Vitamin D

Published by Jessica Jacko on February 17, 2026February 17, 2026

Introduction

Vitamin D (also referred to as calciferol) is a fat-soluble vitamin that is naturally present in a few foods, added to others, and available as a dietary supplement. It is also produced endogenously when ultraviolet (UV) rays from sunlight strike the skin and trigger vitamin D synthesis.

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

Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal bone mineralization and to prevent hypocalcemic tetany (involuntary contraction of muscles, leading to cramps and spasms). It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts [1-3]. Without sufficient vitamin D, bones can become thin, brittle, or misshapen. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults. Together with calcium, vitamin D also helps protect older adults from osteoporosis.

Vitamin D has other roles in the body, including reduction of inflammation as well as modulation of such processes as cell growth, neuromuscular and immune function, and glucose metabolism [1-3]. Many genes encoding proteins that regulate cell proliferation, differentiation, and apoptosis are modulated in part by vitamin D. Many tissues have vitamin D receptors, and some convert 25(OH)D to 1,25(OH)2D.

In foods and dietary supplements, vitamin D has two main forms, D₂ (ergocalciferol) and D₃ (cholecalciferol), that differ chemically only in their side-chain structures. Both forms are well absorbed in the small intestine. Absorption occurs by simple passive diffusion and by a mechanism that involves intestinal membrane carrier proteins [4]. The concurrent presence of fat in the gut enhances vitamin D absorption, but some vitamin D is absorbed even without dietary fat. Neither aging nor obesity alters vitamin D absorption from the gut [4].

Assessing vitamin D status

Serum concentration of 25(OH)D is the main indicator of vitamin D status. However, the serum concentrations of 25(OH)D that are associated with vitamin D deficiency have not been definitively identified. The Food and Nutrition Board at the National Academies of Sciences, Engineering, and Medicine states that levels of 50 nmol/L (20 ng/mL) or more are sufficient for most people, and that the risk of deficiency increases at serum concentrations of less than 30 nmol/L (12 ng/mL).

Assessing vitamin D status by measuring serum 25(OH)D concentrations is complicated by the considerable variability of the available assays (the two most common ones involve antibodies or chromatography) used by laboratories that conduct the analyses [5,6]. As a result, a finding can be falsely low or falsely high, depending on the assay used and the laboratory. The international Vitamin D Standardization Program has developed procedures for standardizing the laboratory measurement of 25(OH)D to improve clinical and public health practice [5,7-10].
In contrast to 25(OH)D, circulating 1,25(OH)2D is generally not a good indicator of vitamin D status because it has a short half-life measured in hours, and serum levels are tightly regulated by parathyroid hormone, calcium, and phosphate [1]. Levels of 1,25(OH)2D do not typically decrease until vitamin D deficiency is severe [2].
Although 25(OH)D functions as a biomarker of exposure, the extent to which 25(OH)D levels also serve as a biomarker of effect on the body (i.e., relating to health status or outcomes) is not clear [1,3].
Researchers have not definitively identified serum concentrations of 25(OH)D associated with deficiency (e.g., rickets), adequacy for bone health, and overall health. After reviewing data on vitamin D needs, an expert committee of the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and Medicine (NASEM) concluded that people are at risk of vitamin D deficiency at serum 25(OH)D concentrations less than 30 nmol/L (12 ng/mL; see Table 1 for definitions of deficiency and inadequacy) [1]. Some people are potentially at risk of inadequacy at 30 to 50 nmol/L (12–20 ng/mL). Levels of 50 nmol/L (20 ng/mL) or more are sufficient for most people. The FNB also noted that serum concentrations greater than 125 nmol/L (50 ng/mL) can be associated with adverse effects [1] (Table 1). The Endocrine Society has not identified 25(OH)D concentrations associated with vitamin D sufficiency, insufficiency, and deficiency and does not recommend routine testing of 25(OH)D concentrations in healthy individuals [11,12].
nmol/L*
ng/mL*
Health status
<30
<12
Associated with vitamin D deficiency, which can lead to rickets in infants and children and osteomalacia in adults
30 to <50
12 to <20
Generally considered inadequate for bone and overall health in healthy individuals
≥50
≥20
Generally considered adequate for bone and overall health in healthy individuals
>125
>50
Linked to potential adverse effects, particularly at >150 nmol/L (>60 ng/mL)
*Serum concentrations of 25(OH)D are reported in both nanomoles per liter (nmol/L) and nanograms per milliliter (ng/mL). One nmol/L = 0.4 ng/mL, and 1 ng/mL = 2.5 nmol/L.
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Optimal serum concentrations of 25(OH)D for bone and general health have not been established because they are likely to vary by stage of life, by race and ethnicity, and with each physiological measure used [1,13,14]. In addition, although 25(OH)D levels rise in response to increased vitamin D intake, the relationship is nonlinear [1]. The amount of increase varies, for example, by baseline serum levels and duration of supplementation.

Recommended Intakes

The Food and Nutrition Board at the National Academies of Sciences, Engineering, and Medicine has established Recommended Dietary Allowances and Adequate Intakes for vitamin D. These values range from 15 to 20 mcg (600–800 IU) for adults and from 10 to 15 mcg (400–600 IU) for infants, children, and adolescents, depending on age.

Age	Male	Female	Pregnancy	Lactation
0–6 months*	10 mcg (400 IU)*	10 mcg (400 IU)*
7–12 months*	10 mcg (400 IU)*	10 mcg (400 IU)*
1–3 years	15 mcg (600 IU)	15 mcg (600 IU)
4–8 years	15 mcg (600 IU)	15 mcg (600 IU)
9–13 years	15 mcg (600 IU)	15 mcg (600 IU)
14–18 years	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)
19–50 years	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)
51–70 years	15 mcg (600 IU)	15 mcg (600 IU)
>70 years	20 mcg (800 IU)	20 mcg (800 IU)
*Adequate Intake (AI)

Sources of Vitamin D

Food

Vitamin D is found naturally in a few foods, such as the flesh of fatty fish, fish liver oils, beef liver, egg yolks, and cheese. In American diets, fortified foods (e.g., milk, breakfast cereals) provide most of the vitamin D.

Few foods naturally contain vitamin D. The flesh of fatty fish (such as trout, salmon, tuna, and mackerel) and fish liver oils are among the best sources [17,1]. An animal’s diet affects the amount of vitamin D in its tissues. Beef liver, egg yolks, and cheese have small amounts of vitamin D, primarily in the form of vitamin D₃ and its metabolite 25(OH)D₃. Mushrooms provide variable amounts of vitamin D₂ [17]. Some mushrooms available on the market have been treated with UV light to increase their levels of vitamin D₂. In addition, the Food and Drug Administration (FDA) has approved UV-treated mushroom powder as a food additive for use as a source of vitamin D₂ in food products [18]. Very limited evidence suggests no substantial differences in the bioavailability of vitamin D from various foods [19].

Animal-based foods typically provide some vitamin D in the form of 25(OH)D in addition to vitamin D₃. The impact of this form on vitamin D status is an emerging area of research. Studies show that 25(OH)D appears to be approximately five times more potent than the parent vitamin for raising serum 25(OH)D concentrations [17,20,21]. One study found that when the 25(OH)D content of beef, pork, chicken, turkey, and eggs is taken into account, the total amount of vitamin D in the food is 2 to 18 times higher than the amount in the parent vitamin alone, depending on the food [20].

Fortified foods provide most of the vitamin D in American diets [1,22]. For example, almost all of the U.S. milk supply is voluntarily fortified with about 3 mcg/cup (120 IU), usually in the form of vitamin D₃ [23]. In Canada, milk must be fortified with 0.88 to 1.0 mcg/100 mL (35–40 IU), and the required amount for margarine is at least 13.25 mcg/100 g (530 IU). Other dairy products made from milk, such as cheese and ice cream, are not usually fortified in the United States or Canada. Plant milk alternatives (such as beverages made from soy, almond, or oats) are often fortified with similar amounts of vitamin D to those in fortified cow’s milk (about 3 mcg [120 IU]/cup); the Nutrition Facts label lists the actual amount [24]. Ready-to-eat breakfast cereals often contain added vitamin D, as do some brands of orange juice, yogurt, margarine, and other food products.

The United States mandates the fortification of infant formula with 1 to 2.5 mcg/100 kcal (40–100 IU) vitamin D; 1 to 2 mcg/100 kcal (40–80 IU) is the required amount in Canada [1].

A variety of foods and their vitamin D levels per serving are listed in Table 3.

Food	Micrograms (mcg) per serving	International Units (IU) per serving	Percent DV*
Cod liver oil, 1 tablespoon	34.0	1,360	170
Trout (rainbow), farmed, cooked, 3 ounces	16.2	645	81
Salmon (sockeye), cooked, 3 ounces	14.2	570	71
Mushrooms, white, raw, sliced, exposed to UV light, ½ cup	9.2	366	46
Milk, 2% milkfat, vitamin D fortified, 1 cup	2.9	120	15
Soy, almond, and oat milks, vitamin D fortified, various brands, 1 cup	2.5–3.6	100–144	13–18
Ready-to-eat cereal, fortified with 10% of the DV for vitamin D, 1 serving	2.0	80	10
Sardines (Atlantic), canned in oil, drained, 2 sardines	1.2	46	6
Egg, 1 large, scrambled**	1.1	44	6
Liver, beef, braised, 3 ounces	1.0	42	5
Tuna fish (light), canned in water, drained, 3 ounces	1.0	40	5
Cheese, cheddar, 1.5 ounce	0.4	17	2
Mushrooms, portabella, raw, diced, ½ cup	0.1	4	1
Chicken breast, roasted, 3 ounces	0.1	4	1
Beef, ground, 90% lean, broiled, 3 ounces	0	1.7	0
Broccoli, raw, chopped, ½ cup	0	0	0
Carrots, raw, chopped, ½ cup	0	0	0
Almonds, dry roasted, 1 ounce	0	0	0
Apple, large	0	0	0
Banana, large	0	0	0
Rice, brown, long-grain, cooked, 1 cup	0	0	0
Whole wheat bread, 1 slice	0	0	0
Lentils, boiled, ½ cup	0	0	0
Sunflower seeds, roasted, ½ cup	0	0	0
Edamame, shelled, cooked, ½ cup	0	0	0
*DV = Daily Value. The U.S. Food and Drug Administration (FDA) developed DVs to help consumers compare the nutrient contents of foods and dietary supplements within the context of a total diet. The DV for vitamin D is 20 mcg (800 IU) for adults and children age 4 years and older [26]. FDA requires food labels to list vitamin D content in mcg per serving. In addition, labels may optionally list the amount in IUs in parentheses. Foods providing 20% or more of the DV are considered to be high sources of a nutrient, but foods providing lower percentages of the DV also contribute to a healthful diet.
** Vitamin D is in the yolk.

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The U.S. Department of Agriculture’s (USDA’s) FoodData Central lists the nutrient content of many foods and provides a comprehensive list of foods containing vitamin D arranged by nutrient content and by food name. However, FoodData Central does not include the amounts of 25(OH)D in foods.

Sun exposure

People can get some of their daily vitamin D through exposure to sunlight, although the season, time of day, length of day, cloud cover, melanin content of the skin, and other factors can affect ultraviolet radiation exposure and vitamin D synthesis.

Most people in the world meet at least some of their vitamin D needs through exposure to sunlight [1]. Type B UV (UVB) radiation with a wavelength of approximately 290 to 320 nanometers penetrates uncovered skin and converts cutaneous 7-dehydrocholesterol to previtamin D₃, which in turn becomes vitamin D₃. 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. Older people and people with dark skin are less able to produce vitamin D from sunlight [1]. UVB radiation does not penetrate glass, so exposure to sunshine indoors through a window does not produce vitamin D [27].

The factors that affect UV radiation exposure, individual responsiveness, and uncertainties about the amount of sun exposure needed to maintain adequate vitamin D levels make it difficult to provide guidelines on how much sun exposure is required for sufficient vitamin D synthesis [15,28]. Some expert bodies and vitamin D researchers suggest, for example, that approximately 5 to 30 minutes of sun exposure, particularly between 10 a.m. and 4 p.m., either daily or at least twice a week to the face, arms, hands, and legs without sunscreen usually leads to sufficient vitamin D synthesis [13,15,28]. Moderate use of commercial tanning beds that emit 2% to 6% UVB radiation is also effective [13,29].

However, despite the importance of the sun for vitamin D synthesis, limiting skin exposure to sunlight and UV radiation from tanning beds is prudent [28]. UV radiation is a carcinogen, and UV exposure is the most preventable cause of skin cancer. Federal agencies and national organizations advise taking photoprotective measures to reduce the risk of skin cancer, including using sunscreen with a sun protection factor (SPF) of 15 or higher, whenever people are exposed to the sun [28,30]. Sunscreens with an SPF of 8 or more appear to block vitamin D-producing UV rays. In practice, however, people usually do not apply sufficient amounts of sunscreen, cover all sun-exposed skin, or reapply sunscreen regularly. Their skin probably synthesizes some vitamin D, even with typically applied sunscreen amounts [1,28].

Dietary supplements

Vitamin D is present in dietary supplements as either vitamin D₂ or vitamin D₃. Both can raise the serum level of 25(OH)D. However, research shows that vitamin D₃ increases serum 25(OH)D levels to a greater extent than vitamin D₂ and can maintain those higher levels for longer periods of time.

Dietary supplements can contain vitamins D₂ or D₃. Vitamin D₂ is manufactured using UV irradiation of ergosterol in yeast, and vitamin D₃ is typically produced with irradiation of 7-dehydrocholesterol from lanolin obtained from the wool of sheep [13,31]. An animal-free version of vitamin D₃ sourced from lichen is also available [32]. People who avoid all animal-sourced products can contact dietary supplement manufacturers to ask about their sourcing and processing techniques.

Both vitamins D₂ and D₃ raise serum 25(OH)D levels, and they seem to have equivalent ability to cure rickets [4]. In addition, most steps in the metabolism and actions of vitamins D₂ and D₃ are identical. However, most evidence indicates that vitamin D₃ increases serum 25(OH)D levels to a greater extent and maintains these higher levels longer than vitamin D₂, even though both forms are well absorbed in the gut [33-36].

Some studies have used dietary supplements containing the 25(OH)D₃ form of vitamin D. Per equivalent microgram dose, 25(OH)D₃ is three to five times as potent as vitamin D₃ [37,38]. However, no 25(OH)D₃ dietary supplements appear to be available to consumers on the U.S. market at this time [32].

Vitamin D Intakes and Status

According to data from the National Health and Nutrition Examination Survey, most people in the United States consume less than the recommended amounts of vitamin D. However, evidence suggests that the majority of people have sufficient serum concentrations of vitamin D based on the thresholds set by the Food and Nutrition Board. Sun exposure is one of the reasons why serum levels of 25(OH)D are generally higher than would be predicted on the basis of vitamin D dietary intakes alone.

Most people in the United States consume less than recommended amounts of vitamin D. An analysis of data from the 2015–2016 National Health and Nutrition Examination Survey (NHANES) found that average daily vitamin D intakes from foods and beverages were 5.1 mcg (204 IU) in men, 4.2 mcg (168 IU) in women, and 4.9 mcg (196 IU) in children age 2 to 19 years [39]. In fact, 2013–2016 NHANES data showed that 92% of men, more than 97% of women, and 94% of people age 1 year and older ingested less than the EAR of 10 mcg (400 IU) of vitamin D from food and beverages [40].

The analysis of 2015–2016 data also showed that 28% of all individuals age 2 years and older in the United States took a dietary supplement containing vitamin D [39]. In addition, 26% of participants age 2 to 5 years and 14% of those age 6 to 11 years took supplements; rates increased with age from 10% of those age 12 to 19 years to 49% of men and 59% of women age 60 and older. Total vitamin D intakes were three times higher with supplement use than with diet alone; the mean intake from foods and beverages alone for individuals age 2 and older was 4.8 mcg (192 IU) but increased to 19.9 mcg (796 IU) when dietary supplements were included.

Some people take very high doses of vitamin D supplements. In 2013–2014, an estimated 3.2% of the U.S. adult population took supplements containing 100 mcg (4,000 IU) or more vitamin D [41].

One might expect a large proportion of the U.S. population to have vitamin D inadequacy on the basis of vitamin D intakes from foods, beverages, and even dietary supplements. However, comparing vitamin D intakes to serum 25(OH)D levels is problematic. One reason is that sun exposure affects vitamin D status, so serum 25(OH)D levels are usually higher than would be predicted on the basis of vitamin D dietary intakes alone [1]. Another reason is that animal foods contain some 25(OH)D. This form of vitamin D is not included in intake surveys and is considerably more potent than vitamins D₂ or D₃ at raising serum 25(OH)D levels [42].

An analysis of NHANES 2011–2014 data on serum 25(OH)D levels found that most people in the United States age 1 year and older had sufficient vitamin D intakes according to the FNB thresholds [43]. However, 18% were at risk of inadequacy (levels of 30–49 nmol/L [12–19.6 ng/mL]), and 5% were at risk of deficiency (levels below 30 nmol/L [12 ng/mL]). Four percent had levels higher than 125 nmol/L (50 ng/mL). Proportions at risk of deficiency were lowest among children age 1 to 5 years (0.5%), peaked at 7.6% in adults age 20 to 39 years, and fell to 2.9% among adults age 60 years and older; patterns were similar for risks of inadequacy. Rates of deficiency varied by race and ethnicity: 17.5% of non-Hispanic Blacks were at risk of vitamin D deficiency, as were 7.6% of non-Hispanic Asians, 5.9% of Hispanics, and 2.1% of non-Hispanic White people. Again, the pattern was similar for the risk of inadequacy. Vitamin D status in the United States remained stable in the decade between 2003–2004 and 2013–2014.

Vitamin D Deficiency

People who are lactose intolerant, allergic to milk, or follow an ovo-vegetarian or vegan diet are at higher risk of vitamin D deficiency. Deficiency may also occur in people who have limited exposure to sunlight, those whose kidneys cannot convert 25(OH)D to its active form, or those who cannot absorb vitamin D efficiently in the digestive tract. Vitamin D deficiency can manifest as rickets in children and as osteomalacia in adolescents and adults.

People can develop vitamin D deficiency when usual intakes are lower over time than recommended levels, 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. Diets low in vitamin D are more common in people who have milk allergy or lactose intolerance and those who consume an ovo-vegetarian or vegan diet [1].

In children, vitamin D deficiency is manifested as rickets, a disease characterized by a failure of bone tissue to become properly mineralized, resulting in soft bones and skeletal deformities [44]. In addition to bone deformities and pain, severe rickets can cause failure to thrive, developmental delay, hypocalcemic seizures, tetanic spasms, cardiomyopathy, and dental abnormalities [45,46].

Prolonged exclusive breastfeeding without vitamin D supplementation can cause rickets in infants, and, in the United States, rickets is most common among breastfed Black infants and children [47]. In one Minnesota county, the incidence rate of rickets in children younger than 3 years in the decade beginning in 2000 was 24.1 per 100,000 [48]. Rickets occurred mainly in Black children who were breastfed longer, were born with low birthweight, weighed less, and were shorter than other children. The incidence rate of rickets in the infants and children (younger than 7) seen by 2,325 pediatricians throughout Canada was 2.9 per 100,000 in 2002–2004, and almost all patients with rickets had been breastfed [49].

The fortification of milk (a good source of calcium) and other staples, such as breakfast cereals and margarine, with vitamin D beginning in the 1930s along with the use of cod liver oil made rickets rare in the United States [28,50]. However, the incidence of rickets is increasing globally, even in the United States and Europe, especially among immigrants from African, Middle-Eastern, and Asian countries [51]. Possible explanations for this increase include genetic differences in vitamin D metabolism, dietary preferences, and behaviors that lead to less sun exposure [45,46].

In adults and adolescents, vitamin D deficiency can lead to osteomalacia, in which existing bone is incompletely or defectively mineralized during the remodeling process, resulting in weak bones [46]. Signs and symptoms of osteomalacia are similar to those of rickets and include bone deformities and pain, hypocalcemic seizures, tetanic spasms, and dental abnormalities [45].

Screening for vitamin D status is becoming a more common part of the routine laboratory bloodwork ordered by primary-care physicians, irrespective of any indications for this practice [6,52-54]. No studies have examined whether such screening for vitamin D deficiency results in improved health outcomes [55]. The U.S. Preventive Services Task Force (USPSTF) found insufficient evidence to assess the benefits and harms of screening for vitamin D deficiency in asymptomatic adults [6]. It added that no national professional organization recommends population screening for vitamin D deficiency.

Groups at Risk of Vitamin D Inadequacy

Certain groups of people are more likely than others to have inadequate vitamin D status. These include breastfed infants, older adults, people with limited sun exposure, people with dark skin, people with conditions that limit fat absorption, and people with obesity or those who have undergone gastric bypass surgery.

Obtaining sufficient vitamin D from natural (nonfortified) food sources alone is difficult. For many people, consuming vitamin D-fortified foods and exposing themselves to some sunlight are essential for maintaining a healthy vitamin D status. However, some groups might need dietary supplements to meet their vitamin D requirements. The following groups are among those most likely to have inadequate vitamin D status.

Breastfed infants

Consumption of human milk alone does not ordinarily enable infants to meet vitamin D requirements, because it provides less than 0.6 to 2.0 mcg/L (25 to 78 IU/L) [1,56,57]. The vitamin D content of human milk is related to the mother’s vitamin D status; studies suggest that the breastmilk of mothers who take daily supplements containing at least 50 mcg (2,000 IU) vitamin D₃ have higher levels of the nutrient [57,58].

Older adults

Older adults are at increased risk of developing vitamin D insufficiency, partly because the skin’s ability to synthesize vitamin D declines with age [1,61]. In addition, older adults are likely to spend more time than younger people indoors, and they might have inadequate dietary intakes of the vitamin [1].

People with limited sun exposure

Homebound individuals; people who wear long robes, dresses, or head coverings for religious reasons; and people with occupations that limit sun exposure are among the groups that are unlikely to obtain adequate amounts of vitamin D from sunlight [62]. The use of sunscreen also limits vitamin D synthesis from sunlight. However, because the extent and frequency of sunscreen use are unknown, the role that sunscreen may play in reducing vitamin D synthesis is unclear [1].

People with dark skin

Greater amounts of the pigment melanin in the epidermal layer of the skin result in darker skin and reduce the skin’s ability to produce vitamin D from sunlight [1]. Black Americans, for example, typically have lower serum 25(OH)D levels than White Americans. However, whether these lower levels in persons with dark skin have significant health consequences is not clear [14]. Those of African American ancestry, for example, have lower rates of bone fracture and osteoporosis than do Whites (see the section below on bone health and osteoporosis).

People with conditions that limit fat absorption

Because vitamin D is fat soluble, its absorption depends on the gut’s ability to absorb dietary fat [4]. Fat malabsorption is associated with medical conditions that include some forms of liver disease, cystic fibrosis, celiac disease, Crohn’s disease, and ulcerative colitis [1,63]. In addition to having an increased risk of vitamin D deficiency, people with these conditions might not eat certain foods, such as dairy products (many of which are fortified with vitamin D), or eat only small amounts of these foods. Individuals who have difficulty absorbing dietary fat might therefore require vitamin D supplementation [63].

People with obesity or who have undergone gastric bypass surgery

Individuals with a body mass index (BMI) of 30 or more have lower serum 25(OH)D levels than individuals without obesity. Obesity does not affect the skin’s capacity to synthesize vitamin D. However, greater amounts of subcutaneous fat sequester more of the vitamin [1]. People with obesity might need greater intakes of vitamin D to achieve 25(OH)D levels similar to those of people with normal weight [1,64,65].

Individuals with obesity who have undergone gastric bypass surgery can also become vitamin D deficient. In this procedure, part of the upper small intestine, where vitamin D is absorbed, is bypassed, and vitamin D that is mobilized into the bloodstream from fat stores might not raise 25(OH)D to adequate levels over time [66,67]. Various expert groups—including the American Association of Metabolic and Bariatric Surgery, The Obesity Society, and the British Obesity and Metabolic Surgery Society—have developed guidelines on vitamin D screening, monitoring, and replacement before and after bariatric surgery [66,68]

Vitamin D and Health

The FNB committee that established DRIs for vitamin D found that the evidence was inadequate or too contradictory to conclude that the vitamin had any effect on a long list of potential health outcomes (e.g., on resistance to chronic diseases or functional measures), except for measures related to bone health. Similarly, in a review of data from nearly 250 studies published between 2009 and 2013, the Agency for Healthcare Research and Quality concluded that no relationship could be firmly established between vitamin D and health outcomes other than bone health [69]. However, because research has been conducted on vitamin D and numerous health outcomes, this section focuses on seven diseases, conditions, and interventions in which vitamin D might be involved: bone health and osteoporosis, cancer, cardiovascular disease (CVD), depression, multiple sclerosis (MS), type 2 diabetes, and weight loss.

Most of the studies described in this section measured serum 25(OH)D levels using various methods that were not standardized by comparing them to the best methods. Use of unstandardized 25(OH)D measures can raise questions about the accuracy of the results and about the validity of conclusions drawn from studies that use such measures and, especially, from meta-analyses that pool data from many studies that use different unstandardized measures [5,9,70]. More information about assay standardization is available from the Vitamin D Standardization Program webpage.

Bone health and osteoporosis

Osteoporosis is characterized by low bone mass and the deterioration of bone tissue, which increases bone fragility and the risk of fractures. Clinical trials have shown that vitamin D and calcium supplements may increase bone mineral density in some postmenopausal women and older men, but it is not clear whether they reduce falls and fracture rates. In addition, the results of studies that have evaluated the effects of supplemental vitamin D on muscle strength and the rate of decline in muscle function have been inconsistent.

Bone is constantly being remodeled. However, as people age—and particularly in women during menopause—bone breakdown rates overtake rates of bone building. Over time, bone density can decline, and osteoporosis can eventually develop [71].

More than 53 million adults in the United States have or are at risk of developing osteoporosis, which is characterized by low bone mass and structural deterioration of bone tissue that increases bone fragility and the risk of bone fractures [72]. About 2.3 million osteoporotic fractures occurred in the United States in 2015 [73]. Osteoporosis is, in part, a long-term effect of calcium and/or vitamin D insufficiency, in contrast to rickets and osteomalacia, which result from vitamin D deficiency. Osteoporosis is most often associated with inadequate calcium intakes, but insufficient vitamin D intakes contribute to osteoporosis by reducing calcium absorption [1].

Bone health also depends on support from the surrounding muscles to assist with balance and postural sway and thereby reduce the risk of falling. Vitamin D is also needed for the normal development and growth of muscle fibers. In addition, inadequate vitamin D levels can adversely affect muscle strength and lead to muscle weakness and pain (myopathy) [1].

Most trials of the effects of vitamin D supplements on bone health also included calcium supplements, so isolating the effects of each nutrient is difficult. In addition, studies provided different amounts of nutrients and used different dosing schedules.

Clinical trial evidence on older adults

Among postmenopausal women and older men, many clinical trials have shown that supplements of both vitamin D and calcium result in small increases in bone mineral density throughout the skeleton [1,74]. They also help reduce fracture rates in institutionalized older people. However, the evidence on the impact of vitamin D and calcium supplements on fractures in community-dwelling individuals is inconsistent.

Vitamin D supplements for bone health in minority populations

Bone mineral density, bone mass, and fracture risk are correlated with serum 25(OH)D levels in White Americans and Mexican Americans, but not in Black Americans [14,83]. Factors such as adiposity, skin pigmentation, vitamin D binding protein polymorphisms, and genetics contribute to differences in 25(OH)D levels between Black and White Americans.

One clinical trial randomized 260 Black women age 60 years and older (mean age 68.2 years) to receive 60 to 120 mcg (2,400 to 4,800 IU) per day vitamin D₃ supplementation to maintain serum 25(OH)D levels above 75 nmol/L (30 ng/mL) for 3 years [84]. The results showed no association between 25(OH)D levels or vitamin D dose and the risk of falling in the 184 participants who completed the study. In fact, Black Americans might have a greater risk than White Americans of falls and fractures with daily vitamin D intakes of 50 mcg (2,000 IU) or more [14]. Furthermore, the bone health of older Black American women does not appear to benefit from raising serum 25(OH)D levels beyond 50 nmol/L (20 ng/mL) [84].

Vitamin D supplements and muscle function

In one clinical trial, 78 frail and near-frail adults aged 65 and older received 800 IU vitamin D3, 10 mcg 25(OH)D, or a placebo daily for six months. The results showed no significant differences in muscle strength or physical performance.

Another study included 100 community-dwelling adults aged 60 and older with low vitamin D levels. Participants received 800 IU vitamin D3 or a placebo for one year.

Some participants required an additional 800 IU per day to raise their vitamin D levels. Although serum vitamin D levels increased, supplementation did not improve lower-extremity strength, power, or lean muscle mass.

Conclusions about vitamin D supplements and bone health

All adults should consume recommended amounts of vitamin D and calcium from foods and supplements if needed. Older women and men should consult their health care providers about their needs for both nutrients as part of an overall plan to maintain bone health and to prevent or treat osteoporosis.

Cancer

Some evidence suggests that vitamin D might inhibit carcinogenesis and slow tumor progression. However, most research has found no relationship between serum 25(OH)D levels and risk of cancer. The results of clinical trials have generally failed to show that vitamin D supplementation with or without calcium supplementation reduces the incidence of cancer. Adequate or higher 25(OH)D levels might reduce cancer mortality rates, but more research is needed to determine the effects of vitamin D supplementation in people with cancer.

Laboratory and animal studies suggest that vitamin D might inhibit carcinogenesis and slow tumor progression by, for example, promoting cell differentiation and inhibiting metastasis. Vitamin D might also have anti-inflammatory, immunomodulatory, proapoptotic, and antiangiogenic effects [1,87]. Observational studies and clinical trials provide mixed evidence on whether vitamin D intakes or serum levels affect cancer incidence, progression, or mortality risk.

Total cancer incidence and mortality

Some observational studies show associations between low serum levels of 25(OH)D and increased risks of cancer incidence and death. In a meta-analysis of 16 prospective cohort studies in a total of 137,567 participants who had 8,345 diagnoses of cancer, 5,755 participants died from cancer [88]. A 50 nmol/L (20 ng/mL) increase in 25(OH)D levels was associated with an 11% reduction in total cancer incidence rates and, in women but not men, a 24% reduction in cancer mortality rates. A meta-analysis of prospective studies that evaluated the association between serum 25(OH)D levels and cancer incidence (8 studies) or cancer mortality (16 studies) found that cancer risk decreased by 7% and cancer mortality rates decreased by 2% with each 20 nmol/L (8 ng/mL) increase in serum 25(OH)D levels [89]. Importantly, not all observational studies found higher vitamin D status to be beneficial, and the studies varied considerably in study populations, baseline comorbidities, and measurement of vitamin D levels.

Clinical trial evidence provides some support for the observational findings. For example, three meta-analyses of clinical trial evidence found that vitamin D supplementation does not affect cancer incidence but does significantly reduce total cancer mortality rates by 12% to 13% [90-92]. In the most recent meta-analysis, 10 randomized clinical trials (including the VITAL trial described below) that included 6,537 cancer cases provided 10 to 50 mcg (400–2,000 IU) vitamin D₃ daily (six trials) or 500 mcg (20,000 IU)/week to 12,500 mcg (500,000 IU)/year boluses of vitamin D₃ (four trials) [91]. The study reports included 3 to 10 years of follow-up data. The vitamin D supplements were associated with serum 25(OH)D levels of 54 to 135 nmol/L (21.6–54 ng/mL). Vitamin D supplementation reduced cancer mortality rates by 13%, and most of the benefit occurred with daily supplementation.

The VITAL clinical trial that investigated the effects of vitamin D supplementation on the primary prevention of cancer in the general population gave 50 mcg (2,000 IU)/day vitamin D₃ supplements with or without 1,000 mg/day marine omega-3 fatty acids or a placebo for a median of 5.3 years [93]. The study included 25,871 men age 50 years and older and women age 55 years and older who had no history of cancer, and most had adequate serum 25(OH)D levels at baseline. Rates of breast, prostate, and colorectal cancer did not differ significantly between the vitamin D and placebo groups. However, normal-weight participants had greater reductions in cancer incidence and mortality rates than those with overweight or obesity.

The Women’s Health Initiative (WHI) clinical trial randomized 36,282 postmenopausal women to receive 10 mcg (400 IU) vitamin D₃ plus 1,000 mg calcium daily or a placebo for a mean of 7 years [94]. Results showed no effect of supplemental vitamin D and calcium on cancer incidence or mortality during the 7-year trial. Similarly, the supplements did not affect cancer incidence over a long-term median follow-up of 22.3 years, but they did reduce cancer mortality by 7% over this period of time [95].

A few studies have examined the effect of vitamin D supplementation on specific cancers. Below are brief descriptions of studies of vitamin D and its association with, or effect on, breast, colorectal, lung, pancreatic, and prostate cancers.

Breast cancer

Some observational studies support an inverse association between 25(OH)D levels and breast cancer risk and mortality, but others do not [96-99]. In the WHI clinical trial desc… Read More

Vitamin D