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Woo TC, Choo R, Jamieson M, Chander S, Vieth R. Pilot study: potential role of vitamin D (Cholecalciferol) in patients with PSA relapse after definitive therapy.Nutr Cancer. 2005;51(1):32-6.PMID: 15749627 [PubMed - indexed for MEDLINE]

Vitamin D: A millenium perspective. Holick MF. J Cell Biochem. 2003 Feb 1;88(2):296-307. Review. PMID: 12520530

Low levels of vitamin D may raise a person's risk of premature death, a study by Johns Hopkins researchers shows. The research followed other recent studies showing low levels of vitamin D are linked to certain cancers, diabetes, and bone and immune system problems, but this is the first research to connect vitamin D deficiency to a higher risk of death

Expression of the multiple sclerosis-associated MHC class II Allele HLA-DRB1*1501 is regulated by vitamin D.\nRamagopalan SV, Maugeri NJ, Handunnetthi L, Lincoln MR, Orton SM, Dyment DA, Deluca GC, Herrera BM, Chao MJ, Sadovnick AD, Ebers GC, Knight JC.\nPLoS Genet. 2009 Feb;5(2):e1000369. Epub 2009 Feb 6.\nPMID: 19197344 [

This critical nutrient builds bones, helps fight infection and may protect against some cancers. Do we get enough?

Vitamin D supplementation during the first year of life and risk of schizophrenia: a Finnish birth cohort study. McGrath J, Saari K, Hakko H, Jokelainen J, Jones P, Järvelin MR, Chant D, Isohanni M. Schizophr Res. 2004 Apr 1;67(2-3):237-45. PMID: 14984883 Conclusion: Vitamin D supplementation during the first year of life is associated with a reduced risk of schizophrenia in males. Preventing hypovitaminosis D during early life may reduce the incidence of schizophrenia.

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 major factor which stimulates weight gain in winter months is vitamin D. Human bodies get vitamin D from sunlight; as the hours of sunlight become less with the onset of fall, so our levels of vitamin D decrease. Low levels of vitamin D affect the brain's production of the hormone leptin. Leptin plays a vital role in controlling appetite and metabolism; so as the amount of vitamin D in our bodies decreases so does the leptin, and this causes an increase in our appetite and a change in our metabolism. Researchers at Aberdeen University found that obese people had 10% less vitamin D than people of average weight. The study also found that excess body fat absorbed vitamin D so the body couldn't use it. Scientists now believe that there is a direct correlation between obesity and low levels of vitamin D.

Evidence for alteration of the vitamin D-endocrine system in obese subjects. Bell NH, Epstein S, Greene A, Shary J, Oexmann MJ, Shaw S. J Clin Invest. 1985 Jul;76(1):370-3. PMID: 2991340 The results provide evidence that alteration of the vitamin D-endocrine system in obese subjects is characterized by secondary hyperparathyroidism which is associated with enhanced renal tubular reabsorption of calcium and increased circulating 1,25(OH)2D. The reduction of serum 25-OHD in them is attributed to feedback inhibition of hepatic synthesis of the precursor by the increased serum 1,25(OH)2D.

Are statins analogues of vitamin D? Grimes DS. Lancet. 2006 Jul 1;368(9529):83-6. Review. PMID: 16815382 doi:10.1016/S0140-6736(06)68971-X There are many reasons why the dietary-heart-cholesterol hypothesis should be questioned, and why statins might be acting in some other way to reduce the risk of coronary heart disease. Here, I propose that rather than being cholesterol-lowering drugs per se, statins act as vitamin D analogues, and explain why. This proposition is based on published observations that the unexpected and unexplained clinical benefits produced by statins have also been shown to be properties of vitamin D. It seems likely that statins activate vitamin D receptors.

The high prevalence of vitamin D insufficiency across Australian populations is only partly explained by season and latitude. van der Mei IA, Ponsonby AL, Engelsen O, Pasco JA, McGrath JJ, Eyles DW, Blizzard L, Dwyer T, Lucas R, Jones G. Environ Health Perspect. 2007 Aug;115(8):1132-9. PMID: 17687438 doi: 10.1289/ehp.9937. Conclusion Vitamin D insufficiency is common over a wide latitude range in Australia. Season appears to be more important than latitude, but both accounted for less than one-fifth of the variation in serum 25(OH)D levels, highlighting the importance of behavioral factors. Current sun exposure guidelines do not seem to fully prevent vitamin D insufficiency, and consideration should be given to their modification or to pursuing other means to achieve vitamin D adequacy.

Seasonality of UV-radiation and vitamin D status at 69 degrees north. Brustad M, Edvardsen K, Wilsgaard T, Engelsen O, Aksnes L, Lund E. Photochem Photobiol Sci. 2007 Aug;6(8):903-8. Epub 2007 Jun 27. PMID: 17668121 The generally high dietary intakes of vitamin D, especially in winter, mask largely the effect of seasonal variation in UV-exposure, causing an atypical seasonal variation in vitamin D status. The UV-hour variable significantly predicted 25(OH)D levels in blood when adjusted for intakes and artificial UV-radiation exposure and sun holidays abroad.

"D-vitamiini on noussut aivan uuteen valoon uusien tutkimusten myötä. Se on monipuolisesti vaikuttava hormoni, joka säätää tuhansien geenien toimintoja. D-vitamiini kohentaa yleiskuntoa, lihasvoimaa, kestävyyttä ja ketteryyttä sekä ehkäisee sikainfluenssaa, kausiflunssaa ja muita infektioita, allergioita (mm. atooppista ihottumaa), astmaa, Chrohnin tautia, diabetesta, MS-tautia, munuaistauteja, reumatauteja, sydän- ja verisuonitauteja sekä syöpää. Riittävä D-vitamiinin saanti ehkäisee ennenaikaista kuolemaa. Maailman Terveysjärjestön tutkimuksen mukaan D-vitamiinilisä voi pidentää tervettä elinaikaa jopa kahdeksalla vuodella. D-vitamiinin vajaus veressä ja kudoksissa johtuu ensisijaisesti auringonvalon puutteesta. Myös yksipuolinen ruokavalio (rasvaisen kalan vähyys) ja geenivirhe ovat puutteen syytekijöitä."

Athletic performance and vitamin D. Cannell JJ, Hollis BW, Sorenson MB, Taft TN, Anderson JJ. Med Sci Sports Exerc. 2009 May;41(5):1102-10. Review. PMID: 19346976 doi: 10.1249/MSS.0b013e3181930c2b Conclusions: Vitamin D may improve athletic performance in vitamin D-deficient athletes. Peak athletic performance may occur when 25(OH)D levels approach those obtained by natural, full-body, summer sun exposure, which is at least 50 ng·mL-1. Such 25(OH)D levels may also protect the athlete from several acute and chronic medical conditions.