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"D-vitamiini näyttäisi suojaavan keskushermoston rappeutumissairauksilta. Viime vuosien aikana on saatu lisävalaistusta normaaliin elimistön vanhenemiseen, kun on selvinnyt, että vanhenemista jarruttavan hormonin (FGF-23) vaikutus perustuu D-vitamiiniin. Sekä koe-eläimillä että ihmisillä on todettu, että FGF-23 jarruttaa D-vitamiinin hormonaalisten muotojen tuottoa. Siten FGF-23:n toimintaa häiritsevät mutaatiot saavat aikaan D-vitamiinin yliaktiivisuuden ja nopeuttavat vanhenemista. Tamperelainen tutkimusryhmä on juuri ilmestyneessä arvostetussa Psychoneuroendocrinology-lehdessä osoittanut, että sekä D-vitamiinin yliaktiivisuus että sen vaikutuksen puutos nopeuttavat fysiologista vanhenemista. Tutkimusryhmä on jo aikaisemmin raportoinut, että eturauhassyövän riski on pienimmillään, kun seerumin D-vitamiinipitoisuus on normaali, mutta riski lisääntyy sekä matalilla että korkeilla veripitoisuuksilla. Sairastumisriski noudattaa U-muotoista riippuvuutta D-vitamiinin veripitoisuudesta. Tällainen U-muotoinen riippuvuus D-vitamiinista näyttäisi olevan melko yleistä, koska sellainen ilmenee myös kokonaiskuolleisuudessa, sydänkuolleisuudessa ja luuston haurastumisessa. On mahdollista, että oikealla D-vitamiinin annostelulla voitaisiin lykätä monien kroonisten sairauksien alkamista jopa vuosilla myöhemmäksi. Tällaisia sairauksia ovat eräät yleiset syövät, sokeritauti, verisuonten kalkkeutuminen, verenpainetauti, keskushermoston rappeutumissairaudet, astma, autoimmuunisairaudet ja osteoporoosi."

Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology. Peterlik M, Cross HS. Eur J Clin Nutr. 2009 Dec;63(12):1377-86. Epub 2009 Sep 2. PMID: 19724293 doi:10.1038/ejcn.2009.105 A compromised vitamin D status, characterized by low 25-hydroxyvitamin D (25-(OH)D) serum levels, and a nutritional calcium deficit are widely encountered in European and North American countries, independent of age or gender. Both conditions are linked to the pathogenesis of many degenerative, malignant, inflammatory and metabolic diseases. Studies on tissue-specific expression and activity of vitamin D metabolizing enzymes, 25-(OH)D-1alpha-hydroxylase and 25-(OH)D-24-hydroxylase, and of the extracellular calcium-sensing receptor (CaR) have led to the understanding of how, in non-renal tissues and cellular systems, locally produced 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and extracellular Ca2+ act jointly as key regulators of cellular proliferation, differentiation and function. Impairment of cooperative signalling from the 1,25-(OH)2D3-activated vitamin D receptor (VDR) and from the CaR in vitamin D and calcium insufficiency causes cellular dysfunction in many organs and biological systems, and, therefore, increases the risk of diseases, particularly of osteoporosis, colorectal and breast cancer, inflammatory bowel disease, insulin-dependent diabetes mellitus type I, metabolic syndrome, diabetes mellitus type II, hypertension and cardiovascular disease. Understanding the underlying molecular and cellular processes provides a rationale for advocating adequate intake of vitamin D and calcium in all populations, thereby preventing many chronic diseases worldwide.

Serum vitamin D concentration and prostate cancer risk: a nested case-control study. Ahn J, Peters U, Albanes D, Purdue MP, Abnet CC, Chatterjee N, Horst RL, Hollis BW, Huang WY, Shikany JM, Hayes RB; Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial Project Team. J Natl Cancer Inst. 2008 Jun 4;100(11):796-804. Epub 2008 May 27. PMID: 18505967 doi:10.1093/jnci/djn152 CONCLUSION: The findings of this large prospective study do not support the hypothesis that vitamin D is associated with decreased risk of prostate cancer; indeed, higher circulating 25(OH)D concentrations may be associated with increased risk of aggressive disease. In summary, results from this large prospective study of men who underwent standardized prostate cancer screening in the context of a screening trial do not support the hypothesis that higher serum vitamin D status is associated with decreased risk of prostate cancer. The study showed no association of vitamin D level with nonaggressive disease; however, it raises the possibility that higher vitamin D level may be associated with increased risks for aggressive disease, although a clear monotonic dose-response relationship was lacking. Along with recent reports of adverse associations for higher vitamin D status and risk of pancreatic (32) and esophageal (33,34) cancer, caution should be taken in recommending high doses of vitamin D or sunlight exposure to the general public for prostate cancer prevention. Future analyses are warranted to confirm these results and to further clarify the effects of vitamin D on aggressive prostate cancer.

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.

"D-vitamiini näyttäisi suojaavan keskushermoston rappeutumissairauksilta. Viime vuosien aikana on saatu lisävalaistusta normaaliin elimistön vanhenemiseen, kun on selvinnyt, että vanhenemista jarruttavan hormonin (FGF-23) vaikutus perustuu D-vitamiiniin. Sekä koe-eläimillä että ihmisillä on todettu, että FGF-23 jarruttaa D-vitamiinin hormonaalisten muotojen tuottoa. Siten FGF-23:n toimintaa häiritsevät mutaatiot saavat aikaan D-vitamiinin yliaktiivisuuden ja nopeuttavat vanhenemista. Tamperelainen tutkimusryhmä on juuri ilmestyneessä arvostetussa Psychoneuroendocrinology-lehdessä osoittanut, että sekä D-vitamiinin yliaktiivisuus että sen vaikutuksen puutos nopeuttavat fysiologista vanhenemista. Tutkimusryhmä on jo aikaisemmin raportoinut, että eturauhassyövän riski on pienimmillään, kun seerumin D-vitamiinipitoisuus on normaali, mutta riski lisääntyy sekä matalilla että korkeilla veripitoisuuksilla. Sairastumisriski noudattaa U-muotoista riippuvuutta D-vitamiinin veripitoisuudesta. Tällainen U-muotoinen riippuvuus D-vitamiinista näyttäisi olevan melko yleistä, koska sellainen ilmenee myös kokonaiskuolleisuudessa, sydänkuolleisuudessa ja luuston haurastumisessa. On mahdollista, että oikealla D-vitamiinin annostelulla voitaisiin lykätä monien kroonisten sairauksien alkamista jopa vuosilla myöhemmäksi. Tällaisia sairauksia ovat eräät yleiset syövät, sokeritauti, verisuonten kalkkeutuminen, verenpainetauti, keskushermoston rappeutumissairaudet, astma, autoimmuunisairaudet ja osteoporoosi"

"Do Your Vitamin D Research Here Links to all the Latest Research Studies Welcome to the Vitamin D Research Library. Here you'll find links to all of the latest Vitamin D Facts and Research studies, clinical trials and other scholarly Vitamin D Facts. The Research Library is Open 24/7 and is always growing. I'll be adding more and more links all of the time. Can't find what you are looking for or just don't want to spend the time doing the research yourself? Chances are, I've already done the Vitamin D Research myself and can answer your question. Read Frequently Asked Questions about Vitamin D OR Ask Your Question About Vitamin D Here and I'll answer your Question about Vitamin D Personally based on the best available Vitamin D Research."

Effects of Atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Pérez-Castrillón JL, Vega G, Abad L, Sanz A, Chaves J, Hernandez G, Dueñas A. Am J Cardiol. 2007 Apr 1;99(7):903-5. Epub 2007 Feb 8. PMID: 17398180 In conclusion, atorvastatin increases vitamin D levels. This increase could explain some of the beneficial effects of atorvastatin at the cardiovascular level that are unrelated to cholesterol levels. The mechanism by which atorvastatin increases vitamin D levels is related to inhibition of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase. Cholesterol is synthesized from 7-dehydrocholesterol, which is also a precursor of vitamin D3. For this reason, we initially observed a statistically significant relation between total cholesterol and vitamin D. HMG-CoA enzyme reductase is key to the synthesis of cholesterol, whereas ultraviolet radiation causes the formation of 25-hydroxyvitamin D. Inhibition of the enzyme may increase levels of 7-dehydrocholesterol and increase the synthesis of 25-hydroxycholecalciferol, thereby increasing vitamin D levels,10 although we observed no relation between lower cholesterol and increased vitamin D. In addition, 25-hydroxyvitamin D has been shown to inhibit HMG-CoA enzyme reductase activity in in vitro studies.11 A greater concentration of vitamin D could increase enzymatic inhibition, acting in synergy with the statin in decreasing total cholesterol.

Vitamin D and type 2 diabetes: are we ready for a prevention trial? Scragg R. Diabetes. 2008 Oct;57(10):2565-6. PMID: 18820212 doi: 10.2337/db08-0879 Despite evidence from the current article (3) and the Finnish study (17), doubts still remain about whether low vitamin status is a cause of type 2 diabetes. Further cohort studies are required, assessing baseline vitamin D status using blood 25(OH)D to be sure that the Ely and Finnish studies are not false-positive results. Glucose clamp studies are also required because we are still not sure of the mechanism influenced by vitamin D-whether it is insulin resistance, secretion, or both. But most importantly, given that nearly three decades have passed since the first studies linking vitamin D with insulin metabolism (6,7), well-designed clinical trials of the effect of vitamin D supplementation on glycemia status and diabetes risk are urgently required to settle this question. And they need to prevent past mistakes. In particular, the vitamin D dose given in such trials needs to be high enough-above 2,000 IU per day (19)-to raise blood 25(OH)D levels above 80 nmol/l because diabetes risk is lowest at this level (9,20). If well-designed trials are carried out and confirm a protective effect from vitamin D, it could be used by the general population as a simple and cheap solution to help prevent the diabetes epidemic.

Hypovitaminosis D in British adults at age 45 y: nationwide cohort study of dietary and lifestyle predictors. Hyppönen E, Power C. Am J Clin Nutr. 2007 Mar;85(3):860-8. PMID: 17344510 Conclusion: Prevalence of hypovitaminosis D in the general population was alarmingly high during the winter and spring, which warrants action at a population level rather than at a risk group level. Data from the 1958 birth cohort suggest that, at different cutoffs for hypovitaminosis D, a substantial public health problem exists in British whites. Obese participants and those living in Scotland were at the highest risk of hypovitaminosis D. However, the prevalence in the general population was very high during the winter and spring, which suggests that, to improve the situation, action is required at a population level rather than at a risk-group level. In the United States, calls have gone out for an increase in vitamin D fortification of foods (11), and the data from the current study suggest that such action is also warranted in the United Kingdom. Vitamin D is currently available without prescription as a dietary supplement only as part of cod liver oil or multivitamin products; hence, a need clearly exists to consider increased availability of over-the-counter supplements. Hypovitaminosis D has been implicated in the development of serious conditions, including diabetes, various types of cancer, and cardiovascular diseases, in addition to its essential role in maintaining bone health (1, 2). The high rates of hypovitaminosis D reported in this study suggest that immediate action is needed to improve the vitamin D status of the British population.

Summary of evidence-based review on vitamin D efficacy and safety in relation to bone health. Cranney A, Weiler HA, O'Donnell S, Puil L. Am J Clin Nutr. 2008 Aug;88(2):513S-519S. Review. PMID: 18689393 We found inconsistent evidence of an association between serum 25-hydroxyvitamin D [25(OH)D] concentration and bone mineral content in infants and fair evidence of an association with bone mineral content or density in older children and older adults. The evidence of an association between serum 25(OH)D concentration and some clinical outcomes (fractures, performance measures) in postmenopausal women and older men was inconsistent, and the evidence of an association with falls was fair. We found good evidence of a positive effect of consuming vitamin D-fortified foods on 25(OH)D concentrations. The evidence for a benefit of vitamin D on falls and fractures varied. We found fair evidence that adults tolerated vitamin D at doses above current dietary reference intake levels, but we had no data on the association between long-term harms and higher doses of vitamin D.

Differences in vitamin D status between countries in young adults and the elderly. McKenna MJ. Am J Med. 1992 Jul;93(1):69-77. PMID: 1385673 PURPOSE: To compare vitamin D status between countries in young adults and in the elderly. MATERIALS AND METHODS: Reports on vitamin D status (as assessed by serum 25-hydroxyvitamin D) from 1971 to 1990 were reviewed. Studies were grouped according to geographic regions: North America (including Canada and the United States); Scandinavia (including Denmark, Finland, Norway, and Sweden); and Central and Western Europe (including Belgium, France, Germany, Ireland, The Netherlands, Switzerland, and the United Kingdom). RESULTS: Vitamin D status varies with the season in young adults and in the elderly, and is lower during the winter in Europe than in both North America and Scandinavia. Oral vitamin D intake is lower in Europe than in both North America and Scandinavia. Hypovitaminosis D and related abnormalities in bone chemistry are most common in elderly residents in Europe but are reported in all elderly populations. CONCLUSIONS: The vitamin D status in young adults and the elderly varies widely with the country of residence. Adequate exposure to summer sunlight is the essential means to ample supply, but oral intake augmented by both fortification and supplementation is necessary to maintain baseline stores. All countries should adopt a fortification policy. It seems likely that the elderly would benefit additionally from a daily supplement of 10 micrograms of vitamin D.

Bioactive vitamin D or calcitriol is a steroid hormone that has long been known for its important role in regulating body levels of calcium and phosphorus, and in mineralization of bone. More recently, it has become clear that receptors for vitamin D are present in a wide variety of cells, and that this hormone has biologic effects which extend far beyond control of mineral metabolism. The active form of vitamin D binds to intracellular receptors that then function as transcription factors to modulate gene expression. Like the receptors for other steroid hormones and thyroid hormones, the vitamin D receptor has hormone-binding and DNA-binding domains. The vitamin D receptor forms a complex with another intracellular receptor, the retinoid-X receptor, and that heterodimer is what binds to DNA. In most cases studied, the effect is to activate transcription, but situations are also known in which vitamin D suppresses transcription. Each of the forms of vitamin D is hydrophobic, and is transported in blood bound to carrier proteins. The major carrier is called, appropriately, vitamin D-binding protein. The halflife of 25-hydroxycholecalciferol is several weeks, while that of 1,25-dihydroxycholecalciferol is only a few hours. The vitamin D receptor binds several forms of cholecalciferol. Its affinity for 1,25-dihydroxycholecalciferol is roughly 1000 times that for 25-hydroxycholecalciferol, which explains their relative biological potencies

"So why is Dr Vieth so frustrated? You might think he'd have cause for celebration. But for him and other vitamin D researchers around the world, the good news comes with a bitter aftertaste. They believe they can prove vitamin D could help millions live longer and be healthier and yet they have not been able to convince their own governments. In the US and Canada, official vitamin D policy is set by the Institute of Medicine. And in the opinion of Vieth, the current recommendations - 200 International Units per day for people under 50, 400 for people aged 51-70, and 600 for those 71 and older - are outrageously low. Bruce Hollis, professor of paediatrics at the Medical University of South Carolina, calls 400 IU a day "a joke". That's because the best research suggests that to achieve the higher vitamin D blood levels associated with disease prevention, most adults in the US would need to take 1,000-2,000 IU a day: five to 10 times more than the current official recommendation for adult In 1999, Reinhold Vieth (pictured right) published a review of vitamin D research in response to the IOM conclusions. In it, he argued that there was no evidence that amounts lower than 20,000 IU a day could be toxic. "Throughout my preparation of this review, I was amazed at the lack of evidence supporting statements about the toxicity of moderate doses of vitamin D," Vieth wrote. Studies have since shown 10,000 IU a day of vitamin D to be safe. While any substance will become toxic in excess, vitamin D researchers today accept that the current vitamin D recommendations could be more than quadrupled with no fear of toxicity.!

"Pohjolan kitsas aurinko tarjoaa D-vitamiinia seuraavan kerran maaliskuussa. Talvella luustovitamiinit pitää tankata ruoasta tai purkista. Kala on D-vitamiininlähteistä parhaita. D on se aurinkovitamiini, jota jokainen muistaa lapsena napsineensa - onnekkaimmat Vitol-helmien tai peräti suklaan muodossa, karskimpien perheiden kasvatit kalanmaksaöljynä. Ilman D-vitamiinia ihmisen elimistö ei kykene käyttämään hyväkseen ruoasta tulevaa kalsiumia, ja se näkyy luustossa. Riisitauti on puutostautien klassikko, jota tavataan meillä yhä. Joka vuosi siihen sairastuu muutama pikkulapsi, jolle ei ole annettu D-vitamiinilisää. D-vitamiinin puute pehmentää aikuistenkin luustoa, mutta silloin taudin nimi on osteomalasia. D:n puutteen katsotaan olevan myös yksi osteoporoosin riskitekijöistä. - D-vitamiinin vajaus ei tunnu olossa eikä näy päälle, ennen kuin luut tosiaan alkavat pehmentyä. Omaa vitamiinitilannettaan kannattaa miettiä, jos ei syö lainkaan kalaa ja käyttää vain vähän D-vitaminoituja maitovalmisteita, toteaa dosentti Christel Lamberg-Allardt Helsingin yliopistosta."

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

(VIDEO) Shedding light on the vitamin D deficiency 'crisis' By GrassRootsHealth.com Oct 11, 2009 - 4:49:39 PM San Diego, CA - Can vitamin D prevent 80% of the incidence of breast cancer? What is its affect on colon cancer and other major illnesses? These questions and more will be addressed when some of the most prominent vitamin D researchers in North America participate in the " Diagnosis & Treatment of Vitamin D Deficiency" seminar presented by GrassrootsHealth at the University of Toronto on Tuesday, November 3 from 8 a.m. - 5 p.m. GrassrootsHealth is the founder of D*action, an international public health project whose goal is to solve the vitamin D deficiency epidemic. GrassrootsHealth and D*action work with over 30 scientists, institutions and individuals committed to educate, test, and study vitamin D levels worldwide. At the conference, a group of physicians and researchers in the vitamin D field will discuss vitamin D's role in the potential prevention of many diseases, including breast cancer, colon cancer, type 1 diabetes and multiple sclerosis, the ultimate reduction in the incidence of infectious diseases and the economic impact of such action

Vitamin D intake to attain a desired serum 25-hydroxyvitamin D concentration. Aloia JF, Patel M, Dimaano R, Li-Ng M, Talwar SA, Mikhail M, Pollack S, Yeh JK. Am J Clin Nutr. 2008 Jun;87(6):1952-8. PMID: 18541590 The mean daily dose was 86 microg (3440 IU). The use of computer simulations to obtain the most participants within the range of 75-220 nmol/L predicted an optimal daily dose of 115 microg/d (4600 IU). No hypercalcemia or hypercalciuria was observed. CONCLUSIONS: Determination of the intake required to attain serum 25(OH)D concentrations >75 nmol/L must consider the wide variability in the dose-response curve and basal 25(OH)D concentrations. Projection of the dose-response curves observed in this convenience sample onto the population of the third National Health and Nutrition Examination Survey suggests a dose of 95 microg/d (3800 IU) for those above a 25(OH)D threshold of 55 nmol/L and a dose of 125 microg/d (5000 IU) for those below that threshold.

Vitamin D intake is low and hypovitaminosis D common in healthy 9- to 15-year-old Finnish girls. Lehtonen-Veromaa M, Möttönen T, Irjala K, Kärkkäinen M, Lamberg-Allardt C, Hakola P, Viikari J. Eur J Clin Nutr. 1999 Sep;53(9):746-51. PMID: 10509773 CONCLUSION: Hypovitaminosis D is fairly common in growing Finnish girls in the wintertime, and three months of vitamin D supplementation with 10 microg/d was insufficient in preventing hypovitaminosis D. The daily dietary vitamin D intake was insufficient (< 5 microg/d) in the majority of participants, while the calcium intake was usually sufficient.

An evaluation of the vitamin D3 content in fish: Is the vitamin D content adequate to satisfy the dietary requirement for vitamin D? Lu Z, Chen TC, Zhang A, Persons KS, Kohn N, Berkowitz R, Martinello S, Holick MF. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):642-4. Epub 2007 Jan 30. PMID: 17267210 doi: 10.1016/j.jsbmb.2006.12.010 Surprisingly, farmed salmon had approximately 25% of the vitamin D content as wild salmon had. The vitamin D content in fish varied widely even within species. These data suggest that the tables that list the vitamin D content are out-of-date and need to be re-evaluated. Little is known about the effect of cooking on the vitamin D content in fish. When farm salmon was baked, almost all of the vitamin D content, i.e. 240 IU of vitamin D3 was recovered from 3.5 oz. of salmon. The initial concentration in the uncooked salmon was 245 IU of vitamin D3. However, when the salmon was fried in vegetable oil, approximately 50% (123 IU of vitamin D3 was recovered.) We also evaluated the vitamin D content in mackerel which is traditionally considered to be an excellent source of vitamin D3 because of its oily content. However, in the one sample that we tested, we only observed 24 IU of vitamin D3 in 3.5 oz.

Food chain as origin of vitamin D in fish D. Sunita Rao and N. Raghuramulu. Comparative Biochemistry and Physiology Part A: Physiology Volume 114, Issue 1, May 1996, Pages 15-19 doi:10.1016/0300-9629(95)02024-1 Plankton, the chief food source of fish, was assessed as the possible dietary origin of vitamin D in fish. The presence of vitamin D compounds were examined in fresh water phytoplankton and zooplankton employing a series of chromatographic procedures. Abundant amounts of provitamins D and vitamins D (D2 and D3) were found in the fresh water plankton. The high amount of vitamin D observed may be due to exposure of plankton to sunlight because the plankton were caught during the summer month. Thus, plankton may be an important contributor to vitamin D in fish.