Overview of vitamin D

Authors
Sassan
Pazirandeh,
MD
David L Burns, MD
Section
Editors
Kathleen
J
Motil,
MD,
PhD
Marc K Drezner, MD
Deputy
Editor
Jean E Mulder, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Aug 2015. | This topic last updated: May 08, 2014.
INTRODUCTION Vitamin D is a fat-soluble vitamin. Very few foods naturally contain vitamin D (fatty
fish livers are the exception), so dermal synthesis is the major natural source of the vitamin. Vitamin D
from the diet or dermal synthesis is biologically inactive and requires enzymatic conversion to active
metabolites (figure 1). Vitamin D is converted enzymatically in the liver to 25-hydroxyvitamin D
(25[OH]D), the major circulating form of vitamin D, and then in the kidney to 1,25-dihydroxyvitamin D,
the active form of vitamin D.
Vitamin D and its metabolites have a significant clinical role because of their interrelationship with
calcium homeostasis and bone metabolism. Rickets (children) and osteomalacia (children and adults)
due to severe vitamin D deficiency are now uncommon except in populations with unusually low sun
exposure, lack of vitamin D in fortified foods, and malabsorptive syndromes. Subclinical vitamin D
deficiency, as measured by low serum 25(OH)D, is very common. In the National Health and Nutrition
Examination Survey (NHANES) 2005 to 2006, 41.6 percent of adult participants (20 years) had
25(OH)D levels below 20 ng/mL (50 nmol/L) [1]. This degree of vitamin D deficiency may contribute to
the development of osteoporosis and an increased risk of fractures and falls in the elderly. Vitamin D
may also regulate many other cellular functions.
This topic review provides an overview of vitamin D. Other reviews discuss specific issues related to
vitamin D:
(See "Causes of vitamin D deficiency and resistance".)
(See "Overview of rickets in children" and "Etiology and treatment of calcipenic rickets in children".)
(See "Epidemiology and etiology of osteomalacia" and "Clinical manifestations, diagnosis, and
treatment of osteomalacia".)
(See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment" and
"Vitamin D insufficiency and deficiency in children and adolescents".)
(See "Vitamin D and extraskeletal health".)
(See "Calcium and vitamin D supplementation in osteoporosis".)
CHEMISTRY Vitamin D, or calciferol, is a generic term and refers to a group of lipid soluble
compounds with a four-ringed cholesterol backbone. 25-hydroxyvitamin D (25[OH]D) is the major
circulating form of vitamin D. It has a half-life of two to three weeks, compared with 24 hours for parent
vitamin D [2]. It has activity at bone and intestine, but is less than 1 percent as potent as 1,25dihydroxyvitamin D, the most active form of vitamin D. The half-life of 1,25-dihydroxyvitamin D is
approximately four to six hours. 1,25-dihydroxyvitamin D binds to intracellular receptors in target
tissues and regulates gene transcription [ 3]. It appears to function through a single vitamin D receptor
(VDR), which is nearly universally expressed in nucleated cells. The receptor is a member of the class II
steroid hormone receptor, and is closely related to the retinoic acid and thyroid hormone receptors [ 4].
Its most important biological action is to promote enterocyte differentiation and the intestinal
absorption of calcium. Other effects include a lesser stimulation of intestinal phosphate absorption,
direct suppression of parathyroid hormone (PTH) release from the parathyroid gland, regulation of
osteoblast function, and permissively allowing PTH-induced osteoclast activation and bone resorption
(figure 1).
SOURCES Very few foods naturally contain vitamin D (fatty fish livers are the exception); dermal
synthesis is the major natural source of the vitamin. Previtamin D3 is synthesized nonenzymatically in
skin from 7-dehydrocholesterol during exposure to the ultraviolet (UV) rays in sunlight. Previtamin D3
undergoes a temperature-dependent rearrangement to form vitamin D3 (cholecalciferol) (figure 1). This
system is exceedingly efficient, and it is estimated that brief casual exposure of the arms and face is
equivalent to ingestion of 200 international units per day [ 5]. However, the length of daily exposure
required to obtain the sunlight equivalent of oral vitamin D supplementation is difficult to predict on an
individual basis and varies with the skin type, latitude, season, and time of day [ 6,7]. Prolonged
exposure of the skin to sunlight does not produce toxic amounts of vitamin D3 because of
photoconversion of previtamin D3 and vitamin D3 to inactive metabolites (lumisterol, tachysterol, 5,6transvitamin D, and suprasterol 1 and 2) [ 8,9]. In addition, sunlight induces production of melanin,
which reduces production of vitamin D3 in the skin.
Infants, disabled persons, and older adults may have inadequate sun exposure, while the skin of those
older than 70 years of age also does not convert vitamin D effectively. In addition, at northern latitudes,

there is not enough radiation to convert vitamin D, particularly during the winter. For these reasons, in
the United States, milk, infant formula, breakfast cereals, and some other foods are fortified with
synthetic vitamin D2 (ergocalciferol), which is derived from radiation of ergosterol found in plants, the
mold ergot, and plankton, or with vitamin D3. In other parts of the world, cereals and bread products
are often fortified with vitamin D.
ABSORPTION Dietary vitamin D is incorporated into micelles, absorbed by enterocytes, and then
packaged into chylomicrons. Disorders associated with fat malabsorption, such as celiac disease, Crohn
disease, pancreatic insufficiency, cystic fibrosis, short gut syndrome, and cholestatic liver disease, are
associated with low serum 25-hydroxyvitamin D (25[OH]D) levels. (See "Causes of vitamin D deficiency
and resistance", section on 'Gastrointestinal disease'.)
METABOLISM Vitamin D from the diet or dermal synthesis is biologically inactive and requires
enzymatic conversion in the liver and kidney to active metabolites.
Hepatic Dietary vitamin D travels to the liver, bound to vitamin Dbinding protein and in continued
association with chylomicrons and lipoproteins, where it and endogenously-synthesized vitamin D3 are
metabolized [10,11]. The hepatic enzyme 25hydroxylase places a hydroxyl group in the 25 position of
the vitamin D molecule, resulting in the formation of 25-hydroxyvitamin D (25[OH]D, calcidiol) (figure
1). 25-hydroxyvitamin D2 has a lower affinity than 25-hydroxyvitamin D3 for vitamin D-binding protein.
Thus, 25-hydroxyvitamin D2 has a shorter half-life than 25-hydroxyvitamin D3, and treatment with
vitamin D2 may not increase serum total 25(OH)D levels as efficiently as vitamin D3. The treatment of
vitamin D deficiency is discussed in detail elsewhere. (See "Vitamin D deficiency in adults: Definition,
clinical manifestations, and treatment", section on 'Preparations'.)
Renal 25-hydroxyvitamin D2 and D3 produced by the liver enter the circulation and travel to the
kidney, again bound to vitamin D-binding protein. This protein has a single binding site, which binds
vitamin D and all of its metabolites. Only 3 to 5 percent of the total circulating binding sites are
normally occupied; as a result, this protein is not rate-limiting in vitamin D metabolism unless large
amounts are lost in the urine, as in the nephrotic syndrome [ 12]. In the renal tubule, entry of the filtered
25(OH)D-vitamin D-binding protein complex into the cells is facilitated by receptor-mediated
endocytosis [13]. At least two proteins working in tandem are involved in this process: cubilin and
megalin [13,14]. Cubilin and megalin, expressed in the renal proximal tubule, are multiligand receptors
that facilitate uptake of extracellular ligands. Deficiency of either of these proteins results in increased
25(OH)D excretion in the urine and, at least in experimental models, 1,25-dihydroxyvitamin D
deficiency and bone disease [13-15].
Within the tubular cell, 25(OH)D is released from the binding protein. The renal tubular cells contain two
enzymes, 1-alpha-hydroxylase (CYP27B1) and 24-alpha-hydroxylase (CYP24), that can further
hydroxylate 25(OH)D, producing 1,25-dihydroxyvitamin D, the most active form of vitamin D, or 24,25dihydroxyvitamin D, an inactive metabolite (figure 1) [ 16-18]. Both enzymes are members of the P-450
system [19]. Studies in vitamin D-deficient animals suggest that the proximal tubule is the important
site of synthesis. In contrast, studies in the normal human kidney indicate that the distal nephron is the
predominant site of 1-alpha-hydroxylase expression under conditions of vitamin D sufficiency [ 18].
The 1-alpha-hydroxylase enzyme is also expressed in extrarenal sites, including the gastrointestinal
tract, skin, vasculature, mammary epithelial cells, osteoblasts, and osteoclasts [ 20,21]. The most widely
recognized manifestation of extrarenal synthesis of 1,25-dihydroxyvitamin D is hypercalcemia and
hypercalciuria in patients with granulomatous diseases, such as sarcoid. In this setting, parathyroid
hormone (PTH)-independent extrarenal production of 1,25-dihydroxyvitamin D from 25(OH)D by
activated macrophages occurs in the lung and lymph nodes. (See "Hypercalcemia in granulomatous
diseases", section on 'Sarcoidosis'.)
The plasma 1,25-dihydroxyvitamin D concentration is a function both of the availability of 25(OH)D and
of the activities of the renal enzymes 1-alpha-hydroxylase and 24-alpha-hydroxylase. The renal 1-alphahydroxylase enzyme is primarily regulated by the following factors [11,19]:
PTH
Serum calcium and phosphate concentrations
Fibroblast growth factor 23 (FGF23)
Increased PTH secretion (most often due to a fall in the plasma calcium concentration) and
hypophosphatemia stimulate the enzyme and enhance 1,25 dihydroxyvitamin D production [ 22]. 1,25dihydroxyvitamin D, in turn, inhibits the synthesis and secretion of PTH, providing negative feedback
regulation of 1,25-diydroxyvitamin D production. 1,25-dihydroxyvitamin D synthesis may also be
modulated by vitamin D receptors (VDRs) on the cell surface; downregulation of these receptors may
play an important role in regulating vitamin D activation [23].
FGF23 inhibits renal production of 1,25-dihydroxyvitamin D by limiting 1-alpha-hydroxylase activity in
the renal proximal tubule and by simultaneously increasing expression of 24-alpha-hydroxylase and
production of 24,25-dihydroxyvitamin D (an inactive metabolite) [ 24]. 1,25-dihydroxyvitamin D
stimulates FGF23, a phosphaturic hormone, creating a feedback loop. Experimental data suggest that
FGF23 decreases renal reabsorption of phosphate, and thereby counteracts the increased
gastrointestinal phosphate reabsorption induced by 1,25-dihydroxyvitamin D, maintaining phosphate
homeostasis [25].

Both 1,25-dihydroxyvitamin D and 25(OH)D are degraded in part by hydroxylation by a 24-hydroxylase

[11,17]. The activity of the 24-hydroxylase gene is increased by 1,25-dihydroxyvitamin D, which
therefore promotes its own inactivation, and decreased by PTH, thereby allowing more active hormone
to be formed [17].
REQUIREMENTS
Adequate intake In 2010, the Institute of Medicine (IOM) released a report on dietary intake
requirements for calcium and vitamin D (table 1) [ 26]. Its Recommended Dietary Allowance (RDA) of
vitamin D for children 1 to 18 years and adults through age 70 years is 600 international units (15 mcg)
daily. Its RDA is 800 international units (20 mcg) daily after age 71 years [ 26]. For pregnant and
lactating mothers, it recommends 600 international units (15 mcg) per day. The intake can be provided
in the diet or as a vitamin D supplement. Vitamin D intake is often low in older adults, who also do not
have regular effective sun exposure. Thus, for older adults, we suggest supplementation with 600 to
800 international units of vitamin D daily. Older persons confined indoors and other high risk groups
may have low serum 25-hydroxyvitamin D (25[OH]D) concentrations at this intake level and may
require higher intakes (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and
treatment", section on 'Groups at high risk for suboptimal intake'.)
The estimated adequate intake for infants up to 12 months is 400 international units (10 mcg) daily
(table 2). Vitamin D supplementation should be given to infants who are exclusively breast fed, because
the vitamin D content of human milk is low. The Lawson Wilkins Pediatric Endocrine Society also
recommends supplementation with 400 international units daily of vitamin D beginning within days of
birth for infants who are exclusively breast-fed [27]. Most infant formulas contain at least 400units/L of
vitamin D, so formula-fed infants will also require supplementation to meet this goal, unless they
consume at least 1000 mL daily of formula. Vitamin D intake of at least 400 units/day is also
recommended for children who do not consume at least one liter of vitamin D-fortified milk daily [ 27].
(See "Vitamin D insufficiency and deficiency in children and adolescents", section on 'Prevention'.)
The recommendations for dietary vitamin D intake were based upon the beneficial effects of calcium
and vitamin D on skeletal health (see "Calcium and vitamin D supplementation in osteoporosis", section
on 'Efficacy'). The evidence supporting a benefit of vitamin D on extraskeletal outcomes was
inconsistent, inconclusive as to causality, and insufficient, and therefore was not used as a basis for
dietary reference intake development [28]. (See "Vitamin D and extraskeletal health".)
Estimates of vitamin D requirements vary and depend in part upon sun exposure and the standards
used to define a deficient state. The IOM committee assumed minimal sun exposure when establishing
the dietary reference intakes for vitamin D. Casual exposure to sunlight provides amounts of vitamin D
that are adequate to prevent rickets in many people, but is influenced by geographic location, season,
use of sun block lotion, and skin pigmentation [ 29]. (See "Vitamin D insufficiency and deficiency in
children and adolescents", section on 'Decreased synthesis'.)
Vitamin D requirements also may depend on disease states and concomitant medications. As an
example, patients undergoing long-term treatment with glucocorticoids may benefit from higher levels
of supplementation of vitamin D and calcium. (See "Prevention and treatment of glucocorticoid-induced
osteoporosis", section on 'Calcium and vitamin D'.)
Optimal serum 25-hydroxyvitamin D The best laboratory indicator of vitamin D adequacy is the
serum 25(OH)D concentration [30]. The lower limit of normal for 25(OH)D levels varies depending on
the geographic location and sunlight exposure of the reference population (range 8 to 15 ng/mL).
However, there is no consensus on the optimal 25(OH)D concentration for skeletal or extraskeletal
health. The IOM concluded that a serum 25(OH)D concentration of 20 ng/mL (50nmol/L) is sufficient for
most individuals [2], but other experts (Endocrine Society, National Osteoporosis Foundation [NOF],
International Osteoporosis Foundation [IOF], American Geriatrics Society [AGS]) suggest that a
minimum level of 30 ng/mL (75nmol/L) is necessary in older adults to minimize the risk of falls and
fracture [31-35]. The serum parathyroid hormone (PTH) level typically is inversely related to 25(OH)D
levels in adults, and may be a useful secondary indicator of vitamin D insufficiency. In general, this
relationship is weak for children. Controversies surrounding the optimal serum 25(OH)D concentration
are reviewed separately. (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and
treatment", section on 'Defining vitamin D sufficiency'.)
DEFICIENCY AND RESISTANCE Vitamin D deficiency or resistance is caused by one of four
mechanisms (see "Causes of vitamin D deficiency and resistance"):
Impaired availability of vitamin D, secondary to inadequate dietary vitamin D, fat malabsorptive
disorders, and/or lack of sunlight (photoisomerization)
Impaired hydroxylation by the liver to produce 25-hydroxyvitamin D (25[OH]D)
Impaired hydroxylation by the kidneys to produce 1,25-dihydroxyvitamin D (vitamin D-dependent
rickets type 1, chronic renal insufficiency)
End organ insensitivity to vitamin D metabolites (hereditary vitamin D-resistant rickets [HVDRR,
vitamin D-dependent rickets type 2])
Several studies have shown suboptimal serum levels of 25(OH)D and vitamin D intake in the United
States and other countries [27,36-40]. (See 'Requirements' above and "Vitamin D insufficiency and

deficiency in children and adolescents" and "Vitamin D deficiency in adults: Definition, clinical
manifestations, and treatment".)
Lack of vitamin D activity leads to reduced intestinal absorption of calcium and phosphorus. Early in
vitamin D deficiency, hypophosphatemia is more marked than hypocalcemia. With persistent vitamin D
deficiency, hypocalcemia occurs and causes secondary hyperparathyroidism, which leads to
phosphaturia, demineralization of bones, and, when prolonged and severe, to osteomalacia in adults
and rickets and osteomalacia in children. (See "Epidemiology and etiology of osteomalacia" and
"Etiology and treatment of calcipenic rickets in children", section on 'Nutritional rickets'.)
Overt vitamin D deficiency resulting in rickets and osteomalacia in children and osteomalacia in adults
is now uncommon in most developed countries. However, subclinical vitamin D deficiency occurs even
in developed countries and is associated with osteoporosis, increased risk of falls, and possibly
fractures. (See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment",
section on 'Clinical manifestations'.)
Glucocorticoids, when used chronically in high doses, inhibit intestinal vitamin D-dependent calcium
absorption, which is one of the mechanisms whereby chronic glucocorticoid excess leads to
osteoporosis and fractures. (See "Pathogenesis, clinical features, and evaluation of glucocorticoidinduced osteoporosis".)
Vitamin D stores decline with age, especially in the winter. Controlled trials have demonstrated that
vitamin D and calcium supplementation can reduce the risk of falls and fractures in the elderly. (See
"Calcium and vitamin D supplementation in osteoporosis" and "Vitamin D deficiency in adults:
Definition, clinical manifestations, and treatment", section on 'Benefits of vitamin D repletion'.)
EXCESS The intake at which the dose of vitamin D becomes toxic is not clear. The Institute of
Medicine (IOM) has defined the "tolerable upper intake level" (UL) for vitamin D as 100 micrograms
(4000 international units) daily for healthy adults and children 9 to 18 years [ 26]. This is also the UL for
pregnant and lactating women. The UL for infants and children up to nine years old is lower (table 2).
For patients with malabsorption (eg, celiac disease, gastrectomy, inflammatory bowel disease), oral
dosing of vitamin D depends upon the absorptive capacity of the individual patient. High doses of
vitamin D of 10,000 to 50,000 units daily may be necessary to replete vitamin D in some patients. Such
patients require careful monitoring to avoid toxicity. Indications for high dose vitamin D
supplementation and the UL for vitamin D supplementation are discussed in more detail separately.
(See "Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment", section on
'Dosing'.)
Vitamin D intoxication generally occurs after inappropriate use of vitamin D preparations. It may occur
in fad dieters who consume "megadoses" of supplements or in patients who take vitamin D
replacement therapy for malabsorption, renal osteodystrophy, osteoporosis, or psoriasis. Vitamin D
intoxication has been documented in adults taking more than 60,000 international units per day [ 41].
Case reports have described hypervitaminosis D due to errors in manufacturing, formulation or
prescription, including milk that was inadvertently excessively fortified with vitamin D [ 42,43].
Prolonged exposure of the skin to sunlight does not produce toxic amounts of vitamin D3
(cholecalciferol) because of photoconversion of previtamin D3 and vitamin D3 to inactive metabolites
[8,9]. Multiple studies reveal that prolonged exposure of the skin to sunlight results in a maximum
serum 25-hydroxyvitamin D (25[OH]D) level of <80 ng/ml (200 nmol/L) [7,44,45].
Symptoms of acute intoxication are due to hypercalcemia and include confusion, polyuria, polydipsia,
anorexia, vomiting, and muscle weakness. Chronic intoxication may cause nephrocalcinosis, bone
demineralization and pain. The diagnosis and treatment of vitamin D toxicity are reviewed separately.
(See "Diagnostic approach to hypercalcemia" and "Treatment of hypercalcemia".)
There is some feedback regulation of the hepatic 25-hydroxylase, and the liver has the capacity to
metabolize 25(OH)D to inactive metabolites. This is accomplished by the P-450 system and is enhanced
by alcohol, barbiturates, and phenytoin. However, it is insufficient to prevent vitamin D intoxication
following the ingestion of large amounts of vitamin D. The liver is the usual storage system for vitamin
D. When large amounts of vitamin D are ingested, much of the excess vitamin D is stored in adipose
tissue [46]. As these sites become saturated, the vitamin D remains in serum and is converted to toxic
levels of 25(OH)D [4]. (See "Etiology of hypercalcemia", section on 'Hypervitaminosis D'.)
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SUMMARY AND RECOMMENDATIONS
Very few foods naturally contain vitamin D; fatty fish and eggs are the exceptions. Dermal
synthesis and foods fortified with vitamin D are the major sources of the vitamin. (See 'Sources'
above.)
Vitamin D3 (cholecalciferol) is synthesized nonenzymatically in skin from 7-dehydrocholesterol
during exposure to the ultraviolet (UV) rays in sunlight. Vitamin D3 from the skin or diet must be 25hydroxylated in the liver, then 1-hydroxylated in the kidneys to the active form, 1,25dihydroxycholecalciferol (calcitriol) (figure 1). (See 'Metabolism' above.)
The Recommended Dietary Allowance (RDA) for vitamin D is 600 international units (units) daily for
adults through age 70 years and for children 1 to 18 years of age (table 2). For adults 71 years and
older, 800 units (20 micrograms) daily is recommended for the prevention and treatment of
osteoporosis. Vitamin D intake and effective sun exposure are often inadequate in older adults. In
older adults, particularly those at increased risk of falls and fracture, we suggest supplementation
with vitamin D (Grade 2B). We administer 600 to 800 international units daily. (See 'Requirements'
above and "Calcium and vitamin D supplementation in osteoporosis".)
Vitamin D deficiency can be caused by unusually low sun exposure combined with lack of vitamin
D-fortified foods or malabsorption. Alternatively, impaired hydroxylation of vitamin D in liver or
kidney can prevent metabolism into the physiologically active form. Rarely, genetic defects may
cause the end organs to be unresponsive to vitamin D, as in hereditary vitamin D-resistant rickets
(HVDRR). (See 'Deficiency and resistance' above and "Causes of vitamin D deficiency and
resistance".)
Vitamin D intoxication generally occurs after inappropriate use of vitamin D preparations. Prolonged
exposure of the skin to sunlight does not produce toxic amounts of vitamin D3 because of
photoconversion of previtamin D3 and vitamin D3 to inactive metabolites. Symptoms of acute
intoxication are due to hypercalcemia and include confusion, polyuria, polydipsia, anorexia, vomiting,
and muscle weakness. Long-term intoxication can cause bone demineralization and pain. In children,
the hypercalcemia can cause brain injury. (See 'Excess' above and "Diagnostic approach to
hypercalcemia" and "Treatment of hypercalcemia".)
The Institute of Medicine (IOM) has defined the "tolerable upper intake level" (UL) for vitamin D as
100 micrograms (4000 units) daily for healthy adults and children 9 to 18 years (table 2). The UL for
infants and children up to nine years old is lower. (See 'Excess' above.)
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REFERENCES
Forrest KY, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res 2011;
31:48.
2 http://books.nap.edu/openbook.php?record_id=13050 (Accessed on December 08, 2010).
Lowe KE, Maiyar AC, Norman AW. Vitamin D-mediated gene expression. Crit Rev Eukaryot Gene Expr 1992;
3
2:65.
4 DeLuca HF. Overview of general physiologic features and functions of vitamin D. Am J Clin Nutr 2004; 80:1689S.
5 Haddad JG. Vitamin D--solar rays, the Milky Way, or both? N Engl J Med 1992; 326:1213.
Terushkin V, Bender A, Psaty EL, et al. Estimated equivalency of vitamin D production from natural sun exposure
6 versus oral vitamin D supplementation across seasons at two US latitudes. J Am Acad Dermatol 2010;
62:929.e1.
Binkley N, Novotny R, Krueger D, et al. Low vitamin D status despite abundant sun exposure. J Clin Endocrinol
7
Metab 2007; 92:2130.
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