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Prospective Study of Serum 25-Hydroxyvitamin D Level, Cardiovascular Disease Mortality, and All-Cause Mortality in Older U.S. Adults. Ginde AA, Scragg R, Schwartz RS, Camargo CA Jr. J Am Geriatr Soc. 2009 Jun 22. [Epub ahead of print] PMID: 19549021 DOI: 10.1111/j.1532-5415.2009.02359.x CONCLUSION: In noninstitutionalized older adults, a group at high risk for all-cause mortality, serum 25(OH)D levels had an independent, inverse association with CVD and all-cause mortality. Randomized controlled trials of vitamin D supplementation in older adults are warranted to determine whether this association is causal and reversible.

Independent association of low serum 25-hydroxyvitamin d and 1,25-dihydroxyvitamin d levels with all-cause and cardiovascular mortality. Dobnig H, Pilz S, Scharnagl H, Renner W, Seelhorst U, Wellnitz B, Kinkeldei J, Boehm BO, Weihrauch G, Maerz W. Arch Intern Med. 2008 Jun 23;168(12):1340-9. PMID: 18574092 Conclusions Low 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels are independently associated with all-cause and cardiovascular mortality. A causal relationship has yet to be proved by intervention trials using vitamin D.

What causes coronary heart disease or coronary atherosclerotic plaque, this thing that we track with heart scans? Well, here are a few little-publicized facts about heart disease that you are unlikely to hear from your When's-the-next-stent? cardiologist or the What is there besides statins? primary care doctor. (Since everybody knows that smoking is a modifiable risk for heart disease that can be readily identified, let's focus on the blood tests that reveal heart disease causes.)

Vitamin D and mortality in older men and women. Pilz S, Dobnig H, Nijpels G, Heine RJ, Stehouwer CD, Snijder MB, van Dam RM, Dekker JM. Clin Endocrinol (Oxf). 2009 Nov;71(5):666-72. Epub 2009 Feb 18. PMID: 19226272 DOI: 10.1111/j.1365-2265.2009.03548.x Conclusions Low 25(OH)D levels are associated with all-cause mortality and even more pronounced with cardiovascular mortality, but it remains unclear whether vitamin D deficiency is a cause or a consequence of a poor health status. Therefore, intervention studies are warranted to evaluate whether vitamin D supplementation reduces mortality and cardiovascular diseases.

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

Low serum 25-hydroxyvitamin D concentrations are associated with greater all-cause mortality in older community-dwelling women. Semba RD, Houston DK, Ferrucci L, Cappola AR, Sun K, Guralnik JM, Fried LP. Nutr Res. 2009 Aug;29(8):525-30. PMID: 19761886 doi:10.1016/j.nutres.2009.07.007 Older community-dwelling women with low 25(OH)D levels are at an increased risk of death.

The Toronto group gave a fixed low dose (2,000 units) of the prehormone, cholecalciferol, a very safe compound that never causes high calcium in the doses used. In fact, the lowest dose of cholecalciferol known to cause high blood calcium is more than 20,000 units. Therefore, the Toronto group got better results with one-tenth the comparable dose of deltanoids! Vieth wanted to use more cholecalciferol but widespread ignorance about the physiology and pharmacology of vitamin D remains and he could not get adequate dosing past the various review committees.

Vitamin D plays a critical role in the human body's response to tuberculosis, according to new research that explains why people of African descent are more susceptible to TB. The research also suggests a new way to fight one of the world's deadliest diseases: with a simple dietary supplement. Tuberculosis, usually caused when a person inhales tuberculosis bacteria, killed an estimated 1.7 million people in 2003 and is the leading cause of death for people afflicted with AIDS, according to the World Health Organization (WHO).

Vitamin D supplementation. Eveleigh B. Can Fam Physician. 2007 Sep;53(9):1435; author reply 1435. PMID: 17872869 My concern regarding vitamin D2 is that it is a synthetic analogue and might interact with the vitamin D receptor differently in various cell systems. It has been reported that vitamin D3 might improve glycemic control.7 Vitamin D2 has been reported to cause worsening of glycemic control in people of East Indian descent.8 Is this because of vitamin D receptor polymorphism, or because of enhanced 24-hydroxylase enzyme activation, or is it due to how vitamin D2 interacts with the receptor? Until this has been sorted out, I feel safest using vitamin D3. There are about 2000 synthetic analogues of vitamin D. The search is on for one that can cross the blood-brain barrier to treat certain types of brain cancers without causing hypercalcemia.9 But then again, what other effects would this compound have? There are still so many unknowns

Paradigms and Paradoxes Last month Dr. Armin Zittermann of Ruhr University, Germany, published the best vitamin D paper of the month. He reviewed the mounting evidence that vitamin D deficiency is a major cause of heart disease. Zittermann A, Schleithoff SS, Koerfer R. Putting cardiovascular disease and vitamin D insufficiency into perspective. Br J Nutr. 2005 Oct;94(4):483-92. Before we start, let's talk about paradigms and paradoxes. A paradigm is a set of assumptions, concepts, and practices that constitutes a way of viewing reality. The current paradigm is that heart disease is caused by a combination of genetics, hypertension, diabetes, cholesterol, smoking, obesity, inactivity, and diet. A paradox is a fact that contradicts the paradigm.

Independent association of low serum 25-hydroxyvitamin d and 1,25-dihydroxyvitamin d levels with all-cause and cardiovascular mortality.\nDobnig H, Pilz S, Scharnagl H, Renner W, Seelhorst U, Wellnitz B, Kinkeldei J, Boehm BO, Weihrauch G, Maerz W.\nArch Intern Med. 2008 Jun 23;168(12):1340-9.\nPMID: 18574092

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.

25-hydroxyvitamin D levels and the risk of mortality in the general population. Melamed ML, Michos ED, Post W, Astor B. Arch Intern Med. 2008 Aug 11;168(15):1629-37. PMID: 18695076 Conclusion The lowest quartile of 25(OH)D level (<17.8 ng/mL) is independently associated with all-cause mortality in the general population.

Vitamin D association with estradiol and progesterone in young women. Knight JA, Wong J, Blackmore KM, Raboud JM, Vieth R. Cancer Causes Control. 2009 Nov 15. [Epub ahead of print] PMID: 19916051 CONCLUSIONS: Higher levels of vitamin D may reduce progesterone and estradiol, providing a potential mechanism for reduction in breast cancer risk from increased vitamin D exposure in young women.

A phase 2 trial exploring the effects of high-dose (10,000 IU/day) vitamin D(3) in breast cancer patients with bone metastases. Amir E, Simmons CE, Freedman OC, Dranitsaris G, Cole DE, Vieth R, Ooi WS, Clemons M. Cancer. 2009 Nov 13. [Epub ahead of print] PMID: 19918922 DOI: 10.1002/cncr.24749 METHODS: Patients with bone metastases treated with bisphosphonates were enrolled into this single-arm phase 2 study. Patients received 10,000 IU of vitamin D3 and 1000 mg of calcium supplementation each day for 4 months. The effect of this treatment on palliation, bone resorption markers, calcium metabolism, and toxicity were evaluated at baseline and monthly thereafter. CONCLUSIONS: Daily doses of 10,000 IU vitamin D3 for 4 months appear safe in patients without comorbid conditions causing hypersensitivity to vitamin D. Treatment reduced inappropriately elevated parathyroid hormone levels, presumably caused by long-term bisphosphonate use. There did not appear to be a significant palliative benefit nor any significant change in bone resorption. Cancer 2010. © 2009 American Cancer Society.

Sunlight regulates the cutaneous production of vitamin D3 by causing its photodegradation. Webb AR, DeCosta BR, Holick MF. J Clin Endocrinol Metab. 1989 May;68(5):882-7. PMID: 2541158 doi:10.1210/jcem-68-5-882 Vitamin D3 proved to be exquisitely sensitive to sunlight, and once formed in the skin, exposure to sunlight resulted in its rapid photodegradation to a variety of photoproducts, including 5,6-transvitamin D3, suprasterol I, and suprasterol II.suprasterol I, and suprasterol II.

Environmental risk factors for autism: Do they help cause de novo genetic mutations that contribute to the disorder? Kinney DK, Barch DH, Chayka B, Napoleon S, Munir KM. Med Hypotheses. 2009 Aug 20. [Epub ahead of print] PMID: 19699591

Prostate cancer risk and prediagnostic serum 25-hydroxyvitamin D levels (Finland). Ahonen MH, Tenkanen L, Teppo L, Hakama M, Tuohimaa P. Cancer Causes Control. 2000 Oct;11(9):847-52. PMID: 11075874 DOI: 10.1023/A:1008923802001 CONCLUSIONS: We conclude that low levels of 25-VD associated with an increased risk for subsequent earlier exposure and more aggressive development of prostate cancer, especially before the andropause.

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

An estimated 50% to 60% of older people have suboptimal vitamin D levels, which is a problem that could affect more than bone health. Recent cross-sectional studies have also shown an association between low vitamin D levels and cardiovascular disease, hypertension, and metabolic syndrome. In a long-term prospective study from Germany, researchers assessed whether 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels were associated with all-cause and cardiovascular mortality among more than 3000 consecutive patients (mean age, 62) referred for coronary angiography.