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Vitamin D

Vitamin D is a fat-soluble vitamin that is naturally present in few foods. Some foods are fortified with vitamin D, and it is available as a dietary supplement. It is also produced endogenously when ultraviolet (UVB) light from the sun strikes the skin and trigger vitamin D synthesis.

Vitamin D3 (cholecalciferol) is derived by the effect of UVB irradiation on 7-dehydrocholesterol- a companion of cholesterol in the skin. The molecule is rearranged with the opening of the B ring on the steroid nucleus. Vitamin D3 is the naturally occurring form of the vitamin in animals. Vitamin D2 (ergocalciferol) is derived from the fungal sterol ergosterol following irradiation with UVB light. The original D1, turned out to be an impure mixture of sterols. As vitamin D is formed in the skin (an organ) and acts on other organs (bones, kidney, gut), it can be considered a hormone.

Vitamin D obtained from sun exposure, food, and supplements is biologically inert and must undergo two hydroxylations in the body for activation. The first occurs in the liver, converting vitamin D to calcidiol (25-hydroxyvitamin D [25(OH)D]). The second, occurs primarily in the kidney and forms the physiologically active calcitriol (1,25-dihydroxyvitamin D [1,25(OH)2D]).

Calcitriol is one of three hormones that act in concert to maintain the extracellular concentration gradient (the other two being parathormone and calcitonin). Calcitriol acts also as a steroid hormone, having a specific receptor in the cell nuclei of a range of tissues and a DNA binding domain. The main effect of the vitamin D receptor is observed in the small intestine, osteoblasts and osteoclasts, and maintains adequate serum calcium and phosphate concentrations to enable normal mineralization of bone. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults. Together with calcium, vitamin D also helps protect older adults from osteoporosis.

Very few foods in nature contain vitamin D. The flesh of fatty fish (such as salmon, tuna, and mackerel) and fish liver oils are among the best sources. Small amounts of vitamin D are found in beef liver, cheese, and egg yolks. Vitamin D in these foods is primarily in the form of vitamin D3 and its metabolite 25(OH)D3. Some mushrooms provide vitamin D2 in variable amounts, enhanced levels through exposure to ultraviolet light.

Most diets provide less 5mcg vitamin D per day unless the milk is fortified (RDA is 15-20mcg/d). Fortified foods provide most of the vitamin D in the western diet. Ready-to-eat breakfast cereals often contain added vitamin D, as do some brands of orange juice, yogurt, margarine and other food products. Plant milk alternatives (such as beverages made from soy, almond, or oats) are often fortified with vitamin D to the amount found in fortified cow’s milk (about 100 IU/cup). Both the United States and Canada mandate the fortification of infant formula with vitamin D: 40–100 IU/100 kcal. Supplements should be D3 (cholecalciferol) D2 (ergocalciferol) is less effective at raising 25(OH)D.

In young people, who’s bones are still growing, a deficiency of vitamin D presents as rickets. In which there is reduced calcification if the growing ends (epiphyses) of bones. The corresponding decalcifying bone disease in adults is osteomalacia; bone density is reduced- the ratio of calcium to organic bone is reduced. In osteoporosis, total bone is reduced, organic as well as calcium. As vitamin D levels fall, there is an increase in parathyroid hormone and increased mobilisation of bone. Deficiency can occur in those who usually stay indoors or those who are fully covered when outdoors. Malabsorption increases risk. Living at high latitudes can increase risk, particularly during the winter months.

Muscular weakness and susceptibility to infections in rickets or osteomalacia may indicate roles of vitamin D in the muscular and immune systems. The vitamin D receptor is expressed in many different cell nuclei, with indications of non-bone actions of vitamin D in tuberculosis, psoriasis, coronary heart disease, hypertension, diabetes, obesity and cancer. Large meta-analysis studies have found an inverse association of 25(OH) D concentrations and death from cardiovascular disease and from cancer.

A growing body of research suggests that vitamin D might play some role in the prevention and treatment of type 1 and type 2 diabetes, hypertension, glucose intolerance, multiple sclerosis, and other medical conditions. However, most evidence for these roles comes from in vitro, animal, and epidemiological studies. Until randomized control trials are conducted, the implications of the available evidence for public health and care will be debated. One meta-analysis found use of vitamin D supplements to be associated with a statistically significant reduction in overall mortality from any cause, but a reanalysis of the data found no association.

The US Institute of Medicine has set the RDA at 15 mcg (600IU) per day for ages 1-70 years, and 20mcg (800IU) per day for infants, and adults over 70 years. Excessive exposure to sunlight will not cause vitamin D toxicity as previtamin D is photoisomerized to biologically inert products. Hypervitaminosis D from dietary intake can cause raised plasma calcium, with a risk of soft tissue calcification and urinary calcium stones. The upper intake level is set at 100mcg or 4000IU per day.


Aloia, J. F. (2011). Clinical Review: The 2011 report on dietary reference intake for vitamin D: where do we go from here? J Clin Endocrinol Metab, 96(10), 2987-2996. doi:10.1210/jc.2011-0090

Chung M, Balk EM, Brendel M, Ip S, Lau J, Lee J, Lichtenstein A, Patel K, Raman G, Tatsioni A, Terasawa T, Trikalinos TA. Vitamin D and calcium: a systematic review of health outcomes. Evid Rep Technol Assess (Full Rep). 2009 Aug;(183):1-420. Review. PubMed PMID: 20629479; PubMed Central PMCID: PMC4781105.

Institute of Medicine, Food and Nutrition Board (2010). Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press.

Mann, J. & Truswell, S. (2017). Essentials of human nutrition. (5th ed.). London, United Kingdom: Oxford University Press.


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