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Vitamin D deficiency is a very serious health problem. Most people tend to think of it only in terms of skeletal problems; however, it is much more than that. Vitamin D deficiency has now been linked with a multitude of neoplasms, autoimmune dysfunction, compromised innate immunity and neurodevelopment in utero. Vitamin D is made in huge amounts when we go into intense sun. A fair-skinned individual can produce approximately 20,000 IU in 10 minutes' time with a total body exposure. A person with significant pigmentation will require up to 10 times the exposure to make an equivalent amount. In the winter at the latitude of Chicago, even a fair person cannot photo-produce vitamin D from mid-October through March. Thus, it is VERY important to have a realistic vitamin D recommendation as the current 200 IU/day recommendation is a joke

Seasonal affective disorder (SAD) is a type of winter-time depression experienced by people those who live in northern latitudes such as those of New York, Seattle, all of Canada, and Northern Europe. I believe it is primarily a disorder of sunlight/vitamin D deficiency. Vitamin D, when administered in late winter, produces a positive effect on mood in only five days.[1] One theory for this is that vitamin D stimulates the brain to produce more serotonin. In a wintertime experiment, serum vitamin D levels doubled in six months through supplementation and dramatically increased scores on a wellbeing assessment.[2] Two groups were given either 1,000 IU or 4,000 IU of vitamin D daily. And although both groups improved, the higher dose produced better results.

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

Cod liver oil, vitamin A toxicity, frequent respiratory infections, and the vitamin D deficiency epidemic. Cannell JJ, Vieth R, Willett W, Zasloff M, Hathcock JN, White JH, Tanumihardjo SA, Larson-Meyer DE, Bischoff-Ferrari HA, Lamberg-Allardt CJ, Lappe JM, Norman AW, Zittermann A, Whiting SJ, Grant WB, Hollis BW, Giovannucci E. Ann Otol Rhinol Laryngol. 2008 Nov;117(11):864-70. Review. PMID: 19102134 Until we have better information on doses of vitamin D that will reliably provide adequate blood levels of 25(OH)D without toxicity, treatment of vitamin D deficiency in otherwise healthy children should be individualized according to the numerous factors that affect 25(OH)D levels, such as body weight, percent body fat, skin melanin, latitude, season of the year, and sun exposure.2 The doses of sunshine or oral vitamin D3 used in healthy children should be designed to maintain 25(OH)D levels above 50 ng/mL. As a rule, in the absence of significant sun exposure, we believe that most healthy children need about 1,000 IU of vitamin D3 daily per 11 kg (25 lb) of body weight to obtain levels greater than 50 ng/mL. Some will need more, and others less. In our opinion, children with chronic illnesses such as autism, diabetes, and/or frequent infections should be supplemented with higher doses of sunshine or vitamin D3, doses adequate to maintain their 25(OH)D levels in the mid-normal of the reference range (65 ng/mL) - and should be so supplemented year round. Otolaryngologists treating children are in a good position to both diagnose and treat vitamin D deficiency.

A few researchers are turning their attention to the sunshine vitamin as a culprit, prompted by the experience of immigrants that have moved from their equatorial country to two northern latitude locations As evidence of widespread vitamin D deficiency grows, some scientists are wondering whether the sunshine vitamin-once only considered important in bone health-may actually play a role in one of neurology's most vexing conditions: autism. The idea, although not yet tested or widely held, comes out of preliminary studies in Sweden and Minnesota. Last summer, Swedish researchers published a study in Developmental Medicine and Child Neurology that found the prevalence of autism and related disorders was three to four times higher among Somali immigrants than non-Somalis in Stockholm. The study reviewed the records of 2,437 children, born between 1988 and 1998 in Stockholm, in response to parents and teachers who had raised concerns about whether children with a Somali background were overrepresented in the total group of children with autism

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.

Diagnosis and treatment of vitamin D deficiency. Cannell JJ, Hollis BW, Zasloff M, Heaney RP. Expert Opin Pharmacother. 2008 Jan;9(1):107-18. PMID: 18076342 The recent discovery - in a randomised, controlled trial - that daily ingestion of 1100 IU of colecalciferol (vitamin D) over a 4-year period dramatically reduced the incidence of non-skin cancers makes it difficult to overstate the potential medical, social and economic implications of treating vitamin D deficiency. Not only are such deficiencies common, probably the rule, vitamin D deficiency stands implicated in a host of diseases other than cancer. The metabolic product of vitamin D is a potent, pleiotropic, repair and maintenance, secosteroid hormone that targets > 200 human genes in a wide variety of tissues, meaning it has as many mechanisms of action as genes it targets. A common misconception is that government agencies designed present intake recommendations to prevent or treat vitamin D deficiency. They did not. Instead, they are guidelines to prevent particular metabolic bone diseases. Official recommendations were never designed and are not effective in preventing or treating vitamin D deficiency and in no way limit the freedom of the physician - or responsibility - to do so. At this time, assessing serum 25-hydroxy-vitamin D is the only way to make the diagnosis and to assure that treatment is adequate and safe. The authors believe that treatment should be sufficient to maintain levels found in humans living naturally in a sun-rich environment, that is, > 40 ng/ml, year around. Three treatment modalities exist: sunlight, artificial ultraviolet B radiation or supplementation. All treatment modalities have their potential risks and benefits. Benefits of all treatment modalities outweigh potential risks and greatly outweigh the risk of no treatment. As a prolonged 'vitamin D winter', centred on the winter solstice, occurs at many temperate latitudes, ≤ 5000 IU (125 μg) of vitamin D/d

"We are fond of grumbling about Britain's grey skies, but there may be a good medical reason for doing so. It seems the dreary weather is bad for our hearts - worse, even, than raised cholesterol and an unhealthy diet. That's the controversial claim being made by Dr David Grimes, a gastroenterologist from Blackburn. He's been gazing at the sky for 20 years for clues about why his patients get more sick than those in the south of the country. And what he's found turns key assumptions about heart disease on their head. 'It's not diet or cholesterol levels that raise your risk of heart disease,' he claims. 'It's where you live. People in the north are more likely to be ill because they get less sunshine Basically they are suffering from 'latitude' sickness. The link is vitamin D. While we get some from our diet, the main source is the sun - sunlight converts a compound in the skin into vitamin D, so the amount you make is directly related to the amount of sunshine you get. In a new book Dr Grimes argues the higher the level of vitamin D in your blood, the lower your risk of heart disease and a range of other illnesses. If he's right, what we need is not diet and lifestyle advice, but food fortified with vitamin D. For years the vitamin was thought to be useful only for preventing rickets. So how does he treat them? 'You can do it with diet,' he says 'One Bangladeshi woman eats oily fish every day and now has a vitamin D blood level of 40. 'We give supplements of 1,000 international units (IU) a day or we can give an injection of 300,000 IU that lasts for a year. 'The patients respond well,' says Grimes 'but what's needed is a proper controlled, long-term trial and who is going to fund that? Not a drug company.'"

An acknowledged benefit of exposure to ultraviolet radiation is synthesis of vitamin D in human skin. Here we have defined a standard vitamin D dose based upon recommended requirements for vitamin D, and present a web-based tool that enables the user to calculate associated exposure times for any time and place ( http://nadir.nilu.no/~olaeng/fastrt/VitD_quartMED.html). The recommended UV exposure times depends on latitude, time, total ozone, clouds, aerosols, surface reflectivity and altitude all of which can be specified by the user. A simpler version for non-experts is available at http://nadir.nilu.no/~olaeng/fastrt/VitD-ez_quartMED.html

"Let's shine some sunlight on these knowledge deficiencies: * Serum vitamin D levels have been dropping (as chronic inflammation has been increasing) over the last three decades -- has something changed in our diets? * Vitamin D deficiencies occur globally (not restricted to Northern latitudes or winter) -- related to diet? * Women are more vulnerable, because of cultural modesty in some countries, but males are still D-deficient. * A subset of people exposed to ample sunshine are still D-deficient. * Vitamin D deficient individuals also have elevated TNF. * Vitamin D deficiency and inflammation are risk factors in the same diseases. It seems that the simplest conclusion is that chronic inflammation leads to vitamin D deficiency, even though vitamin D deficiency may also contribute to inflammation."

Geographic variation of prostate cancer mortality rates in the United States: Implications for prostate cancer risk related to vitamin D. Grant WB. Int J Cancer. 2004 Sep 1;111(3):470-1; author reply 472. No abstract available. PMID: 15221981 10.1002/ijc.20220 The implications of our results and those of Tuohimaa et al.[1] include the following. Vitamin D supplementation should be undertaken in wintertime, a period when it is impossible to produce vitamin D by solar UVB exposure in northeastern states.[13] Given these new results, the optimal vitamin D intake and production and serum 25(OH)-vitamin D3 levels for prostate cancer appear to be lower than for other cancers. However, when developing guidelines for vitamin D fortification, many factors should be included in the analysis, including all of the potential health benefits and possible risks of vitamin D, as well as age, sex, residence, child-bearing status, etc.[14] Also, the suggestion that daily vitamin D3 supplement doses of 100 g (4,000 IU)/day are safe[15] should be reexamined. Finally, in terms of preventing prostate cancer, more attention should be given to diet, which has the greatest environmental impact on risk of prostate cancer, with animal products being important risk factors and vegetable products, especially onions and other allium family members, being important risk-reduction factors.[16]

Evolution and function of vitamin D. Holick MF. Recent Results Cancer Res. 2003;164:3-28. Review. PMID: 12899511

Global vitamin D status and determinants of hypovitaminosis D. Mithal A, Wahl DA, Bonjour JP, Burckhardt P, Dawson-Hughes B, Eisman JA, El-Hajj Fuleihan G, Josse RG, Lips P, Morales-Torres J; on behalf of the IOF Committee of Scientific Advisors (CSA) Nutrition Working Group. Osteoporos Int. 2009 Jun 19. [Epub ahead of print] PMID: 19543765 CONCLUSION: Reports from across the world indicate that hypovitaminosis D is widespread and is re-emerging as a major health problem globally.

The review, published in Osteoporosis International, provides a global perspective of vitamin D status across different regions of the world and identifies common and significant determinants of hypovitaminosis D. Six regions of the world were reviewed-Asia, Europe, Middle East and Africa, Latin America, North America, and Oceania-through a survey of published literature.

Vitamin D and skin physiology: a D-lightful story.\nHolick MF, Chen TC, Lu Z, Sauter E.\nJ Bone Miner Res. 2007 Dec;22 Suppl 2:V28-33.\nPMID: 18290718 \ndoi: 10.1359/jbmr.07s211\n

Ecological Studies Of Ultraviolet B, Vitamin D And Cancer Since 2000. Grant WB, Mohr SB. Ann Epidemiol. 2009 Mar 6. [Epub ahead of print] PMID: 19269856 doi:10.1016/j.annepidem.2008.12.014

Ecological Studies Of Ultraviolet B, Vitamin D And Cancer Since 2000. Grant WB, Mohr SB. Ann Epidemiol. 2009 Mar 6. [Epub ahead of print] PMID: 19269856

Chen TC, Chimeh F, Lu Z, Mathieu J, Person KS, Zhang A, Kohn N, Martinello S, Berkowitz R, Holick MF. Factors that influence the cutaneous synthesis and dietary sources of vitamin D. Arch Biochem Biophys. 2007 Apr 15;460(2):213-7. Epub 2007 Jan 8. PMI

Addressing the health benefits and risks, involving vitamin D or skin cancer, of increased sun exposure.\nMoan J, Porojnicu AC, Dahlback A, Setlow RB.\nProc Natl Acad Sci U S A. 2008 Jan 15;105(2):668-73. Epub 2008 Jan 7.\nPMID: 18180454

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.