on February 26, 2026
Vitamin D for Athletes: Testing, Dosing, and Deficiency
Regulatory note: Vitamin D is an essential fat-soluble micronutrient. The structure/function statements in this article have not been evaluated by the Food and Drug Administration. Vitamin D supplements are not intended to diagnose, treat, cure, or prevent any disease. Dosing guidance in this article is general educational information — consult a qualified healthcare provider before beginning any supplementation protocol, particularly at doses above 2,000 IU/day.
Vitamin D deficiency is one of the most common and most overlooked problems in athletic populations. If you train primarily indoors — in a gym, a CrossFit box, a HYROX facility, or any covered environment — you are producing little to no vitamin D during your training sessions, regardless of how many hours per week you put in. This guide covers what vitamin D actually does, why athletes are at elevated deficiency risk, how to test and interpret your blood levels, how to determine the right dose for your baseline, and what to look for in a supplement worth taking.
What Vitamin D Actually Is
Despite being called a vitamin, vitamin D functions more like a hormone in the body. Unlike true vitamins that must be obtained entirely from food, vitamin D is synthesized endogenously — the skin produces it when exposed to ultraviolet B (UVB) radiation from sunlight. The dietary form accounts for a much smaller proportion of vitamin D status in most populations than sun exposure does.
The process begins when UVB radiation converts 7-dehydrocholesterol in skin cells to previtamin D3, which isomerizes to cholecalciferol (vitamin D3). This travels to the liver where it is hydroxylated to 25-hydroxyvitamin D — the storage form and the biomarker measured in blood tests. The kidneys then convert 25(OH)D to 1,25-dihydroxyvitamin D (calcitriol), the biologically active hormone that interacts with vitamin D receptors (VDRs) in virtually every tissue in the body.
Why "Hormone" Is More Accurate Than "Vitamin"
The vitamin D receptor (VDR) has been identified in over 35 different tissue types — including skeletal muscle, cardiac muscle, immune cells, bone, brain, and the gut. Calcitriol regulates the expression of hundreds of genes. A compound that acts through a nuclear receptor to regulate gene transcription across virtually every tissue in the body is functionally a hormone, not a cofactor in a single metabolic reaction. This is why vitamin D deficiency affects so many physiological systems simultaneously.
Why Athletes Are at Higher Deficiency Risk
The general population has high rates of vitamin D deficiency — estimates suggest 40–50% of US adults have insufficient levels. Athletes, counterintuitively, have rates that are at least as high and in some populations significantly higher. The reasons are specific and addressable.
~40% of US adults estimated to have insufficient vitamin D levels (<30 ng/mL)
56–77% of indoor athletes in research populations found to be vitamin D insufficient
0 IU vitamin D produced during training in a gym, CrossFit box, or any indoor facility regardless of duration
>37°N latitude where meaningful UVB synthesis is unavailable November–March even outdoors
Indoor Training Environment
Glass blocks UVB radiation. Training in any indoor facility — regardless of windows — produces zero vitamin D. An athlete logging 12 hours per week in a gym is spending 12 hours in zero-UVB exposure, while potentially reducing their time for outdoor sun exposure by the same margin.
This is the primary risk factor for the Fathom ICP — CrossFit, HYROX, powerlifting, and functional fitness athletes train predominantly or entirely indoors.
Northern Latitude (above 37°N)
Above approximately 37°N latitude (roughly the level of San Francisco, Denver, or Richmond, VA), the sun's angle from October through March is insufficient for meaningful UVB synthesis regardless of time outdoors. The entire northern half of the US, all of Canada, the UK, and most of Europe experience a 4–6 month window each year where outdoor exposure alone cannot maintain vitamin D status.
High Skin Melanin Concentration
Melanin reduces UVB penetration, requiring 3–10× longer sun exposure to produce equivalent vitamin D compared to lower melanin concentrations. This is a significant biological modifier — athletes with higher melanin concentration require more sun exposure or higher supplemental doses to reach the same serum 25(OH)D level.
Sunscreen and Clothing Coverage
SPF 15 reduces vitamin D synthesis by approximately 99%. Full clothing coverage during outdoor training limits the skin surface area available for synthesis. Athletes who consistently wear sunscreen and/or train covered outdoors effectively eliminate sun-based vitamin D production regardless of exposure time.
Body Composition
Vitamin D is fat-soluble and is sequestered in adipose tissue. Counterintuitively, athletes with high body fat percentage may have lower circulating 25(OH)D despite similar intake, because more vitamin D is stored rather than circulating. This is less relevant for lean athletes, but worth noting for body composition diversity within the population.
Low Dietary Intake
Very few foods contain meaningful vitamin D: fatty fish (salmon, mackerel, sardines), egg yolks, and fortified foods are the primary sources. Athletes not regularly consuming these foods obtain minimal dietary vitamin D. The typical Western diet provides 150–400 IU/day — far below maintenance requirements when sun exposure is absent.
What Vitamin D Does: Evidence-Based Functions
Musculoskeletal Function Most directly relevant to athletes
Vitamin D receptors are present in skeletal muscle tissue. Research has associated adequate vitamin D status with normal muscle function, force production, and muscle fiber composition. Studies in athletic populations have found correlations between vitamin D status and measures of strength and power, though the evidence for causal performance improvement from supplementation in already-sufficient athletes is less consistent than the evidence for restoring function in deficient individuals.
Vitamin D is also essential for calcium absorption in the gut — the primary mechanism through which it supports bone mineral density and structural integrity. In athletes with high impact loading (running, jumping, barbell training), bone health is a direct performance variable.
Immune System Regulation Highly relevant for high-volume training blocks
Vitamin D receptors are expressed on virtually all immune cells including T cells, B cells, and macrophages. Calcitriol modulates both innate and adaptive immune responses. Research has consistently associated lower vitamin D status with increased upper respiratory illness frequency — a well-documented problem in athletes during heavy training phases when immune function is transiently suppressed.
For athletes managing high training loads, adequate vitamin D status may support immune resilience during periods when training stress is high and recovery is compressed. Structure/function claim: vitamin D supports normal immune function.
Inflammatory Response Modulation Recovery-relevant
Vitamin D influences the production of inflammatory cytokines and has been studied in the context of acute and chronic inflammatory responses. Adequate vitamin D status is associated with more regulated inflammatory signaling — relevant to both post-training recovery and chronic systemic inflammation risk in high-volume athletes.
The mechanism involves calcitriol's influence on NF-κB signaling — a central regulator of inflammatory gene expression — and its promotion of anti-inflammatory cytokine production.
Cardiovascular and Metabolic Function General health foundation
VDRs are present in cardiac muscle and vascular smooth muscle. Research has associated vitamin D status with normal blood pressure regulation, cardiac function, and glucose metabolism. For athletes focused on cardiovascular performance, adequate vitamin D may support the vascular and metabolic foundation on which training adaptations are built — though it is not a performance supplement in the direct sense that creatine or citrulline are.
Hormonal Axis Support Relevant for strength athletes
Some research has found associations between vitamin D status and testosterone levels in men, with deficient individuals showing lower testosterone than sufficient individuals. Several intervention studies have found modest increases in testosterone with vitamin D supplementation in deficient men. The relationship is not fully established as causal, and the magnitude of effect is modest — but it represents a mechanistically plausible pathway given VDR expression in Leydig cells and the role of vitamin D in steroidogenesis.
How to Test Your Vitamin D Level
Dosing vitamin D intelligently requires knowing your baseline. Without a blood test, you are supplementing blindly — potentially undertreating deficiency or, in rare cases, contributing to excess accumulation of a fat-soluble vitamin. Testing is inexpensive, widely available, and the single most important step in building a rational vitamin D protocol.
Which Test to Order
The correct test is serum 25-hydroxyvitamin D [25(OH)D] — also written as 25-OH vitamin D or calcidiol. This is the storage form and the accepted clinical marker for vitamin D status. Do not confuse it with 1,25-dihydroxyvitamin D (calcitriol, the active hormone) — calcitriol levels do not accurately reflect vitamin D stores and can be normal or even elevated in deficient individuals due to compensatory upregulation of the converting enzyme.
How to get tested: A standard vitamin D panel is available through your primary care provider, a direct-to-consumer lab service (LabCorp, Quest, or online services), or an annual wellness panel. It typically costs $30–60 without insurance. Many insurance plans cover it, particularly if you have documented risk factors. Home finger-prick tests are also available but show more variability than standard venous draws — use a standard lab test for the baseline reading.
When to test: Test in late winter (February–March in the Northern Hemisphere) for your lowest annual level, and in late summer (August–September) for your highest. This gives you the full seasonal picture. If you supplement, retest 8–12 weeks after beginning a new protocol to assess response.
Interpreting Your Results: The 25(OH)D Scale
Results are reported in ng/mL (US) or nmol/L (most other countries). To convert: multiply ng/mL by 2.5 to get nmol/L. The scale below uses ng/mL.
Serum 25(OH)D Reference Ranges — ng/mL
Deficient < 20 ng/mL Clinical deficiency. Significant impairment of calcium absorption, bone remodeling, immune function, and musculoskeletal performance. Requires aggressive repletion, ideally under medical supervision.
Insufficient 20–29 ng/mL Below optimal. Endocrine Society and many sports medicine organizations consider this insufficient for athletes. Secondary hyperparathyroidism can develop as the body attempts to maintain calcium homeostasis. Supplementation and/or sun exposure protocol warranted.
Sufficient (IOM) 30–49 ng/mL Meets the Institute of Medicine's sufficiency threshold. Adequate for bone health in the general population. Some sports medicine researchers and clinicians argue athletes perform best at the higher end of this range or slightly above it.
Optimal for Athletes 40–60 ng/mL The range most frequently cited in athletic performance and sports medicine literature for optimal musculoskeletal, immune, and metabolic function. The Endocrine Society considers up to 60 ng/mL safe and appropriate. Most supplementation protocols for athletes are designed to target this range.
Excess / Monitoring Zone 60–100 ng/mL Above the target range for most individuals. Not necessarily toxic at this level, but warrants attention and dose adjustment. Higher doses over extended periods can push levels into this range — which is why periodic retesting matters.
Toxicity Risk > 100 ng/mL Vitamin D toxicity risk zone. Hypercalcemia, nausea, weakness, kidney impairment possible. This level is not achievable through sun exposure alone — only through very high prolonged supplemental doses. Requires medical evaluation and cessation of supplementation.
The Athlete Target: 40–60 ng/mL
For the Fathom ICP — a serious athlete training 5–12 hours per week, predominantly indoors, with high physical demand on musculoskeletal and immune systems — the goal of supplementation is to maintain serum 25(OH)D in the 40–60 ng/mL range year-round. This requires knowing your baseline and adjusting dose seasonally. There is no universal dose that achieves this across all individuals — which is why testing is not optional if you want to do this intelligently.
Dosing by Baseline: A Practical Framework
Individual response to vitamin D supplementation varies significantly based on baseline level, body weight, absorption, genetics, and baseline sun exposure. The table below is a general framework — not a medical protocol. Doses above 4,000 IU/day warrant physician oversight and periodic monitoring.
| Baseline 25(OH)D | Starting Dose Range | Retest Timeline | Notes |
|---|---|---|---|
| < 20 ng/mL (Deficient) | 4,000–6,000 IU/day, or physician-directed loading dose | 8–12 weeks | Clinical deficiency — consult a physician. Loading protocols (50,000 IU weekly for 8 weeks) are sometimes prescribed but require monitoring. Daily dosing at 4,000–6,000 IU is a safer self-directed approach with retesting. |
| 20–29 ng/mL (Insufficient) | 2,000–4,000 IU/day | 8–12 weeks | Common starting range for indoor athletes in northern climates during winter. Most individuals in this range reach target (40–60 ng/mL) within 8–12 weeks at 2,000–4,000 IU/day. |
| 30–39 ng/mL (Low-sufficient) | 1,000–2,000 IU/day | 12–16 weeks or annual | Maintenance territory. Lower doses are appropriate; goal is to move to mid-sufficient range and maintain it seasonally. Sun exposure in summer may allow dose reduction or elimination. |
| 40–60 ng/mL (Optimal) | 1,000–2,000 IU/day (maintenance) | Annually (seasonal testing) | Already in target range. Maintenance dosing to prevent seasonal decline. Reduce or pause in peak summer if outdoor exposure is substantial. Retest in late winter to confirm maintenance. |
| > 60 ng/mL (Excess zone) | Pause or reduce significantly | 8 weeks after dose change | No additional supplementation needed. Assess whether previous protocol drove excess. Reduce to 500–1,000 IU/day or pause entirely until retest confirms return to target range. |
The practical rule: As a rough estimate, each 1,000 IU of daily vitamin D3 supplementation raises serum 25(OH)D by approximately 5–10 ng/mL over 8–12 weeks in most adults — though individual response varies significantly. This estimate is useful for planning a protocol, not for replacing actual blood testing.
D3 vs D2: Why the Form Matters
Vitamin D3 (Cholecalciferol)
Preferred form
The form produced naturally by human skin in response to UVB radiation. D3 is also the form found in animal-sourced foods (fatty fish, egg yolks, liver).
- Bioavailability: Raises serum 25(OH)D approximately 2–3× more effectively than equivalent D2 dose
- Half-life: Longer half-life in circulation than D2, meaning it maintains blood levels more consistently
- Stability: More stable in supplement formulations
- Source: Typically derived from lanolin (sheep's wool) or lichen (vegan D3)
For athletes: D3 is the correct form for performance-oriented supplementation. It is what your body makes, it raises levels more effectively, and it maintains those levels more consistently.
Vitamin D2 (Ergocalciferol)
Inferior form
Plant-derived form, found naturally in mushrooms exposed to UV light. D2 is what most prescription-dose vitamin D is dispensed as (50,000 IU capsules) — for historical reasons rather than superiority.
- Bioavailability: Less effective at raising and maintaining serum 25(OH)D compared to D3
- Half-life: Shorter — levels decline faster between doses
- Meta-analysis data: Multiple studies confirm D3 superiority for raising 25(OH)D
- Use case: Appropriate for vegans without access to vegan D3; otherwise no advantage over D3
Vegan athletes: lichen-derived D3 provides the preferred form without animal sourcing.
Oil-Based vs Powder Capsule: Does It Matter?
Vitamin D is fat-soluble, meaning it is absorbed more efficiently in the presence of dietary fat. Research has confirmed that oil-based vitamin D supplements (softgels containing D3 in an oil carrier) produce meaningfully better absorption than dry powder tablet formulations when taken in a fasted state or without a fat-containing meal. The practical recommendation: take vitamin D with your largest meal of the day, or choose an oil-based softgel formulation. Taken with a fat-containing meal, the difference between oil and powder forms narrows substantially.
What Quality Actually Looks Like
Vitamin D is one of the most consistently mislabeled supplement categories. Testing of commercial products has found significant discrepancies between labeled and actual vitamin D content — in both directions. Some products contain less than 50% of labeled dose; others contain substantially more. For a fat-soluble vitamin where toxicity is possible at chronically excessive doses, label accuracy is not a minor concern.
Vitamin D Quality Checklist
Form: Vitamin D3 (cholecalciferol), not D2. Label should specify D3 clearly.
Third-party testing: NSF Certified for Sport, USP Verified, or Informed Sport. Independent batch testing for label accuracy — not just GMP manufacturing certification.
Carrier oil: Oil-based softgel (olive oil, MCT, sunflower) for maximum absorption in the fasted state. Powder capsules work but require co-ingestion with a fat-containing meal.
IU disclosure: Clear IU amount per serving. 1,000 IU and 2,000 IU are the most practical dose increments for home self-management.
No unnecessary additives: Artificial colors, artificial flavors, and unnecessary fillers serve no function in a vitamin D supplement.
Avoid: D2 (ergocalciferol) as the primary form. Labels that don't specify D2 vs D3. Products without independent third-party testing. Proprietary "vitamin D complexes" with undisclosed amounts.
Avoid: Mega-dose products (25,000–100,000 IU per capsule) for self-directed use. These doses require medical supervision and periodic monitoring — they are not appropriate for daily unsupervised supplementation.
Cofactors: K2, Magnesium, and Fat
Vitamin D does not operate in isolation. Three cofactors meaningfully influence either the effectiveness of vitamin D supplementation or the downstream utilization of the vitamin D-regulated calcium it promotes:
Vitamin K2
Vitamin K2 (specifically MK-7 form) activates osteocalcin and matrix Gla protein — two vitamin K-dependent proteins that direct calcium into bone and prevent its accumulation in soft tissue (arteries, kidneys). As vitamin D supplementation increases calcium absorption, adequate K2 ensures that calcium is directed appropriately.
The concern: high-dose D3 supplementation without adequate K2 theoretically increases arterial calcification risk. The evidence for this concern is not definitive, but K2 co-supplementation is widely recommended by clinicians at doses of 90–200 mcg MK-7/day when taking D3 above 2,000 IU.
MK-7 is preferred over MK-4 — longer half-life, better bioavailability at lower doses.
Magnesium
Magnesium is required for the conversion of vitamin D to its active form. Both the hepatic 25-hydroxylation and renal 1α-hydroxylation steps are magnesium-dependent enzymatic reactions. Magnesium deficiency can impair vitamin D activation — meaning adequate supplementation with D3 may produce lower-than-expected blood level response in magnesium-deficient individuals.
Athletes are among the highest-risk populations for magnesium insufficiency due to sweat losses and high metabolic demand. Ensuring adequate magnesium (from food or supplementation) is a prerequisite for effective vitamin D utilization.
Form matters: Magnesium bisglycinate or glycinate — not oxide (~4% absorption).
Dietary Fat
Vitamin D is fat-soluble — it requires bile and dietary fat for emulsification and absorption in the small intestine. Taking vitamin D in a completely fasted state, particularly from a powder capsule, meaningfully reduces absorption compared to taking it with a fat-containing meal.
Practical recommendation: Take vitamin D with your largest meal, which for most people includes dietary fat. If you use an oil-based softgel, this is less critical — but co-ingestion with food remains best practice.
Seasonal Adjustments
Summer (May–September, Northern Hemisphere)
For athletes at latitudes below 50°N with meaningful outdoor exposure, supplementation needs may decrease substantially. 15–30 minutes of midday summer sun on arms and legs without sunscreen can produce 10,000–25,000 IU equivalent in light-skinned individuals — but this depends heavily on skin type, latitude, time of day, and cloud cover.
Practical approach: reduce supplemental dose to 500–1,000 IU/day in summer if you have regular outdoor exposure, and retest in September to confirm levels have been maintained in target range.
For athletes who train exclusively indoors year-round, summer outdoor supplementation may still be warranted — they are not producing vitamin D from their training regardless of season.
Winter (October–April, Northern Hemisphere)
Above 37°N latitude, meaningful UVB synthesis is essentially unavailable from November through February regardless of outdoor time. Supplementation becomes the sole reliable source of vitamin D maintenance during this period.
Athletes should plan for higher winter doses — particularly if autumn testing reveals levels approaching the lower end of sufficient range. A level of 45 ng/mL in September will often decline to 25–30 ng/mL or lower by March without supplementation in northern climates.
Winter dose: whatever is required to maintain 40–60 ng/mL based on your known response rate. For many indoor athletes in northern climates, this is 2,000–4,000 IU/day.
The Upper Limit and Toxicity Risk
Vitamin D toxicity (hypervitaminosis D) is real but is not achievable through sun exposure — the skin has a self-limiting mechanism. It is only possible through supplementation, typically requiring sustained doses above 10,000 IU/day for extended periods or extremely high acute doses.
The Established Upper Limits
The Institute of Medicine's Tolerable Upper Intake Level (UL) for vitamin D is 4,000 IU/day for adults — established as safe for chronic daily intake without monitoring. The Endocrine Society's guidelines for clinically supervised supplementation allow up to 10,000 IU/day in certain clinical contexts. Doses above 4,000 IU/day for self-directed supplementation warrant physician involvement and periodic 25(OH)D testing. The toxicity concern — hypercalcemia and its sequelae — does not appear at blood levels below 100 ng/mL in most individuals. Maintaining 40–60 ng/mL does not approach toxicity territory.
The practical takeaway: the risk of toxicity from self-directed supplementation at 1,000–4,000 IU/day is very low. The risk of inadequate vitamin D status is substantially more common and more consequential for athletic performance and health. The solution to managing the risk of excess is periodic blood testing — not supplementing at doses that are too low to be effective.
FAQ
Do I really need to get a blood test before supplementing?
Technically no — supplementing at 1,000–2,000 IU/day is conservative enough that it is unlikely to cause harm in most adults regardless of baseline. But testing transforms a guess into a protocol. If you are at 15 ng/mL, 1,000 IU/day is woefully inadequate. If you are at 55 ng/mL, 4,000 IU/day could push you into excess territory. The $30–60 test cost is the best investment in making vitamin D supplementation actually accomplish what you are trying to accomplish. At minimum, test once to establish your baseline and understand how your body responds.
Can I get enough vitamin D from sunlight alone?
In summer, at latitudes below 50°N, with direct midday sun exposure on large skin surface areas (arms, legs, torso) without sunscreen — yes, in principle. In practice: most indoor athletes in the northern US and Europe do not achieve this consistently enough to maintain 40–60 ng/mL year-round. Above 37°N in winter, sun exposure cannot maintain adequate levels regardless of time outdoors. Testing tells you whether your actual combination of sun and diet is getting the job done. Most indoor athletes find it is not, particularly from October through March.
I train outdoors sometimes — does that count?
Yes, outdoor training in direct midday sun contributes to vitamin D synthesis, with meaningful caveats: sunscreen largely eliminates synthesis even outdoors; training early morning or late evening when the sun is low produces very little UVB regardless of exposure duration; cloud cover significantly reduces synthesis; and athletic clothing limits the skin surface area available. Blood testing is the only way to know whether your combination of outdoor training, diet, and sun exposure is maintaining adequate status.
What time of day should I take vitamin D?
With your largest meal containing dietary fat — typically breakfast or dinner. The timing relative to training does not matter; vitamin D is not an acute performance supplement. Consistency of daily dosing matters more than specific timing. Some individuals find vitamin D taken close to bedtime disrupts sleep; if this is your experience, morning or midday dosing is preferable.
Do I need to take K2 with vitamin D?
The evidence for K2 co-supplementation is suggestive rather than definitive, but the biological rationale is sound — both nutrients are involved in calcium regulation, and K2's role in directing calcium away from soft tissue while vitamin D increases calcium absorption represents a coherent interaction. Most clinicians recommend K2 (MK-7 form, 100–200 mcg/day) alongside D3 supplementation above 2,000 IU/day, particularly for long-term daily use. It is a low-risk, low-cost addition to a vitamin D protocol for any athlete supplementing consistently.
Will vitamin D improve my athletic performance?
If you are deficient or insufficient, correcting your status may restore normal musculoskeletal function, immune resilience, and hormonal support that deficiency was impairing. Whether supplementation in already-sufficient athletes produces additional performance benefit above the 40–60 ng/mL target range is not well-supported by current evidence. The value of vitamin D for athletes is primarily in ensuring adequate baseline status — not in pushing levels as high as possible. Structure/function claim: vitamin D supports normal muscle function, immune function, and bone health. These statements have not been evaluated by the FDA.
How long does it take to see results from vitamin D supplementation?
Blood levels respond over 8–12 weeks of consistent daily supplementation. The physiological effects that accompany status correction (improved immune function, musculoskeletal support) occur as levels rise — there is no acute effect from a single dose. Think of vitamin D as a foundation to establish and maintain year-round, not an acute supplement to deploy around training sessions.
Conclusion
Vitamin D is not a performance supplement in the way that creatine or citrulline are — it does not directly drive an acute training effect. What it is, for a serious indoor athlete, is a foundational micronutrient whose deficiency is common, consequential, and almost entirely preventable with a $30 blood test and a simple daily protocol.
The path forward is straightforward: test your 25(OH)D level, interpret the result using the scale in this article, select an appropriate D3 dose based on your baseline, take it with a fat-containing meal alongside K2 and adequate magnesium, and retest after 8–12 weeks to confirm your response. Adjust seasonally. The goal is 40–60 ng/mL year-round — not as high as possible, not whatever a standard multivitamin provides, but the specific range associated in the research literature with optimal function across the physiological systems that matter most for athletes.
The Athlete's Summary
You train hard. You train indoors. Your training produces zero vitamin D. The northern winter produces zero vitamin D regardless of outdoor time. Your diet likely provides 150–400 IU/day, far short of maintenance. The result, for the majority of indoor athletes, is chronic insufficiency that impairs the same systems — musculoskeletal, immune, inflammatory, hormonal — that you are training to develop. A blood test and a well-dosed D3 supplement fix this completely. It is one of the highest-leverage, lowest-cost interventions in athlete health — not because vitamin D is magic, but because deficiency is common and unnecessary.
† These statements have not been evaluated by the Food and Drug Administration. Vitamin D is a dietary supplement and is not intended to diagnose, treat, cure, or prevent any disease. The dosing guidance in this article is general educational information. Consult a qualified healthcare provider before beginning any supplementation protocol, particularly at doses above 2,000 IU/day or if you have pre-existing health conditions affecting calcium or kidney function.
Related reading: The Hybrid Athlete Supplement Stack · Creatine and Brain Function · Hybrid Training: A Complete Guide
References (Selected)
- Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266–81. PubMed
- Larson-Meyer DE, Willis KS. Vitamin D and athletes. Curr Sports Med Rep. 2010;9(4):220–6. PubMed
- Holick MF, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2011;96(7):1911–30. PubMed
- Tripkovic L, et al. Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status. Am J Clin Nutr. 2012;95(6):1357–64. PubMed
- Wacker M, Holick MF. Sunlight and vitamin D: a global perspective for health. Dermatoendocrinol. 2013;5(1):51–108. PMC
- Pilz S, et al. Effect of vitamin D supplementation on testosterone levels in men. Horm Metab Res. 2011;43(3):223–5. PubMed
- Dudenkov DV, et al. Changing incidence of serum 25-hydroxyvitamin D values above 50 ng/mL. Mayo Clin Proc. 2015;90(5):577–86. PubMed
- Charoenngam N, Holick MF. Immunologic effects of vitamin D on human health and disease. Nutrients. 2020;12(7):2097. PMC
- Uwitonze AM, Razzaque MS. Role of magnesium in vitamin D activation and function. J Am Osteopath Assoc. 2018;118(3):181–9. PubMed
- Schurgers LJ, et al. Vitamin K and vitamin D: from bone to heart, brain, and beyond. Nutrients. 2023;15(17):3724. PMC
