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A comparison of egg consumption with other modifiable coronary heart disease lifestyle risk factors: a relative risk apportionment study. Barraj L, Tran N, Mink P. Risk Anal. 2009 Mar;29(3):401-15. Epub 2008 Nov 4. PMID: 19000074 DOI: 10.1111/j.1539-6924.2008.01149.x Our analysis shows that the combination of modifiable lifestyle risk factors accounts for less than 40% of the population CHD mortality. For the majority of U.S. adults age 25+, consuming one egg a day accounts for <1% of CHD risk. Hence, focusing on decreasing egg intake as an approach to modify CHD risk would be expected to yield minimal results relative to changing other behaviors such as smoking and other dietary habits.

Egg consumption and risk of type 2 diabetes in men and women. Djoussé L, Gaziano JM, Buring JE, Lee IM. Diabetes Care. 2009 Feb;32(2):295-300. Epub 2008 Nov 18. PMID: 19017774 DOI: 10.2337/dc08-1271 CONCLUSIONS-These data suggest that high levels of egg consumption (daily) are associated with an increased risk of type 2 diabetes in men and women. Confirmation of these findings in other populations is warranted.

Fish consumption and risk of major chronic disease in men. Virtanen JK, Mozaffarian D, Chiuve SE, Rimm EB. Am J Clin Nutr. 2008 Dec;88(6):1618-25. PMID: 19064523 doi:10.3945/ajcn.2007.25816 Conclusions: Modest fish consumption was associated with a lower risk of total cardiovascular disease, consistent with cardiac mortality benefits but not with total cancer or overall major chronic disease; n-6 fatty acid consumption did not influence these relations.

A 22-y prospective study of fish intake in relation to prostate cancer incidence and mortality. Chavarro JE, Stampfer MJ, Hall MN, Sesso HD, Ma J. Am J Clin Nutr. 2008 Nov;88(5):1297-303. PMID: 18996866 Conclusion: These results suggest that fish intake is unrelated to prostate cancer incidence but may improve prostate cancer survival.

Why is it that vitamin D deficiency can manifest in so many different ways in different people? One big reason is something called vitamin D receptor (VDR) genotypes, the variation in the receptor for vitamin D. Why is it that the dose of vitamin D necessary to reach a specific level differs so widely from one person to the next? VDR genotype, again. Variation in blood levels of 25-hydroxy vitamin D from a specific dose of vitamin D can vary three-fold, as shown by a University of Toronto study. In other words, a dose of 4000 units per day may yield a 25-hydroxy vitamin D blood level of 30 ng/ml in Mary, 60 ng/ml in Paul, and 90 ng/ml in Pete--same dose, different blood levels.

Prevention of nonvertebral fractures with oral vitamin D and dose dependency: a meta-analysis of randomized controlled trials. Bischoff-Ferrari HA, Willett WC, Wong JB, Stuck AE, Staehelin HB, Orav EJ, Thoma A, Kiel DP, Henschkowski J. Arch Intern Med. 2009 Mar 23;169(6):551-61. PMID: 19307517 Conclusion Nonvertebral fracture prevention with vitamin D is dose dependent, and a higher dose should reduce fractures by at least 20% for individuals aged 65 years or older.

March 27, 2009 - A significant decrease in serum 25-hydroxyvitamin D (25[OH]D) levels has led to an increase in vitamin D insufficiency in the US population, especially in racial and ethnic groups, according to results of a population-based study reported in the March 23 issue of the Archives of Internal Medicine. "Vitamin D insufficiency has been associated with increases in cardiovascular disease, cancer, and infection," write Adit A. Ginde, MD, from the Department of Emergency Medicine at the University of Colorado Denver School of Medicine, Aurora, Colorado, and colleagues. "Vitamin D supplementation appears to mitigate the incidence and adverse outcomes of these diseases and may reduce all-cause mortality." [...] "These findings have important implications for health disparities and public health," the study authors conclude. "Our data provide additional evidence that current recommendations for vitamin D supplementation (200-600 IU/d) are inadequate to achieve optimal serum 25(OH)D levels in most of the US population." They add that large, randomized controlled trials of higher doses of vitamin D supplementation are needed to evaluate their effect on general health and mortality.

Sulbutiamine is a centrally acting cholinergic vitamin B analogue. One study shows sulbutiamine improve memory in rats. At this time I prefer using a combination of several B vitamins rather than relying on one vitamin B analogue. For more information on B vitamins or to purchase Vitamin B Coenzyme. Even better is to take a multivitamin that has a combination of the B vitamins along with a couple of dozen vitamins and nutrients. In most cases I think it is better to take a small amount of a number of different nutrients as opposed to a large amount of just one. Consider a very popular product that I have formulated called MultiVit-Rx.

Sulbutiamine (brand name: Arcalion) is a precursor to thiamine (i.e., vitamin B1). As a dimer of two structurally modified thiamine residues, sulbutiamine retains many of the features of thiamine. However, the thiazole rings are open, the alcohol groups are esterified, and a disulfide bridge connects the two thiamine analogues. Sulbutiamine is indicated for the treatment of asthenia.[1] Its ability to reduce fatigue is also considered desirable by athletes, and it is available for over-the-counter sale as a nutritional supplement. In one study of chronic fatigue patients, sulbutiamine did not demonstrate sustained benefits over the placebo, which raises doubts about its clinical efficacy.[2] However, the authors of that study suggest that additional research is needed to evalulate the potential usefulness of sulbutiamine in the treatment of chronic fatigue. Sulbutiamine may be beneficial for cognition. Indeed, the demonstrated ability of sulbutiamine to improve memory in rats[3] and patients of schizophrenia[3] suggests that it is a nootropic. Recent research also shows support for the use of sulbutiamine in the treatment of erectile dysfunction

Benfotiamine, a synthetic S-acyl thiamine derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble thiamine disulfide derivatives. Volvert ML, Seyen S, Piette M, Evrard B, Gangolf M, Plumier JC, Bettendorff L. BMC Pharmacol. 2008 Jun 12;8:10. PMID: 18549472 doi:10.1186/1471-2210-8-10 Conclusion Our results show that, though benfotiamine strongly increases thiamine levels in blood and liver, it has no significant effect in the brain. This would explain why beneficial effects of benfotiamine have only been observed in peripheral tissues, while sulbutiamine, a lipid-soluble thiamine disulfide derivative, that increases thiamine derivatives in the brain as well as in cultured cells, acts as a central nervous system drug. We propose that benfotiamine only penetrates the cells after dephosphorylation by intestinal alkaline phosphatases. It then enters the bloodstream as S-benzoylthiamine that is converted to thiamine in erythrocytes and in the liver. Benfotiamine, an S-acyl derivative practically insoluble in organic solvents, should therefore be differentiated from truly lipid-soluble thiamine disulfide derivatives (allithiamine and the synthetic sulbutiamine and fursultiamine) with a different mechanism of absorption and different pharmacological properties.

A popular vitamin supplement is being advertised with claims that are demonstrably untrue, as revealed by research published in the open access journal BMC Pharmacology. Benfotiamine is a synthetic derivative of thiamine (vitamin B1). It is marketed heavily as a dietary supplement using a selection of unsubstantiated, 'not-quite-medical' claims that tend to characterize this field. A large part of this campaign has been built around the belief that benfotiamine is lipid-soluble and, therefore, more physiologically active. Scientific research led by Dr Lucien Bettendorff of the Center for Cellular and Molecular Neurobiology at the University of Liège, Belgium, has entirely disproved these claims.

Benfotiamine (rINN, or S-benzoylthiamine O-monophoshate) is a synthetic S-acyl derivative of thiamine (vitamine B1). After absorption, benfotiamine can be dephosphorylated by cells bearing an ecto-alkaline phosphatase to the lipid-soluble S-benzoylthiamine. The primary use of this antioxidant is as an "anti-AGE" supplement.[3] In a trial, benfotiamine lowered AGE by 40%.[4] However, in Germany doctors have been known to combine benfotiamine with pyridoxine hydrochloride and use it to treat patients with nerve damage and nerve pain such as sciatica. At high doses, benfotiamine was shown to be effective for the treatment of diabetic retinopathy, neuropathy, and nephropathy. I

nightsurfer's Anti-inflammatory Lipid Mediators Diigo list

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nightsurfer's vitamin D related Diigo list