Vitamin D: Is It Really a Vitamin or a Hormone?

An in-depth, evidence-based review for clinicians and informed readers

Executive summary (quick take)

Vitamin D occupies an unusual place in human physiology: it behaves like a micronutrient (we obtain it from diet and sunlight), yet after metabolic activation it acts like a steroid hormone that regulates gene expression across many tissues. The form most commonly measured in clinical practice is 25-hydroxyvitamin D (25(OH)D), which reflects status; the active hormonal form is 1,25-dihydroxyvitamin D (1,25(OH)₂D, calcitriol) produced primarily by the kidney but also locally in many tissues. Because of its endocrine signaling, autocrine/paracrine production, and wide physiologic reach (calcium-phosphate homeostasis, bone health, immune regulation, cell proliferation, cardiovascular effects), many experts consider vitamin D to be a prohormone or fully functioning steroid hormone after activation. Clinically, however, vitamin D deficiency is most important for skeletal health (rickets, osteomalacia) and increasingly for extra-skeletal outcomes under active investigation. Guidelines and authoritative reviews underscore that while vitamin D has hormone-like actions, public health and clinical recommendations must balance benefits, uncertain extra-skeletal effects, and risks of excessive supplementation. NCBIOffice of Dietary SupplementsPMC

Table of contents

1. Introduction: Why the question matters

2. A brief history of vitamin D discovery and naming

3. Chemistry and dietary forms (D₂ vs D₃)

4. Cutaneous synthesis (UVB) and factors that influence production

5. Metabolic activation: liver and kidney steps, relevant enzymes

6. Transport and serum biomarkers (VDBP, 25(OH)D vs 1,25(OH)₂D)

7. Mechanism of action: a steroid nuclear receptor pathway

8. Endocrine versus paracrine/autocrine signaling — implications for classification

9. Physiologic roles: skeletal and extraskeletal (immune, cardio, metabolic, cancer biology)

10. Clinical deficiency: manifestations, prevalence, risk groups

11. Testing: what to measure, interpretation, assay issues

12. Recommended intakes, supplementation, and safety (toxicity)

13. Controversies and evidence for extra-skeletal benefits (what high-quality trials show)

14. Guidelines and consensus statements (IOM/NAS, Endocrine Society, NIH ODS)

15. Practical clinical approach: diagnosing and treating deficiency, monitoring

16. Future research directions and knowledge gaps

17. Conclusion: pragmatic framing — vitamin, prohormone, or hormone?

18. References (key sources and further reading)

1. Introduction: Why this question matters

When clinicians, scientists, or informed members of the public ask whether vitamin D is a vitamin or a hormone, they are not merely indulging semantic curiosity. The answer shapes how we conceptualize testing strategies, supplementation policies, therapeutic uses, and expectations for benefit. If vitamin D is a vitamin in the classic sense (a dietary essential only needed in small amounts), public health emphasis focuses on preventing deficiency for skeletal outcomes. If it is a hormone (produced endogenously, exerting regulatory effects widely), that expands plausible therapeutic roles and biological mechanisms — but also demands rigorous evidence before recommending supplementation for broad disease prevention. Ultimately, vitamin D is best described as a prohormone that, following metabolic activation, functions as a steroid hormone with both endocrine and local (autocrine/paracrine) actions. This hybrid identity underlies ongoing controversies about testing, supplementation, and non-skeletal claims. NCBIPMC

2. A brief history of vitamin D discovery and naming

Historically, the link between sunlight and rickets was noted in the 19th century; cod liver oil and sunlight were among the early effective treatments. The substance isolated and named “vitamin D” followed the pattern of other essential vitamins discovered in the early 20th century. However, as biochemical pathways were elucidated, researchers recognized that the skin produces a cholesterol-derived secosteroid in response to ultraviolet B (UVB) radiation, and that its biologically active metabolite (1,25-dihydroxyvitamin D) functions through a nuclear receptor to regulate gene transcription — behavior that resembles steroid hormones such as cortisol, estrogen, and thyroid hormone. Over decades, the language shifted from “vitamin” to “prohormone” to “hormone,” depending on context. Semantically precise usage matters, but so does physiologic understanding: the molecule can be both an essential nutrient and a hormonally active regulator. PubMedNCBI

3. Chemistry and dietary forms (D₂ vs D₃)

Two major forms are relevant clinically:

• Vitamin D₃ (cholecalciferol): produced in human (and animal) skin from 7-dehydrocholesterol after UVB exposure; also found in oily fish, liver, and in some fortified foods.

• Vitamin D₂ (ergocalciferol): derived from plant sterols (ergosterol) and produced by fungi; historically used in some supplements and fortification.

Chemically both are secosteroids (steroid nucleus with a broken ring). After absorption or cutaneous synthesis, both forms undergo two hydroxylation steps (25-hydroxylation in the liver and 1α-hydroxylation primarily in the kidney) to form the circulating storage form (25(OH)D) and the hormonally active metabolite (1,25(OH)₂D). While D₂ and D₃ are similar, vitamin D₃ appears more effective at raising and maintaining 25(OH)D concentrations in humans. Office of Dietary SupplementsPMC

4. Cutaneous synthesis (UVB) and factors that influence production

Human skin synthesizes previtamin D₃ when 7-dehydrocholesterol absorbs UVB wavelengths (≈290–315 nm). Thermal isomerization converts previtamin D₃ to cholecalciferol (vitamin D₃). This cutaneous production is impacted by:

• Latitude and season: higher latitudes and winter months reduce UVB intensity and vitamin D production.

• Time of day: mid-day sun yields more UVB.

• Skin pigmentation: melanin absorbs UVB; darker skin requires longer exposure for the same vitamin D synthesis.

• Age: elderly skin has less 7-dehydrocholesterol; synthesis declines.

• Clothing, sunscreen, glass, pollution: block UVB and reduce production.

• Body surface area exposed and duration: determine yield.

Because sunlight is the major natural source for many people, public health advice must balance skin cancer risks with vitamin D needs. For many populations, dietary intake and supplementation remain important complements to sunlight. PMC

5. Metabolic activation: liver and kidney steps, relevant enzymes

Vitamin D is a two-step hydroxylation pathway:

1. 25-hydroxylation (liver): Cholecalciferol and ergocalciferol are hydroxylated by hepatic 25-hydroxylases (e.g., CYP2R1 and others) to form 25-hydroxyvitamin D (25(OH)D). 25(OH)D is the main circulating form and the best clinical indicator of vitamin D status because of its longer half-life (~2–3 weeks).

2. 1α-hydroxylation (kidney and extra-renal tissues): 25(OH)D is hydroxylated at the 1α position by CYP27B1 (1α-hydroxylase) to form 1,25-dihydroxyvitamin D (1,25(OH)₂D; calcitriol) — the most biologically active metabolite. Renal production of 1,25(OH)₂D is tightly regulated by parathyroid hormone (PTH), serum calcium and phosphate, and fibroblast growth factor 23 (FGF23). Importantly, other tissues (macrophages, dendritic cells, colon, prostate, breast, and many others) express CYP27B1 and can produce 1,25(OH)₂D locally for autocrine/paracrine functions.

3. Catabolism: CYP24A1 initiates degradation of both 25(OH)D and 1,25(OH)₂D to inactive metabolites.

Because of extra-renal 1α-hydroxylation and tissue-specific actions, the vitamin D system supports both endocrine and local signaling. PMC+1

6. Transport and serum biomarkers (VDBP, 25(OH)D vs 1,25(OH)₂D)

Vitamin D metabolites are lipophilic and circulate bound primarily to vitamin D binding protein (VDBP) and to a lesser extent albumin; only a small fraction (<1%) is free. Clinically:

• 25(OH)D (calcidiol) is measured to assess status (deficiency/insufficiency or sufficiency) because it reflects total input (sunlight + diet/supplement) and has a relatively long half-life.

• 1,25(OH)₂D (calcitriol) is the active hormone, but its serum concentration is tightly regulated and often normal or elevated in early deficiency (due to PTH stimulation) — thus it is not a reliable marker of vitamin D status except in specific disorders (e.g., granulomatous diseases, renal failure, genetic disorders).

Assays vary, and differences between immunoassays and mass spectrometry methods can affect measured values; consensus recommendations call for assay standardization and careful interpretation. NCBIOxford Academic

7. Mechanism of action: a steroid nuclear receptor pathway

1,25(OH)₂D acts primarily through the vitamin D receptor (VDR) — a nuclear receptor member of the steroid-thyroid receptor family. The canonical sequence:

1. Calcitriol diffuses into cells (or enters bound to carrier proteins and undergoes facilitated uptake) and binds VDR in the nucleus.

2. The VDR forms a heterodimer with the retinoid X receptor (RXR).

3. The VDR-RXR complex binds to vitamin D response elements (VDREs) in target gene promoters and modulates transcription — upregulating or downregulating a wide range of genes.

This receptor-mediated genomic action produces effects on calcium transport proteins (e.g., TRPV6, calbindin), bone mineralization genes (osteocalcin, RANKL), cell cycle regulators, and immune-related genes. In addition, non-genomic rapid actions of vitamin D metabolites mediated at the membrane level have been described. This nuclear receptor mechanism is characteristic of steroid hormones, supporting the argument that activated vitamin D behaves as a hormone. PMC

8. Endocrine versus paracrine/autocrine signaling — implications for classification

Vitamin D physiology includes:

• Endocrine signaling: Classic endocrine axis — kidney-derived 1,25(OH)₂D circulates and acts on distant targets (intestine, bone, parathyroid gland) to regulate systemic calcium and phosphate homeostasis.

• Autocrine/paracrine signaling: Many tissues express CYP27B1 and VDR, enabling local conversion of 25(OH)D to 1,25(OH)₂D and signaling within the same tissue or nearby cells. This local production mediates immune modulation, regulation of cell proliferation and differentiation, and antimicrobial peptide expression (e.g., cathelicidin in macrophages).

Because vitamin D metabolites function in both modes (systemic endocrine and local autocrine/paracrine), some authors prefer the term prohormone (a precursor that must be activated to exert hormonal action) while others accept "hormone" for the active metabolite. In either case, the system is more complex than a simple dietary vitamin. PMCOxford Academic

9. Physiologic roles: skeletal and extraskeletal

Skeletal physiology (established)

The classical role — maintaining calcium and phosphate homeostasis and promoting bone mineralization — is the strongest and most consistent effect:

• Intestinal calcium absorption: 1,25(OH)₂D increases expression of calcium transport proteins to enhance dietary calcium uptake.

• Bone mineralization: supports osteoblast function and indirectly modulates osteoclastogenesis (via RANKL and OPG pathways) to remodel bone appropriately.

• Prevention of rickets/osteomalacia: severe deficiency causes defective mineralization in children (rickets) and adults (osteomalacia).

These skeletal effects underpin public health recommendations and clinical uses of supplementation. NCBI+1

Extraskeletal roles (active area of research)

Over the past 20–30 years, numerous non-skeletal actions have been identified in vitro, in animal models, and observational human studies, including:

• Immune modulation: vitamin D influences innate immunity (induction of antimicrobial peptides like cathelicidin) and adaptive immunity (shifting T cell phenotypes); plausible roles in autoimmunity and infection resistance. PMC+1

• Cardiovascular system: associations between low 25(OH)D and hypertension, heart disease, and stroke have been reported, but causality remains unproven. Oxford Academic

• Metabolic health: observational links with insulin resistance, type 2 diabetes risk, and obesity exist; intervention trials are mixed. Office of Dietary Supplements

• Cancer biology: vitamin D signaling affects cell proliferation, differentiation, apoptosis, and angiogenesis; epidemiological studies suggest lower cancer incidence/mortality in higher vitamin D status for some cancers, but randomized trial evidence is inconclusive. PMC

• Neurocognitive and mood outcomes: observational data exist; randomized data limited and inconsistent.

These extraskeletal associations have motivated trials testing supplementation for disease prevention, but results to date are heterogeneous, with robust support strongest for skeletal outcomes and less clear benefit for most extraskeletal endpoints. Recent high-quality guidelines urge caution in over-interpreting observational associations. PubMedPMC

10. Clinical deficiency: manifestations, prevalence, risk groups

Clinical manifestations

• Children: rickets — impaired mineralization of growth plates, bone deformities, growth retardation.

• Adults: osteomalacia — bone pain, muscle weakness, pseudofractures; severe deficiency may increase fracture risk via impaired bone quality.

• Secondary hyperparathyroidism: low vitamin D elevates PTH, driving bone resorption and potential bone loss.

• Nonspecific symptoms: myalgias, weakness, fatigue — common but nonspecific.

Prevalence and at-risk groups

Vitamin D insufficiency and deficiency are common worldwide, with prevalence varying by geography, skin pigmentation, lifestyle (indoor living), dietary patterns, obesity, certain medications, malabsorption syndromes, chronic kidney disease, older age, and institutionalization. Public health surveillance reveals substantial segments of populations below recommended thresholds in many countries; precise estimates depend on cutpoints and assay methods. PubMedOffice of Dietary Supplements

11. Testing: what to measure, interpretation, assay issues

• Best test: serum 25(OH)D (total) — reflects input and stores; longer half-life.

• Not routinely helpful: serum 1,25(OH)₂D — reserved for specific disorders (e.g., renal failure, granulomatous disease, suspected vitamin D receptor anomalies).

• Common cutpoints (examples used in many guidelines, though not universally agreed):

  • Deficiency: 25(OH)D < 20 ng/mL (50 nmol/L)

  • Insufficiency: 20–30 ng/mL (50–75 nmol/L)

  • Sufficiency: ≥30 ng/mL by some groups; others accept ≥20 ng/mL for bone health — there is active debate.

• Assay variation: differences between immunoassays and LC-MS/MS can lead to discordant values; laboratories should participate in standardization programs. Measurement of free 25(OH)D or VDBP-adjusted levels is academically interesting but not yet routine outside research contexts. Oxford AcademicNCBI

12. Recommended intakes, supplementation, and safety (toxicity)

Intake recommendations (selected authoritative sources)

• The Institute of Medicine (IOM/NAS, 2011) established Dietary Reference Intakes: generally 600 IU/day (15 μg) for most adults up to 70, and 800 IU/day (20 μg) for adults over 70 to maintain bone health and normal calcium metabolism. The IOM report considered 25(OH)D ≥ 20 ng/mL as sufficient for most of the population. NCBI

• NIH Office of Dietary Supplements (ODS) provides up-to-date fact sheets, safety information, and acknowledges evolving evidence on extra-skeletal effects. The ODS emphasizes that supplements are important for those with low production from sunlight or dietary sources. Office of Dietary Supplements

• Endocrine Society guidelines (and recent updates) often recommend higher targets (e.g., aiming for 30 ng/mL) in specific clinical contexts and provide treatment regimens for deficiency; the Endocrine Society also issued a 2024 clinical practice guideline on vitamin D for disease prevention that clarifies indications where supplementation might be appropriate. Endocrine SocietyPubMed

Supplementation regimens

• Maintenance dosing: commonly 800–2000 IU/day for adults, with higher doses for those at high risk or with proven deficiency.

• Repletion protocols: may use higher daily doses (e.g., 50,000 IU weekly for 6–8 weeks) or equivalent regimens, followed by maintenance dosing — guided by baseline level and clinical context.

• Form preference: vitamin D₃ (cholecalciferol) is often preferred over D₂ for potency and duration of effect. Office of Dietary Supplements

Safety and toxicity

• Vitamin D toxicity (hypervitaminosis D) is generally due to excessive supplemental intake, not sunlight. It presents with hypercalcemia and its manifestations (nausea, vomiting, polyuria, polydipsia, dehydration, renal impairment, calcification). Toxicity thresholds vary, but sustained intakes of very high doses (e.g., >10,000 IU/day long-term) increase the risk; serum 25(OH)D levels >150 ng/mL are associated with toxicity. Routine supplementation within recommended ranges is safe for most people. Care is needed when combining high-dose vitamin D with calcium supplements. Office of Dietary Supplements

13. Controversies and evidence for extra-skeletal benefits

A substantial portion of research interest concerns whether vitamin D supplementation prevents or improves outcomes outside bone health. The evidence landscape includes:

• Observational studies: many report associations between low 25(OH)D and higher risk of infections, autoimmune diseases, cardiovascular disease, diabetes, cancer, and mortality. Because low vitamin D can be a marker of poor health or low sun exposure rather than a causal factor, observational results require confirmation by randomized controlled trials (RCTs).

• Randomized trials: Mixed results. For some endpoints (e.g., respiratory infections in certain groups), meta-analyses of RCTs suggest modest benefit for individuals with profound deficiency. For major outcomes such as cardiovascular disease, cancer incidence, or diabetes prevention, large RCTs have produced largely null or small effects, with subgroup or secondary analyses sometimes hinting at benefit in deficient subpopulations. High-quality recent trials and meta-analyses underscore modest or no benefit for broad primary prevention in unselected populations, leading many guideline bodies to recommend against routine supplementation solely for non-skeletal disease prevention. PubMedPMC

• Mendelian randomization and genetic studies: provide mixed evidence on causality; some analyses support causal links for certain outcomes (e.g., very low vitamin D and bone disease), while others do not support broad causal effects on cardiovascular disease or cancer.

• Heterogeneity and thresholds: one persistent issue is whether benefits exist only below certain 25(OH)D thresholds (e.g., <12–20 ng/mL). If so, trials enrolling participants with adequate baseline status may dilute potential treatment effects.

Because of this complexity, leading clinical organizations advise targeted testing and supplementation for those at risk of deficiency and caution against mass supplementation for disease prevention without clear indications. Recent guideline updates (e.g., Endocrine Society 2024) attempt to synthesize the trial data and provide conditional recommendations. PubMedPMC

14. Guidelines and consensus statements (IOM/NAS, Endocrine Society, NIH ODS, others)

Key authorities and their positions:

• Institute of Medicine (IOM/NAS), 2011: focused on bone health and concluded that 25(OH)D ≥20 ng/mL suffices for most—set RDAs as described earlier. The IOM committee was cautious about endorsing higher thresholds without stronger evidence for extraskeletal outcomes. NCBI

• Endocrine Society: often issues more clinically oriented guidance with higher target levels in specific situations (e.g., patients with osteopenia/osteoporosis, malabsorption, obesity, older adults). The Endocrine Society also released a 2024 clinical practice guideline addressing vitamin D for disease prevention that evaluates recent trial data and provides recommendations. Endocrine SocietyPubMed

• NIH Office of Dietary Supplements (ODS): provides accessible fact sheets and periodic updates summarizing evidence and safety information; it supports targeted supplementation in at-risk groups and highlights the need for more research on extraskeletal outcomes. Office of Dietary Supplements

• Consensus statements and reviews: recent expert panels and review articles (e.g., endocrine review articles, consensus statements on status assessment) emphasize assay standardization, cautious interpretation, and targeted strategies rather than universal high-dose supplementation. Oxford AcademicPMC

15. Practical clinical approach: diagnose, treat, monitor

A pragmatic approach for clinicians:

1. Who to test: test patients with risk factors (malabsorption, chronic kidney disease, liver disease, obesity, older adults with falls/fractures, certain medications that affect vitamin D metabolism, dark skin with limited sun exposure, institutionalized patients). Routine screening of the general, healthy population is not universally recommended. PubMed

2. What to measure: serum 25(OH)D (total). Consider calcium, phosphate, creatinine, and PTH in complex cases. Measure 1,25(OH)₂D only when indicated. Oxford Academic

3. Treatment of deficiency: typical repletion regimens range from 50,000 IU weekly for 6–8 weeks (ergocalciferol or cholecalciferol) to daily high doses, followed by maintenance dosing (800–2000 IU/day or individualized dosing) to maintain target 25(OH)D. Verify repletion with repeat 25(OH)D measurement after 8–12 weeks. In malabsorption or bariatric surgery, higher doses or intramuscular formulations may be necessary. Office of Dietary Supplements

4. Monitoring and safety: monitor for biochemical signs of toxicity if very high doses are used. Avoid excessive supplementation without clear indication. Be cautious with combined calcium supplementation in patients with cardiovascular risk. Office of Dietary Supplements

5. Counseling: encourage safe sun exposure balanced with skin cancer prevention, dietary sources (fatty fish, fortified dairy/alternatives), and adherence to supplementation when indicated. Discuss uncertainty around extraskeletal benefits but emphasize the well-established skeletal benefits in deficient individuals. NCBIOffice of Dietary Supplements

16. Future research directions and knowledge gaps

Key unresolved questions:

• Causal relationships for extraskeletal diseases: Do low vitamin D levels cause disease, or are they markers of ill health? Large, well-designed RCTs in deficient populations are needed to clarify causality for cardiovascular disease, cancer, autoimmunity, and metabolic disorders. PubMed

• Optimal serum targets: consensus on a single universal target is lacking; whether higher thresholds benefit specific subpopulations remains an open question. NCBI

• Personalized dosing: the role of genetics (polymorphisms in VDBP, CYP2R1, CYP27B1, VDR) and individual factors (obesity, absorption) in determining optimal dosing needs further study.

• Local production and tissue-specific effects: mechanistic studies to link autocrine/paracrine production of 1,25(OH)₂D to clinically meaningful outcomes.

• Assay standardization and free vs total 25(OH)D: measuring bioavailable vitamin D and developing clinically useful thresholds.

High-quality, targeted trials and mechanistic research will remain essential to inform practice beyond bone health. Oxford AcademicPubMed

17. Conclusion — pragmatic framing: vitamin, prohormone, or hormone?

• Vitamin (nutrient) aspect: Humans require vitamin D (or adequate UVB exposure) to prevent rickets and osteomalacia. In that sense, vitamin D is a nutrient essential to health — the classical reason it was named a vitamin.

• Prohormone/hormone aspect: After 25-hydroxylation and renal (or local) 1α-hydroxylation, the resulting calcitriol (1,25(OH)₂D) binds the VDR and regulates gene expression with endocrine and autocrine/paracrine effects. This steroid-receptor mechanism and widespread tissue distribution of VDR/CYP27B1 define it as a hormone or at least a prohormone whose active form is a hormone.

Practical answer: Vitamin D should be considered a prohormone that becomes a hormone after enzymatic activation — it is both a necessary nutrient (vitamin) and a hormonally active signaling molecule. Clinicians and policymakers should therefore (a) prevent and treat deficiency to protect bone health, (b) use supplementation judiciously where evidence supports benefit, and (c) await stronger randomized evidence before recommending widescale supplementation for unproven extraskeletal outcomes. NCBIOffice of Dietary SupplementsPubMed

18. References and selected further reading

(Key, authoritative sources cited in the article — click titles if you want to read the original documents.)

1. NIH Office of Dietary Supplements — Vitamin D (Health Professional Fact Sheet). Updated regularly; practical overview of sources, function, deficiency, and safety. Office of Dietary Supplements
   — NIH ODS fact sheet (Health Professional): https://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/

2. Holick MF. Vitamin D deficiency. New England Journal of Medicine. 2007;357(3):266–281. Seminal clinical review on deficiency and physiology. PubMed
   — NEJM review: https://pubmed.ncbi.nlm.nih.gov/17634462/

3. Vitamin D: Production, Metabolism, and Mechanism of Action. (NCBI Bookshelf/Physiology chapter). Detailed mechanistic overview of activation, enzymes, and actions. NCBI
   — NCBI Bookshelf chapter: https://www.ncbi.nlm.nih.gov/books/NBK278935/

4. Dietary Reference Intakes for Calcium and Vitamin D (Institute of Medicine, 2011). Authoritative review establishing RDAs and population targets for bone health. NCBI
   — IOM report summary: https://www.ncbi.nlm.nih.gov/books/NBK56070/

5. Consensus Statement: Vitamin D status assessment and recommendations (Endocrine Reviews / Academic consensus articles; see recent consensus 2023–2024). Focus on assay standardization and interpretation. Oxford Academic

6. Endocrine Society — Clinical Practice Guideline: Vitamin D for the Prevention of Disease (2024). Recent guideline synthesizing trial data and offering practice recommendations. PubMedEndocrine Society

7. Guidelines for Preventing and Treating Vitamin D Deficiency. Review of repletion regimens and target levels (systematic review/guideline). PMC

8. Vitamin D Metabolism, Mechanism of Action, and Clinical Applications (PMCID review, 2014). Comprehensive review of metabolism and clinical roles. PMC

Notes on citations and how I used them

• I relied primarily on reviews, guideline statements, and evidence syntheses from the NIH, peer-reviewed journals (NEJM, J Clin Endocrinol Metab, Endocrine Reviews), and consensus guidance because these sources best represent current, authoritative understanding.

• Wherever I described fundamental physiology (metabolic steps, enzymes, receptor mechanism) I cited textbook/review material (NCBI Bookshelf, PMCID reviews).

• For contemporary guideline positions and the most recent evaluations of evidence for disease prevention, I cited the Endocrine Society’s clinical practice guideline (2024) and consensus reviews.

• For public health intake recommendations and rationale, I cited the IOM (2011) and NIH ODS.

• For clinical issues such as toxicity, supplementation regimens, and monitoring I cited NIH ODS and guideline reviews.

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