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How to optimize vitamin D supplementation to prevent cancer, based on cellular adaptation and hydroxylase enzymology. Vieth R. Anticancer Res. 2009 Sep;29(9):3675-84. Review. PMID: 19667164

How to optimize vitamin D supplementation to prevent cancer, based on cellular adaptation and hydroxylase enzymology. Vieth R. Anticancer Res. 2009 Sep;29(9):3675-84. Review. PMID: 19667164

Vitamin D A Key Player In Overall Health Of Several Body Organs, Says Biochemist In a paper published in the August issue of the American Journal of Clinical Nutrition, Norman identifies vitamin D's potential for contributions to good health in the adaptive and innate immune systems, the secretion and regulation of insulin by the pancreas, the heart and blood pressure regulation, muscle strength and brain activity. In addition, access to adequate amounts of vitamin D is believed to be beneficial towards reducing the risk of cancer. Norman also lists 36 organ tissues in the body whose cells respond biologically to vitamin D. The list includes bone marrow, breast, colon, intestine, kidney, lung, prostate, retina, skin, stomach and the uterus.

How to optimize vitamin D supplementation to prevent cancer, based on cellular adaptation and hydroxylase enzymology. Vieth R. Anticancer Res. 2009 Sep;29(9):3675-84. PMID: 19667164

Incidence of reported cold/influenza symptoms according to season. The 104 subjects in the placebo group (light shade) reported cold and flu symptoms year around with the most symptoms in the winter. While on 800 IU per day (intermediate shade) the 104 test subjects were as likely to get sick in the summer as the winter. Only one of the 104 test subjects had cold/influenza symptoms during the final year of the trial, when they took 2,000 IU of vitamin D per day (dark shading). Adapted from: Aloia JF, Li-Ng M: Epidemic influenza and vitamin D. Epidemiol Infect 2007; 135: 1095-1096

Robert P. Heaney is John A. Creighton University Professor, Creighton University, Omaha, Nebraska, United States. Hominid evolution took place in an environment (equatorial East Africa) that provided a superabundance of both calcium and vitamin D, the first in available foods and the second through conversion of 7-dehydrocholesterol to pre-vitamin D in the skin, a reaction catalysed by the intense solar ultraviolet (UV) radiation. Seemingly as a consequence, the evolving human physiology incorporated provisions to prevent the potential of toxic excesses of both nutrients. For vitamin D the protection was of two sorts: skin pigmentation absorbed the critical UV wavelengths and thereby limited dermal synthesis of cholecalciferol; and slow delivery of vitamin D from the skin into the bloodstream left surplus vitamin in the skin, where continuing sun exposure led to its photolytic degradation to inert compounds. For calcium, the adaptation consisted of very inefficient calcium absorption, together with poor to absent systemic conservation. The latter is reflected in unregulated dermal calcium losses, a high sensitivity of renal obligatory calcium loss to other nutrients in the diet and relatively high quantities of calcium in the digestive secretions. Today, chimpanzees in the original hominid habitat have diets with calcium nutrient densities in the range of 2 to 2.5 mmol per 100 kcal, and hunter-gatherer humans in Africa, South America and New Guinea still have diets very nearly as high in calcium (1.75 to 2 mmol per 100 kcal) (Eaton and Nelson, 1991). With energy expenditure of 3 000 kcal per day (a fairly conservative estimate for a contemporary human doing physical work), such diets would provide substantially in excess of 50 mmol of calcium per day. By contrast, median intake in women in North America and in many European countries today is under 15 mmol per day. Two factors altered the primitive situation: the migration of humans from Africa to higher latitude

Vitamin D deficiency is the cause of common obesity. Foss YJ. Med Hypotheses. 2009 Mar;72(3):314-21. Epub 2008 Dec 2. PMID: 19054627 doi:10.1016/j.mehy.2008.10.005 Common obesity and the metabolic syndrome may therefore result from an anomalous adaptive winter response. The stimulus for the winter response is proposed to be a fall in vitamin D. The synthesis of vitamin D is dependent upon the absorption of radiation in the ultraviolet-B range of sunlight. At ground level at mid-latitudes, UV-B radiation falls in the autumn and becomes negligible in winter. It has previously been proposed that vitamin D evolved in primitive organisms as a UV-B sensitive photoreceptor with the function of signaling changes in sunlight intensity. It is here proposed that a fall in vitamin D in the form of circulating calcidiol is the stimulus for the winter response, which consists of an accumulation of fat mass (obesity) and the induction of a winter metabolism (the metabolic syndrome). Vitamin D deficiency can account for the secular trends in the prevalence of obesity and for individual differences in its onset and severity. It may be possible to reverse the increasing prevalence of obesity by improving vitamin D status.

The vitamin D-antimicrobial peptide pathway and its role in protection against infection. Gombart AF. Future Microbiol. 2009 Nov;4:1151-65. PMID: 19895218 Vitamin D deficiency has been correlated with increased rates of infection. Since the early 19th century, both environmental (i.e., sunlight) and dietary sources (cod liver) of vitamin D have been identified as treatments for TB. The recent discovery that vitamin D induces antimicrobial peptide gene expression explains, in part, the 'antibiotic' effect of vitamin D and has greatly renewed interest in the ability of vitamin D to improve immune function. Subsequent work indicates that this regulation is biologically important for the response of the innate immune system to wounds and infection and that deficiency may lead to suboptimal responses toward bacterial and viral infections. The regulation of the cathelicidin antimicrobial peptide gene is a human/primate-specific adaptation and is not conserved in other mammals. The capacity of the vitamin D receptor to act as a high-affinity receptor for vitamin D and a low-affinity receptor for secondary bile acids and potentially other novel nutritional compounds suggests that the evolutionary selection to place the cathelicidin gene under control of the vitamin D receptor allows for its regulation under both endocrine and xenobiotic response systems. Future studies in both humans and humanized mouse models will elucidate the importance of this regulation and lead to the development of potential therapeutic applications

Back to the future: a new look at 'old' vitamin D. Chun RF, Adams JS, Hewison M. J Endocrinol. 2008 Aug;198(2):261-9. Epub 2008 May 21. PMID: 18495944 DOI: 10.1677/JOE-08-0170

Vitamin D in defense of the human immune response.\nAdams JS, Liu PT, Chun R, Modlin RL, Hewison M.\nAnn N Y Acad Sci. 2007 Nov;1117:94-105. Epub 2007 Jul 26. Review.\nPMID: 17656563\nDOI: 10.1196/annals.1402.03