Vitamin D (Calciferol)
1. Identity, Chemical Nature, and Natural Sources
Chemical Identity
Vitamin D, also known as calciferol, comprises a group of fat-soluble seco-sterols. Vitamin D, first identified as a vitamin early in the 20th century, is now recognized as a prohormone. A unique aspect of vitamin D as a nutrient is that it can be synthesized by the human body through the action of sunlight.
The two major forms are vitamin D2 and vitamin D3. Vitamin D2 (ergocalciferol) is largely human-made and added to foods, whereas vitamin D3 (cholecalciferol) is synthesized in the skin of humans from 7-dehydrocholesterol and is also consumed in the diet via the intake of animal-based foods. The D2 and D3 forms differ only in their side chain structure.
Cholecalciferol (vitamin D3) is the naturally occurring form of vitamin D that is synthesized in the skin from endogenous or dietary cholesterol upon exposure to ultraviolet radiation (sunlight). Ergocalciferol (vitamin D2) is a plant-derived form used as a food additive.
Both forms increase vitamin D in your blood, but D3 might raise it higher and for longer than D2. Both vitamin D3 and vitamin D2 are synthesized commercially and found in dietary supplements or fortified foods.
Natural Food Sources
Very few foods in nature contain vitamin D. The flesh of fatty fish (such as salmon, tuna, and mackerel) and fish liver oils are among the best sources. Small amounts of vitamin D are found in beef liver, cheese, and egg yolks. Mushrooms provide some vitamin D. Some mushrooms you buy in the store have higher vitamin D content because they have been exposed to ultraviolet light. Most milk in the United States is fortified with 400 IU vitamin D per quart. Most of the time, foods made from milk, such as cheese and ice cream, are not fortified.
Cutaneous (Endogenous) Synthesis
Your body makes vitamin D when your bare skin is exposed to the sun. Most people get at least some vitamin D this way. However, clouds, smog, old age, and having dark-colored skin reduce the amount of vitamin D your skin makes. Also, your skin does not make vitamin D from sunlight through a window.
Sun is the main source of vitamin D and is produced endogenously when skin is exposed to solar ultraviolet radiation. Synthesis of vitamin D depends on the amount and type of melanin present in the skin, and the darker the skin the higher the amount of sunlight required to produce vitamin D.
Forms and Preparations
Vitamin D is found in multivitamin/mineral supplements. It is also available in dietary supplements containing only vitamin D or vitamin D combined with a few other nutrients. Because vitamin D is fat soluble, it is best absorbed when taken with a meal or snack that includes some fat.
Beyond D2 and D3, pharmaceutical forms include calcifediol (25-hydroxyvitamin D3, also known as calcidiol), which is the immediate metabolic precursor to the active hormone, and calcitriol (1,25-dihydroxyvitamin D3), the biologically active hormonal form prescribed for specific medical conditions. Calcitriol is a hormonally active synthetic vitamin D analog prescribed to manage hypocalcemia and renal osteodystrophy. FDA-approved indications include treating hypocalcemia in patients undergoing chronic renal dialysis, secondary hyperparathyroidism in those with chronic kidney disease not yet requiring dialysis, and hypocalcemia in patients with hypoparathyroidism or pseudohypoparathyroidism.
2. Historical and Traditional Use
Pre-Modern Observations and Folk Use
Rickets was a common disease in 17th century England. Frances Glisson's treatise on rickets published in 1650, a glorious contribution to English medicine, described the clinical and anatomic features of rickets in great detail. The exact etiology of rickets had been elusive until the 1920s. During the Glissonian era, rickets was a mysterious disease. By the late 19th and early 20th century, faulty diet or faulty environment (poor hygiene, lack of fresh air and sunshine) or lack of exercise was implicated in its causation.
It was common folklore in the 19th century in fishing communities on the coast of England to give their children cod liver oil as a way of preventing rickets. Bretonneau in 1827 treated a 15-month-old child with severe rickets with cod liver oil and noted the incredible speed at which the patient was cured. His student Trousseau further demonstrated that oils from aquatic mammals including seals and whales as well as oily fish including herring were also effective in treating rickets. These observations suggested that rickets was caused by a nutritional deficiency.
The first association relating inadequate sunlight exposure as a cause for rickets was made by the Polish physician scientist Sniadecki in 1822. He connected the dots and realized that children living in industrialized Warsaw who were not exposed to direct sunlight were plagued with rickets, whereas children who lived in rural farm areas and were outdoors and exposed to sunlight had no evidence of this bone-deforming disease.
This was followed by Palm who in 1890 recognized that the lack of sunlight was a common denominator that could be associated with the high incidence of rickets in children living in the inner cities in Great Britain when compared to children living in underdeveloped countries. He encouraged systematic sunbathing as a means for preventing and curing rickets, as did Sniadecki.
The Industrial Revolution and the Rise of Rickets
The growing incidence of rickets with the Industrial Revolution raised speculations about its origin and treatment. The characterization of solar light and luminous spectrum led to the identification of the biological effects of ultraviolet radiation, and to the discovery of phototherapy as an alternative therapeutic process to the solar irradiation.
At the turn of the 20th century, rickets was rampant among the poor children living in the industrialized and polluted northern cities of the United States. By the late 1700s, Percival (1789) was advocating the use of cod-liver oil for the treatment of rickets and therefore suggesting the nutritional nature of vitamin D. But soon after, in the early 1800s, Sniadecki (1840) in Poland was documenting the differential incidence of rickets in city-dwelling children versus rural-dwellers and suggesting some environmental factor was involved.
Scientific Discovery in the Early 20th Century
Finally, in 1918, Mellanby reported that he could produce rickets in beagles by placing them on an oatmeal diet and then reversing the disease by giving them cod liver oil. This observation convinced the scientific community that rickets was caused by a nutritional deficiency, and the hunt was on to determine what nutrient was deficient. It was originally concluded that vitamin A in cod liver oil was responsible for its antirachitic activity. However, Elmer McCollum, who had discovered vitamin B, was not convinced that the antirachitic factor was vitamin A.
The discovery of a fat-soluble nutrient that had antirachitic activity and no vitamin A activity by McCollum has had far reaching health benefits for children and adults. He named this nutrient vitamin D.
McCollum showed that the anti-rachitic substance in cod-liver oil was distinct from vitamin A and named it Vitamin D. The dilemma about why both light and a dietary substance cured rickets was eventually resolved by the work of Harriette Chick and Harry Steenbock who independently investigated the dual role of nutrition and sunlight exposure in the prevention of rickets. Steenbock and Black (1924) performed the definitive experiment when they showed that irradiation of certain foods (e.g., plant oils or yeast) increased their vitamin D activity.
Steenbock patented the process, and with this patent was able to attract industry to use this discovery to eliminate rickets as a major medical problem.
Irradiated ergosterol from yeast became the major vitamin D source for food fortification and the treatment of rickets, leading to a public health campaign to eradicate rickets by the 1930s. With the discovery of vitamin D and the delineation of the anti-rachitic properties of cod-liver oil by the 1930s, it became possible to not only treat but also eradicate rickets in the United States.
3. Key Constituents, Metabolites, and Mechanisms of Action
The Vitamin D Endocrine System
Vitamin D undergoes serial metabolic transformations to an active entity, 1,25(OH)₂D. Thus, vitamin D, produced in skin as cholecalciferol (vitamin D3), or absorbed from the gut as vitamin D3 or as ergocalciferol (vitamin D2), is transported in the circulation, bound to a vitamin D binding protein (DBP). Vitamin D may be obtained by sunlight exposure or absorption from the gut and metabolized sequentially, by liver CYP2R1 and kidney (or extrarenal) CYP27B1, to calcitriol (1,25(OH)₂D).
In the liver, vitamin D3 undergoes hydroxylation to produce 1,25-dihydroxyvitamin D (calcitriol), the active form of vitamin D. Calcitriol, a small lipophilic molecule with superior cellular penetration, then binds to the vitamin D receptor (VDR). Calcitriol binds to vitamin D receptors in the kidneys, parathyroid glands, intestines, and bones to increase serum blood calcium levels by promoting absorption in the intestines, renal tubular reabsorption in the kidneys, and release from bone.
Blood levels of vitamin D status are assessed via the intermediate metabolite, 25-hydroxyvitamin D [25(OH)D]. In the blood, a form of vitamin D known as 25-hydroxyvitamin D is measured in either nanomoles per liter (nmol/L) or nanograms per milliliter (ng/mL).
Genomic and Non-Genomic Mechanisms
The vitamin D system is unique in that distinct calcium homeostatic functions and cell growth regulatory activities are mediated through a single ligand, calcitriol, acting through a specific receptor exhibiting ubiquitous tissue expression, the vitamin D receptor (VDR). The VDR is a member of a superfamily of nuclear steroid hormone receptors which regulate gene transcription by interacting with response elements in gene promoters.
Calcitriol, like other steroid hormones, may function through both genomic and non-genomic mechanisms. In the traditional function, the interaction between the biologically active form of vitamin D and the vitamin D receptor (VDR) affects the transcription of thousands of genes by binding to repeated sequences present in their promoter region, named vitamin D-responsive elements (VDREs). Non-transcriptional effects, on the other hand, occur quickly and are unaffected by inhibitors of transcription and protein synthesis.
With the finding of the vitamin D receptor (VDR) in nearly every tissue and the more recent discovery of thousands of VDR binding sites throughout the genome controlling hundreds of genes, the interest in vitamin D and its impact on multiple biologic processes has accelerated tremendously.
Calcium and Phosphate Homeostasis
Both global and tissue-specific deletion studies leading to decreases of the active form of vitamin D, calcitriol [1,25(OH)₂D], and/or of the vitamin D receptor (VDR), have demonstrated the primary role of calcitriol and VDR in bone, cartilage and tooth development and in the regulation of mineral metabolism and of parathyroid hormone (PTH) and FGF23, which modulate calcium and phosphate fluxes.
They have also extended the spectrum of actions of calcitriol and the VDR to include, among others: modulation of skin metabolism; joint regulation of adipose tissue metabolism; cardiovascular function; and immune function.
Vitamin D Degradation
1,25(OH)₂D limits CYP27B1 activity by inhibiting PTH and increasing FGF23 production as well as reducing 1,25(OH)₂D levels by inducing the catalytic enzyme CYP24A1. Degradation of calcitriol occurs primarily through the CYP24A1 enzyme system, which creates 24,25-dihydroxyvitamin D and other inactive catabolites that are excreted.
4. Scientific Evidence by Health Area
4.1 Bone Health: Rickets and Osteomalacia
The relationship between vitamin D and bone disease is the most firmly established in nutrition science and medicine. In children, vitamin D deficiency causes rickets, a disease in which the bones become soft, weak, deformed, and painful. In teens and adults, vitamin D deficiency causes osteomalacia, a disorder that causes bone pain and muscle weakness.
The evidence base here is not only strong but historically definitive: the entire discovery of vitamin D arose from the clinical observation and experimental reversal of rickets with cod liver oil and sunlight. The identification of the chemical nature of an essential dietary factor with anti-rickets effect (ergocalciferol or vitamin D2), together with another factor with identical properties, but more potent, produced in the skin exposed to sunlight (cholecalciferol or vitamin D3), was essential to the elucidation, prevention and therapy of the disease.
4.2 Bone Health: Osteoporosis and Fracture Prevention
Although rickets and osteomalacia are extreme examples of the effects of vitamin D deficiency, osteoporosis is an example of a long-term effect of calcium and vitamin D insufficiency. Adequate storage levels of vitamin D maintain bone strength and might help prevent osteoporosis in older adults, non-ambulatory individuals who have difficulty exercising, postmenopausal women, and individuals on chronic steroid therapy.
However, evidence from large recent trials on fracture prevention through supplementation in generally vitamin D-sufficient populations is less clear. Three recently-completed, large clinical trials in the U.S., New Zealand, and Australia, referred to as the "mega-trials," were conducted to determine the impact of supplemental vitamin D on a variety of outcomes including falls and fractures. The trials were similar in design and collectively included over 50,000 generally vitamin D-replete, older men and women. The mega-trials established that vitamin D supplementation with the equivalent of 2,000 to 3,300 IU/d of vitamin D3 had no favorable effect on risk of falls or fractures.
While these trials were in progress, evidence emerged that circulating 25-hydroxyvitamin D levels have a U-shaped association with risk of falling, raising concern about a potential untoward effect of high-dose supplementation.
By contrast, a meta-analysis of dosage-specific data found that vitamin D supplementation with daily dose of 800 to 1,000 IU was associated with lower risks of osteoporotic fracture and fall. This discrepancy between meta-analyses of earlier trials (which generally enrolled more deficient populations) and the recent mega-trials (enrolling largely replete participants) suggests that baseline deficiency is a key modifier of response to supplementation.
4.3 Cancer
Preclinical models support calcitriol's antiproliferative and neuroprotective functions, and its synergistic effects with chemotherapy, although large-scale randomized controlled trials (RCTs) have yielded mixed or inconclusive results, particularly in cancer, cardiovascular events, and cognitive decline.
The VITAL trial was the most definitive large RCT to date on this question. The VITamin D and OmegA-3 TriaL (VITAL) was a nationwide, randomized, placebo-controlled, 2×2 factorial trial of vitamin D3 (cholecalciferol, 2,000 IU/day) and marine omega-3 fatty acids (1 g/day) for the prevention of cancer and cardiovascular disease. There were 25,871 U.S. men aged ≥50 and women aged ≥55, including 5,106 African Americans, who participated. Primary endpoints were total invasive cancer and major cardiovascular events (composite of myocardial infarction, stroke, and cardiovascular mortality). Vitamin D supplementation did not reduce either of the primary endpoints.
Evidence strength: Preclinical data are suggestive. Large RCT data (VITAL) do not support a primary preventive role for supplemental vitamin D3 at 2,000 IU/day for cancer incidence in a largely vitamin D-sufficient general population.
4.4 Cardiovascular Disease
Observational studies consistently associate low 25(OH)D concentrations with increased risk of hypertension, atherosclerosis, myocardial infarction, heart failure, arrhythmias, stroke, and cardiovascular mortality. Mechanistic investigations have revealed that vitamin D modulates cardiomyocyte calcium handling, endothelial function, vascular smooth muscle proliferation, inflammation, oxidative stress, and renin–angiotensin–aldosterone system activity, establishing biologically plausible links to cardiovascular outcomes.
Despite these associations, large randomized trials of vitamin D supplementation have failed to demonstrate reductions in major cardiovascular events, likely due to heterogeneity in baseline status, dosing regimens, intervention timing, genetic variability, and underlying comorbidities. Vitamin D may function more effectively as a biomarker of cardiovascular risk rather than a universal therapeutic agent, with deficiency reflecting systemic vulnerability rather than acting as a dominant causal factor.
A 2024 systematic review and meta-analysis of 29 RCTs (>134,000 individuals) and 30 prospective cohort studies (>157,000 individuals) found that in clinical trial studies, the incidence of CVDs among the vitamin D-consuming group was not significantly different from that in the placebo group (RR: 0.99, 95% CI: 0.95–1.03; P=0.77). CVD mortality was also not significantly different between the two groups (RR: 0.97, 95% CI: 0.90–1.05; P=0.72). In cohort studies, however, low circulating 25(OH)D increased the risk of CVD incidence by 31% and CVD mortality by 37%.
Evidence strength: Observational evidence is consistently associative. RCT evidence does not support supplementation reducing cardiovascular events in the general population, though research into severely deficient subgroups is ongoing.
4.5 Immune Function and Autoimmune Disease
Your immune system needs vitamin D to fight off invading bacteria and viruses. The actions of calcitriol and the VDR have been extended to include modulation of immune function.
Systematic review analyses have examined the antioxidant and anti-inflammatory effects of vitamin D against acute and chronic diseases, focusing particularly on cancer, immune-related diseases, cardiomyopathies, and infectious diseases.
Regarding multiple sclerosis (MS): scientists have not actually studied whether vitamin D supplements can prevent MS. In people who have MS, clinical trials show that taking vitamin D supplements does not keep symptoms from getting worse or coming back.
Evidence strength: Mechanistic and observational data for immune modulation are robust. Clinical trial evidence for supplementation reducing the incidence or severity of specific autoimmune diseases remains limited or unsupportive in well-powered studies.
4.6 Mental Health and Depression
Some studies have found links between low blood levels of vitamin D and an increased risk of depression. However, clinical trials show that taking vitamin D supplements does not prevent or reliably treat depression.
A 2025 meta-analysis of RCTs found nuance in this area: vitamin D supplementation significantly alleviates depressive symptoms (SMD = −0.36), particularly in subgroups with baseline deficiency (<20 ng/mL) and comorbid chronic inflammatory conditions. The therapeutic mechanism likely involves dual modulation of the neuro-immune axis and achievement of a threshold serum 25(OH)D level (>30 ng/mL).
A large RCT nested within the VITAL study found that results were consistent with evidence of lack of benefit in smaller-scale shorter-term trials. Even among RCTs that featured doses of 800 IU/d or greater of vitamin D3 and 12 months or longer of treatment, no benefits were observed for late-life mental health or well-being measures.
Evidence strength: Mixed. Some meta-analyses suggest modest benefit in deficient individuals, but large high-quality RCTs in general populations do not support a robust anti-depressant effect.
4.7 Blood Sugar Regulation and Type 2 Diabetes
Vitamin D helps your body regulate blood sugar levels. However, clinical trials in people with and without diabetes show that supplemental vitamin D does not improve blood sugar levels, insulin resistance, or hemoglobin A1c levels.
High-dose vitamin D3 has demonstrated benefits in specific populations, including improved bone mineral density, immune homeostasis, glycemic control, and reduced inflammation. In patients with chronic kidney disease, cystic fibrosis, and inflammatory bowel disease, targeted supplementation has been associated with clinical improvements. These findings highlight the importance of disease-specific context and baseline deficiency status in evaluating supplementation outcomes.
Evidence strength: Evidence from general-population RCTs is not supportive of glycemic benefit. Evidence in specific deficient or high-risk subpopulations (e.g., chronic kidney disease, inflammatory bowel disease) is more favorable but requires further study.
4.8 Skin Conditions (Psoriasis)
Calcipotriol and 22-oxa calcitriol (OCT) are approved for the treatment of psoriasis. Vitamin D treats plaque-type psoriasis in some people. Vitamin D or a cream that has a form of vitamin D called calcipotriene can be used on the skin. This represents one of the best-established clinical applications of topical vitamin D analogs, with regulatory approval in multiple jurisdictions.
Evidence strength: Strong for topical vitamin D analogs (calcipotriol) in plaque psoriasis, with regulatory approvals in multiple countries.
5. Body Systems Associated with Vitamin D
- Skeletal system: Vitamin D helps the body absorb calcium, one of the main building blocks for strong bones. Together with calcium, vitamin D helps protect against osteoporosis, a disease that thins and weakens the bones and makes them more likely to break.
- Muscular system: Muscles need vitamin D to move.
- Nervous system: Nerves need vitamin D to carry messages between the brain and the body.
- Immune system: The immune system needs vitamin D to fight off invading bacteria and viruses.
- Cardiovascular system: Hyperlipidemia, increased atherogenic plaques, cardiac inflammation, hypertension, myocarditis, myocardial infarction, and heart failure are some of the commonly known conditions connected with vitamin D deficiency.
- Endocrine system: Vitamin D regulates PTH and FGF23, both critical to mineral homeostasis. Calcitriol and the VDR play primary roles in the regulation of mineral metabolism and of parathyroid hormone (PTH) and FGF23, which modulate calcium and phosphate fluxes.
- Integumentary system (skin): The actions of calcitriol and the VDR include modulation of skin metabolism. Topical analogs have clinically proven roles in psoriasis management.
6. Dosage Forms and Doses Reported in Studies
Recommended Dietary Allowances (RDAs) and Reference Values
The recommended daily amount of vitamin D is 400 international units (IU) for children up to age 12 months, 600 IU for people ages 1 to 70 years, and 800 IU for people over 70 years. RDAs for vitamin D are listed in both micrograms (mcg) and International Units (IU); 1 mcg vitamin D is equal to 40 IU.
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.
Sufficiency Thresholds
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.
Doses Used in Major Clinical Trials
- VITAL trial: Vitamin D3 (cholecalciferol, 2,000 IU/day) for the prevention of cancer and cardiovascular disease.
- Falls and fracture mega-trials: Vitamin D supplementation with the equivalent of 2,000 to 3,300 IU/d of vitamin D3.
- Fracture/fall meta-analysis: Vitamin D supplementation with daily dose of 800 to 1,000 IU was associated with lower risks of osteoporotic fracture and fall.
- Safety trial: In a trial including 373 62-year-old healthy and vitamin D-replete subjects, 400, 4,000 and 10,000 IU were administered daily for 3 years. Hypercalcemia occurred in 0, 3 and 9% in the 400, 4,000 and 10,000 IU/day groups, respectively.
- Depression meta-analysis: A randomized, triple-blind, placebo-controlled trial found that patients who received 50,000 IU of vitamin D every two weeks and 4.5×10¹¹ CFU of probiotics daily showed a significant improvement in depressive symptoms after 12 weeks.
Clinical Guidelines for Supplementation
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. The Endocrine Society does not recommend specific doses but notes that all individuals should adhere to the RDA.
The prevention and/or correction of vitamin D deficiency/insufficiency with 800–1,000 IU/daily of vitamin D or 10 µg/day of calcifediol are safe.
7. Safety, Toxicity, and Drug Interactions
Upper Tolerable Intake Level and Toxicity
Excess intake of vitamin D — but not sun exposure — can lead to a state of vitamin D "intoxication" or "hypervitaminosis D." Chemically synthesized vitamin D became available late in the third decade of the 20th century; reports of vitamin D intoxication were first found from 1928 to 1932. The condition of hypervitaminosis D leads to hypercalcemia and eventually to soft tissue calcification and resultant renal and cardiovascular damage.
Vitamin D overdosing includes hypercalcemia, hypercalciuria, and mineral deposits in soft tissues. A safety upper limit of 4,000 IU/day, which is consistently accepted, has been challenged, since the risk of adverse events in other systems than calcium-phosphate homeostasis may depend not only on the dose, but on the outcome, the treatment regimen, and possibly the age, sex, and vitamin D status.
Vitamin D-mediated hypercalcemia occurs as a result of diverse mechanisms including excessive ingestion of vitamin D and its metabolites, ectopic enzyme overexpression, and mutations of inactivating enzymes.
Increased public awareness of vitamin D–related health benefits might increase the risk of vitamin D toxicity due to self-administration of vitamin D in doses higher than recommended for age and body weight or even higher than the established upper limit intake values.
Drug Interactions
Orlistat (Xenical and alli) is a weight-loss drug. It can reduce the amount of vitamin D the body absorbs from food and supplements. Cholesterol-lowering statins might not work as well if you take high-dose vitamin D supplements (including atorvastatin, lovastatin, and simvastatin). Steroids such as prednisone can lower blood levels of vitamin D. Thiazide diuretics (such as Hygroton, Lozol, and Microzide) could raise blood calcium levels too high if taken with vitamin D supplements.
Other potential biologic mechanisms for drug–vitamin D interactions include: altered absorption of fat-soluble vitamin D when taken concurrently with drugs that inhibit absorption or enhance elimination of dietary fat, and exacerbation of risk of hypercalcemia when taken with calcium-sparing medications.
Use of thiazide diuretics in combination with calcium and vitamin D supplements may cause hypercalcemia in the elderly, or those with compromised renal function or hyperparathyroidism.
Absorption and At-Risk Populations
People with conditions that limit fat absorption, such as Crohn's disease, celiac disease, or ulcerative colitis, have impaired vitamin D absorption. This is because the vitamin D consumed is absorbed in the gut along with fat. People with obesity or who have undergone gastric bypass surgery may need more vitamin D than other people.
Clouds, smog, old age, and having dark-colored skin reduce the amount of vitamin D the skin makes. The darker the skin, the higher the amount of sunlight required to produce vitamin D. Pooled prevalence of vitamin D deficiency in dark-skinned migrants, adjusted for latitude of study country, was estimated at 77% (95% confidence interval, 70%–84%).
In several countries, calcifediol (25-hydroxyvitamin D) is often prescribed for the prevention and/or treatment of vitamin D deficiency. Calcifediol appears to display a higher rate of intestinal absorption compared with cholecalciferol. This compound could be particularly useful in liver failure, in drug-induced alterations of liver cytochrome enzymes activity, in genetic disorders of 25-hydroxylase, and in gastrointestinal diseases.
References
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- NIH Office of Dietary Supplements — Vitamin D: Consumer Fact Sheet
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