Vitamin D is fat-soluble vitamin requiring bile for absorption, and occurs naturally in animal foods such as salmon, herring, sardines, egg yolks, cod liver oil and dairy products. It can be acquired either by ingestion or by exposure to sunlight.
The combination of low sunlight and inadequate sources of the vitamin D rich foods has made rickets a large concern. Interestingly, the first discovered "Neanderthal men" were diagnosed as "ancient" men who died of rickets. This accounted for the posture and facial features as bone defects. After years of debate about the origin of Neanderthals, this is still one of the most viable explanations. As darker skinned men and women left the sunny climates of the southern hemisphere, they were able to convert less Vitamin D from their skin, rickets set in changing bone structure and eventually killing them. It should be noted that most "Neanderthals" are found in areas of reduced sunlight. In the United States, milk is fortified with Vitamin D to prevent this from happening, especially in the darker skinned population, where more sunlight is required to convert pre-vitamin D to vitamin D.
This fat-soluble vitamin can be obtained two major ways. The first is through exposure to sunlight. Our skin has pre-vitamin D (7-dehydroxycholesterol) present in the epidermis. As sunlight or ultraviolet light hits the skin, the pre-vitamin D is converted to the vitamin form called D3 (cholecalciferol). Dietary vitamin D can be obtained from salt water fish, and fish oils, although small amounts can be found in eggs, beef, butter and some vegetable oils.
Vitamin D is found primarily in foods of animal origin, unless they are fortified. Vegetables are usually low in vitamin D, except leafy dark green vegetables and mushrooms which are significant sources of vitamin D.
Vitamin D2 (ergocalciferol) is obtained from plants. Vegetables are usually low in vitamin D, but leafy dark green vegetables and mushrooms are significant non-animal sources.
Vitamin D3 (cholecalciferol) is stable to heat, light, and storage and is derived from animal products. It promotes calcium absorption for proper heart muscle function.
The major function of vitamin D is as a regulator of calcium. Cholecalciferol (D3) is converted to active forms by hydroxylation, which then play crucial roles on the absorption, metabolism, and cellular use of calcium. Active forms of vitamin D3 are now known to initiate biological responses via the regulation of protein synthesis at the level of the gene. The health of the human skeletal system is dependent on the proper amount of vitamin D; a lack of which causes weak and brittle bones, bone malformations and rickets.
The RDA for vitamin D for adults is 200 IU; for children, teens and pregnant or lactating women it is 400 IU; for the elderly or those with poor sunlight exposure or living in high northern or southern latitudes, it is 400 – 800 IU. It can be supplied by eating approximately 1.5kg of beef, 2.0kg of corn oil – or 100kg of cabbage! The RDA can also be supplied by eating roughly 50gm of salmon or 2.0gm of cod liver oil, and since fortified milk contains 400 IU per quart, half a quart of milk provides the RDA. For comparison, human breast milk contains only 4 to 60 IU per quart. One IU (International Unit) is equal to 0.025mcg of crystalline cholecalciferol.
It is estimated that the RDA can be achieved through the exposure of 30% of a persons skin surface to the sun for 30 minutes at moderate latitudes. The darker the skin, the less vitamin D will be produced (up to 95% of UV light is blocked). If longer exposure times are had, even with the darkest skin color, sufficient levels of vitamin D are produced. Glass blocks UV light, so indoor exposure does not help. During the winter months especially, it is advisable to supplement vitamin D if sun exposure is low and dietary sources are in question. The vitamin D in human milk varies with sun exposure and vitamin D intake.
Care must be taken in treating vitamin D deficiency, since high doses of vitamin D are toxic and can result in the permanent deposit of minerals in the heart, lungs and kidneys. Symptoms of toxicity include nausea, vomiting, joint pain, and lack of interest in eating food. In adults, vitamin D toxicity occurs with eating 50,000 IU or more per day. In infants, toxicity occurs with 1,000 IU per day. The continued intake of toxic doses results in death.
Vitamin D can inhibit the inflammatory mediators that develop in the intestinal wall after a gastrointestinal infection, and helps ease the symptoms of IBS. A 2012 study involving 37 patients found that 26 reported easing of IBS symptoms following supplementation with vitamin D.
The Children's Memorial Hospital in Chicago studied five vitamin D-deficient infants; at least two cases were caused by low vitamin D levels during pregnancy. Health problems ranged from seizures and growth failure to rickets. [Daaboul J, et al. J of Perinat 1997;17(1): 10-4] Congenital cataracts have also been linked to low levels of vitamin D. [Blau EB. The Lancet 1996;347: p.626] Other research points to vitamin D as a possible adjunct therapy for premature babies with respiratory distress syndrome [Nguyen TM, et al. Am J of Physiol 1996; 271(3): L392-9] and for women with gestational diabetes. [Rudnicki PM, Molsted-Pedersen L. Diabetologia 1997; 40(1): 40-4]
The U.S. RDA is 400 IU or 10mg.
Rickets heals promptly with 4,000 IU of oral vitamin D per day administered for approximately one month. During this treatment, the doctor should monitor the levels of 25-OH-D in the plasma to make certain they are raised to a normal value. The bone abnormalities (visible by X-ray) generally disappear gradually over a period of 3-9 months. Parents are instructed to take their infants outdoors for approximately 20 minutes per day with their faces exposed. Children should also be encouraged to play outside.
Osteomalacia is treated by eating 2,500 IU per day of vitamin D for about three months. Measurements of 25-OH-D, calcium, and parathyroid hormone should be obtained after the treatment period to make sure the therapy did, in fact, result in normal blood values.
In patients with advanced hormone refractory prostate cancer with bone metastases, 2000 IU of vitamin D with 500mg of calcium per day for three months was found to reduce bone pain, increase muscle strength, and improve the quality of life. [J. Urology 2000; 163: pp.187-190]
According to researchers, women who have mutations in their vitamin D receptor gene are nearly twice as likely to develop breast cancer as are women who do not have the mutation. These findings support previous studies showing vitamin D may offer protection against the disease. Researchers have found that Caucasian women with certain versions of this gene not only have an increased risk of breast cancer, but also may suffer from a more aggressive form of the disease if it spreads.
If true, this suggests that vitamin D does indeed play a part in protecting the body against breast cancer. It also shows that different versions of the vitamin D receptor gene will influence the way in which vitamin D protects the female body against this disease. [Colston, K., et al. Vitamin D receptor gene polymorphisms and breast cancer risk. Clinical Cancer Research August 14, 2004; 10(16)]
Administration of activated vitamin D (1,25 dihydroxycholecalciferol) may be beneficial in non-Hodgkin's lymphoma. Experimental Study: In a small trial, patients with non-Hodgkin's lymphoma who were found to have high levels of vitamin D receptors responded to activated vitamin D. [Cunningham D, Gilcrist NL, Cowan RA, et al. Vitamin D as a modulator of tumour growth in low grade lymphomas. Abstract. Scot Med J 30: p.193, 1985]
Evidence of vitamin D's protective effect against cancer is compelling. Since the 1950s, documentation in medical literature has suggested regular sun exposure is associated with substantial decreases in death rates from certain cancers and a decrease in overall cancer death rates. More recent research suggests this is a causal relationship that acts through the body's vitamin D metabolic pathways. For instance, some evidence points to a prostate, breast and colon cancer belt in the United States, which lies in northern latitudes under more cloud cover than other regions during the year. Rates for these cancers are two to three times higher than in sunnier regions.
Dark-skinned people require more sun exposure to make vitamin D. The thickness of the skin layer called the stratum corneum affects the absorption of UV radiation. Dark human skin is thicker than white skin and thus transmits only about 40% of the UV rays for vitamin D production. Darkly pigmented individuals who live in sunny equatorial climates experience a higher mortality (not incidence) rate from breast and prostate cancer when they move to geographic areas that are deprived of sunlight exposure in winter months. The rate of increase varies, and researchers hesitate to quote figures because many migrant black populations also have poor nutrition and deficient health care that confound statistics somewhat.
Although excessive sun exposure may give rise to skin cancer, researchers as early as 1936 were aware that skin cancer patients have reduced rates of other cancers. One researcher estimates moderate sunning would prevent 30,000 annual cancer deaths in the United States.
Vitamin D may also go beyond cancer prevention and provide tumor therapy. Much has been made of pharmaceutical angiogenesis inhibitors – agents that help inhibit the growth of new, undesirable blood vessels that tumors require for nutrient supply and growth. Laboratory tests have shown vitamin D to be a potent angiogenesis inhibitor.
Vitamin D also works at another stage of cancer development. Tumor cells are young, immortal cells that never grow up, mature and die off. Because vitamin D derivatives have been shown to promote normal cell growth and maturation, drug companies today are attempting to engineer patentable forms of vitamin D for anti-cancer therapy.
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