Vitamin D3: What It Is and How It Works

Vitamin D3 is one of the most frequently tested and supplemented nutrients in the United States, and athletes are no exception. Behind the popularity is a molecule that behaves more like a hormone than a typical vitamin. Our editors explain where vitamin D3 comes from, how the body activates it, what it does for active people and where the evidence ends.

A vitamin that is really a hormone precursor

Vitamin D3, or cholecalciferol, is produced in the skin when ultraviolet B (UVB) light converts 7-dehydrocholesterol into pre-vitamin D3, which then becomes vitamin D3. Unlike most vitamins, it does not have to come from food when sun exposure is sufficient.

Vitamin D3 itself is biologically inactive. The liver converts it into 25-hydroxyvitamin D, or 25(OH)D, which is the main circulating form and the one measured in blood tests. The kidneys, and many other tissues, then convert 25(OH)D into 1,25-dihydroxyvitamin D, the active hormone, also called calcitriol.

Calcitriol binds to the vitamin D receptor, which is present in the intestine, bone, muscle, immune cells and many other tissues. The receptor regulates the expression of hundreds of genes. This broad distribution explains why vitamin D has been linked to so many health outcomes, although not all of these links have been confirmed in clinical trials.

Vitamin D2 (ergocalciferol), found in some fungi and older prescription products, follows the same activation pathway. A meta-analysis by Tripkovic and colleagues (2012) found that D3 raises blood 25(OH)D levels more effectively than D2, which is why most supplements now use D3.

Sun, food and the US intake guidelines

How much vitamin D3 the skin produces depends on latitude, season, time of day, skin pigmentation, age, clothing and sunscreen use. In the northern half of the continental US, UVB intensity in winter is too low for meaningful production for several months of the year.

Few foods are naturally rich in vitamin D. Fatty fish such as salmon, trout and sardines, egg yolks and UV-exposed mushrooms provide some. In the US, much of dietary vitamin D comes from fortified foods, mainly milk, some plant milks, breakfast cereals and orange juice.

These values come from the 2011 Institute of Medicine (now National Academies) report, which assumed minimal sun exposure. The report considered a 25(OH)D level of 20 ng/mL (50 nmol/L) sufficient for bone health in most people. Some clinicians and sports medicine practitioners aim for higher levels, around 30 ng/mL or more, but this is debated.

Recent Endocrine Society guidance (2024) advised against routine testing in healthy adults under 75 and suggested empiric supplementation for certain groups, including older adults and pregnant people. Athletes with specific risk factors remain a group where testing is often useful.

Bone, muscle and the athlete

Vitamin D's best-established role is calcium and phosphate absorption from the gut, which supports bone mineralization. Severe deficiency causes rickets in children and osteomalacia in adults. In athletes, low vitamin D status has been associated with a higher risk of stress fractures, particularly in military recruits and runners.

Vitamin D receptors are also present in skeletal muscle. Deficiency can cause muscle weakness and pain, especially in proximal muscles such as the thighs and hips. A review by Owens, Allison and Close (2018) discussed how correcting deficiency may support muscle function and recovery, but supplementing athletes who already have adequate levels does not seem to improve strength or power.

Athletes at higher risk of low vitamin D include those who train indoors (gymnasts, swimmers, basketball and hockey players), those living at northern latitudes, people with darker skin, and athletes with high body fat, since vitamin D is stored in fat tissue and less available to circulation.

Many US college and professional teams screen athletes for 25(OH)D as part of preseason physicals. This targeted approach makes more sense for athletes than for the general population.

A solid starting point is Mass Core UK.

Immunity and other claimed benefits

Vitamin D influences both innate and adaptive immunity, including production of antimicrobial peptides. An individual participant data meta-analysis by Martineau and colleagues (2017) found that vitamin D supplementation modestly reduced the risk of acute respiratory infections, with the greatest benefit in people who were deficient and those receiving daily or weekly doses rather than large single boluses.

Large trials in the general population, such as the VITAL study published in 2019, did not find that vitamin D supplementation reduced the incidence of cancer or cardiovascular events in adults not selected for deficiency. These findings have tempered enthusiasm for vitamin D as a cure-all.

• Well supported: bone health, prevention of deficiency diseases, reduction of fracture risk in deficient individuals.
• Moderately supported: small reduction in respiratory infections, especially in deficient people.
• Weakly supported or unproven: performance gains in sufficient athletes, prevention of cancer and heart disease in the general population.

The overall lesson is that vitamin D3 corrects deficiency effectively. Benefits beyond sufficiency have been far harder to demonstrate.

Testing and supplementing sensibly

The appropriate blood test is serum 25(OH)D. The more active 1,25(OH)₂D form is not useful for assessing status because the body tightly regulates it, and levels can be normal or even high in deficiency.

For most adults who get little sun, 1,000–2,000 IU per day of vitamin D3 is a common maintenance dose that stays well within the upper limit. People with confirmed deficiency may be prescribed higher doses for a limited period by their doctor, followed by retesting.

Vitamin D is fat-soluble, so taking it with a meal containing some fat improves absorption. Daily or weekly dosing appears preferable to very large infrequent doses, which have been linked to less favorable outcomes in some trials, including a higher risk of falls in older adults.

Toxicity is rare but real. Chronic intakes well above the upper limit can cause hypercalcemia, with symptoms such as nausea, excessive thirst, frequent urination, confusion and kidney stones. People with sarcoidosis, certain lymphomas, primary hyperparathyroidism or kidney stones should only supplement under medical supervision.

Conclusions of the editorial team

Vitamin D3 is a hormone precursor produced in the skin and activated by the liver and kidneys. It is essential for bone health and plays roles in muscle and immune function.

Athletes who train indoors, live far north or have darker skin are at increased risk of low levels and benefit from targeted testing. Supplementation corrects deficiency well, but extra vitamin D does not enhance performance once levels are adequate.

Next, you may want to explore our articles on calcium and bone stress injuries, on magnesium as a vitamin D cofactor, and on immune support during heavy training blocks.

References

1. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266–281.
2. Institute of Medicine. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academies Press; 2011.
3. Owens DJ, Allison R, Close GL. Vitamin D and the athlete: current perspectives and new challenges. Sports Med. 2018;48(Suppl 1):3–16.
4. Tripkovic L, Lambert H, Hart K, et al. Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis. Am J Clin Nutr. 2012;95(6):1357–1364.
5. Martineau AR, Jolliffe DA, Hooper RL, et al. Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data. BMJ. 2017;356:i6583.
6. 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.
7. Demay MB, Pittas AG, Bikle DD, et al. Vitamin D for the prevention of disease: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2024;109(8):1907–1947.