Vitamin D

Vitamin D is something of a misnomer — it’s more accurately described as a prohormone than a vitamin. Unlike true vitamins, the body can make it from sunlight; it has to be activated in two steps before it works; it travels in the blood on a dedicated carrier protein; and its active form (calcitriol) binds to receptors inside the nucleus of cells throughout the body to directly regulate genes — the way steroid hormones work. Vitamin D may influence the activity of hundreds to a few thousand genes, involved in calcium absorption, immune cell development, muscle function, insulin secretion, and cell growth. That breadth explains why low vitamin D has been linked to so many conditions in observational studies — though, as large trials have since shown, correcting low levels doesn’t fix all of them.

The Activation Pathway — How Sunlight Becomes a Hormone

Step 1 — Making it in the skin: when UVB rays (wavelength 290–315nm) hit exposed skin, they convert 7-dehydrocholesterol — a cholesterol relative stored in the skin — into previtamin D3, which then becomes vitamin D3 (cholecalciferol). This is the form made by sunlight and the form in most supplements.

Step 2 — Liver conversion: vitamin D3 travels to the liver, where an enzyme (CYP2R1) converts it to 25-hydroxyvitamin D [25(OH)D], or calcidiol. This is the main circulating form, and the one measured by standard blood tests. It lasts around 2–3 weeks in the blood, so it reflects vitamin D status over recent weeks.

Step 3 — Kidney activation: in the kidneys, another enzyme (CYP27B1) converts 25(OH)D into 1,25-dihydroxyvitamin D [1,25(OH)₂D] — calcitriol, the active hormone. This step is tightly controlled by parathyroid hormone (PTH), calcium, phosphate, the bone hormone FGF23, and calcitriol itself, so the body controls how much active vitamin D it makes, regardless of how much 25(OH)D is available.

The key point: sun exposure and supplements both raise 25(OH)D, the raw material for activation. The kidneys then decide how much becomes active calcitriol, which is why vitamin D supplements don’t simply raise the active hormone in proportion to the dose.

The vitamin D receptor (VDR): calcitriol works by binding to the vitamin D receptor, found in almost every type of cell — in the intestine, kidney, bone, immune cells, muscle, heart, brain, pancreas, reproductive organs, and skin. The receptor teams up with a partner receptor (RXR) and binds to specific stretches of DNA, switching target genes on or off. This is how vitamin D influences calcium handling, immune function, insulin secretion, and muscle.

Calcium and Phosphorus Regulation

Vitamin D’s best-established job is enabling the absorption of calcium and phosphorus:

Intestinal absorption: calcitriol switches on the production of calcium transport proteins in the gut lining. With adequate vitamin D, the body absorbs roughly 30–40% of dietary calcium; with severe deficiency, absorption falls to around 10–15%. That’s the main reason vitamin D deficiency causes bone disease — not because people don’t eat calcium, but because they can’t absorb enough of it.

The PTH feedback loop: when blood calcium falls, the parathyroid glands release PTH, which signals the kidneys to make more calcitriol. Calcitriol then increases calcium absorption from the gut and calcium recovery in the kidneys. As calcium returns to normal, PTH falls, and calcitriol and FGF23 help switch off further activation.

Vitamin D RDA (Recommended Dietary Allowance)

Source: US National Academies, via the NIH Office of Dietary Supplements. The daily value used on food labels is 20µg (800 IU). 1µg = 40 IU.

The debate over how much is enough: vitamin D has been one of the most debated nutrients of the past 15 years. The RDA was set in 2010 to keep blood 25(OH)D at or above 20ng/mL (50nmol/L), the level judged adequate for bone health. In 2011, the Endocrine Society argued for a higher target of 30ng/mL, and many practitioners still aim for 40–60ng/mL. Since then, several very large trials have tested whether extra vitamin D prevents disease. The biggest, VITAL, gave about 26,000 US adults 2,000 IU a day for around five years and found no reduction in cancer, heart disease, fractures, falls, or depression — though most participants weren’t deficient to begin with. In response, the Endocrine Society’s 2024 guideline no longer endorses the 30ng/mL target or specific cut-offs for “sufficiency” and “insufficiency,” and it suggests against routine vitamin D testing in healthy people, including people with darker skin or obesity.

What remains clear is that genuine deficiency — particularly below about 12ng/mL (30nmol/L) — harms bones and muscles, and that some groups benefit from more than the RDA. The 2024 guideline suggests vitamin D above the RDA, without testing, for children and teenagers aged 1–18, adults aged 75 and over, pregnant women, and adults with high-risk prediabetes.

Interpreting a 25(OH)D blood test: testing is most useful for people with symptoms of deficiency, bone disease, malabsorption, or other medical reasons. These are the commonly used ranges:

ODA (Optimal Daily Allowance)

Get at least the RDA — 600 IU (15µg) a day, or 800 IU (20µg) over age 70 — from sensible sun exposure in summer, food, and a supplement when sun exposure is low. In practice, that means most people living far from the equator benefit from a supplement in autumn and winter: the UK, for example, advises everyone to take 400 IU (10µg) a day from October to March, and many people take 1,000–2,000 IU a day — a safe, reasonable amount below the 4,000 IU upper limit. People who get little sun all year round (who spend most of their time indoors, cover most of their skin, or have darker skin at high latitudes) may need a supplement year-round, and people with obesity often need more to reach the same blood levels. For people who aren’t deficient, large trials have found little benefit from going higher, and very high doses carry their own risks.

Found In (per 100g)

Few foods contain much vitamin D, and for most people, food alone can’t reliably supply enough without sun exposure or a supplement. Oily fish is the standout:

* Value from USDA’s SR Legacy data, where the Foundation Foods entry doesn’t include it. Cod liver oil is shown per 100g for comparison — a tablespoon (about 13.6g) provides about 34µg (1,360 IU), though products vary.

Fortified foods — such as milk and plant-based milks, some breakfast cereals, yogurts, and spreads — can be important sources, but fortification rules and amounts vary a lot between countries, so check the label. Ordinary mushrooms, grown in the dark, contain very little vitamin D. But mushrooms exposed to UV light — some are sold labeled as “high in vitamin D” — can contain far more, enough for a serving to provide a large share of the daily value. Their vitamin D is D2, which is somewhat less effective than D3 at raising blood levels.

Vitamin D Helps With

• Calcium and phosphorus absorption for building and maintaining bone
• Preventing rickets in children and osteomalacia in adults
• Fracture prevention — mainly when combined with calcium in older adults who are deficient or living in care homes; in generally healthy adults, trials haven’t shown fewer fractures
• Muscle function and strength — particularly when correcting a deficiency
• Immune function — daily supplements modestly reduced respiratory infections in trials, mainly in people with low levels
• Autoimmune disease — in the VITAL trial, 2,000 IU a day was linked with about 22% fewer new autoimmune diseases over five years
• Blood sugar — in people with prediabetes, trials suggest vitamin D modestly reduces the risk of progressing to type 2 diabetes
• Cancer — supplements haven’t reduced how often people develop cancer, but analyses of trials suggest a possible modest reduction in cancer deaths
• Mood — low vitamin D is linked with depression, but in VITAL, supplements didn’t prevent depression in adults
• Brain development — vitamin D is important during pregnancy and early childhood

Vitamin D for Athletes and Active People

Vitamin D matters for athletes mainly through bone health, muscle function, and immunity — and low levels are common in athletes who train indoors or through the winter.

Muscle function: vitamin D receptors are found in muscle, and vitamin D influences calcium handling and the development of muscle fibers. In athletes and others who are deficient, some trials have found improvements in muscle strength and function after correcting the deficiency. In people with adequate levels, extra vitamin D hasn’t been shown to improve strength or performance.

Bone stress injuries: low vitamin D is linked with a higher risk of stress fractures, which are common in runners, military recruits, and dancers. In a large trial in female US Navy recruits, daily calcium (2,000mg) plus vitamin D (800 IU) reduced stress fractures by about a fifth during basic training.

Immune protection: intense training temporarily weakens immune defenses, and athletes with low vitamin D tend to have more upper respiratory infections, particularly in winter. Trials across the general population found that regular daily vitamin D modestly reduces respiratory infections, with the clearest benefit in people with low levels.

Athletes at higher risk of low vitamin D:

• Indoor athletes and gym-based exercisers who get little sun
• Athletes living far from the equator or training through winter
• Athletes with darker skin, who make less vitamin D from the same sun exposure
• Athletes with higher body fat, who tend to have lower blood levels

Target levels for athletes: some sports scientists suggest aiming for 40–50ng/mL or more, citing associations with muscle power and lower injury rates. These are associations rather than proven cause and effect, and trials haven’t shown that pushing levels this high improves performance in athletes who aren’t deficient. For athletes at risk of low levels, a winter supplement — and, where there’s a medical reason, a blood test — is a sensible approach.

Sunshine and Vitamin D

How much sun:

• Only UVB rays (290–315nm) produce vitamin D — UVA doesn’t
• The more skin that’s exposed, the more vitamin D you make — arms and legs make a much bigger contribution than face and hands alone
• Midday sun (roughly 10am–3pm) is most effective, because UVB is strongest when the sun is high
• For lighter-skinned people, a short spell of midday summer sun on the arms and legs — often around 10–30 minutes, well short of burning — can produce a substantial amount of vitamin D. People with darker skin need considerably longer, often several times as long
• Window glass blocks almost all UVB, and clothing blocks it too. Sunscreen reduces vitamin D production, though in real-world use, most people who wear sunscreen still make some
• Avoid sunburn: it’s a major risk factor for skin cancer, and you don’t need to burn — or even tan — to make vitamin D

Latitude and season:

• Above roughly 35° latitude (much of Europe, the northern US, and northern Asia), there’s too little UVB in winter for the skin to make meaningful vitamin D — roughly November to February at around 40°, and longer further north. In the UK (about 50–58°N), the skin can make vitamin D only from about late March or April to the end of September.
• This “vitamin D winter” is why health authorities in many northern countries recommend a vitamin D supplement during the darker months.

Age reduces production: the skin contains less 7-dehydrocholesterol as we age, so older adults make much less vitamin D from the same sun exposure — up to about 75% less in people over 70 than in young adults.

Skin pigmentation: melanin in darker skin absorbs UVB, reducing vitamin D production. People with darker skin living far from the equator are at the highest risk of low vitamin D — a mismatch between skin evolved for strong equatorial sun and life in low-UV regions.

Vitamin D Deficiency

Deficiency risk is higher in:

• People with little sun exposure — those who work or stay mostly indoors, live far from the equator, cover most of their skin, or always use high-factor sunscreen outdoors
• People with darker skin living far from the equator
• Older adults — who make less vitamin D in their skin, and are more often housebound
• People with obesity — vitamin D is stored in and diluted by fat tissue, so they tend to have lower blood levels and need more to raise them
• People with fat malabsorption — from conditions such as Crohn’s disease, celiac disease, or short bowel syndrome, or after weight-loss surgery
• Breastfed babies — breast milk contains little vitamin D, so the American Academy of Pediatrics recommends 400 IU a day for breastfed infants, starting soon after birth
• People with chronic kidney disease — the kidney’s activation step is impaired
• People taking medicines that speed up vitamin D breakdown, such as some anti-seizure drugs and long-term glucocorticoids

Rickets and osteomalacia:

Rickets occurs in children when growing bones fail to mineralize properly. Signs include bowed legs or knock knees, a prominent forehead, thickened wrists and ankles, a groove across the lower chest (Harrison’s sulcus), delayed tooth eruption, and weak bones. Rickets was common in 19th-century industrial cities, where smoke-filled air blocked sunlight and many children spent their days indoors — until cod liver oil, sunlight, and later food fortification largely eliminated it.

Osteomalacia is the adult equivalent: bones become soft and poorly mineralized. It causes widespread bone pain (particularly in the spine, pelvis, and legs), weakness in the muscles of the hips and shoulders, and a waddling walk. It’s sometimes mistaken for fibromyalgia, arthritis, or depression, and responds well to treatment.

General symptoms of vitamin D deficiency:

• Fatigue and general weakness
• Bone pain and tenderness
• Muscle weakness, aches, and cramps
• More frequent infections, particularly respiratory
• Low mood — low vitamin D is linked with depression, though the direction of the link isn’t clear
• Hair loss, in some cases of severe deficiency
• Fractures from minor falls or injuries

Excessive Doses of Vitamin D

Upper limit (UL): 4,000 IU (100µg) a day for adults. The limits are lower for babies and young children:

Source: US National Academies, via the NIH Office of Dietary Supplements. Doctors sometimes prescribe higher doses for a limited time to treat a diagnosed deficiency.

Vitamin D toxicity: toxicity comes from taking too much in supplements — not from sun exposure, since the skin limits its own production, and not from normal food. It usually involves very high doses taken for a long time (typically well over 10,000 IU a day for months), or dosing mistakes with high-strength products. Toxicity works through hypercalcemia — too much calcium in the blood:

• Symptoms of high calcium: nausea, vomiting, poor appetite, excessive thirst, frequent urination, confusion, and weakness
• Kidney damage and kidney stones
• If prolonged, calcium deposits in soft tissues such as the blood vessels, kidneys, and heart

Higher isn’t automatically better, even below toxic levels: in a three-year Canadian trial, healthy adults taking 4,000 or 10,000 IU a day lost slightly more bone density than those taking 400 IU. And in a trial in older women, a single very large yearly dose (500,000 IU) increased falls and fractures. That’s part of why current guidelines prefer daily, moderate doses over large, infrequent ones.

A caution for some medical conditions: in people with sarcoidosis, tuberculosis, some lymphomas, and certain other conditions, immune cells can activate vitamin D on their own, so supplements can cause high calcium. People with these conditions should only take vitamin D on medical advice.

Magnesium and vitamin D: magnesium is involved in vitamin D metabolism, including the enzymes that activate it. In one randomized trial, magnesium supplements helped normalize vitamin D levels — raising them in people whose levels were low. Low magnesium may be one reason some people respond poorly to vitamin D, though how often this matters isn’t known. Getting enough magnesium from food (or a supplement, if your diet is low) is a sensible part of supporting vitamin D status.

Types of Vitamin D

• Vitamin D3 (cholecalciferol): the form made by human skin and found in animal foods. It raises and maintains blood levels more effectively than D2, and is the preferred supplement form for most people. Vegan D3, made from lichen, is also available.
• Vitamin D2 (ergocalciferol): made by exposing yeast or mushrooms to UV light. Used in some prescription products. Less effective than D3 at raising blood levels per dose, but still effective, and suitable for vegans.
• Calcifediol [25(OH)D3]: the already liver-converted form. It raises blood levels faster and more predictably than D3, and is used medically, including for people with liver disease. Available on prescription in some countries.
• Calcitriol [1,25(OH)₂D3]: the fully active hormone. Used medically for people with advanced kidney disease, whose kidneys can’t activate vitamin D. It bypasses the body’s controls on activation, so it can easily raise calcium too much and needs close monitoring. Prescription only.

Which form for your goal:

How to Take Vitamin D

Take it with a meal that contains fat: vitamin D is fat-soluble, and studies have found noticeably better absorption — roughly a third to a half more — when it’s taken with a fat-containing meal rather than on an empty stomach.

Choose daily, moderate doses: daily supplements give steadier blood levels than large weekly or monthly doses, and current guidelines prefer them. Avoid very large single doses (such as a yearly mega-dose) unless prescribed.

Typical doses: 400–1,000 IU (10–25µg) a day covers the RDA and the winter shortfall for most people, and many people take 1,000–2,000 IU (25–50µg). Stay below the 4,000 IU (100µg) upper limit unless a doctor advises a higher dose. People with obesity often need more to reach the same blood levels.

Winter supplementation: if you live far from the equator, take a supplement through the darker months — in the UK, for example, the official advice is 400 IU (10µg) a day from October to March, and year-round for people who get little sun.

Testing: routine testing isn’t recommended for healthy people, but a 25(OH)D test makes sense if you have symptoms of deficiency, bone problems, a malabsorption condition, or another medical reason. If you’re being treated for a deficiency, your doctor may retest after about three months.

Magnesium: make sure your diet provides enough magnesium, which supports vitamin D metabolism.

Vitamin K2: some practitioners pair vitamin D with vitamin K2 (MK-7), on the theory that K2 helps direct calcium into bones and away from arteries by activating calcium-binding proteins. The theory is plausible, but trials haven’t shown that the combination prevents arterial calcification or fractures at typical doses. If you take warfarin or another vitamin K-sensitive blood thinner, don’t take K2 without medical advice.

Interactions

Long-term glucocorticoids (such as prednisone) reduce calcium absorption and speed bone loss, so people taking them often need more vitamin D and calcium. Some anti-seizure medicines (such as phenytoin, phenobarbital, and carbamazepine) speed up vitamin D breakdown. Orlistat and cholestyramine reduce absorption of fat-soluble vitamins. Thiazide diuretics reduce calcium loss in urine, so combining them with high-dose vitamin D raises the risk of high calcium. High calcium levels also increase the risk of side effects from digoxin, a heart medicine.

Synergy

• Works with calcium and phosphorus for bone — vitamin D enables calcium absorption, but bones can’t be built without enough calcium in the diet.
• Works with magnesium, which is involved in vitamin D metabolism and activation.
• Often paired with vitamin K2, which activates proteins that bind calcium in bone and in artery walls — a plausible partnership, though the combination’s benefits haven’t been proven in trials.
• Works with vitamin A — the vitamin D receptor and vitamin A’s receptors both team up with the same partner receptor (RXR), and very high vitamin A intake can work against vitamin D’s effects on bone.
• Works with zinc in immune function and bone metabolism.

Antagonistic Interactions

• Very high vitamin A intake can work against vitamin D in bone.
• Excess vitamin D raises calcium too much, which can lead to calcium deposits in soft tissues.
• Low magnesium may blunt the response to vitamin D.
• Glucocorticoids and some anti-seizure medicines reduce vitamin D’s effectiveness.
• Thiazide diuretics combined with high-dose vitamin D raise the risk of high calcium.
• Obesity lowers blood vitamin D levels, as vitamin D is stored in fat tissue.

Food values: USDA FoodData Central — cod liver oil (SR Legacy, FDC ID 173577); sockeye salmon, cooked (SR Legacy, 173692); pink salmon, canned (SR Legacy, 175175); Atlantic salmon, farmed, cooked (SR Legacy, 175168); Pacific mackerel, cooked (SR Legacy, 171994); Atlantic herring, cooked (SR Legacy, 175117); sardines, canned in oil (SR Legacy, 175139); egg, hard-boiled (SR Legacy, 173424); light tuna, canned in water (Foundation Foods, 334194); cheddar cheese (Foundation Foods, 328637, vitamin D from SR Legacy); shiitake mushrooms, cooked (SR Legacy, 168437); white mushrooms, boiled (SR Legacy, 169252). RDA and upper limits from the US National Academies, via the NIH Office of Dietary Supplements. % Daily Values use the FDA’s current Daily Value of 20µg; 1µg = 40 IU.