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Quest Diagnostics

Vitamin D Testing

Test code(s) 17306, 92888, 91935

Vitamin D is a fat-soluble prohormone, 2 forms of which are relevant to human nutrition: vitamin D3 (also known as cholecalciferol) and vitamin D2 (ergocalciferol). Vitamin D3 is produced in sunlight-exposed skin, from the conversion of 7-dehydrocholesterol. Vitamin D2 is derived from sunlight acting on fungal and plant sources. Despite the fact that the biological activities of vitamins D3 and D2 are comparable, a meta-analysis showed that vitamin D3 supplementation is more efficacious at raising serum levels than vitamin D2 supplementation.

Both vitamin D3 and D2 are converted to 25-hydroxy vitamin D (25[OH]D) (calcidiol) in the liver by the enzyme CYP2R1. 25(OH)D is later hydroxylated to 1,25-dihydroxy vitamin D (1,25[OH]2D) (calcitriol) in kidneys by the enzyme CYP27B1. Both 25(OH)D and 1,25(OH)2D are degraded into inactive metabolites by CYP24A1, an enzyme with 24-hydroxylase activity.

Mutations that inactivate the enzymes regulating vitamin D metabolism can cause serious abnormalities. Inactivation of CYP2R1 or CYP27B1 leads to rickets,2,3 and inactivation of CYP24A1 leads to idiopathic infantile hypercalcemia in children and recurrent kidney stone formation in adults.4

25(OH)D has a circulating half-life of 2 to 3 weeks and is the major circulating form of vitamin D. It is the best indicator for monitoring vitamin D status in patients not suffering from renal disease.1

1,25(OH)2D is the biologically active form of vitamin D. It has a circulating half-life of approximately 4 hours and circulates at one one-thousandth the concentration of 25(OH)D. Thus, serum 1,25(OH)2D does not reflect vitamin D reserves, and measurement of 1,25(OH)2D is not useful for monitoring the vitamin D status of most patients. Serum levels are tightly regulated by serum levels of parathyroid hormone (PTH), calcium, and phosphate.1 Serum 1,25(OH)2D is frequently either normal or even elevated in those with vitamin D deficiency, due to secondary hyperparathyroidism.1

Measurement of 1,25(OH)2D is useful only for patients with disorders of 25(OH)D and phosphate metabolism. Disorders include chronic kidney disease, hereditary phosphate-losing disorders, oncogenic osteomalacia, pseudovitamin D-deficiency rickets, vitamin D-resistant rickets, and chronic granuloma-forming disorders, such as sarcoidosis and some lymphomas.1

The active form of vitamin D, 1,25(OH)2D, is critical for maintaining healthy calcium and phosphorus levels, thus helping the body form and maintain strong bones. Calcitriol helps regulate plasma calcium by acting synergistically with parathyroid hormone (PTH) to enhance (1) renal calcium reabsorption, (2) intestinal calcium and phosphate absorption, and (3) the release of calcium stores out of the bone. Calcitriol also increases reabsorption of phosphate in the kidney, while PTH stimulates phosphate excretion. Calcitriol also modulates neuromuscular, immune, and other cellular functions.

The reference range of vitamin D levels is controversial.1,5,6,7 According to different professional societies, vitamin D sufficiency ranges between >20 ng/dL5,6  to ≥30 ng/dL.1,7,8  In line with the Endocrine Society,1 the National Osteoporosis Foundation,8 and the American Geriatric Society,7 Quest defines vitamin D sufficiency as a value of ≥30 ng/dL.  

According to National Health and Nutrition Examination Survey (NHANES) data, 42% of the US population has a vitamin D level of <20 ng/mL, qualifying for vitamin D deficiency.9

The different causes of Vitamin D deficiency are classified as exogenous or endogenous.

Exogenous causes

  • Inadequate exposure to sunlight, especially common in winter and northern latitudes10
  • Inadequate absorption of sunlight through the skin in people with darker skin color10
  • Inadequate absorption of sunlight in people who regularly use sunscreen10
  • Wearing protective clothing and veils

Endogenous causes

  • Decreased hepatic synthesis11
  • Obesity12
  • Malabsorption (from celiac disease,13 pancreatic insufficiency, post bariatric surgery,14 or gastrectomy)
  • Aging15
  • Chronic kidney disease (CKD)16,17
  • Cystic fibrosis18
  • Chronic hospitalization19
  • Internalization in nursing homes20
  • Postmenopausal females receiving therapy for osteoporosis21
  • Taking medications that accelerate vitamin D metabolism (eg, phenytoin, phenobarbital, and carbamazepine)22

Vitamin D levels of <10 ng/dL put individuals at risk for rickets and osteomalacia. Nonspecific musculoskeletal pain is a common and frequently unrecognized symptom of vitamin D deficiency.23 Vitamin D deficiency has also been associated with various conditions, including muscle weakness, cardiovascular disease, hypertension, diabetes, and cancer.

Most individuals with moderate vitamin D deficiency (15-20 ng/dL) are asymptomatic; however, these low concentrations are usually associated with a compensatory rise in parathyroid hormone (PTH).24 This condition, known as secondary hyperparathyroidism, leads to impaired intestinal calcium absorption, negative calcium balance, and excess bone resorption. 

The RDA is 600 international units (IU) (15 mcg) per day for most adults before age 70 and 800 IU (20 mcg per day) after age 70. These RDAs are based on a 2010 IOM (American Institute of Medicine, now National Academy of Medicine) meta-regression analysis. Several other national committees recommend similar RDAs.6,25-26 Other professional societies have endorsed higher RDAs,1,7 but larger doses that increase serum 25(OH)D concentrations to over 30 ng/mL do not reduce disease burden and appear to cause harm in older populations.27  

Vitamin D replacement is recommended for high-risk adults with serum 25(OH)D levels of <20 ng/mL (50 nmol/L).

  • <12 ng/mL: The typical dose is 25,000 to 50,000 IU (625 and 1,250 mcg) of vitamin D2 or D3 orally once per week for 6 to 8 weeks, and then 800 IU (20 mcg) of vitamin D2 or D3 daily thereafter.
  • 12 to <20 ng/mL: The typical dose is 800 to 1,000 IU (20 to 25 mcg) daily.

General conclusions from studies of vitamin D supplementation are mixed; conclusions related to skeletal and non-skeletal conditions are discussed below.

Most of these studies were conceived after it became clear that the vitamin D receptor (VDR) and the vitamin D enzyme system exist in most cells in the body, and that activation of this signaling pathway causes the ubiquitous transcription of several vitamin D-dependent genes. Based on this, investigators asked if vitamin D could prevent skeletal and non-skeletal conditions and conducted randomized clinical trials comparing patients who received vitamin D supplements to those who received placebo.

Skeletal conditions

Population-based studies have shown that higher levels of serum 25(OH)D are associated with higher bone mineral density,28-31 while low serum concentrations of 25(OH)D are associated with hip fracture risk, particularly among individuals with serum 25(OH)D <12 compared to those with ≥30 ng/mL.32-35 In contrast, prospective, randomized, placebo-controlled trials have shown either that vitamin D does not prevent fractures27,36-39 or, if given at high doses, increases fracture rate.40

Results of vitamin D combined with calcium are more variable and are either associated with decreased fracture rate41 or have no effect on fracture rate.36,42 However, most such studies have found an association of calcium and vitamin D supplementation with increased bone mineral density.43-45

The majority of these trials evaluated a generally healthy population of older adults not selected for vitamin D deficiency or a diagnosis of osteoporosis; such an approach may not have captured the effect of supplementation in vitamin D deficient patients. Thus, future investigations should include more senior people at higher risk for vitamin D deficiency (eg, living in nursing homes, housebound, or with a heavy burden of chronic disease).

Non-skeletal conditions

Despite an epidemiological association between vitamin D deficiency and various non-skeletal conditions, studies have not conclusively established that vitamin D supplementation has an effect in preventing falls,27  cardiovascular diseases,27,46,47 diabetes,27,48 respiratory infections,49 tuberculosis,50 COVID-19,51 or cancer.27,47,52

However, it may reduce cancer mortality53 and help prevent autoimmune diseases.54 Despite supplementation not being associated with beneficial effects on some endpoints, patients with overt vitamin D deficiency (serum 25[OH]D <20 ng/mL [50 nmol/L]) should receive vitamin D supplementation to treat the deficiency.

Vitamin D3 can be obtained through exposure to sunlight and from diet. The best food source for vitamin D3 is cod liver or halibut liver. It is also present in salmon, mackerel, herring, cheese, egg yolk, beef liver, and canned fish.1

For vitamin D2, the best food source is shiitake mushrooms.1

Both forms of vitamin D are also found in over-the-counter and prescription supplement forms or fortified foods, including milk and orange juice.

None of these sources may be adequate for patients with liver or kidney disease; these patients may need supplementation with the active form of vitamin D: 1,25(OH)2D.

Prevalence of vitamin D deficiency is highest at the end of winter (48% of individuals) and lowest at the end of summer (21% of individuals).55

Measuring serum 25(OH)D levels is not indicated for healthy individuals. Screening is indicated for individuals at risk for deficiency. These include patients who have the following conditions1:

  • Osteoporosis
  • Osteomalacia
  • Rickets
  • Chronic kidney disease
  • Diseases that require certain medications (anti-seizure medications, glucocorticoids, AIDS medications, antifungals, cholestyramine)
  • Malabsorption syndromes, including inflammatory bowel disease, Crohn disease, cystic fibrosis, history of bariatric surgery, pancreatic insufficiency, or gastrectomy
  • Hyperparathyroidism
  • Hepatic failure

Screening is also recommended for the following1:

  • African American and Hispanic children and adults
  • Pregnant and lactating women
  • Older adults with history of falls or nontraumatic fractures
  • Older adults or indigent people who are housebound or have heavy burden of chronic disease
  • Obese children and adults

If a patient is at risk for vitamin D deficiency and has not been tested recently, the patient should be tested to assess levels. Some physicians may wish to monitor people receiving vitamin D therapy to evaluate compliance and expected change in concentration. 

Vitamin D tests measure the total concentration of 25(OH)D. Vitamin D tests that use liquid chromatography with tandem mass spectrometry (LC-MS/MS) can measure the concentrations of vitamin D2 and D3; when added together, these equal the total vitamin D concentration. 

Quest offers 2 methods: immunoassay and liquid chromatography-tandem mass spectrometry (LC-MS/MS). Both methods are considered accurate and reliable.

Immunoassay is suitable for most patients and measures total 25(OH)D concentrations, not its separate components. This method provides high-quality quantitative results that meet the National Institute of Standards and Technology (NIST Standard Reference Material [SRM] 972) requirements and is certified by the Centers for Disease Control and Prevention Vitamin D Standardization Certification Program.

LC-MS/MS measures 25(OH)D2, 25(OH)D3, and total 25(OH) concentrations. LC-MS/MS is the reference method endorsed by experts at the National Institute of Standards and Technology, the Centers for Disease Control and Prevention, and the National Institutes of Health.

Infants (birth up to 3 years) may have circulating levels of the 25(OH)D C3-epimer, a low-activity form of vitamin D. The immunoassay method does not detect the C3-epimer. The LC-MS/MS method does detect it but overestimates total vitamin D if the C3-epimer is not accounted for. To address this, Quest offers a separate LC-MS/MS test for infants (test code 91935), which involves separation of the 25(OH)D C3-epimer and exclusion of it from the 25(OH)D results reported.

25(OH)D, Immunoassay (test code 17306): This test measures total serum 25(OH)D concentrations, which provide a good index of circulating vitamin D activity in patients not affected by renal disease. Low 25(OH)D levels can result from a dietary deficiency, poor absorption of the vitamin, or impaired metabolism of the sterol in the liver. 25(OH)D deficiency can lead to bone diseases such as rickets and osteomalacia. Above-normal levels can lead to hypercalcemia.

QuestAssureDTM 25(OH)D (D2, D3), LC-MS/MS (test code 92888): This test is used in patients >3 years of age on D2 supplementation or those who require separate D2 and D3 measurement.

QuestAssureDTM for Infants (test code 91935):  While measurements of 25(OH)D provide a good index of circulating vitamin D activity in patients not affected by renal disease, for patients <3 years of age, it is important to remove circulating levels of the inactive C3-epimer of vitamin D from the sample so that total vitamin D levels are not falsely elevated. Falsely elevated results could erroneously make the result appear to be within normal limits and lead to potential under-treatment. Levels of C3-epimer in older children and adults are usually negligible and do not cause falsely elevated vitamin D results.

Quest vitamin D test reports provide the concentration of total 25(OH)D in a patient’s serum, the total 25(OH)D reference range, and the suggested cut points to define optimal, insufficient, and deficient vitamin D statuses.

Tests using the liquid chromatography-tandem mass spectrometry (LC-MS/MS) method also provide the concentration of 25(OH)D2 and 25(OH)D3. Neither reference nor interpretative ranges have been established for these components of total 25(OH)D.

No. Special patient preparations are not required prior to testing.

Medicare includes coverage for vitamin D testing in patients at high risk for deficiency.

At-risk categories for vitamin D deficiency include the following:

  • Osteoporosis
  • Osteomalacia
  • Rickets
  • Obesity
  • Chronic kidney disease (CKD) stage III or greater
  • Long-term use of medications known to lower vitamin D levels (anti-seizure medications, glucocorticoids, AIDS medications, antifungals, cholestyramine)
  • Malabsorption syndromes including inflammatory bowel disease, Crohn disease, cystic fibrosis, history of bariatric surgery
  • Hyperparathyroidism
  •  Liver cirrhosis
  • Certain lymphomas

In some jurisdictions, coverage for at-risk patients includes testing up to 3 times per year.

In most jurisdictions, Medicare has expanded coverage for vitamin D testing for obese patients (BMI ≥30). When ordering tests for these patients, be sure to include the appropriate ICD-10 code to support accurate payment and reduce disruptions. For obesity, these include Z68.30–Z68.45. For a list of top diagnosis codes used by ordering physicians, visit QuestDiagnostics.com/MLCP.

References

  1. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2011;96:1911-1930. doi:10.1210/jc.2011-0385
  2. Thacher TD, Fischer PR, Singh RJ, et al. CYP2R1 mutations impair generation of 25-hydroxyvitamin D and cause an atypical form of vitamin D deficiency. J Clin Endocrinol Metab. 2015;100(7):E1005-13. doi:10.1210/jc.2015-1746
  3. Fu GK, Lin D, Zhang MY, et al. Cloning of human 25-hydroxyvitamin D-1 alpha-hydroxylase and mutations causing vitamin D-dependent rickets type 1. Mol Endocrinol. 1997;11(13):1961-1970. doi:10.1210/mend.11.13.0035
  4. Schlingmann KP, Kaufmann M, Weber S, et al. Mutations in CYP24A1 and idiopathic infantile hypercalcemia. N Engl J Med. 2011;365(5):410-421. doi:10.1056/NEJMoa1103864
  5. Institute of Medicine (US) Committee to Review Dietary Reference Intakes for Vitamin D and Calcium. Dietary reference intakes for calcium and vitamin D. National Academies Press (US); 2011. Accessed August 3, 2023.
  6. EFSA Panel on Dietetic Products Nutrition and Allergies (NDA). Dietary reference values for vitamin D. EFSA J. 2016;14:e04547.
  7. American Geriatrics Society Workgroup on Vitamin DSfOA. Recommendations abstracted from the American Geriatrics Society Consensus Statement on Vitamin D for Prevention of Falls and Their Consequences. J Am Geriatr Soc. 2014;62(1):147-152. doi:10.1111/jgs.12631
  8. Cosman F, de Beur SJ, LeBoff MS, et al. Clinician's guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):2359-2381. doi:10.1007/s00198-014-2794-2
  9. Forrest KY, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res. 2011;31(1):48-54. doi:10.1016/j.nutres.2010.12.001
  10. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-81. doi:10.1056/NEJMra070553
  11. Compston JE. Hepatic osteodystrophy: vitamin D metabolism in patients with liver disease. Gut. 1986;27(9):1073-1090. doi:10.1136/gut.27.9.1073
  12. Roizen JD, Long C, Casella A, et al. Obesity decreases hepatic 25-hydroxylase activity causing low serum 25-hydroxyvitamin D. J Bone Miner Res. 2019;34(6):1068-1073. doi:10.1002/jbmr.3686
  13. Shaker JL, Brickner RC, Findling JW, et al. Hypocalcemia and skeletal disease as presenting features of celiac disease. Arch Intern Med. 1997;157(9):1013-1016.
  14. Peterson LA, Zeng X, Caufield-Noll CP, et al. Vitamin D status and supplementation before and after bariatric surgery: a comprehensive literature review. Surg Obes Relat Dis. 2016;12(3):693-702. doi:10.1016/j.soard.2016.01.001
  15. Tsai KS, Wahner HW, Offord KP, et al. Effect of aging on vitamin D stores and bone density in women. Calcif Tissue Int. 1987;40(5):241-243. doi:10.1007/BF02555255
  16. Nitta K, Nagano N, Tsuchiya K. Fibroblast growth factor 23/klotho axis in chronic kidney disease. Nephron Clin Pract. 2014;128(1-2):1-10. doi:10.1159/000365787
  17. LaClair RE, Hellman RN, Karp SL, et al. Prevalence of calcidiol deficiency in CKD: a cross-sectional study across latitudes in the United States. Am J Kidney Dis. 2005;45(6):1026-1033. doi:10.1053/j.ajkd.2005.02.029
  18. Donovan DS, Jr., Papadopoulos A, Staron RB, et al. Bone mass and vitamin D deficiency in adults with advanced cystic fibrosis lung disease. Am J Respir Crit Care Med. 1998;157(6 Pt 1):1892-1899. doi:10.1164/ajrccm.157.6.9712089
  19. Thomas MK, Lloyd-Jones DM, Thadhani RI, et al. Hypovitaminosis D in medical inpatients. N Engl J Med. 1998;338(12):777-783. doi:10.1056/NEJM199803193381201
  20. Lips P, Wiersinga A, van Ginkel FC, et al. The effect of vitamin D supplementation on vitamin D status and parathyroid function in elderly subjects. J Clin Endocrinol Metab. 1988;67(4):644-650. doi:10.1210/jcem-67-4-644
  21. Guardia G, Parikh N, Eskridge T, et al. Prevalence of vitamin D depletion among subjects seeking advice on osteoporosis: a five-year cross-sectional study with public health implications. Osteoporos Int. 2008;19(1):13-19. doi:10.1007/s00198-007-0456-3
  22. Meier C, Kraenzlin ME. Antiepileptics and bone health. Ther Adv Musculoskelet Dis. Oct 2011;3(5):235-243. doi:10.1177/1759720X11410769
  23. Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc. 2003;78(12):1463-1470. doi:10.4065/78.12.1463
  24. Valcour A, Blocki F, Hawkins DM, et al. Effects of age and serum 25-OH-vitamin D on serum parathyroid hormone levels. J Clin Endocrinol Metab. 2012;97(11):3989-3995. doi:10.1210/jc.2012-2276
  25. Scientific Advisory Committee on Nutrition. Vitamin D and Health. Scientific Advisory Committee on Nutrition; 2016. https://assets.publishing.service.gov.uk/media/5a804e36ed915d74e622dafa/SACN_Vitamin_D_and_Health_report.pdf
  26. LeBoff MS, Greenspan SL, Insogna KL, et al. The clinician's guide to prevention and treatment of osteoporosis. Osteoporos Int. 2022;33(10):2049-2102. doi:10.1007/s00198-021-05900-y
  27. Gallagher JC, Rosen CJ. Vitamin D: 100 years of discoveries, yet controversy continues. Lancet Diabetes Endocrinol. 2023;11(5):362-374. doi:10.1016/S2213-8587(23)00060-8
  28. Villareal DT, Civitelli R, Chines A, et al. Subclinical vitamin D deficiency in postmenopausal women with low vertebral bone mass. J Clin Endocrinol Metab. 1991;72(3):628-634. doi:10.1210/jcem-72-3-628
  29. Kuchuk NO, van Schoor NM, Pluijm SM, et al. Vitamin D status, parathyroid function, bone turnover, and BMD in postmenopausal women with osteoporosis: global perspective. J Bone Miner Res. 2009;24(4):693-701. doi:10.1359/jbmr.081209
  30. Bischoff-Ferrari HA, Dietrich T, Orav EJ, et al. Positive association between 25-hydroxy vitamin D levels and bone mineral density: a population-based study of younger and older adults. Am J Med. 2004;116(9):634-639. doi:10.1016/j.amjmed.2003.12.029
  31. Looker AC. Serum 25-hydroxyvitamin D and risk of major osteoporotic fractures in older U.S. adults. J Bone Miner Res. 2013;28(5):997-1006. doi:10.1002/jbmr.1828
  32. Cauley JA, Lacroix AZ, Wu L, et al. Serum 25-hydroxyvitamin D concentrations and risk for hip fractures. Ann Intern Med. 2008;149(4):242-250. doi:10.7326/0003-4819-149-4-200808190-00005
  33. Ensrud KE, Taylor BC, Paudel ML, et al. Serum 25-hydroxyvitamin D levels and rate of hip bone loss in older men. J Clin Endocrinol Metab. 2009;94(8):2773-2780. doi:10.1210/jc.2008-2786
  34. LeBoff MS, Kohlmeier L, Hurwitz S, et al. Occult vitamin D deficiency in postmenopausal US women with acute hip fracture. JAMA. 1999;281(16):1505-1511. doi:10.1001/jama.281.16.1505
  35. Cauley JA, Parimi N, Ensrud KE, et al. Serum 25-hydroxyvitamin D and the risk of hip and nonspine fractures in older men. J Bone Miner Res. 2010;25(3):545-553. doi:10.1359/jbmr.090826
  36. Grant AM, Avenell A, Campbell MK, et al. Oral vitamin D3 and calcium for secondary prevention of low-trauma fractures in elderly people (Randomised Evaluation of Calcium Or vitamin D, RECORD): a randomised placebo-controlled trial. Lancet. 2005;365(9471):1621-1628. doi:10.1016/S0140-6736(05)63013-9
  37. Bischoff-Ferrari HA, Vellas B, Rizzoli R, et al. Effect of Vitamin D Supplementation, Omega-3 Fatty Acid Supplementation, or a Strength-Training Exercise Program on Clinical Outcomes in Older Adults: The DO-HEALTH Randomized Clinical Trial. JAMA. 2020;324(18):1855-1868. doi:10.1001/jama.2020.16909
  38. LeBoff MS, Chou SH, Ratliff KA, et al. Supplemental Vitamin D and Incident Fractures in Midlife and Older Adults. N Engl J Med. 2022;387(4):299-309. doi:10.1056/NEJMoa2202106
  39. Smith H, Anderson F, Raphael H, et al. Effect of annual intramuscular vitamin D on fracture risk in elderly men and women--a population-based, randomized, double-blind, placebo-controlled trial. Rheumatology (Oxford). 2007;46(12):1852-1857. doi:10.1093/rheumatology/kem240
  40. Sanders KM, Stuart AL, Williamson EJ, et al. Annual high-dose oral vitamin D and falls and fractures in older women: a randomized controlled trial. JAMA. 2010;303(18):1815-1822. doi:10.1001/jama.2010.594
  41. Dawson-Hughes B, Harris SS, Krall EA, Dallal GE. Effect of calcium and vitamin D supplementation on bone density in men and women 65 years of age or older. N Engl J Med. 1997;337(10):670-676. doi:10.1056/NEJM199709043371003
  42. Jackson RD, LaCroix AZ, Gass M, et al. Calcium plus vitamin D supplementation and the risk of fractures. N Engl J Med. 2006;354(7):669-683. doi:10.1056/NEJMoa055218
  43. Daly RM, Brown M, Bass S, et al. Calcium- and vitamin D3-fortified milk reduces bone loss at clinically relevant skeletal sites in older men: a 2-year randomized controlled trial. J Bone Miner Res. 2006;21(3):397-405. doi:10.1359/JBMR.051206
  44. Meier C, Woitge HW, Witte K, et al. Supplementation with oral vitamin D3 and calcium during winter prevents seasonal bone loss: a randomized controlled open-label prospective trial. J Bone Miner Res. 2004;19(8):1221-1230. doi:10.1359/JBMR.040511
  45. Peacock M, Liu G, Carey M, et al. Effect of calcium or 25OH vitamin D3 dietary supplementation on bone loss at the hip in men and women over the age of 60. J Clin Endocrinol Metab. 2000;85(9):3011-3019. doi:10.1210/jcem.85.9.6836
  46. Barbarawi M, Kheiri B, Zayed Y, et al. Vitamin D Supplementation and Cardiovascular Disease Risks in More Than 83 000 Individuals in 21 Randomized Clinical Trials: A Meta-analysis. JAMA Cardiol. 2019;4(8):765-776. doi:10.1001/jamacardio.2019.1870
  47. Manson JE, Cook NR, Lee IM, et al. Vitamin D Supplements and Prevention of Cancer and Cardiovascular Disease. N Engl J Med. 2019;380(1):33-44. doi:10.1056/NEJMoa1809944
  48. Pittas A, Dawson-Hughes B, Staten M. Vitamin D Supplementation and Prevention of Type 2 Diabetes. Reply. N Engl J Med. 2019;381(18):1785-1786. doi:10.1056/NEJMc1912185
  49. Camargo CA, Sluyter J, Stewart AW, et al. Effect of Monthly High-Dose Vitamin D Supplementation on Acute Respiratory Infections in Older Adults: A Randomized Controlled Trial. Clin Infect Dis. 2020;71(2):311-317. doi:10.1093/cid/ciz801
  50. Ganmaa D, Uyanga B, Zhou X, et al. Vitamin D Supplements for Prevention of Tuberculosis Infection and Disease. N Engl J Med. 2020;383(4):359-368. doi:10.1056/NEJMoa1915176
  51. Jolliffe DA, Holt H, Greenig M, et al. Effect of a test-and-treat approach to vitamin D supplementation on risk of all cause acute respiratory tract infection and covid-19: phase 3 randomised controlled trial (CORONAVIT). BMJ. 2022;378:e071230. doi:10.1136/bmj-2022-071230
  52. Goulao B, Stewart F, Ford JA, et al. Cancer and vitamin D supplementation: a systematic review and meta-analysis. Am J Clin Nutr. 2018;107(4):652-663. doi:10.1093/ajcn/nqx047
  53. Keum N, Lee DH, Greenwood DC, Manson JE, Giovannucci E. Vitamin D supplementation and total cancer incidence and mortality: a meta-analysis of randomized controlled trials. Ann Oncol. 2019;30(5):733-743. doi:10.1093/annonc/mdz059
  54. Hahn J, Cook NR, Alexander EK, et al. Vitamin D and marine omega 3 fatty acid supplementation and incident autoimmune disease: VITAL randomized controlled trial. BMJ. 2022;376:e066452. doi:10.1136/bmj-2021-066452
  55. Hansen L, Tjonneland A, Koster B, et al. Vitamin D Status and Seasonal Variation among Danish Children and Adults: A Descriptive Study. Nutrients. 2018;10(11):1801. doi:10.3390/nu10111801


This FAQ is provided for informational purposes only and is not intended as medical advice. Test selection and interpretation, diagnosis, and patient management decisions should be based on the clinician’s education, clinical expertise, and assessment of the patient.

 

Document FAQS.199 Version: 1

Version 1: Effective 12/21/2023 to present

Version 0: Effective 07/31/2018 to 12/21/2023

 

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