mineral
Zinc
Canonical supplement identityModeled ingredients
No ingredient relationship is modeled in this pilot.
Modeled forms
No form relationship is modeled in this pilot.
Evidence-grounded comparison · non-production preview
Review two canonical supplement records topic by topic, with evidence availability, source boundaries, and limitations kept explicit—without rankings or recommendations.
This comparison organizes two separately sourced supplement records. It describes evidence structure and availability without ranking supplements or recommending use.
Reference counts are descriptive. More references do not necessarily mean better or stronger evidence.
Identity boundaries
mineral
No ingredient relationship is modeled in this pilot.
No form relationship is modeled in this pilot.
vitamin
Source boundaries
Zinc — Fact Sheet for Health Professionals
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Vitamin D — Fact Sheet for Health Professionals
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Structural orientation
26 structural observations are available. Topic states remain visible in the aligned comparison below.
Topic-by-topic evidence
Evidence topic
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Washington, DC: National Academy Press; 2001.
Government reference · Population basis: unknown · Directness: not assessedRyu M-S, Aydemir TB. Zinc. In: Marriott BP, Birt DF, Stallings VA, Yates AA, eds. Present Knowledge in Nutrition. 11th ed. Cambridge, Massachusetts: Wiley-Blackwell; 2020:393-408.
Study type could not be determined · Population basis: unknown · Directness: not assessedKing JC, Cousins RJ. Zinc. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014:189-205.
Study type could not be determined · Population basis: unknown · Directness: not assessedMacDonald RS. The Role of Zinc in Growth and Cell Proliferation. The Journal of Nutrition 2000;130:1500S-8S. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedNagraj SK, Naresh S, Srinivas K, George RP, Shetty N, Levenson D, et al. Interventions for the managing taste disturbances. Cochrane Database Syst Rev 2017:CD010470. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedZinc, an essential mineral, is naturally present in some foods, added to others, and available as a dietary supplement. Zinc is also found in some cold lozenges, over-the-counter drugs sold as cold remedies, and some denture adhesive creams.
Zinc is involved in many aspects of cellular metabolism. It is required for the catalytic activity of hundreds of enzymes, and it plays a role in enhancing immune function, protein and DNA synthesis, wound healing, and cell signaling and division [1-4]. Zinc also supports healthy growth and development during pregnancy, infancy, childhood, and adolescence and is involved in the sense of taste [2,3,5].
The total amount of zinc in the body is approximately 1.5 grams (g) in women and 2.5 g in men [2]. Most of this zinc is stored in skeletal muscle and bone [1-3].
Zinc homeostasis is maintained through absorption of zinc from the diet, excretion into the gastrointestinal tract, and reabsorption in the gastrointestinal lumen [2,3]. In general, as zinc intakes rise, the amount of zinc absorbed also increases, but its fractional absorption drops [2,3].
Zinc — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessedNorman AW, Henry HH. Vitamin D. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition, 10th ed. Washington DC: Wiley-Blackwell, 2012.
Study type could not be determined · Population basis: unknown · Directness: not assessedJones G. Vitamin D. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease, 11th ed. Philadelphia: Lippincott Williams & Wilkins, 2014.
Study type could not be determined · Population basis: unknown · Directness: not assessedSilva MC, Furlanetto TW. Intestinal absorption of vitamin D: A systematic review. Nutr Rev 2018;76:60-76. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedVitamin 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].
Vitamin D — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Washington, DC: National Academy Press; 2001.
Government reference · Population basis: unknown · Directness: not assessedRyu M-S, Aydemir TB. Zinc. In: Marriott BP, Birt DF, Stallings VA, Yates AA, eds. Present Knowledge in Nutrition. 11th ed. Cambridge, Massachusetts: Wiley-Blackwell; 2020:393-408.
Study type could not be determined · Population basis: unknown · Directness: not assessedKing JC, Cousins RJ. Zinc. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014:189-205.
Study type could not be determined · Population basis: unknown · Directness: not assessedNations SP, Boyer PJ, Love LA, Burritt MF, Butz JA, Wolfe GI, et al. Denture cream: an unusual source of excess zinc, leading to hypocupremia and neurologic disease. Neurology 2008;71:639-43. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedDoherty K, Connor M, Cruickshank R. Zinc-containing denture adhesive: a potential source of excess zinc resulting in copper deficiency myelopathy. Br Dent J 2011;210:523-5. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedPlum LM, Rink L, Haase H. The essential toxin: impact of zinc on human health. Int J Environ Res Public Health 2010;7:1342-65. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedSpencer H, Norris C, Williams D. Inhibitory effects of zinc on magnesium balance and magnesium absorption in man. J Am Coll Nutr 1994;13:479-84. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedGetting excessive amounts of zinc can cause nausea, dizziness, headaches, gastric distress, vomiting, and loss of appetite. Doses of 50 mg of zinc or more over a period of weeks can inhibit copper absorption, reduce immune function, and lower high-density lipoprotein cholesterol levels; however, it is unlikely that a person would obtain this much zinc from food alone. The Tolerable Upper Intake Level for zinc is 40 mg for adults, and it ranges from 4 to 34 mg for infants, children, and adolescents, depending on age.
High zinc intakes can cause nausea, dizziness, headaches, gastric distress, vomiting, and loss of appetite [2,3]. If used for weeks, doses of 50 mg zinc or more—typically from supplements or excessive use of denture adhesive creams that contain zinc—can interfere with copper absorption (which can cause low copper status), reduce immune function, and lower HDL cholesterol levels [1-3,101]. The amount of zinc obtained from food is rarely as high as 50 mg, so the zinc in foods is unlikely to cause zinc toxicity. Very high doses of zinc from supplements (142 mg/day) might also interfere with magnesium absorption and disrupt magnesium balance [102].
According to a few reports, overuse of denture adhesive creams that contain up to 34 mg zinc per gram of product can lead to neurological symptoms (including sensory ataxia and myelopathy) and anemia. Zinc-free formulations are available to prevent these effects [2,20,21].
The FNB has established ULs for zinc from food and supplements for healthy individuals based on the levels of zinc that have an adverse effect on copper status (Table 3) [1]. The ULs do not apply to individuals who are receiving zinc for medical treatment, but such individuals should be under the care of a physician.
| Age | Male | Female | Pregnancy | Lactation |
|---|---|---|---|---|
| 0–6 months | 4 mg | 4 mg | ||
| 7–12 months | 5 mg | 5 mg | ||
| 1–3 years | 7 mg | 7 mg | ||
| 4–8 years | 12 mg | 12 mg | ||
| 9–13 years | 23 mg | 23 mg | ||
| 14–18 years | 34 mg | 34 mg | 34 mg | 34 mg |
| 19+ years | 40 mg | 40 mg | 40 mg | 40 mg |
Zinc — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessedGalior K, Grebe S, Singh R. Development of vitamin D toxicity from overcorrection of vitamin D deficiency: A review of case reports. Nutrients 2018, 10, 953. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedAuguste BL, Avila-Casado C, Bargman JM. Use of vitamin D drops leading to kidney failure in a 54-year-old man. CMAJ 2019;191:E390-4. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedVogiatzi MG, Jacobson-Dickman E, DeBoer MD. Vitamin D supplementation and risk of toxicity in pediatrics: A review of current literature. J Clin Endocrinol Metab 2014;99:1132-41. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSingh P, Trivedi N. Tanning beds and hypervitaminosis D: A case report. Ann Intern Med 2014;160:810-1. [PubMed abstract]
Case report · Population basis: unknown · Directness: not assessedLaurent MR, Gielen E, Pauwels S, Vanderschueren D, Bouillon R. Hypervitaminosis D associated with tanning bed use: A case report. Ann Intern Med 2017;166:155-6. [PubMed abstract]
Case report · Population basis: unknown · Directness: not assessedPerez-Castrillon JL, Vega G, Abad L, Sanz A, Chaves J, Hernandez G, Duenas A. Effects of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Am J Cardiol 2007;99:903-5. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedJackson RD, LaCroix AZ, Gass M, Wallace RB, Robbins J, Lewis CE, et al. Calcium plus vitamin D supplementation and the risk of fractures. N Engl J Med 2006;354:669-82. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedMalihi Z, Lawes CMM, Wu Z, Huang Y, Waayer D, Toop L, et al. Monthly high-dose vitamin D supplementation does not increase kidney stone risk or serum calcium: Results from a randomized controlled trial. Am J Clin Nutr 2019;109:1578-87. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessedMalihi Z, Wu Z, Stewart AW, Lawes CMM, Scragg R. Hypercalcemia, hypercalciuria, and kidney stones in long-term studies of vitamin D supplementation: A systematic review and meta-analysis. Am J Clin Nutr 2016;104:1039-51. [PubMed abstract]
Meta-analysis · Population basis: unknown · Directness: not assessedVitamin D toxicity can cause hypercalcemia, hypercalciuria, and high serum 25(OH)D concentrations; in extreme cases, it may lead to renal failure, calcification of soft tissues, cardiac arrhythmias, and death. Vitamin D toxicity is almost always a result of excessive intakes of vitamin D through supplements. Taking calcium supplements in combination with vitamin D supplements may increase the risk of certain adverse effects. The Tolerable Upper Intake Level for vitamin D ranges from 25 to 100 mcg (1,000–4,000 IU), depending on age.
Excess amounts of vitamin D are toxic. Because vitamin D increases calcium absorption in the gastrointestinal tract, vitamin D toxicity results in marked hypercalcemia (total calcium greater than 11.1 mg/dL, beyond the normal range of 8.4–10.2 mg/dL), hypercalciuria, and high serum 25(OH)D levels (typically >375 nmol/l [150 ng/mL]) [158]. Hypercalcemia, in turn, can lead to nausea, vomiting, muscle weakness, neuropsychiatric disturbances, pain, loss of appetite, dehydration, polyuria, excessive thirst, and kidney stones.
In extreme cases, vitamin D toxicity causes renal failure, calcification of soft tissues throughout the body (including in coronary vessels and heart valves), cardiac arrhythmias, and even death. Vitamin D toxicity has been caused by consumption of dietary supplements that contained excessive vitamin D amounts because of manufacturing errors, that were taken inappropriately or in excessive amounts, or that were incorrectly prescribed by physicians, [158-160].
Experts do not believe that excessive sun exposure results in vitamin D toxicity because thermal activation of previtamin D3 in the skin gives rise to various non-vitamin D forms that limit formation of vitamin D3. Some vitamin D3 is also converted to nonactive forms [1]. However, frequent use of tanning beds, which provide artificial UV radiation, can lead to 25(OH)D levels well above 375 to 500 nmol/L (150–200 ng/mL) [161-163].
The combination of high intakes of calcium (about 2,100 mg/day from food and supplements) with moderate amounts of vitamin D (about 19 mcg [765 IU]/day from food and supplements) increased the risk of kidney stones by 17% over 7 years among 36,282 postmenopausal women who were randomly assigned to take 1,000 mg/day calcium and 10 mcg (400 IU)/day vitamin D or a placebo [164]. However, other, shorter (from 24 weeks to 5 years) clinical trials of vitamin D supplementation alone or with calcium in adults found greater risks of hypercalcemia and hypercalciuria, but not of kidney stones [165,166].
The FNB established ULs for vitamin D in 2010 (Table 4) [1]. While acknowledging that signs and symptoms of toxicity are unlikely at daily intakes below 250 mcg (10,000 IU), the FNB noted that even vitamin D intakes lower than the ULs might have adverse health effects over time. The FNB recommended avoiding serum 25(OH)D levels above approximately 125 to 150 nmol/L (50–60 ng/mL), and it found that even lower serum levels (approximately 75–120 nmol/L [30–48 ng/mL]) are associated with increases in rates of all-cause mortality, risk of cancer at some sites (e.g., pancreas), risk of cardiovascular events, and number of falls and fractures among older adults.
| Age | Male | Female | Pregnancy | Lactation |
|---|---|---|---|---|
| 0–6 months | 25 mcg (1,000 IU) | 25 mcg (1,000 IU) | ||
| 7–12 months | 38 mcg (1,500 IU) | 38 mcg (1,500 IU) | ||
| 1–3 years | 63 mcg (2,500 IU) | 63 mcg (2,500 IU) | ||
| 4–8 years | 75 mcg (3,000 IU) | 75 mcg (3,000 IU) | ||
| 9–13 years | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | ||
| 14–18 years | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) |
| 19–50 years | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) |
| 51–70 years | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | ||
| >70 years | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) |
Vitamin D — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Donaldson M, Touger-Decker R. Vitamin and mineral supplements: friend or foe when combined with medications? J Am Dent Assoc 2014;145:1153-8. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedLomaestro BM, Bailie GR. Absorption interactions with fluoroquinolones. 1995 update. Drug Saf 1995;12:314-33. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedChen JC, Chuang CH, Wang JD, Wang CW. Combination therapy using chelating agent and zinc for Wilson's isease. J Med Biol Eng 2015;35:697-708. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSuliburska J, Skrypnik K, Szulinska M, Kupsz J, Markuszewski L, Bogdanski P. Diuretics, ca-antagonists, and angiotensin-converting enzyme inhibitors affect zinc status in hypertensive patients on monotherapy: a randomized trial. Nutrients 2018;10. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedZinc may interact with certain medications, such as quinolone antibiotics, tetracycline antibiotics, and penicillamine. In addition, some diuretics can decrease serum zinc concentrations by increasing zinc excretion in urine.
Zinc has the potential to interact with certain medications. In addition, several types of medications might adversely affect zinc levels. A few examples are provided below. Individuals who are taking these and other medications on a regular basis should discuss their zinc status with their health care providers.
Both quinolone antibiotics (such as Cipro) and tetracycline antibiotics (such as Achromycin and Sumycin) might interact with zinc in the gastrointestinal tract, which could inhibit the absorption of both zinc and the antibiotic if they are taken at the same time [103,104]. Taking the antibiotic at least 2 hours before or 4 to 6 hours after the zinc supplement minimizes this interaction [103].
Zinc can reduce the absorption and action of penicillamine, a drug used to treat rheumatoid arthritis and Wilson disease [105]. To minimize this interaction, people should take zinc supplements and penicillamine at least 1 hour apart.
Thiazide diuretics, such as chlorthalidone (e.g., Hygroton, Thalitone) and hydrochlorothiazide (e.g., Esidrix, HydroDIURIL), increase zinc excretion in the urine. This increased excretion, in turn, decreases serum zinc concentrations [106].
Zinc — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Gotfredsen A, Westergren Hendel H, Andersen T. Influence of orlistat on bone turnover and body composition. Int J Obes Relat Metab Disord 2001;25:1154-60. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedJames WP, Avenell A, Broom J, Whitehead J. A one-year trial to assess the value of orlistat in the management of obesity. Int J Obes Relat Metab Disord 1997;21:S24-30. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedMcDuffie JR, Calis KA, Booth SL, Uwaifo GI, Yanovski JA. Effects of orlistat on fat-soluble vitamins in obese adolescents. Pharmacotherapy 2002;22:814-22. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedRobien K, Oppeneer SJ, Kelly JA, Hamilton-Reeves JM. Drug-vitamin D interactions: A systematic review of the literature. Nutr Clin Pract 2013;28:194-208. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedSchwartz JB. Effects of vitamin D supplementation in atorvastatin-treated patients: A new drug interaction with an unexpected consequence. Clin Pharmacol Ther 2009;85:198-203. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedPerez-Castrillon JL, Vega G, Abad L, Sanz A, Chaves J, Hernandez G, Duenas A. Effects of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Am J Cardiol 2007;99:903-5. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedAloia JF, Li-Ng M, Pollack S. Statins and vitamin D. Am J Cardiol 2007;100:1329. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedBuckley LM, Leib ES, Cartularo KS, Vacek PM, Cooper SM. Calcium and vitamin D3 supplementation prevents bone loss in the spine secondary to low-dose corticosteroids in patients with rheumatoid arthritis. A randomized, double-blind, placebo-controlled trial. Ann Intern Med 1996;125:961-8. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedde Sevaux RGL, Hoitsma AJ, Corstens FHM, Wetzels JFM. Treatment with vitamin D and calcium reduces bone loss after renal transplantation: a randomized study. J Am Soc Nephrol 2002;13:1608-14. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessedLukert BP, Raisz LG. Glucocorticoid-induced osteoporosis: pathogenesis and management. Ann Intern Med 1990;112:352-64. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSkversky AL, Kumar J, Abramowitz MK, Kaskel FJ, Melamed ML. Association of glucocorticoid use and low 25-hydroxyvitamin D levels: Results from the National Health and Nutrition Examination Survey (NHANES): 2001-2006. J Clin Endocrinol Metab 2011;96:3838-45. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedDrinka PJ, Nolten WE. Hazards of treating osteoporosis and hypertension concurrently with calcium, vitamin D, and distal diuretics. J Am Geriatr Soc 1984;32:405-7. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedCrowe M, Wollner L, Griffiths RA. Hypercalcaemia following vitamin D and thiazide therapy in the elderly. Practitioner 1984;228:312-3. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedVitamin D supplements may interact with medications, and some medications may affect vitamin D levels. These medications include orlistat, statins, steroids, and thiazide diuretics.
Vitamin D supplements may interact with several types of medications. A few examples are provided below. Individuals taking these and other medications on a regular basis should discuss their vitamin D intakes and status with their health care providers.
The weight-loss drug orlistat (Xenical and alli), together with a reduced-fat diet, can reduce the absorption of vitamin D from food and supplements, leading to lower 25(OH)D levels [167-170].
Statin medications reduce cholesterol synthesis. Because endogenous vitamin D is derived from cholesterol, statins may also reduce vitamin D synthesis [170]. In addition, high intakes of vitamin D, especially from supplements, might reduce the potency of atorvastatin (Lipitor), lovastatin (Altoprev and Mevacor), and simvastatin (FloLipid and Zocor), because these statins and vitamin D appear to compete for the same metabolizing enzyme [170-173].
Corticosteroid medications, such as prednisone (Deltasone, Rayos, and Sterapred), are often prescribed to reduce inflammation. These medications can reduce calcium absorption and impair vitamin D metabolism [174-176]. In the NHANES 2001–2006 survey, 25(OH)D deficiency (less than 25 nmol/L [10 ng/mL]) was more than twice as common among children and adults who reported oral steroid use (11%) than in nonusers (5%) [177].
Thiazide diuretics (e.g., Hygroton, Lozol, and Microzide) decrease urinary calcium excretion. The combination of these diuretics with vitamin D supplements (which increase intestinal calcium absorption) might lead to hypercalcemia, especially among older adults and individuals with compromised renal function or hyperparathyroidism [170,178,179].
Vitamin D — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Office of Dietary Supplements, National Institutes of Health. Dietary Supplement Label Database. 2021.
Study type could not be determined · Population basis: unknown · Directness: not assessedBrnic M, Wegmuller R, Melse-Boonstra A, Stomph T, Zeder C, Tay FM, et al. Zinc absorption by adults is similar from intrinsically labeled zinc- biofortified rice and from rice fortified with labeled zinc sulfate. J Nutr 2016;146:76-80. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedWegmuller R, Tay F, Zeder C, Brnic M, Hurrell RF. Zinc absorption by young adults from supplemental zinc citrate is comparable with that from zinc gluconate and higher than from zinc oxide. J Nutr 2014;144:132-6. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedSolomons NW. Competitive interaction of iron and zinc in the diet: consequences for human nutrition. J Nutr 1986;116:927-35. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedWhittaker P. Iron and zinc interactions in humans. Am J Clin Nutr 1998;68:442s-6s. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedEuropean Food Safety Authority. Scientific Opinion on Dietary Reference Values for zinc. 2014.
Study type could not be determined · Population basis: unknown · Directness: not assessedArredondo M, Martínez R, Núñez MT, Ruz M, Olivares M. Inhibition of iron and copper uptake by iron, copper and zinc. Biol Res 2006;39:95-102. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedForms of zinc that are commonly found in dietary supplements include zinc sulfate, zinc acetate, and zinc gluconate. Taking supplements that contain a substantial amount of iron (≥25 mg) at the same time as zinc supplements can reduce zinc absorption and plasma concentrations of zinc.
Zinc is available in supplements that only contain zinc, supplements that contain zinc in combination with other ingredients, and in many multivitamin/mineral products [13]. Supplements can contain any of a variety of forms of zinc, including zinc sulfate, zinc acetate, and zinc gluconate [14]. The Supplement Facts panel on a dietary supplement label declares the amount of elemental zinc in the product, not the weight of the entire zinc-containing compound.
Absorption of zinc from supplements that contain zinc citrate or zinc gluconate is similar, at approximately 61% in young adults; the absorption from supplements that contain zinc oxide is 50% [15]. Taking supplements containing 25 mg elemental iron or more at the same time as zinc supplements can reduce zinc absorption and plasma zinc concentrations [16-19]. However, the iron added to enriched or fortified foods does not significantly interfere with zinc absorption because the chemical form of iron used in fortification is typically poorly soluble in the gut and does not compete strongly with zinc for absorpion.
Zinc — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Silva MC, Furlanetto TW. Intestinal absorption of vitamin D: A systematic review. Nutr Rev 2018;76:60-76. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedHolick MF. Vitamin D deficiency. N Engl J Med 2007;357:266-81. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedHirsch AL. Industrial Aspects of Vitamin D. In: Feldman D, Pike JW, Adams JS, eds. Vitamin D. 3rd ed. Academic Press; 2011:73-93.
Study type could not be determined · Population basis: unknown · Directness: not assessedNational Institutes of Health. Dietary Supplement Label Database. 2020.
Study type could not be determined · Population basis: unknown · Directness: not assessedTripkovic L, Lambert H, Hart K, Smith CP, Bucca G, Penson S, et al. Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: A systematic review and meta-analysis. Am J Clin Nutr 2012;95:1357-64. [PubMed abstract]
Meta-analysis · Population basis: unknown · Directness: not assessedLehmann U, Hirche F, Stangl GI, Hinz K, Westphal S, Dierkes J. Bioavailability of vitamin D2 and D3 in healthy volunteers, a randomised placebo-controlled trial. J Clin Endocrin Metab 2013;98:4339-45. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedLogan VF, Gray AR, Peddie MC, Harper MJ, Houghton LA. Long-term vitamin D3 supplementation is more effective than vitamin D2 in maintaining serum 25-hydroxyvitamin D status over the winter months. Br J Nutr 2013;109:1082-8. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedTripkovic L, Wilson LR, Hart K, Johnsen S, de Lusignan S, Smith CP, et al. Daily supplementation with 15 µg vitamin D2 compared with vitamin D3 to increase wintertime 25-hydroxyvitamin D status in healthy South Asian and white European women: A 12-wk randomized, placebo-controlled food-fortification trial. Am J Clin Nutr 2017;106:481-90. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedGraeff-Armas LA, Bendik I, Kunz I, Schoop R, Hull S, Beck M. Supplemental 25-hydroxycholecalciferol is more effective than cholecalciferol in raising serum 25-hydroxyvitamin D concentrations in older adults. J Nutr 2020;150:73-81. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedQuesada-Gomez JM, Bouillon R. Is calcifediol better than cholecalciferol for vitamin D supplementation? Osteoporos Int 2018;29:1697-1711. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedVitamin 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 — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Washington, DC: National Academy Press; 2001.
Government reference · Population basis: unknown · Directness: not assessedThe Food and Nutrition Board at the National Academies of Sciences, Engineering, and Medicine has established Recommended Dietary Allowances and Adequate Intakes for zinc. These values range from 8 to 12 mg for adults and from 2 to 13 mg for infants, children, and adolescents, depending on age, sex, and life stage.
Intake recommendations for zinc and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and Medicine [1]. DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values include the following:
Table 1 lists the current zinc RDAs. For infants from birth to 6 months, the FNB established an AI for zinc that is equivalent to the mean intake of zinc in healthy, breastfed infants.
| Age | Male | Female | Pregnancy | Lactation |
|---|---|---|---|---|
| 0–6 months* | 2 mg | 2 mg | ||
| 7–12 months | 3 mg | 3 mg | ||
| 1–3 years | 3 mg | 3 mg | ||
| 4–8 years | 5 mg | 5 mg | ||
| 9–13 years | 8 mg | 8 mg | ||
| 14–18 years | 11 mg | 9 mg | 12 mg | 13 mg |
| 19+ years | 11 mg | 8 mg | 11 mg | 12 mg |
*Adequate Intake (AI)
Zinc — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessedSempos CT, Binkley N. 25-hydroxyvitamin D assay standardisation and vitamin D guidelines paralysis. Public Health Nutrition 2020;23:1153-64. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedDemay MB, Pittas AG, Bikle DD, Diab DL, Kiely ME, et al. Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1907-1947. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedShah VP, Nayfeh T, Alsawaf Y, Saadi S, Farah M, et al. A Systematic Review Supporting the Endocrine Society Clinical Practice Guidelines on Vitamin D. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1961-1974. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedBouillon R. Comparative analysis of nutritional guidelines for vitamin D. Nat Rev Endocrinol 2017;13:466-79. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedScientific Advisory Committee on Nutrition. Vitamin D and Health. 2016.
Study type could not be determined · Population basis: unknown · Directness: not assessedThe 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.
Intake recommendations for vitamin D and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by expert committees of NASEM [1]. DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values include the following:
The FNB established RDAs for vitamin D to indicate daily intakes sufficient to maintain bone health and normal calcium metabolism in healthy people. RDAs for vitamin D are listed in both micrograms (mcg) and International Units (IU); 1 mcg vitamin D is equal to 40 IU (Table 2). Even though sunlight is a major source of vitamin D for some people, the FNB based the vitamin D RDAs on the assumption that people receive minimal sun exposure [1]. For infants from birth to 12 months, the FNB developed AIs based on the amount of vitamin D that maintains serum 25(OH)D levels above 20 ng/mL (50 nmol/L) and supports bone development.
| 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) |
Many other countries around the world and some professional societies have somewhat different guidelines for vitamin D intakes [15]. These differences are a result of an incomplete understanding of the biology and clinical implications of vitamin D, different purposes for the guidelines (e.g., for public health in a healthy population or for clinical practice), and/or the use in some guidelines of observational studies in addition to randomized clinical trials to establish recommendations [9,15]. For example, the United Kingdom Scientific Advisory Committee on Nutrition recommends intakes of 10 mcg (400 IU)/day for individuals age 4 years and older [16]. The Endocrine Society recommends routine vitamin D supplementation for children and teens age 1 to 18 years, pregnant women, adults with pre-diabetes, and adults age 75 years and older, but not for healthy adults age 19 to 74 [11,12]. The Endocrine Society does not recommend specific doses but notes that all individuals should adhere to the RDA.
Vitamin D — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Washington, DC: National Academy Press; 2001.
Government reference · Population basis: unknown · Directness: not assessedRyu M-S, Aydemir TB. Zinc. In: Marriott BP, Birt DF, Stallings VA, Yates AA, eds. Present Knowledge in Nutrition. 11th ed. Cambridge, Massachusetts: Wiley-Blackwell; 2020:393-408.
Study type could not be determined · Population basis: unknown · Directness: not assessedKing JC, Cousins RJ. Zinc. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014:189-205.
Study type could not be determined · Population basis: unknown · Directness: not assessedBailey RL, Pac SG, Fulgoni VL, 3rd, Reidy KC, Catalano PM. Estimation of total usual dietary intakes of pregnant women in the United States. JAMA Netw Open 2019;2:e195967. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedSiva S, Rubin DT, Gulotta G, Wroblewski K, Pekow J. Zinc deficiency is associated with poor clinical outcomes in patients with inflammatory bowel disease. Inflamm Bowel Dis 2017;23:152-7. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedEhrlich S, Mark AG, Rinawi F, Shamir R, Assa A. Micronutrient Deficiencies in Children With Inflammatory Bowel Diseases. Nutr Clin Pract 2020;35:315-22. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedWierdsma NJ, van Bokhorst-de van der Schueren MA, Berkenpas M, Mulder CJ, van Bodegraven AA. Vitamin and mineral deficiencies are highly prevalent in newly diagnosed celiac disease patients. Nutrients 2013;5:3975-92. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedRondanelli M, Faliva MA, Gasparri C, Peroni G, Naso M, Picciotto G, et al. Micronutrients dietary supplementation advices for celiac patients on long-term gluten-free diet with good compliance: a review. Medicina (Kaunas) 2019;55. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedBakaloudi DR, Halloran A, Rippin HL, Oikonomidou AC, Dardavesis TI, Williams J, et al. Intake and adequacy of the vegan diet. A systematic review of the evidence. Clin Nutr 2021;40:3503-21. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedFoster M, Chu A, Petocz P, Samman S. Effect of vegetarian diets on zinc status: a systematic review and meta- analysis of studies in humans. J Sci Food Agric 2013;93:2362-71. [PubMed abstract]
Systematic review · Population basis: human · Directness: not assessedAgnoli C, Baroni L, Bertini I, Ciappellano S, Fabbri A, Papa M, et al. Position paper on vegetarian diets from the working group of the Italian Society of Human Nutrition. Nutr Metab Cardiovasc Dis 2017;27:1037-52. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedFoster M, Samman S. Vegetarian diets across the lifecycle: impact on zinc intake and status. Adv Food Nutr Res 2015;74:93-131. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedWilson RL, Grieger JA, Bianco-Miotto T, Roberts CT. Association between maternal zinc status, dietary zinc intake and pregnancy complications: a systematic review. Nutrients 2016;8. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedHe L, Lang L, Li Y, Liu Q, Yao Y. Comparison of serum zinc, calcium, and magnesium concentrations in women with pregnancy-induced hypertension and healthy pregnant women: A meta- analysis. Hypertens Pregnancy 2016;35:202-9. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedOta E, Mori R, Middleton P, Tobe-Gai R, Mahomed K, Miyazaki C, et al. Zinc supplementation for improving pregnancy and infant outcome. Cochrane Database Syst Rev 2015:Cd000230. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedBzikowska-Jura A, Sobieraj P, Michalska-Kacymirow M, Wesołowska A. Investigation of iron and zinc concentrations in human milk in correlation to maternal factors: an observational pilot study in Poland. Nutrients 2021;13:303. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedKeikha M, Shayan-Moghadam R, Bahreynian M, Kelishadi R. Nutritional supplements and mother's milk composition: a systematic review of interventional studies. Int Breastfeed J 2021;16:1. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedAumeistere L, Ciproviča I, Zavadska D, Bavrins K, Borisova A. Zinc content in breast milk and its association with maternal diet. Nutrients 2018;10. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedAbe SK, Balogun OO, Ota E, Takahashi K, Mori R. Supplementation with multiple micronutrients for breastfeeding women for improving outcomes for the mother and baby. Cochrane Database Syst Rev 2016;2:Cd010647. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedKatayama K, Hosui A, Sakai Y, Itou M, Matsuzaki Y, Takamori Y, et al. Effects of zinc acetate on serum zinc concentrations in chronic liver diseases: a multicenter, double-blind, randomized, placebo-controlled trial and a dose adjustment trial. Biol Trace Elem Res 2020;195:71-81. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessedAckland ML, Michalczyk AA. Zinc and infant nutrition. Arch Biochem Biophys 2016;611:51-7. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedMartyres DJ, Vijenthira A, Barrowman N, Harris-Janz S, Chretien C, Klaassen RJ. Nutrient insufficiencies/deficiencies in children with sickle cell disease and its association with increased disease severity. Pediatr Blood Cancer 2016;63:1060-4. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedSwe KM, Abas AB, Bhardwaj A, Barua A, Nair NS. Zinc supplements for treating thalassaemia and sickle cell disease. Cochrane Database Syst Rev 2013:Cd009415. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSkalny AV, Skalnaya MG, Grabeklis AR, Skalnaya AA, Tinkov AA. Zinc deficiency as a mediator of toxic effects of alcohol abuse. Eur J Nutr 2018;57:2313-22. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedKang YJ, Zhou Z. Zinc prevention and treatment of alcoholic liver disease. Mol Aspects Med 2005;26:391-404. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedMcClain C, Vatsalya V, Cave M. Role of zinc in the development/progression of alcoholic liver disease. Curr Treat Options Gastroenterol 2017;15:285-95. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedNavarro S, Valderrama R, To-Figueras J, Gimenez A, Lopez JM, et al. Role of zinc in the process of pancreatic fibrosis in chronic alcoholic pancreatitis. Pancreas 1994;9:270-74. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedMenzano E, Carlen PL. Zinc deficiency and corticosteroids in the pathogenesis of alcoholic brain dysfunction--a review. Alcohol Clin Exp Res 1994;18:895-901. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedCertain groups of people are more likely than others to have zinc inadequacy. These include people with gastrointestinal disorders and those who have had bariatric surgery, people who follow vegetarian or vegan diets, and women who are pregnant or lactating. In addition, infants who are exclusively breastfed after 6 months of age and children with sickle cell disease have a higher risk of zinc inadequacy, as do people with alcohol use disorder.
The following groups are among those most likely to have inadequate zinc status.
Zinc inadequacy is common in people with inflammatory bowel disease (IBD, which includes ulcerative colitis and Crohn’s disease) and those who have had bariatric surgery that involved a resection of the gastrointestinal tract. This is due to poor dietary intake, decreased zinc absorption, or increased urinary excretion as a result of inflammation [31,32]. Approximately 15% to 40% of people with IBD have zinc deficiency during active disease states and while in remission [31,32]. In patients with zinc deficiency, the risk of IBD-related symptoms (e.g., anemia, hemorrhage, abdominal or perianal fistula) increases, and these patients are more likely to need hospitalization or surgery. Zinc supplementation might reduce these risks [31].
Approximately 50% of people with newly diagnosed celiac disease have a high risk of zinc inadequacy or deficiency; potential contributors to this risk might include zinc malabsorption and mucosal inflammation [33,34]. These deficiencies sometimes persist even when people with celiac disease avoid foods containing gluten [34].
The bioavailability of zinc from vegetarian diets is often lower than from nonvegetarian diets because people who follow vegetarian diets typically eat large amounts of legumes and whole grains, which contain phytates that bind zinc and inhibit its absorption [2]. In addition, meat is high in bioavailable zinc [35]. As a result, people who follow vegetarian diets and vegan diets usually have lower dietary intakes of zinc and lower serum zinc levels than those who include animal products in their diet [36].
People who follow vegetarian or vegan diets might benefit from using certain food preparation techniques that reduce the binding of zinc by phytates and increase its bioavailability, such as soaking beans, grains, and seeds in water for several hours before cooking them [37]. Canned and pre-cooked items are another option. In addition, organic acids in fermented foods might increase zinc absorption [37]. People who follow vegetarian or vegan diets might also benefit from zinc supplements [38].
During pregnancy, the amount of zinc needed increases to accommodate fetal growth, and the FNB therefore recommends that pregnant women consume 3 mg/day more zinc than nonpregnant women in the same age group [1,3]. Similarly, the zinc requirement increases by 4 mg/day during lactation.
NHANES data from 2001 to 2014 show that 11% of pregnant women in the United States have total zinc intakes from foods and supplements that are below the EAR [25]. Low serum zinc concentrations during pregnancy might increase the risk of preeclampsia and low-birthweight infants [39,40]. Routine zinc supplementation during pregnancy does not appear to reduce the risk of low birthweight, stillbirth, or neonatal death, but it might lower the risk of preterm birth [41].
During lactation, some [42,43] but not all [44] studies show that adequate intakes of foods rich in zinc increase concentrations of the mineral in breast milk. Evidence is also conflicting on whether zinc supplementation during lactation increases the zinc content of breast milk [45,46].
Zinc concentrations in breast milk peak during the first month after birth and then decline by approximately 75% by the ninth month [3]. Because of this sharp drop, human breast milk alone is not sufficient to meet the infant’s zinc requirement after age 6 months [3,47]. The FNB recommends that in addition to breast milk, infants age 7 to 12 months consume age-appropriate foods or formula that contains zinc [1].
Children with sickle cell disease (SCD) have a high risk of zinc insufficiency or deficiency, possibly as a result of the chelation therapy used to treat iron overload [3,48]. Children with SCD and low zinc status often are shorter and weigh less than age-matched peers, and they also have a higher risk of maturation delays, vaso-occlusive pain crises (blockages of blood flow to an area of the body), and associated hospitalizations [48]. Supplemental zinc might enhance growth in children with SCD and decrease the risk of bacterial infections, hospitalizations, and vaso-occlusive pain crises [3,48,49].
Low zinc status has been observed in 30% to 50% of people with alcohol use disorder [1,50]. Ethanol consumption decreases intestinal absorption of zinc and increases urinary zinc excretion [1,50,51,52]. In addition, the variety and amount of food consumed by many people with alcohol use disorder is limited, leading to inadequate zinc intake [53,54].
Zinc — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessedSilva MC, Furlanetto TW. Intestinal absorption of vitamin D: A systematic review. Nutr Rev 2018;76:60-76. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedBrown LL, Cohen B, Tabor D, Zappala G, Maruvada P, Coates PM. The vitamin D paradox in Black Americans: A systems-based approach to investigating clinical practice, research, and public health—expert panel meeting report. BMC Proceedings, 2018;12(Suppl 6):6. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedPicciano MF. Nutrient composition of human milk. Pediatr Clin North Am 2001;48:53-67. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedWagner CL, Greer FR, American Academy of Pediatrics Section on Breastfeeding, American Academy of Pediatrics Committee on Nutrition. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Pediatrics 2008;122:1142-52. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedDawodu A, Tsang RC. Maternal vitamin D status: Effect on milk vitamin D content and vitamin D status of breastfeeding infants. Adv Nutr 2012;3:353-61. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedDavis CD, Dwyer JT. The 'sunshine vitamin': benefits beyond bone? J Natl Cancer Inst 2007;99:1563-5. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSimon AE, Ahrens KA. Adherence to vitamin D intake guidelines in the United States. Pediatrics 2020;145:e20193574. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedChalcraft JR, Cardinal LM, Wechsler PJ, Hollis BW, Gerow KG, Alexander BM, et al. Vitamin D synthesis following a single bout of sun exposure in older and younger men and women. Nutrients 2020; 12, 2237; doi:10.3390/nu12082237. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedSowah D, Fan X, Dennett L, Hagtvedt R, Straube S. Vitamin D levels and deficiency with different occupations: A systematic review. BMC Public Health 2017;17:519. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedPappa HM, Bern E, Kamin D, Grand RJ. Vitamin D status in gastrointestinal and liver disease. Curr Opin Gastroenterol 2008;24:176-83. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedDrincic A, Fuller E, Heaney RP, Armas LAG. 25-hydroxyvitamin D response to graded vitamin D3 supplementation among obese adults. J Clin Endocrinol Metab 2013;98:4845-51. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedEkwaru JP, Zwicker JD, Holick MF, Giovannucci E, Veugelers PJ. The importance of body weight for the dose response relationship of oral vitamin D supplementation and serum 25-hydroxyvitamin D in healthy volunteers. PLOS ONE 2014;9:e111265. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedChakhtoura M, Rahme M, Fuleihan E-H. Vitamin D metabolism in bariatric surgery. Endocrinol Metab Clin North Am 2017;46:947-82. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedPeterson L, Zeng X, Caufield-Noll CP, Schweitzer MA, Magnuson TH, Steele KE. Vitamin D status and supplementation before and after bariatric surgery: A comprehensive literature review. Surg Obes Relat Dis 2016;12:693-702. [PubMed abstract]
Narrative review · Population basis: unknown · Directness: not assessedChakhtoura MT, Nakhoul N, Akl EA, Mantzoros CS, El Hajj Guleihan GA. Guidelines on vitamin D replacement in bariatric surgery? Identification and systematic appraisal. Metabolism 2016;65:586-97. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedCertain 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.
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].
Although UVB exposure can produce vitamin D in infants, the American Academy of Pediatrics (AAP) advises parents to keep infants younger than 6 months out of direct sunlight, dress them in protective clothing and hats, and apply sunscreen on small areas of exposed skin when sun exposure is unavoidable [59]. The AAP recommends 10 mcg (400 IU)/day vitamin D supplements for exclusively and partially breastfed infants starting shortly after birth and lasting until they are weaned and consume at least 1,000 mL/day vitamin D-fortified formula or whole milk [57]. The AAP also recommends 10 mcg (400 IU)/day supplemental vitamin D for all infants who are not breastfed and ingest less than 1,000 mL/day vitamin D-fortified formula or milk. An analysis of NHANES 2009–2016 data found that only 20.5% of breastfed infants and 31.1% of infants who were not breastfed ingested these recommended amounts of supplements [60].
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].
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].
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).
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].
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 — Fact Sheet for Health Professionals
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Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Washington, DC: National Academy Press; 2001.
Government reference · Population basis: unknown · Directness: not assessedRyu M-S, Aydemir TB. Zinc. In: Marriott BP, Birt DF, Stallings VA, Yates AA, eds. Present Knowledge in Nutrition. 11th ed. Cambridge, Massachusetts: Wiley-Blackwell; 2020:393-408.
Study type could not be determined · Population basis: unknown · Directness: not assessedKing JC, Cousins RJ. Zinc. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014:189-205.
Study type could not be determined · Population basis: unknown · Directness: not assessedHennigar SR, Lieberman HR, Fulgoni VL, 3rd, McClung JP. Serum Zinc Concentrations in the US population are related to sex, age, and time of blood draw but not dietary or supplemental zinc. J Nutr 2018;148:1341-51. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSerum or plasma zinc concentrations are often used to assess zinc status, and concentrations in healthy people typically range from 80 to 120 mcg/dL. However, these measures have important limitations. For example, zinc concentrations in serum can be affected by age, sex, and time of day, and they do not always correlate with dietary or supplemental zinc intakes.
Serum or plasma zinc concentrations are typically used in clinical practice to assess zinc status. In healthy people, the amount of zinc in serum or plasma is 80 to 120 micrograms/deciliter (mcg/dL) (12 to 18 micromoles/liter [mcmol/L]) [2]. Serum zinc concentrations below 70 mcg/dL in women and 74 mcg/dL in men indicate inadequate zinc status. However, both serum and plasma measures have important limitations. Zinc concentrations in serum are associated with the patient’s sex and age as well as the time of the blood draw (morning vs. evening) and do not always correlate with dietary or supplemental zinc intakes [6]. Zinc concentrations also fluctuate in response to other factors, including infections, changes in steroid hormones, and muscle catabolism during weight loss or illness [1,3]. When assessing a patient's zinc status, clinicians also consider risk factors for zinc deficiency, such as inadequate caloric intake, chronic alcohol use, and malabsorptive digestive diseases, as well as signs of zinc deficiency, such as impaired growth in infants and children [1].
Zinc — Fact Sheet for Health Professionals
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Source attribution does not imply NIH or ODS endorsement of MEDucated.
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessedNorman AW, Henry HH. Vitamin D. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition, 10th ed. Washington DC: Wiley-Blackwell, 2012.
Study type could not be determined · Population basis: unknown · Directness: not assessedJones G. Vitamin D. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease, 11th ed. Philadelphia: Lippincott Williams & Wilkins, 2014.
Study type could not be determined · Population basis: unknown · Directness: not assessedSempos CT, Heijboer AC, Bikle DD, Bollerslev J, Bouillon R, Brannon PM, et al. Vitamin D assays and the definition of hypovitaminosis D. Results from the First International Conference on Controversies in Vitamin D. Br J Clin Pharmacol 2018;84:2194-207. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedLeFevre ML. Screening for vitamin deficiency in adults: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2015;162:133-40. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedBrooks SPJ, Sempos CT. The importance of 25-hydroxyvitamin D assay standardization and the Vitamin D Standardization Program. Journal of AOAC International 2017;100:1223-4.
Study type could not be determined · Population basis: unknown · Directness: not assessedTaylor CL, Sempos CT, Davis CD, Brannon PM. Vitamin D: moving forward to address emerging science. Nutrients 2017, 9, 1308; doi:10.3390/mu9121308. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSempos CT, Binkley N. 25-hydroxyvitamin D assay standardisation and vitamin D guidelines paralysis. Public Health Nutrition 2020;23:1153-64. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedOffice of Dietary Supplements, National Institutes of Health. Vitamin D Standardization Program (VDSP).
Study type could not be determined · Population basis: unknown · Directness: not assessedDemay MB, Pittas AG, Bikle DD, Diab DL, Kiely ME, et al. Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1907-1947. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedShah VP, Nayfeh T, Alsawaf Y, Saadi S, Farah M, et al. A Systematic Review Supporting the Endocrine Society Clinical Practice Guidelines on Vitamin D. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1961-1974. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedHolick MF. Vitamin D deficiency. N Engl J Med 2007;357:266-81. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedBrown LL, Cohen B, Tabor D, Zappala G, Maruvada P, Coates PM. The vitamin D paradox in Black Americans: A systems-based approach to investigating clinical practice, research, and public health—expert panel meeting report. BMC Proceedings, 2018;12(Suppl 6):6. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSerum 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).
Serum concentration of 25(OH)D is currently the main indicator of vitamin D status. It reflects vitamin D produced endogenously and that obtained from foods and supplements [1]. In serum, 25(OH)D has a fairly long circulating half-life of 15 days [1]. Serum concentrations of 25(OH)D are reported in both nanomoles per liter (nmol/L) and nanograms per milliliter (ng/mL). One nmol/L is equal to 0.4 ng/mL, and 1 ng/mL is equal to 2.5 nmol/L.
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. |
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.
Vitamin D — Fact Sheet for Health Professionals
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