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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.

Maresins: novel macrophage mediators with potent antiinflammatory and proresolving actions. Serhan CN, Yang R, Martinod K, Kasuga K, Pillai PS, Porter TF, Oh SF, Spite M. J Exp Med. 2009 Jan 16;206(1):15-23. Epub 2008 Dec 22. PMID: 19103881 doi:10.1084/jem.20081880

Antioxidative and anti-inflammatory actions of docosahexaenoic acid and eicosapentaenoic acid in renal epithelial cells and macrophages. Kim YJ, Chung HY. J Med Food. 2007 Jun;10(2):225-31. PMID: 17651056 doi:10.1089/jmf.2006.092.

Resolvin E2: identification and anti-inflammatory actions: pivotal role of human 5-lipoxygenase in resolvin E series biosynthesis. Tjonahen E, Oh SF, Siegelman J, Elangovan S, Percarpio KB, Hong S, Arita M, Serhan CN. Chem Biol. 2006 Nov;13(11):1193-202. PMID: 17114001 doi:10.1016/j.chembiol.2006.09.011

Murck H, Manku M. Ethyl-EPA in Huntington disease: potentially relevant mechanism of action. Brain Res Bull. 2007 Apr 30;72(2-3):159-64. Epub 2006 Nov 15. Review. PMID: 17352940 [PubMed - indexed for MEDLINE]

Effects of pistachios on cardiovascular disease risk factors and potential mechanisms of action: a dose-response study. Gebauer SK, West SG, Kay CD, Alaupovic P, Bagshaw D, Kris-Etherton PM. Am J Clin Nutr. 2008 Sep;88(3):651-9. PMID: 18779280

"We are aware of substantial scientific evidence supporting the role of vitamin D in prevention of cancer. It has been reasonably established that adequate serum vitamin D metabolite levels are associated with substantially lower incidence rates of several types of cancer, including those of the breast, colon, and ovary, and other sites. We have concluded that the vitamin D status of most individuals in North America will need to be greatly improved for substantial reduction in incidence of cancer. Epidemiological studies have shown that higher vitamin D levels are also associated with lower risk of Type I diabetes in children and of multiple sclerosis. Several studies have found that markers of higher vitamin D levels are associated with lower incidence and severity of influenza and several other infectious diseases."

I believe as we start running we need to get the fundamentals of our running action right then we can build on that.

I believe as we start running we need to get the fundamentals of our running action right then we can build on that.

Use of vitamin D in clinical practice. Cannell JJ, Hollis BW. Altern Med Rev. 2008 Mar;13(1):6-20. PMID: 18377099 The recent discovery--from a meta-analysis of 18 randomized controlled trials--that supplemental cholecalciferol (vitamin D) significantly reduces all-cause mortality emphasizes the medical, ethical, and legal implications of promptly diagnosing and adequately treating vitamin D deficiency. Not only are such deficiencies common, and probably the rule, vitamin D deficiency is implicated in most of the diseases of civilization. Vitamin D's final metabolic product is a potent, pleiotropic, repair and maintenance, seco-steroid hormone that targets more than 200 human genes in a wide variety of tissues, meaning it has as many mechanisms of action as genes it targets. One of the most important genes vitamin D up-regulates is for cathelicidin, a naturally occurring broad-spectrum antibiotic. Natural vitamin D levels, those found in humans living in a sun-rich environment, are between 40-70 ng per ml, levels obtained by few modern humans. Assessing serum 25-hydroxy-vitamin D (25(OH)D) is the only way to make the diagnosis and to assure treatment is adequate and safe. Three treatment modalities exist for vitamin D deficiency: sunlight, artificial ultraviolet B (UVB) radiation, and vitamin D3 supplementation. Treatment of vitamin D deficiency in otherwise healthy patients with 2,000-7,000 IU vitamin D per day should be sufficient to maintain year-round 25(OH)D levels between 40-70 ng per mL. In those with serious illnesses associated with vitamin D deficiency, such as cancer, heart disease, multiple sclerosis, diabetes, autism, and a host of other illnesses, doses should be sufficient to maintain year-round 25(OH)D levels between 55 -70 ng per mL. Vitamin D-deficient patients with serious illness should not only be supplemented more aggressively than the well, they should have more frequent monitoring of serum 25(OH)D and serum calcium. Vitamin D should always be

Today, after close to 6000 years of folklore, scientific research shows that garlic is an amazing resource of phytochemicals (botanicals) whose wide range of actions can benefit health. Studies show that garlic protects against infection and inflammation, lowers the risk of heart disease, and has anticancer and antiaging effects. Scientific studies also show that garlic does not have to be eaten raw or fresh to be effective. The potent odor of garlic may not be necessary for its health benefits. Research shows that aged, deodorized garlic extract sometimes works even better than fresh garlic without causing digestive disorders and "garlic breath" that may haunt the fresh garlic eater.

The combination effects index (CI) analysis confirmed the synergy of clioquinol and clofibrate on inhibiting cancer cell viability. Using inhibitors to block PPARalpha signaling diminished the synergistic cytotoxicity of clioquinol and DHA. These results provide pharmacological evidence that the synergistic anticancer action of clioquinol and DHA is mediated by PPARalpha signaling in human cancer cells. PPARalpha signaling mediates the synergistic cytotoxicity of clioquinol and docosahexaenoic acid in human cancer cells. Tuller ER, Brock AL, Yu H, Lou JR, Benbrook DM, Ding WQ. Biochem Pharmacol. 2009 May 1;77(9):1480-6. Epub 2009 Feb 13. PMID: 19426685

Not enough vitamin D: health consequences for Canadians. Schwalfenberg G. Can Fam Physician. 2007 May;53(5):841-54. Review PMID: 17872747 Conclusion Low levels of VTD are considered a major public health problem in Canada, especially during the winter. Those with risk factors should be screened for low 25(OH)D levels and repletion therapy instituted if needed. Researchers have estimated that the oral dose of vitamin D3 to attain and maintain 25(OH)D levels >80 nmol/L is 2200 IU/d if baseline levels are 20 to 40 nmol/L, 1800 IU/d if levels are 40 to 60 nmol/L, and 1160 IU/d if levels are between 60 and 80 nmol/L.64 We need to ensure that patients have healthy blood levels of 25(OH)D to prevent levels of parathyroid hormone from rising and to maximize absorption of calcium, magnesium, and phosphate. Positive effects on bone are marginal at best unless patients consume at least 800 IU/d of VTD. The emerging and exciting role of the VTD receptor and the actions of VTD in maintaining health in other cell types have become more apparent during the last decade.

Vitamin D may suppress infections which lead to development of Multiple Sclerosis Steven R Brenner, None (16 August 2007) J Neurol Neurosurg Psychiatry 2008 I read the article with reference to the inverse relationship between multiple sclerosis clinical activity and deficiency of vitamin D by Soilu-Hannienen (1) with interest, and was considering what mechanism could be in play to cause such a relationship. 25-hydroxylated metabolites of vitamin D act as intracellular regulators of the synthesis and action of defensin (2) molecules against bacterial antigens, defensin being an endogenously synthesized antimicrobial substance (2). Human cathelicidin antimicrobial peptide gene is a target of vitamin D receptor and is strongly up-regulated by 1,25-dihydroxyvitamin D3, indicating vitamin D receptor and the 1,25-dihydroxyvitaminD3 regulate primate innate immunity (3)

Strong correlations have been noted between cardiovascular diseases and low bone density / osteoporosis-connections so strong that the presence of one is considered a likely predictor of the other. This relationship has led to the hypothesis that these conditions share core pathophysiological mechanisms. Recent advances in our understanding of the complimentary roles played by vitamin D3 and vitamin K2 in vascular and bone health provide support for this hypothesis, along with insight into key metabolic dysfunctions underlying cardiovascular disease and osteoporosis. Part II, The Vitamin K Connection to Cardiovascular Health, reviews the ways in which vitamin K regulates calcium utlization, preventing vascular and soft tissue calcification while complimenting the bone-building actions of vitamin D, and also discusses vitamin K safety and dosage issues, and the necessity of providing vitamin K and vitamin A along with vitamin D to preclude adverse effects associated with hypervitaminosis D.

David Feldman, MD, professor of medicine at Stanford, explores the biological action of Vitamin D beyond its widely understood role in the information and maintenance of bone. Emerging therapeutic uses of the vitamin include the prevention and treatment of breast, prostate and colon cancer, chronic kidney disease and arthritis, among other conditions.

Vitamin D2 is much less effective than vitamin D3 in humans. Armas LA, Hollis BW, Heaney RP. J Clin Endocrinol Metab. 2004 Nov;89(11):5387-91. PMID: 15531486 Vitamin D2 potency is less than one third that of vitamin D3. Physicians resorting to use of vitamin D2 should be aware of its markedly lower potency and shorter duration of action relative to vitamin D3.

Despite inadequacies in information concerning the minimum prophylactic requirement of vitamin D for all age groups beyond infancy, there is no doubt that a total intake of 400 I.U. per day is adequate to prevent vitamin D deficiency in substantially all normal children from birth through adolescence. Evidence derived from the study of idiopathic hypercalcemia suggests that certain infants excessively sensitive to the toxic action of vitamin D may, on rare occasions, be adversely affected by daily intakes of 3,000 to 4,000 I.U. and sometimes considerably less. Because of the prevalent practice of food fortification in the United States and Canada, there is now a definite possibility that the individual, even the young infant, may ingest considerably more than the recommended vitamin D allowance, and intakes of 2,000 to 3,500 I.U. per day are possible, particularly beyond infancy. Although there has been no specific evidence that intakes of this order produce deleterious effects beyond infancy, it is pointed out that the long-term consequences of this new nutritional situation on older children or adults are entirely unknown.

It is well known that eating green vegetables, beans, nuts, cereals and fruits prevents cancer, now it is found that beans and wheat bran contains an enzyme inhibitor Inositol // pentakisphosphate which is found to have anti-cancer effects by blocking the action of enzyme Phosphoinositide 3 kinase.