Early registration is now open for APHA 2024! Join us in Minneapolis ×

Call for Education and Research Into Vitamin D Deficiency/Insufficiency

  • Date: Oct 28 2008
  • Policy Number: 20081

Key Words: Healthy People, Nutrition

Vitamin D deficiency/insufficiency is recognized as a major public health concern for both children and adults in the United States.1 Deficiency is defined as less than 20 ng/mL, and insufficiency is greater than or equal to 20 ng/mL but less than 30 ng/mL. Vitamin D sufficiency is 30 to 100 ng/mL.3 It has been estimated that 30% to 40% of children and 40% to 50% of adults in the United States are at risk of vitamin D deficiency.2 It has also been estimated worldwide that 1 billion people are at risk of vitamin D deficiency.3 Four populations in the United States are at highest risk for vitamin D deficiency: (1) women of childbearing age; (2) breastfed infants not receiving vitamin D supplements; (3) people with dark or brown skin type, including a large portion of African Americans and Mexican American adolescents and adults; and (4) elderly people.4–9 It is also recognized from studies in other countries that people whose cultural or religious practices require extensive covering, which can impede subcutaneous vitamin D synthesis,10 may also be at risk, although this theory has not been adequately studied in North America. Factors such as low sunlight exposure, age-related decreases in vitamin D formation through the skin, and diets low in vitamin D all contribute to the high prevalence of vitamin D deficiency.11 

Vitamin D is a fat-soluble vitamin that is provided either through the diet or by syntheses through exposure to sunlight. The vitamin has two major forms: D2 (or ergocalciferol) and D3 (or cholecalciferol).12 The vitamin D produced from its precursor under the skin after exposure to sunlight or intake from vitamin D-rich or enriched foods such as wild salmon, milk, and orange juice is typically not enough to maintain adequate levels of vitamin D.13 The interventions for this widespread public health problem are simple, safe, effective, accessible, and affordable supplemental doses of the vitamin and increased availability of vitamin D fortified food staples.13–14

Vitamin D Synthesis and Metabolism

Once vitamin D3 is made in the skin, or provided from the diet (as vitamin D2 or D3), it is converted in the liver to 25-hydroxyvitamin D [25(OH)D], which is the major circulating form of vitamin D.15 This 25(OH)D is the substrate for production of the active form, 1,25-dihydroxyvitamin D, via two pathways. In the endocrine pathway, 1,25-dihydroxyvitamin D is made in the kidney under tight regulatory control.3 In the paracrine/autocrine pathway, 1,25-dihydroxyvitamin D is made and used locally by a variety of cells in most tissues of the body, including those of the immune system.16 

Factors Affecting Vitamin D Deficiency/Insufficiency and Metabolism

A person’s vitamin D status depends on several factors.3 The time and length of sun exposure, the season, the latitude, the percentage of skin covered by clothing, and the skin pigmentation all can affect how much vitamin D a person’s body will produce.3 Ultraviolet B (UVB) irradiation of the skin for photochemical production of vitamin D is highest at noon time.3 Vitamin D levels, that is, 25(OH)D—the major circulating form, markedly fluctuate with the change of seasons because the angle of the sun’s rays, which is critical to the amount of UVB radiation reaching the surface of the earth, changes during the seasons as well.3 Therefore, maximum vitamin D production occurs in the summer months, and, depending on the latitude, little or no vitamin D may be generated in winter months.17 Latitude defines distance from the equator. The higher the latitude at which a person lives is, the less effective or sufficient the solar ultraviolet radiation from the sun will be for vitamin D production.3 Clothing can be a significant factor as well.3 Vitamin D deficiency is rampant among women in Saudi Arabia, despite sunlight exposure, because the traditional clothing nearly completely covers their skin.3,10 Skin pigmentation or melanin is a dominant factor in regulating the production of vitamin D under conditions of low sunlight exposure. Melanin acts as a sunscreen, so a person with dark skin (type 5 or 6) requires 10 to 50 times the exposure to sunlight to produce the same amount of vitamin D3 in his or her skin as does a lighter-skinned person with skin type 1 or 2.11 Subsequently, in the United States, African Americans have low levels of 25(OH)D, which typically are more severe the further north a person resides.3,4

Functions of Vitamin D

The most well known biologic function of vitamin D is to maintain normal blood levels of calcium and phosphorus.18 The 1,25-dihydroxyvitamin D acts to promote active calcium and phosphorous absorption, and, working with parathyroid hormone, it helps regulate bone metabolism and kidney reabsorption of calcium. By promoting calcium absorption, vitamin D helps to form and maintain strong bones.7,19–20 In addition, vitamin D helps by maintaining a healthy immune system, regulating cell growth and differentiation (thereby exhibiting antitumor activity), and stimulating insulin production from the pancreas.21 Evidence-based research also shows that vitamin D is increasingly recognized as having a role in the health of the cardiovascular system, neurodevelopment, immunomodulation, and regulation of cell growth.12,21

Sources of Vitamin D

Sun Exposure

As previously mentioned, vitamin D3 is synthesized in the skin by exposure to direct sunlight (UVB) and is absorbed from foods. Once vitamin D is produced in the skin or absorbed from food, it requires chemical conversion in the liver to form 25(OH)D, the main circulating form of vitamin D, which is also referred to as the intermediate metabolite. This form of vitamin D is carried in the blood to the kidney where 1,25 dihydroxyvitamin D and the physiologically active form of vitamin D are synthesized and may be released to the circulation. The intermediate form or 25OHD can also be carried in the blood to other tissues that possess the ability to synthesize the active form of vitamin D, which usually acts within the cells where it is synthesized in nearby tissues.15 Sunscreen use and dark skin pigmentation also reduce skin synthesis of vitamin D.

Dietary Sources

Only a few foods naturally contain vitamin D as ergocalciferol and cholecalciferol. Human breast milk is typically low in vitamin D in temperate climates.22 Vitamin D is found in fortified foods such as milk, breakfast cereals, and juices. Vitamin D is also obtained from foods like fish liver oils and cold water fish.11 In the wild, fish are part of a food chain that allows for concentration of vitamin D in the flesh of fatty fish (e.g., salmon, sardines, mackerel); however, in lean fish, vitamin D is concentrated in the liver (e.g., cod liver oil). Land animals that are exposed to sunlight or have vitamin D in their feed may be a source of vitamin D, but the amount of vitamin D provided in meat is not well documented except for liver.23 Eggs are a natural source of vitamin D that can be increased when vitamin D is added to chicken feed, but the level is not usually significant. However, eggs processed to remove cholesterol and saturated fats in the United States have a restored vitamin D content of approximately 6% of the Daily Value. Currently, neither the United States nor Canada require the vitamin D content of foods to be listed on the required nutrition facts panel of food labels.24 Fortification of milk and other foods with vitamin D, such as selected cereals, margarines, juices, and a few selected brands of cheese, provide the majority (66% to 84% of the food sources) of vitamin D dietary intake of Americans.8 Plant foods such as cultivated edible mushrooms that when briefly exposed to UVB produce significant amounts of vitamin D325 and some fortified foods may contain vitamin D2. The biological equivalency of the two forms of vitamin D, ergocalciferol and cholecalciferol, in humans has been challenged recently.26 The effective widespread use of vitamin D2 supplements supports the contention that ergocalciferol-based supplements or food sources are efficacious. Physiologic evidence to support the equivalency of vitamin D2 and vitamin D3 was recently reported.26


Supplements provide another source of vitamin D intake. Vitamin D3 (or cholecalciferol) or vitamin D2 (or ergocalciferol) is usually (but not always) found in multivitamin preparations at 10 µg (400 IU) per tablet, with some having only 5 µg (200 IU) but new formulations are being introduced with 25 µg (1000 IU). In addition to multivitamins, single vitamin D supplements are largely available as cholecalciferol in 10 µg (400 IU), 25 µg (1000 IU) and 50 µg (2000 IU) dosages. Further, some calcium supplements contain various amounts of cholecalciferol or ergocalciferol, which are in the range of 10 to 25 µg (400 to 1000 IU) per tablet. These supplements are intended for maintenance of vitamin D status or for people who have less-than-adequate vitamin D intakes. They are not intended for repletion of vitamin D deficiency. For that purpose, higher dosage forms are available through prescription.21

Symptoms and Consequences of Vitamin D Deficiency

It has long been known that vitamin D is crucial for healthy bones. The presence of active vitamin D in the small intestine aids in the absorption of dietary calcium. Individuals with vitamin D deficiency are able to absorb only one third to one half as much calcium as those with sufficient levels. Calcium is vital to the mineralization of bone. The two diseases traditionally associated with severe vitamin D deficiency are rickets in children, characterized by deformation or softening of bone, and osteomalacia in adults.19,27 Vitamin D deficiency will not only cause rickets in children but also prevent growing children from reaching their maximal genetically determined bone mineral density.28

However, vitamin D deficiency is not the only cause of rickets in children. Rickets can be an outcome of inborn errors of phosphorus metabolism such as phosphate wasting,19 dietary deficiencies of calcium or phosphorus, vitamin C deficiency, and other dietary deficiencies, all of which may result in rickets despite normal circulating levels of 25(OH)D in children.29–30

Prevention of Rickets and Evaluation of Patients With Rickets

Although vitamin D deficiency is a major cause of rickets in children, it is not the only cause. Rickets can result because of dietary deficiencies of calcium or phosphorus, vitamin C deficiency and other dietary deficiencies. Also, rarer causes, such as an inborn error of phosphorus metabolism, leads to phosphate wasting,31 which results in rickets, despite normal circulating levels of 25(OH)D in children.29–30 [AQ: The first several sentences are redundant and could be deleted; however, the next sentence would need to be reworded.]Therefore, during the initial evaluation of patients with rickets, it is important to assess for deficiencies in calcium and phosphorus in addition to 25(OH)D levels. The differential diagnosis of rickets includes conditions that lead to hypocalcemia or hypophosphatemia through decreased intake, malabsorption, or increased excretion of calcium, phosphate, or vitamin D.32 Chronic vitamin D deficiency is strongly linked to osteoporosis and fractures.7,20 In adults, vitamin D deficiency precipitates and exacerbates osteoporosis and increases the risk of bone fracture.19 Vitamin D deficiency in adults also causes osteomalacia, which is a painful bone disease that is often misdiagnosed as fibromyalgia or chronic fatigue syndrome, all of which may explain the underlying mechanism for the role of vitamin D in the prevention of falls.27,33 In addition to the adverse bone health consequences of vitamin D deficiency, it is now recognized that vitamin D deficiency may increase the risk of chronic diseases other than osteomalacia and osteoporosis.34–48 Vitamin D deficiency/insufficiency has also been associated with increased risk of type I35 and type II diabetes mellitus,38,49 multiple sclerosis,40,50 rheumatoid arthritis,39 age-related macular degeneration, and diabetes-related macular edema.76 Hypertension and heart disease may also be associated with vitamin D deficiency.34, 36–37, 44

Vitamin D Inadequacy Detection

To identify vitamin D inadequacy, a simple blood test is required to detect the level of 25(OH)D. Blood testing for vitamin D has only become available in the last 20 years and has been undergoing refinement since that time.13 Recent studies have shown that adequate levels of 25(OH)D are in the range of 30 to 100 ng/mL, as opposed to the older standard of less than 20 ng/mL defining deficiency.3 To reflect this adjustment, the newer term “insufficiency” is being used to reflect levels lower than 30 ng/mL. Specifically, insufficiency is defined as vitamin D levels that are equal to or greater than 20 ng/mL but lower than 30 ng/mL.43,51–52 One concern is the availability of the vitamin D test in laboratories and its cost, particularly when used on a population level. Vitamin D testing is not a routine part of medical care.

Effects of Vitamin D Deficiency on Special Populations

Women of Child-Bearing Age

Vitamin D deficiency in US women of childbearing age has been described as a serious public health matter53 and has been associated with low birth weight babies54 and other health problems for mother and child. Vitamin D deficiency is disproportionately seen in infants of mothers with dark skin55 or who wear concealing clothes (i.e., veils).56 A recent study found that 29% of Black and 5% of White pregnant women residing in the northeastern United States had vitamin D deficiency, despite taking prenatal vitamins that contain approximately 400 IU of vitamin D.57 Furthermore, in utero or early life vitamin D deficiency has been associated with skeletal problems, type I diabetes mellitus, and schizophrenia,57 yet the prevalence of vitamin D deficiency in pregnant women in the United States has been largely unexplored.57 A 2004 review of studies that investigated maternal and neonatal outcomes of vitamin D deficiency or supplementation during pregnancy concluded that there was no evidence of a benefit of supplementation during pregnancy above amounts routinely required to prevent vitamin D deficiency.58 However, a recent study that examined the disparity in vitamin D deficiency of newborns infants of mothers at high risk of being deficient concluded that the clinical implications are unknown and further research is necessary to determine the long-term consequences of maternal and neonatal vitamin D deficiency so that guidelines on vitamin D supplementation during pregnancy can be issued.56

Breastfed Infants

Infants are capable of producing all of the vitamin D they need in their skin during casual exposure to sunlight, provided that the sunlight is of sufficient intensity.59 However, heavy skin pigmentation reduces the amount of vitamin D formed in the skin, which is why infants with dark skin pigmentation tend to have less satisfactory vitamin D status than infants with light skin pigmentation and why they are at increased risk of vitamin D deficiency rickets.59 A lack of supplemental vitamin D or inadequate sunlight exposure in breastfed infants results in increased risk of developing vitamin D deficiency or rickets.60 The recommended intake of vitamin D cannot be met with human milk as the sole source of vitamin D for the breastfed infant because it contains approximately 25 IU/L or less of vitamin D.60 In light of growing concerns about sunlight and skin cancer and the various factors that negatively affect sunlight exposure, the American Academy of Pediatrics recommends that all breastfed infants be given supplemental vitamin D.60

Supplementation should begin within the first 2 months of life.60 A daily intake of 400 IU of vitamin D is believed to prevent rickets reliably and is considered to be free of adverse effects.59 The Institute of Medicine considers 200 IU per day to be an adequate intake for infants.59 The following countries recommend higher levels of supplementation for infants: Bulgaria recommends 20 µg (800 IU) of vitamin D per day, Romania 10 µg (400 IU), and Canada 10 µg (400) (and 20 µg [800 IU] per day in the winter).61 Canada has had this recommendation for more than 10 years.61

Although prevention of rickets is the primary reason vitamin D supplements should be provided to breastfed infants, there is literature suggesting that supplementation during infancy has other health benefits such as protection against type I diabetes mellitus and promotion of higher bone mineral mass in prepubertal girls.59

African Americans

African Americans and other persons of color are at the highest risk of vitamin D deficiency. A 2004 study revealed that 52% of African American and Hispanic adolescent boys and girls were vitamin D deficient.62 Even when adults and children of color reside in sunnier locations such as Florida, Arizona, and Georgia, there is a greater prevalence of vitamin D insufficiency.63 Higher prevalence of vitamin D insufficiency and deficiency among African Americans and Hispanics (as identified by the NHANES III survey) has been observed in small regional surveys as well as the nationally representative NHANES III survey.4 Analyses of the NHANES III survey results revealed that 42% of African American women ages 15 to 49 years were found to be vitamin D deficient throughout the United States at the end of the winter.62 When specific geographic regions are surveyed, the prevalence of vitamin D insufficiency is often greater. Another study in 2004 reported that 76% of African American women at the time they gave birth were vitamin D deficient, and 81% of their infants were also deficient in vitamin D. Healthy men and women older than the age of 65 in Boston were surveyed for vitamin D status, which revealed that a surprising 34% of White, 42% of Hispanic, and 84% of African American men and women were vitamin D deficient.21 These statistics point to the importance of both latitude and skin pigmentation (melanin) in persons of color in hindering vitamin D synthesis. From another perspective, melanin can be a potent sunscreen that provides protection from the damaging effects of sunlight and decreases the amount of UVB that penetrates the skin.64 The UVB radiation is what the skin uses to make vitamin D. Therefore, persons of color living in higher latitudes around the world are at particular risk, as are people living in Canada, Scandinavia, Russia, and all those whose lifestyles keep them from adequate access to sunlight when and where the sun is high in the sky.

A typical African American with a skin type 6 (refers to more melanin pigmentation and lowest risk of skin cancer)13 has a 90% reduced capacity to produce vitamin D in his or her skin compared with the average White person.64 In addition, African Americans often have a lactase deficiency and avoid drinking milk, which is one of the few foods that are fortified with vitamin D.65–66 It has also been suggested that the increased risks of diabetes mellitus, hypertension, and heart disease in African Americans may be associated with their higher prevalence of vitamin D deficiency.11, 14, 21 Although vitamin D deficiency/insufficiency is more prevalent among African Americans, the majority of whom do not achieve optimal 25(OH)D concentrations at any time of year, they experience a much lower incidence of osteoporotic bone fracture than their White counterparts.66 A number of adaptive mechanisms through which African Americans maintain higher bone mineral density in the face of low vitamin D status have been proposed.66 However, most researchers agree that skeletal resistance to parathyroid hormone (PTH) action on bone and intestinal resistance to the action of 1,25 (OH)2D are key factors in the adaptation. Recent studies have failed to show inverse correlations between bone mineral density and 25OHD levels in African American men compared with White men67 or significantly higher bone turnover markers in African American men compared with White and Hispanic men.68 Such adaptive mechanisms may not fully correct skeletal effects of low vitamin D status, especially among elderly African Americans. It is important to encourage clinicians and health educators to promote improved vitamin D status among African Americans of all ages and possibly other racial and ethnic groups. Dietary intervention with vitamin D is low cost and low risk with potentially broad health effects.13, 66

The Elderly

Older adults (ages > 50 years) are at greater risk of vitamin D deficiency than younger adults for several reasons. Physiologically, there are two concerns. The enzyme responsible for synthesis of 1,25(OH)2D in the kidney (the endocrine pathway) is resistant to PTH.28 This means that the 1-alpha-hydroxylase is not increased by PTH when there is need for calcium, so there is prolonged secondary hyperparathyroidism leading to increased bone loss. A low level of 25(OH)D exacerbates this hyperparathyroidism. In addition, skin cells are less able to make cholecalciferol because there are fewer molecules of 7-dehydrocholesterol (provitamin D3) in the epidermis. Skin production of vitamin D after a standard exposure to UVB light decreases with age because of decreased levels of 7-dehydrocholesterol. When young and old subjects are exposed to the same amount of UVB, elderly subjects produce only one third the amount of cholecalciferol.28

Upward of 80% of the elderly are thought to be vitamin D deficient.3,7 Deficiency causes muscle weakness and osteoporosis that leads to falls with devastating vertebral, hip, and other bone fractures. Clinical studies have demonstrated that vitamin D with and without calcium supplementation reduces fracture risk and falls in the institutionalized elderly and in individuals older than age 65 living at home.33,69

Problems Associated With Excess Vitamin D

Intoxication of vitamin D is very rare but can be caused by ingestion of excessively high doses, whether intentional or not.19 Doses of more than 50 000 IU per day raise levels of 25(OH)D to more than 150 ng/mL (374 nmol/L) and are associated with hypercalcemia and hyperphosphatemia.19 Doses of 10 000 IU of vitamin D3 per day for up to 5 months, however, do not cause any signs of toxicity.19 In 2006, a major review of the literature on vitamin D and health reported that vitamin D intake above current dietary reference intakes was not reported to be associated with an increased risk of adverse events.70 However, this report did raise the concern that more methodologically sound research is needed regarding assessment of higher doses of vitamin D supplementation for long-term effects. A tolerable upper intake level (UL) for vitamin D was set in 1997 as 1000 IU for infants 0 to 1 year and 2000 IU for all others. ULs were established to discourage potentially dangerous self-medication. The UL represents a safe intake (i.e., zero risk of adverse effects in an otherwise healthy person). When a patient is undergoing therapeutic treatment under a health professional’s care, this amount can be exceeded. The primary adverse effect that is expected at very high levels of vitamin D is hypercalcemia, which can lead, over time, to calcification of soft tissues such as arteries (arteriosclerosis) and kidney (nephrocalcinosis). A less specific indicator is hypercalciuria, which may lead to increased risk of kidney stones. The value for children and adults has been criticized as being based on a single study of dubious quality.71 A recent risk assessment for vitamin D used new data (post-1997) to derive a more realistic estimate of an UL.72 A thorough examination of studies indicated there was an absence of any signs of toxicity when healthy adults were given more than 250 µg (10 000 IU) daily. Thus, a reasonable estimate of a UL for adults is 10 000 IU. The result of vitamin D intoxication is primarily elevation of the calcium levels in the blood, which could cause stone formation in the body tissues (over time), including urinary stones. With very high calcium levels, people develop a type of diabetes mellitus, or frequent urination, in which calcium causes the same effect on the urinary system as does sugar in diabetes mellitus. The hypercalcemia is corrected by stopping vitamin D supplementation.73

Vitamin D Dietary Reference Intakes

Dietary reference intakes established by the National Academy of Sciences, Institute of Medicine, Food and Nutrition Board recommend daily values of 200 IU (International Units) for children and adults up to age 50, 400 IU for adults ages 51 to 70, and 600 IU for adults older than 70.74 However, many experts believe that a daily dosage of 1000 IU or greater may be more beneficial.2 The growing awareness of the need for greater consumption of vitamin D, beyond those recommended by the National Academy of Sciences with the 1997 Dietary Reference Intakes,74 particularly by African Americans and the elderly, was conveyed to the public as a key recommendation in the 2005 Dietary Guidelines for Americans.74 The 2005 recommendation advised older adults, people with dark skin, and people exposed to insufficient UVB (i.e., sunlight) to consume extra vitamin D from fortified foods and or supplements and stated a daily goal of 1000 IU vitamin D intake for those at risk. A 2000 study examined the estimated amount of oral vitamin D intake necessary to maintain adequate vitamin D status in sunlight exposure in sunlight deprived individuals living in Denmark and suggested that the daily oral intake of vitamin D should probably be 1000 IU per day.75 The National Academy of Sciences has set 2000 IU daily as the UL for vitamin D.74

Why Are Current Efforts to Address Vitamin D Deficiency Not Sufficient?

In addition to sun exposure, the body gets vitamin D in two other ways—from foods and from supplements. The reality is that very few foods are rich in vitamin D except fatty fish such as salmon and mackerel and fortified foods such as milk and some brands of orange juice.24 The few food staples such as milk that are fortified are not uniformly consumed by all racial and ethnic groups.24 Also, studies show that the elderly may particularly benefit from vitamin D supplementation to maintain strong bones and to prevent falls.43,50 However, those populations at greatest risk of vitamin D insufficiency, African American adults and children, have significantly lower use of supplements in the United States and may require higher doses. Daily supplementation of African American children with 400 IU of vitamin D was inadequate to raise circulating levels of 25OHD to a level of sufficiency.43, 50 A 3-year randomized, double-blind, placebo-controlled study found that daily vitamin D supplementation of 800 IU for the first 2 years and 2000 IU for the third and final year in postmenopausal African American women failed to increase serum 25OHD levels to the optimal range in 40% of the study subjects.6 In both of these recent studies, the dose of vitamin D was well above the National Academy of Sciences recommendations of 200 and 600 IU of vitamin D, respectively.

Supplementation as an Intervention

Besides adequate exposure to sunlight and eating food rich in vitamin D, dietary supplements provide another source of intake as noted earlier for populations at highest risk for vitamin D deficiency and insufficiency. For neonates, there is liquid vitamin D, and for children and adults there is a tablet form that is easily tolerated with no significant side effects. In 2006, it was noted that the cost of 1000 IU of vitamin D3 is less than $0.05 per day [AQ: Acceptable as edited?], balanced against the human and economic costs of treating cancer attributable to vitamin D insufficiency.42 Many other examples can be cited to underscore the benefits of adequate levels of vitamin D.42

Need for More Research

Further research is necessary, particularly as questions remain regarding the truly causal role of vitamin D. The Women’s Health Initiative trial of vitamin D plus calcium reports a 17% increase in kidney stones in the intervention group, compared with placebo.77 A recent comprehensive review of more than 160 studies concluded that most trials of higher dose vitamin D were not adequately designed to assess long-term harms and that sensitive and specific indices of the risk of toxicity need to be developed.70

Many studies have shown the power of vitamin D.3,42 It is not known what levels of vitamin D are therapeutic or optimal. More research is needed to look for levels of vitamin D that would be effective in preventing disease in the population, especially high-risk groups. Another area of research that would shed light on the subject is food fortification, although research is needed to determine the optimal foods and fortification levels to reduce the chance of toxicity.

Previous APHA Statements

Previously, APHA put out a statement that briefly mentioned vitamin D in relation to infant feeding (1980, policy statement 80-22) and urging mothers and caretakers of infants to provide vitamin D and fluoride as the only vitamin–mineral supplements. Yet, too few health care practitioners, public health professionals, and the public-at-large have adequate information and knowledge about the benefits of vitamin D in protecting against many chronic diseases and its promise in decreasing health disparities.

Action Statements

Therefore the American Public Health Association—

  1. Urges the Centers for Disease Control and Prevention to advocate and provide funding for a coordinated and integrated approach to educating health care providers, practitioners, public health professionals, and others, such as patient advocates and community health workers, about the science and benefits of adequate levels of vitamin D.
  2. Urges the United States Department of Agriculture (USDA) and other federal agencies to promote the 2005 Dietary Guidelines for Americans as the basis for increased public awareness using current nutrition guidance for healthy eating, notably for populations at highest risk for vitamin D deficiency/insufficiency.
  3. Recommends to the Department of Health and Human Services and USDA that the APHA have organizational representation on the panel of the 2010 Dietary Guidelines for Americans for strategies to improve vitamin D intake.
  4. Requests that it become a participating organization in planning Healthy People 2020 to promote national awareness of the magnitude of the problem of poor vitamin D status and the associated increased risk for chronic disease development by introducing specific objectives in planning Healthy People 2020 goals.
  5. Recommends that Congress appropriate funds to conduct research in diverse populations to determine population specific vitamin D intakes associated with reduced risk of chronic diseases and other conditions.
  6. Recommends that Congress appropriate funds to refine methodology for assessing vitamin D levels in the population.
  7. Recommends that the Food and Drug Administration add vitamin D to the list of required nutrients appearing on the Nutrition Facts Panel that is required on all foods in the US market place.
  8. Urges the Department of Health and Human Services and the USDA to begin a campaign now aimed directly at the general public and based on scientific data currently available, without waiting for the professional publications referred to previously.


  1. Calvo MS, Whiting SJ, Barton CN. Vitamin D intake: a global perspective of current status. J Nutr. 2005;135:310–316.
  2. Holick MF. High prevalence of vitamin D inadequacy and implications for health. Mayo Clin Proc. 2006; 81:353–373.
  3. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357:266–281.
  4. Looker AC, Dawson-Hughes B, Calvo MS, Gunter EW, Sahyoun NR. Serum 25-hydroxyvitamin D status of adolescents and adults in two seasonal subpopulations from NHANES III. Bone. 2002;30:771–777.
  5. Weisberg P, Scanlon KS, Li R, Cogswell ME. Nutritional rickets among children in the United States: review of cases reported between 1986 and 2003. Am J Clin Nutr. 2004;80(6 suppl):1697S–19705S.
  6. Aloia JF, Talwar SA, Pollack S, Yeh J. A randomized controlled trial of vitamin D3 supplementation in African American women. Arch Intern Med. 2005;165:1618–1623.
  7. Holick MF, Siris ES, Binkley N, et al. Prevalence of vitamin D inadequacy among postmenopausal North American women receiving osteoporosis therapy. J Clin Endocrinol Metab. 2005;90:3215–3224.
  8. Moore CE, Murphy MM, Holick MF. Vitamin D intakes by children and adults in the United States differ among ethnic groups. J Nutr. 2005;135:2478–2485.Zadshir A, Tareen N, Pan D, Norris K, Martins D. The prevalence of hypovitaminosis D among US adults: data from the NHANES III. Ethn Dis. 2005;15(4 suppl 5):S5–97–101.
  9. Andersen R, Molgaard C, Skovgaardet LT, et al. Effect of vitamin D supplementation on bone and vitamin D status among Pakistani immigrants in Denmark: a randomised double blinded placebo-controlled intervention study. Br J Nutr. 2008;100:197–207.
  10. Holick MF. Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis. Am J Clin Nutr. 2004;79:362–371.
  11. Holick MF. The UV Advantage. New York, NY: Simon & Schuster; 2003.
  12. Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr. 2003;77: 204–210.
  13. Calvo MS, Whiting SJ. Public health strategies to overcome barriers to optimal vitamin D status in populations with special needs. J Nutr. 2006;136:1135–1139.
  14. Lips P. Vitamin D physiology. Prog Biophys Mol Biol. 2006;92(1):4–8.
  15. Goldstein DR. Toll-like receptors and graft rejection. Transpl Immunol. 2006;16(1):25–31.
  16. Norman AW. Sunlight, season, skin pigmentation, vitamin D, and 25 hydroxyvitamin D: integral components of the vitamin D endocrine system. Am J Clin Nutr. 1998;67:1108–1110.
  17. DeLuca HF. Overview of general physiologic features and functions of vitamin D. Am J Clin Nutr. 2004;80(6 suppl):1689S–16896S.
  18. Heaney RP. Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr. 2003;78:912–919.
  19. Holick MF. The role of vitamin D for bone health and fracture prevention. Curr Osteoporos Rep. 2006;4(3):96–102.
  20. Holick MF. Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease. Am J Clin Nutr. 2004;80(6 suppl):1678S–1688S.
  21. Hollis BW, Wagner CL. Vitamin D requirements during lactation: high-dose maternal supplementation as therapy to prevent hypovitaminosis D for both the mother and the nursing infant. Am J Clin Nutr. 2004;80(6 suppl):1752S–1758S.
  22. Holden JM, Lemar LE, Exler J. Vitamin D in foods: development of the US Department of Agriculture database. Am J Clin Nutr. 2008;87:1092S–1096S.
  23. Calvo MS, Whiting SJ, Barton CN. Vitamin D fortification in the United States and Canada: current status and data needs. Am J Clin Nutr. 2004;80(6 suppl):1710S–1716S.
  24. Calvo M , Garthoff LH, Raybourne RB, et al. FDA’s Center for Food Safety and Applied Nutrition and the Mushroom Council Collaborate to Optimize the Natural Vitamin D Content of Edible Mushrooms and to Examine their Health Benefits in Different Rodent Models of Innate Immunity. Paper presented at: 2006 FDA Science Forum A Century of FDA Science: Pioneering the Future of Public Health; April 18–20, 2006; Washington, DC.
  25. Houghton LA, Vieth R. The case against ergocalciferol (vitamin D2) as a vitamin supplement. Am J Clin Nutr. 2006;84:694–647.
  26. Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc. 2003;78:1463–1470.
  27. Holick MF. Resurrection of vitamin D deficiency and rickets. J Clin Invest. 2006;116:2062–2072.
  28. DeLucia MC, Mitnick ME, Carpenter TO. Nutritional rickets with normal circulating 25-hydroxyvitamin D: a call for reexamining the role of dietary calcium intake in North American infants. J Clin Endocrinol Metab. 2003;88:3539–3545.
  29. Pettifor JM. Nutritional rickets: deficiency of vitamin D, calcium, or both? Am J Clin Nutr. 2004;80(6 suppl):1725S–1729S.
  30. Calvo M, Carpenter T. Influence of phosphorus on the skeleton. In: SA New, J-P Bonjour, eds. Nutritional Aspects of Bone Health. Cambridge, UK: Royal Society of Chemistry; 2003:229–265.
  31. Rauch, F. Overview of Rickets in Children. Up to Date. 2007. Available at: www.uptodate.com/patients/content/topic.do?topicKey=~6iuBwXfMQ7fQa8.
  32. Broe KE, Chen TC, Weinberg J, Bischoff-Ferrari HA, Holick MF, Kiel DP. A higher dose of vitamin D reduces the risk of falls in nursing home residents: a randomized, multiple-dose study. J Am Geriatr Soc. 2007;55:234–239.
  33. Lind L, Hänni A, Lithell H, Hvarfner A, Sörensen OH, Ljunghall S. Vitamin D is related to blood pressure and other cardiovascular risk factors in middle-aged men. Am J Hypertens. 1995;8:894–901.
  34. Hyppönen E, Läärä E, Reunanen A, Järvelin M-R, Virtanen SM. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001;358(9292):1500–1503.
  35. Fahrleitner A, Dobnig H, Obernosterer A. Vitamin D deficiency and secondary hyperparathyroidism are common complications in patients with peripheral arterial disease. J Gen Intern Med. 2002;17:663–669.
  36. Li YC. Vitamin D regulation of the renin-angiotensin system. J Cell Biochem. 2003;88:327–331.
  37. Chiu KC, Chu A, Go VL, Saad MF. Hypovitaminosis D is associated with insulin resistance and beta cell dysfunction. Am J Clin Nutr. 2004;79:820–825.
  38. Merlino LA, Curtis J, Mikuls TR, Cerhan JR, Criswell LA, Saag KG; Iowa Women’s Health Study. Vitamin D intake is inversely associated with rheumatoid arthritis: results from the Iowa Women’s Health Study. Arthritis Rheum. 2004;50(1):72–77.
  39. Munger KL, Zhang SM, O’Reilly E. Vitamin D intake and incidence of multiple sclerosis. Neurology. 2004;62(1):60–65.
  40. Mathieu C, Gysemans C, Giulietti A, Bouillon R. Vitamin D and diabetes. Diabetologia. 2005;48:1247–1257.
  41. Garland CF, Garland FC, Gorham ED. The role of vitamin D in cancer prevention. Am J Public Health. 2006;96:252–261.
  42. Giovannucci E, Liu Y, Rimm EB, et al. Prospective study of predictors of vitamin D status and cancer incidence and mortality in men. J Natl Cancer Inst. 2006;98:451–459.
  43. Vieth R, Kimball S. Vitamin D in congestive heart failure. Am J Clin Nutr. 2006;83:731–732.
  44. Freedman DM, Looker AC, Chang S-C, Graubard BI. Prospective study of serum vitamin D and cancer mortality in the United States. J Natl Cancer Inst. 2007;99:1594–1602.
  45. Garland CF, Gorham ED, Mohr SB. Vitamin D and prevention of breast cancer: pooled analysis. J Steroid Biochem Mol Biol. 2007;103:708–711.
  46. Lappe JM, Travers-Gustafson D, Davies KM, Recker RR, Heaney RP. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007;85:1586–1591.
  47. Pittas AG, Lau J, Hu F, Dawson-Hughes B. The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis. J Clin Endocrinol Metab. 2007;92:2017–2029.
  48. Isaia G, Giorgino R, Adami S. High prevalence of hypovitaminosis D in female type 2 diabetic population. Diabetes Care 2001;24:1496.
  49. Munger KL, Levin LI, Hollis BW, Howard NS, Ascherio A . Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. JAMA. 2006;296:2832–2838.
  50. González EA, Sachdeva A, Oliver DA, Martin KJ. Vitamin D insufficiency and deficiency in chronic kidney disease. A single center observational study. Am J Nephrol. 2004;24:503–510.
  51. Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr. 2006;84:18–28.
  52. Bodnar, LM, Catov JM, Simhan HN, Holick MF, Powers RW, Roberts JM. Maternal vitamin D deficiency increases the risk of preeclampsia. J Clin Endocrinol Metab. 2007;92:3517–2352.
  53. Mannion, CA, Gray-Donald K, Koski KG. Association of low intake of milk and vitamin D during pregnancy with decreased birth weight. CMAJ. 2006;174:1273–1277.
  54. Nesby-O’Dell S, Scanlon KS, Cogswell ME. Hypovitaminosis D prevalence and determinants among African American and white women of reproductive age: third National Health and Nutrition Examination Survey, 1988–1994. Am J Clin Nutr. 2002;76:187–192.
  55. Dijkstra SH, van Beek A, Janssen JW, de Vleeschouwer LHM, Huysman WA, van den Akker ELT. High prevalence of vitamin D deficiency in newborn infants of high-risk mothers. Arch Dis Child. 2007;92:750–753.
  56. Bodnar LM, Simhan HN, Powers RW, Frank MP, Cooperstein E, Roberts JM. High prevalence of vitamin D insufficiency in black and white pregnant women residing in the northern United States and their neonates. J Nutr. 2007;137:447–452.
  57. Specker B. Vitamin D requirements during pregnancy. Am J Clin Nutr. 2004;80(6 suppl):1740S–1747S.
  58. Ziegler EE, Hollis BW, Nelson SE, Jeter JM . Vitamin D deficiency in breastfed infants in Iowa. Pediatrics. 2006;118:603–610.
  59. Gartner LM, Greer FR. Prevention of rickets and vitamin D deficiency: new guidelines for vitamin D intake. Pediatrics. 2003;111(4 pt 1):908–910.
  60. Vitamin D Expert Panel. (2001). Summary of the proceedings of a meeting of scientists, health practitioners, and policy makers from the Centers for Disease Control and Prevention, the American Academy of Pediatrics, and other US academic and professional institutions and government agencies. [AQ: This is not a complete reference. Please provide publication information or where this can be accessed on the Internet.]
  61. Gordon CM, DePeter KC, Feldman HA, Grace E, Emans SJ. Prevalence of vitamin D deficiency among healthy adolescents. Arch Pediatr Adolesc Med. 2004;158:531–537.
  62. Levis S, Gomez A, Jimenez C, et al. Vitamin D deficiency and seasonal variation in an adult South Florida population. J Clin Endocrinol Metab. 2005;90:1557–1562.
  63. Clemens TL, Adams JS, Henderson SL, Holick MF, et al. Increased skin pigment reduces the capacity of skin to synthesise vitamin D3. Lancet. 1982;1(8263):74–76.
  64. Adolfsson O, Meydani SN, Russell RM, et al. Yogurt and gut function. Am J Clin Nutr. 2004;80:245–256.
  65. Harris SS. Vitamin D and African Americans. J Nutr. 2006;136:1126–1129.
  66. Bohannon AD, Hanlon JT, Landerman R, Gold DT, et al. Association of race and other potential risk factors with nonvertebral fractures in community-dwelling elderly women. Am J Epidemiol. 1999;149:1002–1009.
  67. Hannan MT, Litman HJ, Araujo AB, et al. Serum 25-hydroxyvitamin D and bone mineral density in a racially and ethnically diverse group of men. J Clin Endocrinol Metab. 2008;93(1):40–46.
  68. Moseklide L. Vitamin D in the Elderly. Clin Endocrinol. 2005;62:265–281.
  69. Cranney A, Horsley T, O’Donnell S, et al. Effectiveness and safety of vitamin D in relation to bone health. Evid Rep Technol Assess (Full Rep). 2007;(158):1–235.
  70. Vieth, R. Critique of the consideration for establishing the tolerable upper intake level for vitamin D: critical need for revision upwards. J Nutr 2006;136:1117–1122.
  71. Hathcock JN, Shao A, Vieth R, Heaney R, et al. Risk assessment for vitamin D. Am J Clin Nutr. 2007;85(1):6–18.
  72. Sigmundsdottir H, Pan J, Debes GF, et al. DCs metabolize sunlight-induced vitamin D3 to “program” T cell attraction to the epidermal chemokine CCL27. Nat Immunol. 2007;8:285–293.
  73. Institute of Medicine. Dietary Reference Intake for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride, Washington, DC: National Academies Press, 1997.
  74. Glerup H, Mikkelsen K, Poulsen L, et al. Commonly recommended daily intake of vitamin D is not sufficient if sunlight exposure is limited. J Intern Med. 2000;247:260–268.
  75. Parekh N, Chapell RJ, Millen AE, et al. Association between vitamin D and age-related macular degeneration in the Third National Health and Nutrition Examination Survey, 1988–1994. Arch Opthalmol. 2007;125:661–669.
  76. Wactawski-Wende J, Kotchen JM, Anderson GL, et al. Calcium plus vitamin D supplementation and the risk of colorectal cancer. N Engl J Med. 2006;354:684–696.