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Vitamin D is a group of fat-soluble prohormones, the two major forms of which are vitamin D₂ (or ergocalciferol) and vitamin D₃ (or cholecalciferol).^[2] Vitamin D obtained from sun exposure, food, and supplements is biologically inert and must undergo two hydroxylation reactions to be activated in the body. Calcitriol (1,25-Dihydroxycholecalciferol) is the active form of vitamin D found in the body. The term vitamin D also refers to these metabolites and other analogues of these substances.

Calcitriol plays an important role in the maintenance of several organ systems.^[3] However, its major role is to increase the flow of calcium into the bloodstream, by promoting absorption of calcium and phosphorus from food in the intestines, and reabsorption of calcium in the kidneys; enabling normal mineralization of bone and preventing hypocalcemic tetany. It is also necessary for bone growth and bone remodeling by osteoblasts and osteoclasts.^[4]^[5]

Up until 51 years of age 200IU is an adequate intake of vitamin D to maintain bone health and normal calcium metabolism in healthy people assuming no synthesis by exposure to sunlight.^[6]^[7]

Vitamin D plays a number of other roles including inhibition of calcitonin release from the thyroid gland. Calcitonin acts directly on osteoclasts, resulting in inhibition of bone resorption and cartilage degradation. Vitamin D can also inhibit parathyroid hormone secretion from the parathyroid gland and modulate neuromuscular and immune function.^[8]^[9]^[10]

Forms

Name	Chemical composition	Structure
Vitamin D₁	molecular compound of ergocalciferol with lumisterol, 1:1
Vitamin D₂	ergocalciferol (made from ergosterol)
Vitamin D₃	cholecalciferol (made from 7-dehydrocholesterol in the skin).
Vitamin D₄	22-dihydroergocalciferol
Vitamin D₅	sitocalciferol (made from 7-dehydrositosterol)	File:VitaminD5 structure.png

Several forms (vitamers) of vitamin D have been discovered (see table). The two major forms are vitamin D₂ or ergocalciferol, and vitamin D₃ or cholecalciferol. These are known collectively as calciferol.^[11] Vitamin D₂ was chemically characterized in 1932. In 1936 the chemical structure of vitamin D₃ was established and resulted from the ultraviolet irradiation of 7-dehydrocholesterol.^[12]

Chemically, the various forms of vitamin D are secosteroids; i.e., steroids in which one of the bonds in the steroid rings is broken.^[13] The structural difference between vitamin D₂ and vitamin D₃ is in their side chains. The side chain of D₂ contains a double bond between carbons 22 and 23, and a methyl group on carbon 24.

Vitamin D₂ (made from ergosterol) is produced by invertebrates, fungus and plants in response to UV irradiation; it is not produced by vertebrates. Little is known about the biologic function of vitamin D₂ in nonvertebrate species. Because ergosterol can more efficiently absorb the ultraviolet radiation that can damage DNA, RNA and protein it has been suggested that ergosterol serves as a sunscreening system that protects organisms from damaging high energy ultraviolet radiation.^[14]

Vitamin D₃ is made in the skin when 7-dehydrocholesterol reacts with UVB ultraviolet light at wavelengths between 270–300 nm, with peak synthesis occurring between 295-297 nm.^[15]^[16] These wavelengths are present in sunlight when the UV index is greater than 3. At this solar elevation, which occurs daily within the tropics, daily during the spring and summer seasons in temperate regions, and almost never within the arctic circles, vitamin D₃ can be made in the skin, with prolonged exposure to UVB rays an equilibrium is achieved in the skin, and excess vitamin D simply degrades as fast as it is generated.^[17]

Production in the skin

The epidermal strata of the skin. Production is greatest in the stratum basale (colored red in the illustration) and stratum spinosum (colored orange).

The skin consists of two primary layers: the inner layer called the dermis, composed largely of connective tissue, and the outer, thinner epidermis. The epidermis consists of five strata; from outer to inner they are: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale.

Cholecalciferol is produced photochemically in the skin from 7-dehydrocholesterol; 7-dehydrocholesterol is produced in relatively large quantities in the skin of most vertebrate animals, including humans.^[18] The naked mole rat appears to be naturally cholecalciferol deficient as serum 25-OH vitamin D levels are undetectable^[19] interestingly the naked mole rat is resistant to aging, maintains healthy vascular function^[20]and is the longest lived of all rodents.^[21]^[22]

In some animals, the presence of fur or feathers blocks the UV rays from reaching the skin. In birds and fur-bearing mammals, vitamin D is generated from the oily secretions of the skin deposited onto the fur and obtained orally during grooming.^[23]

In 1923, it was established that when 7-dehydrocholesterol is irradiated with light, a form of a fat-soluble vitamin is produced. Alfred Fabian Hess showed that "light equals vitamin D".^[24] Adolf Windaus, at the University of Göttingen in Germany, received the Nobel Prize in Chemistry in 1928, for his work on the constitution of sterols and their connection with vitamins.^[25] In the 1930s he clarified further the chemical structure of vitamin D.

Synthesis mechanism (form 3)

7-dehydrocholesterol, a derivative of cholesterol, is photolyzed by ultraviolet light in 6-electron conrotatory electrocyclic reaction. The product is pre-vitamin D₃.
Pre-vitamin D₃ then spontaneously isomerizes to Vitamin D₃ in a antarafacial hydride [1,7] Sigmatropic shift. At room temperature the transformation of previtamin-D₃ to vitamin D₃ takes about 12 days to complete.^[14]
Whether it is made in the skin or ingested, vitamin D₃ (cholecalciferol) is then hydroxylated in the liver to 25-hydroxycholecalciferol (25(OH)D₃ or calcidiol) by the enzyme 25-hydroxylase produced by hepatocytes. This hydroxylation reaction occurs in the endoplasmic reticulum and requires NADPH, O₂ and Mg²⁺ yet it is not a cytochrome P450 enzyme. Once made the product is stored in the hepatocytes until it is needed and then can be released into the plasma where it will be bound to an α-globulin. 25-hydroxycholecalciferol is then transported to the proximal tubules of the kidneys where it can be hydroxylated by one of two enzymes to different forms of vitamin D, one of which is active vitamin D (1,25-OH D) and another which is inactive vitamin D (24,25-OH D). The enzyme 1α-hydroxylase which is activated by parathyroid hormone (and additionally by low calcium or phosphate) forms the main biologically active vitamin D hormone with a C1 hydroxylation forming 1,25-dihydroxycholecalciferol (1,25(OH)2D₃, also known as calcitriol). A separate enzyme hydroxylates the C24 atom forming 24R,25(OH)2D₃ when 1α-hydroxylase is not active, this inactivates the molecule from any biological activity. Calcitriol is represented below right (hydroxylated Carbon 1 is on the lower ring at right, hydroxylated Carbon 25 is at the upper right end).

Mechanism of action

After vitamin D is produced in the middle layers of skin or consumed in food, it is converted in the liver and kidney to form 1,25 dihydroxyvitamin D, (1,25(OH)₂D), the physiologically active form of vitamin D (when "D" is used without a subscript it refers to either D₂ or D₃). This physiologically active form of vitamin D is known as calcitriol. Following this conversion, calcitriol is released into the circulation, and by binding to a carrier protein in the plasma, vitamin D-binding protein (VDBP), it is transported to various target organs.^[13]

The physiologically active form of vitamin D mediates its biological effects by binding to the vitamin D receptor (VDR), which is principally located in the nuclei of target cells.^[13] The binding of calcitriol to the VDR allows the VDR to act as a transcription factor that modulates the gene expression of transport proteins (such as TRPV6 and calbindin), which are involved in calcium absorption in the intestine.

The vitamin D receptor belongs to the nuclear receptor superfamily of steroid/thyroid hormone receptors, and VDRs are expressed by cells in most organs, including the brain, heart, skin, gonads, prostate, and breast. VDR activation in the intestine, bone, kidney, and parathyroid gland cells leads to the maintenance of calcium and phosphorus levels in the blood (with the assistance of parathyroid hormone and calcitonin) and to the maintenance of bone content.^[26]

The VDR is known to be involved in cell proliferation and differentiation. Vitamin D also affects the immune system, and VDRs are expressed in several white blood cells, including monocytes and activated T and B cells.^[27]

Apart from VDR activation, various alternative mechanisms of action are known. An important one of these is its role as a natural inhibitor of signal transduction by hedgehog (a hormone involved in morphogenesis).^[28]^[29]

Nutrition

Vitamin D is naturally produced by the human body when exposed to direct sunlight. In many countries, such foods as milk, yogurt, margarine, oil spreads, breakfast cereal, pastries, and bread are fortified with vitamin D₂ and/or vitamin D₃.^[30] In the United States and Canada, for example, fortified milk typically provides 100 IU per cup, or a quarter of the estimated adequate intake for adults over age 50.^[2]^[31]

Natural sources

Natural sources of vitamin D include:^[2]

Fatty fish species, such as:
- Herring, 85 g (3 ounces (oz)) provides 1383 IU
- Catfish, 85 g (3 oz) provides 425 IU
- Salmon, cooked, 100 g (3.5 oz) provides 360 IU
- Mackerel, cooked, 100 g (3.5 oz), 345 IU
- Sardines, canned in oil, drained, 50 g (1.75 oz), 250 IU
- Tuna, canned in oil, 85 g (3 oz), 200 IU
- Eel, cooked, 100 g (3.5 oz), 200 IU
- Fish liver oils, such as cod liver oil, 1 Tbs. (15 ml) provides 1,360 IU (one IU equals 25 ng)
A whole egg, provides 20 IU
Beef liver, cooked, 100 g (3.5 oz), provides 15 IU
Mushrooms (after UV light exposure)^[32]^[33]

In the United States (U.S.), typical diets provide about 100 IU/day, the NIH has set the safe upper limit at 2000 IU/day.^[34]^[35]

Measuring vitamin D status

A blood calcidiol (25-hydroxy-vitamin D) level is a satisfactory way to determine the cumulative effect of sun and diet in relation to vitamin D^[36] although serum 25(OH)D levels do not indicate the amount of vitamin D stored in other body tissues.^[37] A concentration of over 15 ng/ml (>37.5 nmol/L) is recommended. Higher levels (>30 ng/ml or >75 nmol/L) are proposed by some as desirable for achieving optimum health but there is not enough evidence to support them.^[38]^[39]^[40]^[41] A study of highly sun exposed young people in Hawaii concluded that as the highest 25(OH)D concentration produced by natural UV exposure seems to be approximately 60 ng/ml (150nmol/L) this value ought to be seen as the upper limit when prescribing vitamin D supplementation.^[42] In a multiethnic cohort there was an increased risk of prostate cancer for those with plasma 25-hydroxyvitamin D of 50ng/ml (125nmol/L)^[43]

Deficiency

Low blood calcidiol (25-hydroxy-vitamin D) can result from avoiding the sun although deficiency may also exist in those with abundant exposure to bright sunlight.^[44] Dietary intake supplies a modest amount of vitamin D as few foods contain a significant quantity of vitamin D relative to synthesis in the skin which can supply a large amount. Some genetic diseases have the appearance of rickets,^[45]^[46]^[47] these are associated with consanguineous marriage.^[48]^[49]^[50]^[51]^[52]^[53]^[54] and possibly founder effect.^[55] In Kashmir, India patients with pseudovitamin D deficiency rickets had grossly raised 25-hydroxyvitamin D concentrations.^[56] Skin colour has also been associated with low 25(OH)D, especially in Africans living in countries with a temperate climate. For example 25-OHD under 10ng/mL (25 nmol/l) in 44% of asymptomatic East African children living in Melbourne^[57]^[58] However a study of healthy young Ethiopians living in Addis Ababa (10 degrees N) found average 25(OH)D levels of 23.5nmol/L.^[59] A review of Vitamin D in Africa^[60] gives the median levels for equatorial countries: Kenya 65.5 nmol/L and Zaire 65nmol/L, concluding that it remains to be established if associations between vitamin D status and health outcomes identified in Western countries can be replicated in African countries.

Vitamin D levels are approximately 30% higher in northern Europe than in central and southern Europe, higher vitamin D concentrations in northern countries may have a genetic basis.^[61]^[62] In a meta-analysis of cross-sectional studies on serum 25(OH)D concentrations globally the levels averaged 54 nmol/l and were higher in women than men, and higher in Caucasians than in non-Caucasians. There was no trend in serum 25(OH)D level with latitude.^[63] African Americans often have a very low circulating 25(OH)D level, however those of African descent have higher parathyroid hormone and 1,25-Dihydroxycholecalciferol associated with lower 25-hydroxyvitamin D than other ethnic groups, moreover they have the greatest bone density^[64] and lowest risk of fragility fractures compared to other populations.^[65]^[66]^[67] African American adults are less likely to be diagnosed with coronary heart disease,^[68] in 2006, 9.4% of white men, 7.8% of black men, and 5.3% of Mexican American men had coronary heart disease,^[69] the NHANES I Epidemiologic Follow-up Study concluded African-American men aged 25 to 74 years had lower age-adjusted rates of coronary heart disease and acute myocardial infarction than white men of the same ages,^[70] African Americans have a lower prevalence and extent of coronary artery calcium (CAC) than whites.^[71] The incidence of testicular cancer among African Americans was calculated to be one quarter of that among whites.^[72] Frank deficiency of vitamin D can result from a number of hereditary disorders.^[3] Deficiency results in impaired bone mineralization, and leads to bone softening diseases^[73] including:

Rickets, a childhood disease characterized by impeded growth, and deformity, of the long bones which can be caused by calcium or phosphorus deficiency as well as a lack of vitamin D, today it is largely found in low income counties in Africa, Asia or the Middle East.^[74]^[75]^[76] Rickets was first described in the 17th century by Francis Glisson who stated in 1650 that it had first appeared about 30 years previously in the counties of Dorset and Somerset.^[77] In 1857 John Snow (physician) suggested the rickets then widespread in Britain was being caused by the adulteration of bakers bread with alum.^[78] The role of diet in the development of rickets^[79]^[80] was determined by Edward Mellanby between 1918–1920.^[81] By altering the diets of dogs raised in the absence of sunlight, he was able to establish unequivocally that rickets was linked with diet, and identified cod liver oil as an excellent anti-rachitic agent and phytic acid as a rachitic agent.^[82]^[83]^[84] Nutritional rickets exists in countries with intense year round sunlight such as Nigeria and can occur without vitamin D deficiency.^[85]^[86] In 1921 Elmer McCollum identified a substance found in certain fats that could prevent rickets. Prior to the fortification of milk products with vitamin D, rickets was a major public health problem, in Denver where ultraviolet rays are approximately 20% stronger than at sea level on the same latitude^[87] almost two thirds of 500 children had mild rickets in the late 1920's.^[88] An increase in the amount of animal protein^[89] in the 20th century American diet coupled with consumption of milk^[90]^[91] fortified with relatively small quantities of vitamin D led to a dramatic decline in the number of rickets cases.^[26] Although rickets is now rare in Britain there have been outbreaks in some immigrant communities but^[92] the sufferers did not conform to the stereotype of concealing clothing. Having darker skin and reduced exposure to sunshine did not produce rickets unless the diet deviated from a Western omnivore pattern characterized by high intakes of meat, fish and eggs, and low intakes of high-extraction cereals.^[93] The dietary risk factors for rickets are independent of the low vitamin D content of most foods and appear to result from interactions between constituents of animal foods and the intermediary metabolism of endogenously-synthesized vitamin D.^[94]
Osteomalacia, a bone-thinning disorder that occurs exclusively in adults and is characterized by proximal muscle weakness and bone fragility. The effects of osteomalacia are thought to contribute to chronic musculoskeletal pain.^[95]^[96] but of the five small double-blind randomized controlled trials, only one found a reduction in pain after supplementation, and there is no persuasive evidence of lower vitamin D status in chronic pain sufferers compared to controls.^[97]

There are associations between low 25(OH)D levels and many diseases,^[98]including several autoimmune diseases.^[10]^[26]^[99] However such associations were found in observational studies and are not conclusive evidence of a causal link, (see correlation does not imply causation), a systemic review^[100] found no significant effect of vitamin D supplements.

One leading^[101] proponent of the view that the optimal concentration of 25(OH)D is at least 30 ng/ml^[102] defines vitamin D deficiency as a 25(OH)D level of under 20 ng/ml (50 nmol/l), applying this criterion he regards 30% to 50% of the United States population as suffering from vitamin D deficiency.^[103] This includes areas with abundant sun exposure, such as Hawaii and southern Arizona where over 50% of inhabitants have 25(OH)D level of under 20 ng/ml.^[104]^[105] Such metrics^[106] depart from more typical definitions of vitamin deficiency which are based on prevention of overt deficiency symptoms or comparable biologic indicators.^[107]^[108]

Overdose by ingestion

In healthy adults, sustained intake of 1250 micrograms/day (50,000 IU) can produce overt toxicity within months,^[109] those with certain medical conditions are far more sensitive to vitamin D and develop hypercalcaemia in response to any increase in vitamin D nutrition while maternal hypercalcaemia during pregnancy may increase foetal sensitivity to effects of vitamin D and lead to a syndrome of mental retardation and facial deformities.^[110]^[111] If you have a medical condition, are pregnant or think you may be, or are breastfeeding, you must consult your doctor before taking a vitamin D supplement. For infants (birth to 12 months) the tolerable Upper Limit, (maximum amount that can be tolerated without harm) is set at 25 micrograms/day (1000 IU). 1000 micrograms/day (40,000 IU) in infants has produced toxicity within 1 month.^[3] The U.S. Dietary Reference Intake Tolerable Upper Intake Level (upper limit) of vitamin D for children and adults is set at 50 micrograms/day (2,000 IU). Serum levels of calcidiol (25-hydroxy-vitamin D) are typically used to diagnose vitamin D overdose which is known to cause hypercalcemia (an elevated level of calcium in the blood) caused by increased intestinal calcium absorption. Vitamin D toxicity is known to be a cause of high blood pressure.^[112] anorexia, nausea, and vomiting. These symptoms are often followed by polyuria (excessive production of urine), polydipsia (increased thirst), weakness, nervousness, pruritus (itch), and eventually renal failure. Other signals of kidney disease including elevated protein levels in the urine, urinary casts, and a build up of wastes in the blood stream can also develop.^[3] In one study, hypercalciuria and bone loss occurred in four patients with documented vitamin D toxicity.^[113] Vitamin D toxicity is treated by discontinuing vitamin D supplementation, and restricting calcium intake. If the toxicity is severe blood calcium levels can be further reduced with corticosteroids or bisphosphonates. Kidney damage may be irreversible.

Exposure to sunlight for extended periods of time does not normally cause vitamin D toxicity.^[114] This is because within about 20 minutes of ultraviolet exposure in light skinned individuals (3–6 times longer for pigmented skin) the concentration of vitamin D precursors produced in the skin reach an equilibrium, and any further vitamin D that is produced is degraded.^[17] According to some sources, endogenous production with full body exposure to sunlight is approximately 250 µg (10,000 IU) per day.^[114] According to Holick, "the skin has a large capacity to produce cholecalciferol"; his experiments indicate that,

"[W]hole-body exposure to one minimal erythemal dose of simulated solar ultraviolet radiation is comparable with taking an oral dose of between 250 and 625 micrograms (10 000 and 25 000 IU) vitamin D."^[17]

It is on the basis of the supposedly similar effect of supplementation and whole body exposure to one erythemal dose that a leading researcher ^[115] has suggested that 250 micrograms/day (10,000 IU) in healthy adults should be adopted as the tolerable upper limit.^[115] Supplements and skin synthesis have a different effect on on serum 25(OH)D concentrations;^[116] endogenously synthesized vitamin D3 travels in plasma almost exclusively on vitamin D-binding protein (VDBP), providing for a slower hepatic delivery of the vitamin D and the more sustained increase in plasma 25-hydroxycholecalciferol observed after depot, parenteral administration of vitamin D. Yet the orally administered route vitamin D produces swift hepatic delivery of vitamin D, and transient, but nonetheless abrupt, increases in plasma 25-hydroxycholecalciferol. The richest food source of vitamin D — wild salmon — would require 35 ounces a day to provide 10,000IU.^[117] It has been argued^[118] that ingestion of vitamin D in large amounts was achieved in the process of grooming by furry human ancestors and that from UV-exposed human skin secretions early humans ingested vitamin D by licking the skin, however this putative ingestion of vitamin D by early humans is not quantified. A study^[119] found 34% of its sample of healthy western Canadians to be be under 40nmol/L at some point and 97% to be under 80nmol/L at least once. It has been questioned.^[120] whether to ascribe a state of sub-optimal vitamin D status when the annual variation in ultraviolet will naturally produce a period of falling levels, and such a seasonal decline has been a part of Europeans' adaptive environment^[121] for 1000 generations,^[122] is clear thinking.

Still more contentious is recommending supplementation when those supposedly in need of it are labeled healthy and serious doubts exist as to the long term effect of attaining and maintaining serum 25(OH)D of at least 80nmol/L by supplementation.^[123] Possible ethnic differences in physiological pathways for ingested vitamin D, such as Inuit have, may confound across the board recommendations for vitamin D levels. Inuit compensate for lower production of vitamin D by converting more of this vitamin to its most active form^[124] Another study by the Toronto group^[125] did have 'young Canadian adults of diverse ancestry ' but applied a standard of serum 25(OH)D levels that was significantly higher than official recommedations.^[126]^[127], 75 nmol/L as "optimal", between 75 nmol/L and 50 nmol/L as "insufficient" and < 50 nmol/L as "deficient". The results were ' 22% of individuals of European ancestry had 25(OH)D levels less than the 40 nmol/L cutoff, which is comparable to the values observed in previous studies. 78% of individuals of East Asian ancestry and 77% of individuals of South Asian ancestry had 25(OH)D concentrations lower than 40 nmol/L. The East Asians in the Toronto sample had low 25(OH)D levels when compared to whites. Lipps (2010)^[128] in a world wide review says 'vitamin D deficiency (serum 25(OH)D<25nmol/l) is highly prevalent in China: "A survey in Beijing indicated that Vitamin D-deficiency (plasma 25(OH)D concentration <12.5 nmol/l) occurred in more than 40% of adolescent girls in winter." In a Chinese population at particular risk for esophageal cancer, those with the highest serum 25(OH)D concentrations have a significantly increased risk of the precursor lesion.^[129] Inuit have relatively high rates of esophageal cancer and there are ethnic differences in the metabolism of vitamin D between Caucasians and Inuit.^[130]^[131]

In South Asians Harinarayan (2009^[132] found "All studies uniformly point to low 25(OH)D levels in the populations studies despite abundant sunshine in our country". For example rural men around Delhi average 44nmol/L. Healthy Indians living at the latitude they are presumably best adapted to seem have low 25(OH)D levels which are not very different from healthy South Asians living in Canada. South Indian patients with ischemic heart disease have serum 25-hydroxyvitamin D3 levels which are extremely high — above 222.5 nmol/l.^[133] The Toronto group conclude -"skin pigmentation, assessed by measuring skin melanin content, showed an inverse relationship with serum 25(OH)D". The uniform occurence of very low serum 25(OH)D in Indians living in India and Chinese in China does not support the hypothesis that the low levels seen in the more pigmented are due to lack of synthesis from the sun at higher latitudes, the leader of the study has urged dark-skinned immigrants to take vitamin D supplements nonetheless; "I see no risk, no downside, there's only a potential benefit".^[134]^[135] A study of French Canadians^[136] found that a significant minority did not maximize ingested serum 25(OH)D for genetic reasons; vitamin D-binding protein polymorphisms explained as much of the variation in circulating 25(OH)D as did total ingestion of vitamin D.^[137] Oral vitamin D intake,^[138] is lower in Europe than both North America and Scandinavia.^[139] Whether the toxicity of oral intake of vitamin D is due to that route being unnatural as suggested by Fraser.^[140]^[141] is not known, but there is a certain amount of evidence to suggest that dietary vitamin D may be carried by lipoprotein particles^[142] into cells of the artery wall and atherosclerotic plaque, where it may be converted to active form by monocyte-macrophages.^[143] These findings raise questions regarding the effects of vitamin D intake on atherosclerotic calcification and cardiovascular risk. Dietary vitamin D may be causing vascular^[144] calcification.

Health effects

Immune system

The hormonally active form of vitamin D mediates immunological effects by binding to nuclear vitamin D receptors (VDR).^[145] VDR ligands have been shown to increase the activity of natural killer cells, and enhance the phagocytic activity of macrophages.^[27] Active vitamin D hormone also increases the production of cathelicidin, an antimicrobial peptide that is produced in macrophages triggered by bacteria, viruses, and fungi.^[146]^[147]^[148]

A 2006 study published in the Journal of the American Medical Association, reported evidence of a link between Vitamin D deficiency and the onset of multiple sclerosis; the authors posit that this is due to the immune-response suppression properties of Vitamin D.^[149] Further research conducted in 2009 indicates that vitamin D is required to activate a histocompatibility gene (HLA-DRB1*1501) necessary for differentiating between self and foreign proteins in a subgroup of individuals genetically predisposed to MS.^[150] It has been suggested that pregnant women take vitamin D during their pregnancy, to lessen the likelihood of the child developing MS later in life.^[151]^[152] However vitamin D fortification has been suggested to have caused a pandemic of allergic disease,^[153] a study of infants who received supplemental vitamin D found an association between vitamin D supplementation in infancy and an increased risk of atopy and allergic rhinitis later in life.^[154] A 2010 study by veteran vitamin D researcher Hector DeLuca has cast doubt on whether the vitamin D sythesizing effect of UVB is the feature of sunlight that affects MS.^[155] Ultraviolet- A radiation (which is not involved in synthesis of vitamin D) is known to affect the immune system.^[156]^[157]^[158]

Influenza

In the 1918 flu pandemic most of the fatalities were healthy young adults and the outbreak was widespread in the summer and autumn (in the Northern Hemisphere). Neither of these facts suggest high vitamin D levels gave any protection, they are actually suggestive of increased mortality for those with higher 25(OH) D concentrations.

Cancer

The molecular basis for thinking vitamin D has the potential to prevent cancer lies in its role as a nuclear transcription factor that regulates cell growth, differentiation, apoptosis and a wide range of cellular mechanisms central to the development of cancer.^[159] These effects may be mediated through vitamin D receptors expressed in cancer cells.^[27]

A 2005 metastudy found correlations between vitamin D levels and and cancer. Drawing from a meta-analysis of 63 observational studies of vitamin D status , the authors suggested that intake of an additional 1,000 international units (IU) (or 25 micrograms) of vitamin D daily reduced an individual's colon cancer risk by 50%, and breast and ovarian cancer risks by 30%.^[160]^[161]^[162]^[163]

A 2006 study using data on over 4 million cancer patients from 13 different countries showed a marked difference in cancer risk between countries classified as sunny and countries classified as less–sunny for a number of different cancers, it has been disputed whether the predictive models used in such studies are accurate in estimating 25(OH)D levels^[164]^[165] Research has also suggested that cancer patients who have surgery or treatment in the summer — and therefore make more endogenous vitamin D — have a better chance of surviving their cancer than those who undergo treatment in the winter when they are exposed to less sunlight.^[166] However vitamin D levels do not depend on regional solar irradiance^[167] Another 2006 study found that taking the U.S. RDA of vitamin D (400 IU per day) cut the risk of pancreatic cancer by 43% in a sample of more than 120,000 people from two long-term health surveys.^[168]^[169] However in male smokers a 3-fold increased risk for pancreatic cancer in the highest compared to lowest quintile of serum 25-hydroxyvitamin D concentration has been found.^[170] Research is being done on the use of calcitriol in the medical treatment of patients with advanced prostate cancer.^[171]

Polymorphisms of the vitamin D receptor (VDR) gene have been associated with an increased risk of breast cancer.^[172] Impairment of the VDR-mediated gene expression is thought to alter mammary gland development or function and may predispose cells to malignant transformation. Women with homozygous FOK1 mutations in the VDR gene had an increased risk of breast cancer compared with the women who did not. FOK1 mutation has also been associated with decreasing bone mineral density which in turn may be associated with an increase in the risk of breast cancer.^[173]While low levels of vitamin D in serum have been correlated with breast cancer disease progression and bone metastases^[172] and studies suggest that increased intake of vitamin D reduces the risk of breast cancer in premenopausal women,^[174]other studies found no effect on breast or colorectal cancers.^[175]^[176]

A randomized intervention study involving 1,200 women, published in June 2007, reports that vitamin D supplementation (1,100 international units (IU)/day) resulted in a 60% reduction in cancer incidence, during a four-year clinical trial, rising to a 77% reduction for cancers diagnosed after the first year (and therefore excluding those cancers more likely to have originated prior to the vitamin D intervention).^[177]^[178] Although the study was criticized on several grounds^[179] including failing to take into account a long term overall increase in cancer found in a another study of vitamin D intake^[180] in 2007 the Canadian Cancer Society, (a national community-based organization of volunteers) recommended that all adults begin taking 1,000 IU per day (five times more than the government says they need) .^[181]^[182] A US National Cancer Institute study analyzed data from the third national Health and Nutrition Examination Survey to examine the relationship between levels of circulating vitamin D in the blood and cancer mortality in a group of 16,818 participants aged 17 and older. It found no support for an association between 25(OH)D and total cancer mortality,^[183] unlike other studies it was done prospectively – meaning that participants were followed looking forward, and actual blood tests were used to measure the amount of vitamin D in their blood rather than than by trying to infer vitamin D levels from predictive models which may be inaccurate.^[184]^[185]^[186]

Cardiovascular disease

There is a certain amount of evidence to suggest that dietary vitamin D may be carried by lipoprotein particles^[187] into cells of the artery wall and atherosclerotic plaque, where it may be converted to active form by monocyte-macrophages.^[188] These findings raise questions regarding the effects of vitamin D intake on atherosclerotic calcification and cardiovascular risk. Dietary vitamin D may be causing vascular^[189] calcification. Low levels of vitamin D are associated with an increase in high blood pressure and cardiovascular risk. Numerous observational studies show this link, but of two systemic reviews one found only weak evidence of benefit from supplements and the other found no evidence of a beneficial effect whatsoever.^[190]^[191]^[192] The precise mechanism for cardiovascular regulation is still under investigation; possibilities include blood pressure regulation through the renin-angiotensin system, parathyroid hormone levels, direct impact on heart muscle function, inflammation, and vascular calcification.^[193]

When researchers monitored the vitamin D levels, blood pressure and other cardiovascular risk factors of 1739 people, of an average age of 59 years for 5 years, they found that those people with low levels of vitamin D had a 62% higher risk of a cardiovascular event than those with normal vitamin D levels.^[194] Low levels of vitamin D have also been correlated with hypertension, elevated VLDL triglycerides, and impaired insulin metabolism.^[195]

A report from the National Health and Nutrition Examination Survey (NHANES) involving nearly 5,000 participants found that low levels of vitamin D were associated with an increased risk of peripheral artery disease (PAD). The incidence of PAD was 80% higher in participants with the lowest vitamin D levels (<17.8 ng/mL).^[98] Cholesterol levels were found to be reduced in gardeners in the UK during the summer months.^[196] Heart attacks peak in winter and decline in summer in temperate^[197] but not tropical latitudes.^[198] Calcifediol (25-hydroxy-vitamin D) is implicated in the etiology of atherosclerosis, especially in non-Caucasians.^[140]^[199]^[133]^[200] Vitamin D levels are generally higher in the physically fit but are lower in those of tropical origin, this is a confound for any attempt to make a worldwide recommendation for vitamin D.^[201] 1,25-Dihydroxycholecalciferol(active serum vitamin D) levels are inversely correlated with coronary calcification^[202] moreover one-alpha-hydroxy-cholecalciferol, an active vitamin D analog^[203] therapy seems to protect patients from developing vascular calcification.^[204] African Americans have higher active serum vitamin D levels.^[205]^[206]^[207] There are racial differences in the association of coronary calcified plaque^[208] in that there is less calcified atherosclerotic plaque in the coronary arteries of African-Americans than in whites. One study found an elevated risk of ischaemic heart disease in Southern India in individuals whose vitamin D levels were above 89 ng/mL.^[133] Freedman et al. (2010) have found that serum vitamin D correlates in African Americans, but not in Euro-Americans, with calcified atheroscleratic plaque. Pharmacokinetics of vitamin D toxicity states - "Early assumptions that 1,25(OH)2D3 might cause hypercalcemia in vitamin D toxicity have been replaced by the theories that 25(OH)D3 at pharmacologic concentrations can overcome vitamin D receptor affinity disadvantages to directly stimulate transcription or that total vitamin D metabolite concentrations displace 1,25(OH)2D from vitamin D binding".^[37] Freedman et al. (2010) states - "Higher levels of 25-hydroxyvitamin D seem to be positively correlated with aorta and carotid CP in African Americans but not with coronary CP. These results contradict what is observed in individuals of European descent".^[209] Recommendations stemming for a single standard for optimal serum 25(OH)D concentrations ignores the differing genetically mediated determinates of serum 25(OH)D and may result in ethnic minorities in Western countries having the results of studies done with subjects not representative of ethnic diversity applied to them. Vitamin D levels vary for genetically mediated reasons as well as environmental ones.^[210]^[211]^[212]^[62]^[213]^[214]^[215]^[208]^[216] Among descent groups with heavy sun exposure during their evolution, taking supplemental vitamin D to attain the 25(OH)D level associated with optimal health in studies done with mainly European populations may have deleterious outcomes.^[217] A review of vitamin D status in India concluded that studies uniformly point to low 25(OH)D levels in Indians despite abundant sunshine, and suggested a public health need to fortify Indian foods with vitamin D might exist. However the levels found in India are consistent with many other studies of tropical populations which have found that even an extreme amount of sun exposure, such as incured by rural Indians,^[218] does not raise 25(OH)D levels to the levels typically found in Europeans,^[219]^[220]^[221]^[222]^[223]^[224]^[225]

Mortality

Using information from the National Health and Nutrition Examination Survey a group of researchers concluded that having low levels of vitamin D (<17.8 ng/ml) was independently associated with an increase in all-cause mortality in the general population.^[226] The study evaluated whether low serum vitamin D levels were associated with all-cause mortality, cancer, and cardiovascular disease (CVD) mortality among 13,331 diverse American adults who were 20 years or older. Vitamin D levels of these participants were collected over a 6-year period (from 1988 through 1994), and individuals were passively followed for mortality through the year 2000. Shortening of leukocyte telomeres is a marker of aging. Leukocyte telomere length (LTL) predicts the development of aging-related disease, and length of these telomeres decreases with each cell division and with increased inflammation (more common in the elderly). Vitamin D can inhibit proinflammatory overeaction and slow the turnover of leukocytes, longer leukocyte telomere length is achieved by the body maintaining the optimal vitamin D concentration.^[227]

Complex regulatory mechanisms control metabolism, recent epidemiologic evidence suggests that there is a narrow range of vitamin D levels in which vascular function is optimized. Levels above or below this natural homeostasis of vitamin D increase mortality.^[228] Overall, excess or deficiency in the calcipherol system appear to cause abnormal functioning and premature aging.^[229]^[230]^[231]

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^ ^a ^b ^c ^d Vitamin D at The Merck Manual of Diagnosis and Therapy Professional Edition
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^ ^a ^b ^c Vitamin D The Physicians Desk Reference. 2006 Thompson Healthcare.
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^ http://www.medscape.com/viewarticle/713649_3 Hedgehog signaling and Vitamin D
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^ Vitamin D and rickets By Z. Hochberg
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^ Office of Minority Health[5]
^ Dept. Of Health and Human Services [6]
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^ History of Vitamin D University of California, Riverside, Vitamin D Workshop.
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^ US National Institutes Of Health, National cancer Institute[7]
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^ Garrison, R., Jr., Somer, E., The nutrition desk reference(1997)
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^ Stewart B. Leavitt. "Vitamin D – A Neglected 'Analgesic' for Chronic Musculoskeletal Pain" (PDF). Pain-Topics.org. Retrieved 2009-03-25.
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^ Holick., M., The Vitamin D Solution: A 3- Step Strategy to Cure Our Most Common Health Problem (2010) ISBN 1594630674
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^ Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride(1997)., ISBN 978-0-309-06350-0. [8] page 235[9]
^ Vitamin D. The Merck Manuals Vitamin D [10]
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^ [11]European Food and Safety authority., Tolerable Upper Intake Limits for Vitamins And Minerals(2006) ISBN 92-9199-014-0
^ "Complete Guide to Vitamins, Minerals and Supplements", Fisher Books, Tucsan AZ, 1988, p42
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^ [Effects Of Vitamin D and the Natural selection of skin colour:how much vitamin D nutrition are we talking about http://www.direct-ms.org/pdf/VitDVieth/Vieth%20Anthropology%20vit%20D.pdf]
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^ [Tseng, Lisa. (2003). Controversies in Vitamin D Supplementation. Nutrition Bytes, 9(1) http://escholarship.org/uc/item/4m84d4fn] (Peer reviewed)
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^ [Tseng, Lisa. (2003). Controversies in Vitamin D Supplementation. Nutrition Bytes, 9(1) http://escholarship.org/uc/item/4m84d4fn]
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^ Scientific Advisory Committee on Nutrition (2007) Update on Vitamin D Position Statement by the Scientific Advisory Committee on Nutrition 2007 ISBN 9780112431145
^ Office of Dietary Supplements • National Institutes of Health Dietary Supplement Fact Sheet: Vitamin D [12]
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^ Harinarayan Vitamin D Status in India – Its Implications and Remedial Measures (2009) [cite http://www.japi.org/january_2009/R-1.html]a review of over 50 studies of 25(OH)D
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^ CBC Dark-skinned immigrants urged to take vitamin DTuesday, February 16, 2010 CBC news
^ STEPHEN STRAUSS: SCIENCE FRICTION The vitamin D debate Feb. 13, 2008 [13] CBC Analysis and viewpoint
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^ Janet Raloff, The Antibiotic Vitamin Science News, Vol 170, November 11, 2006, pages 312-317
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^ "Science News / Molecular Link Between Vitamin D Deficiency And MS". Retrieved 2009-02-25.
^ Vitamin D helps control MS gene. BBC News. 5 February 2009.
^ Genetic Study Supports Vitamin D Deficiency as an Environmental Factor in MS Susceptibility. Multiple Sclerosis Society of Canada. 5 February 2009
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^ "Vitamin D 'can lower cancer risk'". BBC News. 28 December 2005. Retrieved 2006-03-23.
^ Gorham ED, Garland CF, Garland FC et al. (2007). "Optimal vitamin D status for colorectal cancer prevention: a quantitative meta analysis. Am J Prev Med. 32:210-216.
^ Garland CF, Mohr SB, Gorham ED et al. (2006). "Role of ultraviolet B irradiance and vitamin D in prevention of ovarian cancer." Am J Prev Med. 31:512-514.
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^ BBC NEWS | Health | Vitamin D 'slashes cancer risk'
^ doi:10.1158/0008-5472.CAN-06-1876
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^ ^a ^b Buyru N, Tezol A;,Yosunkaya-Fenerci E, Dalay, N. Vitamin D receptor gene polymorphisms in breast cancer. Experimental and Molecular Medicine. 2003; 35(6):550-555.
^ Chen WY, Bertone-Johnson ER, Hunter DJ, Willett WC, Hankinson SE. Associations Between Polymorphisms in the Vitamin D Receptor and Breast Cancer Risk. Cancer Epidemiology, Biomarkers, & Prevention. 2005; 14(10):2335-2339.
^ Lin J, Manson JE, Lee IM, Cook NR, Buring JE, Zhang SM. Intakes of calcium and vitamin D and breast cancer risk in women. Archives of Internal Medicine.2007; 167(10):1050-9,
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^ Martin Mittelstaedt (28 April 2007). "Vitamin D casts cancer prevention in new light". Global and Mail. Retrieved 2007-04-28.
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^ Canadian Cancer Society announces Vitamin D recommendation, 08 June 2007.
^ Canadian Cancer Society recommends vitamin D. CTV.ca News Staff
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^ Maybe Vitamin D Isn't The Answer After All[14]
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^ Tseng, Lisa (2003). "Controversies in Vitamin D Supplementation". Nutrition Bytes. 9 (1).
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External links

[1] Walter F., PhD. Boron (2003). "The Parathyroid Glands and Vitamin F". Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. p. 1094. ISBN 978-1-4160-2328-9.

[FactD-2] "Dietary Supplement Fact Sheet: Vitamin D". National Institutes of Health. Archived from the original on 2007-09-10. Retrieved 2007-09-10.

[Merck-3] Vitamin D at The Merck Manual of Diagnosis and Therapy Professional Edition

[4] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 9023488, please use {{cite journal}} with |pmid=9023488 instead.

[5] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 18088161, please use {{cite journal}} with |pmid=18088161 instead.

[6] Scientific Advisory Committee on Nutrition (2007) Update on Vitamin D Position Statement by the Scientific Advisory Committee on Nutrition 2007 ISBN 9780112431145

[7] Office of Dietary Supplements • National Institutes of Health Dietary Supplement Fact Sheet: Vitamin D [1]

[8] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 3858880, please use {{cite journal}} with |pmid=3858880 instead.

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[11] Dorland's Illustrated Medical Dictionary, under Vitamin (Table of Vitamins)

[12] History of Vitamin D University of California, Riverside, Vitamin D Workshop.

[River-13] About Vitamin D Including Sections: History, Nutrition, Chemistry, Biochemistry, and Diseases. University of California Riverside

[Holick_2004-14] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 14985208, please use {{cite journal}} with |pmid=14985208 instead.

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[23] Sam D. Stout; Sabrina C. Agarwal; Stout, Samuel D. (2003). Bone loss and osteoporosis: an anthropological perspective. New York: Kluwer Academic/Plenum Publishers. ISBN 0-306-47767-X.{{cite book}}: CS1 maint: multiple names: authors list (link)

[24] UNRAVELING THE ENIGMA OF VITAMIN D U.S. National Academy of Sciences

[25] Windaus biography at nobelprize.org

[Sun-26] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 15585788, please use {{cite journal}} with |pmid=15585788 instead.

[PDR-27] Vitamin D The Physicians Desk Reference. 2006 Thompson Healthcare.

[28] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 16895439, please use {{cite journal}} with |pmid=16895439 instead.

[29] ttp://www.medscape.com/viewarticle/713649_3 Hedgehog signaling and Vitamin D

[Nowson-30] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 12149085, please use {{cite journal}} with |pmid=12149085 instead.

[Holick2-31] Holick, Michael (2007). The Vitamin D Pandemic and its Health Consequences. 34th European Symposium on Calcified Tissues. Copenhagen. {{cite conference}}: Unknown parameter |month= ignored (help)

[32] ttp://articles.latimes.com/2008/mar/31/health/he-eat31

[33] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 19281276, please use {{cite journal}} with |pmid=19281276 instead.

[34] Dietary Supplement Fact Sheet: Vitamin D

[35] Dietary Reference Intakes for Vitamin D and Calcium

[36] Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride(1997)., ISBN 978-0-309-06350-0. [2] page 235[3]

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[38] Scientific Advisory Committee on Nutrition (2007) Update on Vitamin D Position Statement by the Scientific Advisory Committee on Nutrition 2007 ISBN 9780112431145

[39] Office of Dietary Supplements • National Institutes of Health Dietary Supplement Fact Sheet: Vitamin D [4]

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[54] Vitamin D and rickets By Z. Hochberg

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[68] Office of Minority Health[5]

[69] Dept. Of Health and Human Services [6]

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[87] US National Institutes Of Health, National cancer Institute[7]

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[93] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 6970590, please use {{cite journal}} with |pmid=6970590 instead.

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[95] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 12520530, please use {{cite journal}} with |pmid=12520530 instead.

[pain-topics-96] Stewart B. Leavitt. "Vitamin D – A Neglected 'Analgesic' for Chronic Musculoskeletal Pain" (PDF). Pain-Topics.org. Retrieved 2009-03-25.

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[100] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 20194237, please use {{cite journal}} with |pmid=20194237 instead.

[101] Holick., M., The Vitamin D Solution: A 3- Step Strategy to Cure Our Most Common Health Problem (2010) ISBN 1594630674

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[108] Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride(1997)., ISBN 978-0-309-06350-0. [8] page 235[9]

[109] Vitamin D. The Merck Manuals Vitamin D [10]

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[111] [11]European Food and Safety authority., Tolerable Upper Intake Limits for Vitamins And Minerals(2006) ISBN 92-9199-014-0

[112] "Complete Guide to Vitamins, Minerals and Supplements", Fisher Books, Tucsan AZ, 1988, p42

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[117] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 17267210, please use {{cite journal}} with |pmid=17267210 instead.

[118] [Effects Of Vitamin D and the Natural selection of skin colour:how much vitamin D nutrition are we talking about http://www.direct-ms.org/pdf/VitDVieth/Vieth%20Anthropology%20vit%20D.pdf]

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[120] [Tseng, Lisa. (2003). Controversies in Vitamin D Supplementation. Nutrition Bytes, 9(1) http://escholarship.org/uc/item/4m84d4fn] (Peer reviewed)

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[123] [Tseng, Lisa. (2003). Controversies in Vitamin D Supplementation. Nutrition Bytes, 9(1) http://escholarship.org/uc/item/4m84d4fn]

[124] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 14708040, please use {{cite journal}} with |pmid=14708040 instead.

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[126] Scientific Advisory Committee on Nutrition (2007) Update on Vitamin D Position Statement by the Scientific Advisory Committee on Nutrition 2007 ISBN 9780112431145

[127] Office of Dietary Supplements • National Institutes of Health Dietary Supplement Fact Sheet: Vitamin D [12]

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[132] Harinarayan Vitamin D Status in India – Its Implications and Remedial Measures (2009) [cite http://www.japi.org/january_2009/R-1.html]a review of over 50 studies of 25(OH)D

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[134] CBC Dark-skinned immigrants urged to take vitamin DTuesday, February 16, 2010 CBC news

[135] STEPHEN STRAUSS: SCIENCE FRICTION The vitamin D debate Feb. 13, 2008 [13] CBC Analysis and viewpoint

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[146] Janet Raloff, The Antibiotic Vitamin Science News, Vol 170, November 11, 2006, pages 312-317

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[Science_News-150] "Science News / Molecular Link Between Vitamin D Deficiency And MS". Retrieved 2009-02-25.

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[161] "Vitamin D 'can lower cancer risk'". BBC News. 28 December 2005. Retrieved 2006-03-23.

[162] Gorham ED, Garland CF, Garland FC et al. (2007). "Optimal vitamin D status for colorectal cancer prevention: a quantitative meta analysis. Am J Prev Med. 32:210-216.

[163] Garland CF, Mohr SB, Gorham ED et al. (2006). "Role of ultraviolet B irradiance and vitamin D in prevention of ovarian cancer." Am J Prev Med. 31:512-514.

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[165] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 17540555, please use {{cite journal}} with |pmid=17540555 instead.

[166] "Vitamin D 'aids lung cancer ops'". BBC News. 22 April 2005. Retrieved 2006-03-23.

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[169] BBC NEWS | Health | Vitamin D 'slashes cancer risk'

[170] :10.1158/0008-5472.CAN-06-1876

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[Buyru-172] Buyru N, Tezol A;,Yosunkaya-Fenerci E, Dalay, N. Vitamin D receptor gene polymorphisms in breast cancer. Experimental and Molecular Medicine. 2003; 35(6):550-555.

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[176] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 16467233, please use {{cite journal}} with |pmid= 16467233 instead.,

[GlobeAndMail-177] Martin Mittelstaedt (28 April 2007). "Vitamin D casts cancer prevention in new light". Global and Mail. Retrieved 2007-04-28.

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[180] Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 17549593, please use {{cite journal}} with |pmid=17549593 instead.

[181] Canadian Cancer Society announces Vitamin D recommendation, 08 June 2007.

[182] Canadian Cancer Society recommends vitamin D. CTV.ca News Staff

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[186] Maybe Vitamin D Isn't The Answer After All[14]

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[199] Tseng, Lisa (2003). "Controversies in Vitamin D Supplementation". Nutrition Bytes. 9 (1).

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[217] Tseng, L., (2003) Controversies in Vitamin D Supplementation

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