemical changes (e.g., protein oxidation, glycation, AGE formation, and cross-linking) that accompany aging and associated pathologies. Glycation, generation of advanced glycosylation end- products (AGEs), and formation of protein carbonyl groups play important roles in aging, diabetes, its secondary complications, and neurodegenerative conditions. Due to carnosine's antiglycating activity, reactivity toward deleterious carbonyls, zinc- and copper- chelating activity and low toxicity, carnosine and related structures could be effective against age-related protein carbonyl stress. It is suggested that carnivorous diets could be beneficial because of their carnosine content, as the dipeptide has been shown to suppress some diabetic complications in mice. It is also suggested that carnosine's therapeutic potential should be explored with respect to neurodegeneration. Olfactory tissue is normally enriched in carnosine, but olfactory dysfunction is frequently associated with neurodegeneration. Olfactory administration of carnosine could provide a direct route to compromised tissue, avoiding serum carnosinases. PMID: 16804013 Glycation, ageing and carnosine: are carnivorous diets beneficial? Non-enzymic protein glycosylation (glycation) plays important roles in ageing and in diabetes and its secondary complications. Dietary constituents may play important roles in accelerating or suppressing glycation. It is suggested that carnivorous diets contain a potential anti-glycating agent, carnosine (beta-alanyl-histidine), whilst vegetarians may lack intake of the dipeptide. The possible beneficial effects of carnosine and related structures on protein carbonyl stress, AGE formation, secondary diabetic complications and age- related neuropathology are discussed. PMID: 15955546 --- In , Novick <jnovickrd@...> wrote: > The REAL Culprits > > Cream cheese, 3,265 > Mayonnaise 9470 > Butter 1,324 > > Beef > furter, boiled 7 min 6,736 > furter, broiled 5 min 10,143 > Hamburger, fried 6 min 2,375 > Hamburger, fast food 4,876 > Meatball, boiled in sauce 2,567 > > Shoulder cut, broiled 5,367 > Bacon, microwave 1,173 > Deli ham, smoked 2,114 > Pork chop, pan fried 4,277 > > Chicken breast, skinless cubes > Steamed 10 min and broiled 12 min 5,071 > Pan fried 10 min and boiled 12 min 5,706 > > Chicken breast, skinless cutlet > Raw 692 > Boiled 1 h 1,011 > Broiled 15 min 5,245 > Fried 8 min 6,651 > Roasted, barbecue sauce 4,291 > Roasted, breaded 4,102 > Roasted, breaded, microwave, 1 min 55,157 > > > Fish > Salmon, raw 502 > Salmon, smoked 515 > Trout, raw 705 > Trout, roasted 25 min 1,924 > > Cheese > American, processed 2,603 > American, processed,e low fat 1,425 > Brie 1,679 > Cottage cheese, 1,744 > Feta 2,527 > Mozzarella,e part skim 503 > Parmesan,e grated 2,535 > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 24, 2008 Report Share Posted August 24, 2008 Inhibition of protein glycation by extracts of culinary herbs and spices. We tested whether polyphenolic substances in extracts of commercial culinary herbs and spices would inhibit fructose-mediated protein glycation. Extracts of 24 herbs and spices from a local supermarket were tested for the ability to inhibit glycation of albumin. Dry samples were ground and extracted with 10 volumes of 50% ethanol, and total phenolic content and ferric reducing antioxidant potential (FRAP) were measured. Aliquots were incubated in triplicate at pH 7.4 with 0.25 M fructose and 10 mg/mL fatty acid-free bovine albumin. Fluorescence at 370 nm/440 nm was used as an index of albumin glycation. In general, spice extracts inhibited glycation more than herb extracts, but inhibition was correlated with total phenolic content (R(2) = 0.89). The most potent inhibitors included extracts of cloves, ground Jamaican allspice, and cinnamon. Potent herbs tested included sage, marjoram, tarragon, and rosemary. Total phenolics were highly correlated with FRAP values (R(2) = 0.93). The concentration of phenolics that inhibited glycation by 50% was typically 4-12 microg/mL. Relative to total phenolic concentration, extracts of powdered ginger and bay leaf were less effective than expected, and black pepper was more effective. Prevention of protein glycation is an example of the antidiabetic potential for bioactive compounds in culinary herbs and spices. PMID: 18598169 Quote Link to comment Share on other sites More sharing options...
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