Vitamin D is a fat-soluble vitamin that is naturally present in very few foods, added to others, and available as a dietary supplement.
It is also produced endogenously when ultraviolet rays from sunlight strike the skin and trigger vitamin D synthesis. 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 and converts vitamin D to hydroxyvitamin D [25 OH D], also known as calcidiol.
The second occurs primarily in the kidney and forms the physiologically active 1,dihydroxyvitamin D [1,25 OH 2 D], also known as calcitriol [ 1 ]. Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal mineralization of bone and to prevent hypocalcemic tetany. It vitamin d deficiency and metabolism also needed for bone growth and bone remodeling by osteoblasts and osteoclasts [ 12 ].
Without sufficient vitamin D, bones can become thin, brittle, or misshapen. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults [ 1 ]. Together with calcium, vitamin D also helps protect older adults from osteoporosis.
Vitamin D has other roles in the body, including modulation of cell growth, neuromuscular and immune function, and reduction of inflammation [ 134 ]. Many genes encoding proteins that regulate cell proliferation, differentiation, and apoptosis are modulated in part by vitamin D [ 1 ]. Serum concentration of 25 OH D is the best indicator of vitamin D status. It reflects vitamin D produced cutaneously and that obtained from food and supplements [ 1 ] and has a fairly long circulating half-life of 15 days [ 5 ].
Serum 25 OH D levels do not indicate the amount of vitamin D stored in body tissues. In contrast to 25 OH D, circulating 1,25 OH 2 D is generally not a good indicator of vitamin D status because it has a short half-life of 15 hours and serum concentrations are vitamin d deficiency and metabolism regulated by parathyroid hormone, calcium, and phosphate [ 5 ]. Levels of 1,25 OH 2 D do not typically decrease until vitamin D deficiency is severe [ 26 ], vitamin d deficiency and metabolism.
There is considerable discussion of the serum concentrations of 25 OH D associated with deficiency e. An additional complication in assessing vitamin D status is in the actual measurement of serum 25 OH D concentrations. Considerable variability exists among the various assays available the two most common methods being antibody based and liquid chromatography based and among laboratories that conduct the analyses [ 178 ].
This means that compared with the actual concentration of 25 OH D in a sample of blood serum, a falsely low or falsely high value may be obtained depending on the assay or laboratory used [ 9 ]. A standard reference material for 25 OH D became available in July that permits standardization of values across laboratories and may improve method-related variability [ 110 ].
DRI is the general term for a set of reference values used to plan and assess nutrient intakes of healthy people. These values, which vary by age and gender, include:.
The FNB established an RDA for vitamin D representing a daily intake that is sufficient to maintain bone health and normal calcium metabolism in healthy people. Even though sunlight may be a major source of vitamin D for some, the vitamin D RDAs are set on the basis of minimal sun exposure [ 1 ]. 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 [ 111 ].
Small amounts of vitamin D are found in beef liver, cheese, and egg yolks. Vitamin D in these foods is primarily in the vitamin d deficiency and metabolism of vitamin D 3 and its metabolite 25 OH D 3 [ 12 ].
Some mushrooms provide vitamin D 2 in variable amounts [ 1314 ]. Mushrooms with enhanced levels of vitamin D 2 from being exposed to ultraviolet light under controlled conditions are also available. Fortified foods provide most of the vitamin D in the American diet [ 114 ]. For example, almost all of the U. In the s, a milk fortification program was implemented in the United States to combat rickets, then a major public health problem [ 1 ].
Other dairy products made from milk, such as cheese and ice cream, are generally not fortified. Ready-to-eat breakfast cereals often contain added vitamin D, as do some brands of orange juice, vitamin d deficiency and metabolism, yogurt, margarine and other food products. Both the United States and Canada mandate the fortification of infant formula with vitamin D: Food and Drug Administration FDA developed DVs to help consumers compare the nutrient contents of products within the context of a total diet.
This DV, however, is changing to 20 mcg as the updated Nutrition and Supplement Facts labels are implemented [ 16 ], vitamin d deficiency and metabolism. The updated labels and DVs must appear on food products and dietary supplements beginning in Januarybut they can be used now [ 17 ]. FDA does not currently require food labels to list vitamin D content unless a food has been fortified with this nutrient, but it requires vitamin D content to be listed on the updated labels. A growing number of foods are being analyzed for vitamin D content, vitamin d deficiency and metabolism.
Simpler and faster methods to measure vitamin D in foods are needed, as are vitamin d deficiency and metabolism standard reference materials with certified values for vitamin D to ensure accurate measurements [ 18 ]. Animal-based foods can provide some vitamin D in the form of 25 OH D, which appears to be approximately five times more potent than the parent vitamin in raising serum 25 OH D concentrations [ 19 ]. One study finds that taking into account the serum 25 OH D content of beef, pork, chicken, turkey, and eggs can increase the estimated levels of vitamin D in the food from two to 18 times, depending upon the food [ 19 ].
Actual vitamin D intakes in the U. Most people meet at least some of their vitamin D needs through exposure to sunlight [ 12 ], vitamin d deficiency and metabolism. Ultraviolet UV B radiation with a wavelength of — nanometers penetrates uncovered skin and converts cutaneous 7-dehydrocholesterol to previtamin D 3vitamin d deficiency and metabolism in turn becomes vitamin D 3 [ 1 ].
Season, time of day, length of day, cloud cover, smog, skin melanin content, and sunscreen are among the factors that affect UV radiation exposure and vitamin D synthesis [ 1 ]. Perhaps surprisingly, geographic latitude does not consistently predict average serum 25 OH D levels in a population.
Ample opportunities exist to form vitamin D and store it in the liver and fat from exposure to sunlight during the spring, vitamin d deficiency and metabolism, summer, and fall months even in the far north latitudes [ 1 ], vitamin d deficiency and metabolism.
UVB radiation does not penetrate glass, so exposure to sunshine indoors through a window does not produce vitamin D [ 21 ]. Sunscreens with a sun protection factor SPF of 8 or more appear to block vitamin D-producing UV rays, although in practice people generally do not apply sufficient amounts, cover all sun-exposed skin, or reapply sunscreen regularly [ 122 ].
Therefore, skin likely synthesizes some vitamin D even when it is protected by sunscreen as typically applied. The factors that affect UV radiation exposure and research to date on the amount of sun exposure needed to maintain adequate vitamin D levels make it difficult to provide general guidelines.
Individuals with limited sun exposure need to include good sources of vitamin D in their diet or take a supplement to achieve recommended levels of intake. Despite the importance of the sun for vitamin D synthesis, it is prudent to limit exposure of skin to sunlight [ 22 ] and UV radiation from tanning beds [ 24 ], vitamin d deficiency and metabolism. UV radiation is a carcinogen responsible for most of the estimated 1. Lifetime cumulative UV damage to skin is also largely responsible for some vitamin d deficiency and metabolism dryness and other cosmetic changes.
The American Academy of Dermatology advises that photoprotective measures be taken, including the use of sunscreen, whenever one is exposed to the sun [ 25 ]. Assessment of vitamin D requirements cannot address the level of sun exposure because of these public health concerns about skin cancer, and there are no studies to determine whether UVB-induced synthesis of vitamin D can occur without increased risk of skin cancer [ 1 vitamin d deficiency and metabolism. In supplements and fortified foods, vitamin D is available in two forms, D 2 ergocalciferol and D 3 cholecalciferol that differ chemically only in their side-chain structure.
Vitamin D 2 is manufactured by the UV irradiation of ergosterol in yeast, and vitamin D 3 vitamin d deficiency and metabolism manufactured by the irradiation of 7-dehydrocholesterol from lanolin and the chemical conversion of cholesterol [ 6 ]. The two forms have traditionally been regarded as equivalent based on their ability to cure rickets and, indeed, most steps involved in the metabolism and actions of vitamin D 2 and vitamin D 3 are identical.
Both forms as well as vitamin D in foods and from cutaneous synthesis effectively raise serum 25 OH D levels [ 2 ], vitamin d deficiency and metabolism.
Firm conclusions about any different effects of these two forms of vitamin D cannot be drawn. However, it appears that at nutritional doses vitamins D 2 and D 3 are equivalent, but at high doses vitamin D 2 is less potent. The most marked increase was among older women, vitamin d deficiency and metabolism. Comparing vitamin D intake estimates from foods and dietary supplements to serum 25 OH D concentrations is problematic. One reason is that comparisons can only be made on group means rather than on data linked to individuals.
Another is the fact that sun exposure affects vitamin D status; serum 25 OH D levels are generally higher than would be predicted on the basis of vitamin D intakes alone [ vitamin d deficiency and metabolism ], vitamin d deficiency and metabolism. The highest mean was Generally, younger people had higher levels than older people, and males had slightly higher levels than females.
Over the past 20 years, mean serum 25 OH D concentrations in the United States have slightly declined among males but not females. This decline is likely due to simultaneous increases in body weight, reduced milk intake, and greater use of sun protection when outside [ 28 ], vitamin d deficiency and metabolism. Nutrient deficiencies are usually the result of dietary inadequacy, impaired absorption and use, increased requirement, or increased excretion.
A vitamin D deficiency can occur when usual intake is lower than recommended levels over vitamin d deficiency and metabolism, exposure to sunlight is limited, the kidneys cannot convert 25 OH D to its active form, or absorption of vitamin D from the digestive tract is inadequate. Vitamin D-deficient diets are associated with milk allergy, lactose intolerance, vitamin d deficiency and metabolism, ovo-vegetarianism, and veganism [ 1 ].
Rickets and osteomalacia are the classical vitamin D deficiency diseases. In children, vitamin D deficiency causes rickets, a disease characterized by a failure of bone tissue to properly mineralize, resulting in soft bones and skeletal deformities [ 20 ]. Rickets was first described in the midth century by British researchers [ 2029 ].
The fortification of milk with vitamin D beginning in the s has made rickets a rare disease in the United States, although it is still reported periodically, vitamin d deficiency and metabolism, particularly among African American infants and children [ 32025 ]. Prolonged exclusive breastfeeding without the AAP-recommended vitamin D supplementation is a significant cause of rickets, particularly in dark-skinned infants vitamin d deficiency and metabolism by mothers who are not vitamin D replete [ 30 ].
Additional causes of rickets include extensive use of sunscreens and placement of children in daycare programs, where they often have less outdoor activity and sun exposure [ 2029 ]. Rickets is also more prevalent among immigrants from Asia, Africa, and the Middle East, possibly because of genetic differences in vitamin D metabolism and behavioral differences that lead to less sun exposure. In adults, vitamin D deficiency can lead to osteomalacia, resulting in weak bones [ 15 ].
Symptoms of bone pain and muscle weakness can indicate inadequate vitamin D levels, but such symptoms can be subtle and go undetected in the initial stages. Obtaining sufficient vitamin D from natural food sources alone is difficult. For many people, consuming vitamin D-fortified foods and, arguably, being exposed to some sunlight are essential for maintaining a healthy vitamin D status. In some groups, dietary supplements might be required to meet the daily need for vitamin D.
A review of reports of nutritional rickets found that a majority of cases occurred among young, breastfed African Americans [ 32 ]. A survey of Canadian pediatricians found the incidence of rickets in their patients to be 2.
While the sun vitamin d deficiency and metabolism a potential source of vitamin D, the AAP advises keeping infants out of direct sunlight and having them wear protective clothing and sunscreen [ 34 ].
As noted earlier, the AAP recommends that exclusively and partially breastfed infants be supplemented with IU of vitamin D per day [ 26 ], the RDA for this nutrient during infancy. Older adults are at increased risk of developing vitamin D insufficiency in part because, vitamin d deficiency and metabolism, as they age, skin cannot synthesize vitamin D as efficiently, they are likely to spend more time indoors, and they may have inadequate intakes of the vitamin [ 1 ].
Homebound individuals, women who wear long vitamin d deficiency and metabolism and head coverings for religious reasons, and people with occupations that limit sun exposure are unlikely to obtain adequate vitamin D from sunlight [ 3536 ]. Because the extent and frequency of use of sunscreen are unknown, the significance of the role that sunscreen may play in reducing vitamin D synthesis is unclear [ 1 ].
Various reports consistently show lower serum 25 OH D levels in persons identified as black compared with those identified as white.