Vitamin D and Cognitive Function: The Sunshine Nutrient

Short answer: In observational studies, low vitamin D is linked to faster cognitive decline and higher dementia risk. Large trials (VITAL-Cog, DO-HEALTH) found supplements did not help cognition, mostly in people who weren’t deficient. Get the recommended intake (600 IU a day, 800 IU over 70) from fatty fish, fortified foods and sun; don’t exceed 4,000 IU a day without a doctor.

Vitamin D has not been shown to protect thinking or memory. The evidence is preliminary: low levels are consistently linked to cognitive decline, but randomized trials of supplements have found no cognitive benefit.

So the practical advice is about general health, not brain boosting. Get the recommended intake from food, sun and, where advised, a supplement. Correcting a deficiency diagnosed by a doctor matters for bone and general health, but it has not been shown to protect cognition.

How much vitamin D you need

The Institute of Medicine (IOM) set the recommended dietary allowance (RDA) at 600 IU a day for adults aged 19–70 and 800 IU a day over 70. These amounts correspond to a blood level of at least 50 nmol/L (20 ng/mL), which the IOM judged enough for nearly everyone. It found the evidence for benefits beyond bone health inconsistent (Ross 2011).

The Endocrine Society once recommended more: in 2011 it set a target above 75 nmol/L (30 ng/mL). The newer guideline (Demay 2024) replaced that advice. It suggests:

• not taking vitamin D above the recommended intake to prevent disease in healthy adults under 75;
• vitamin D supplements for adults aged 75 and older, pregnant people, people with high-risk prediabetes, and children and adolescents;
• no routine blood tests, including for people with obesity or darker skin, because no trial evidence supports testing and the best target level is unknown.

This advice does not apply to people with a medical reason for vitamin D treatment or testing, such as malabsorption or osteoporosis. If a doctor diagnoses a deficiency, they may prescribe a higher dose for a limited time.

Safety

The Tolerable Upper Intake Level for adults is 4,000 IU a day. Doses above it should only be taken under medical supervision. Too much vitamin D can raise blood calcium (hypercalcemia), causing nausea, confusion, kidney stones and heart rhythm problems.

Vitamin D supplements can interact with some medicines, including thiazide diuretics, steroids and some anticonvulsants. Ask a doctor or pharmacist before starting, especially if you are pregnant, breastfeeding, take medication, or have kidney disease or a health condition. There is no evidence that high doses improve cognition.

D3 or D2?

Supplements come as vitamin D3 (cholecalciferol, from animal sources or lichen) or D2 (ergocalciferol, from fungi). A meta-analysis of trials (Tripkovic 2012) found D3 raised blood levels more than D2. The difference was clear with large occasional doses but was lost with daily dosing. D3 is often preferred, and vegan D3 made from lichen is widely available.

Testing

The standard test measures 25-hydroxyvitamin D, or 25(OH)D, the storage form in blood. Labs report it in nmol/L or ng/mL (1 ng/mL = 2.5 nmol/L). The IOM considered 50 nmol/L adequate and noted risks at both low and high levels. The Endocrine Society found no clear evidence for a best target.

Routine testing is not advised for people without a medical reason. Whether you need a test is a question for your doctor, for example if you have a malabsorption condition or take medicines that affect vitamin D.

Food sources of vitamin D

Few foods contain much vitamin D. Sunlight on skin is the body’s main natural source, but for people who spend most of their time indoors, food and supplements often matter more.

• Fatty fish: The richest natural source, and it comes with omega-3 fats. Values vary between fish. Salmon and sardines two to three times a week give a useful base.
• Cod liver oil: It also provides vitamin A and omega-3s. The high vitamin A content means intake should be limited, especially in pregnancy.
• Eggs: A modest source. Eggs from hens exposed to sunlight or fed more vitamin D can contain more.
• UV-exposed mushrooms: The only substantial plant source. Mushrooms exposed to UVB light, from the sun or commercial treatment, make vitamin D2. Some are sold with the vitamin D content on the label. D2 may raise blood levels less than D3, but these mushrooms are a good option for vegetarians and vegans.
• Fortified foods: Many countries add vitamin D to milk, orange juice, cereals and plant milks, typically 100-150 IU per serving. Nordic countries fortify dairy and margarine as public health policy. These amounts help, but are generally too small to correct a deficiency on their own.

Sun exposure

Sunlight is the most efficient source of vitamin D. Exposing large areas of skin to midday summer sun can produce more than typical diets provide. The skin needs UVB light (wavelength 290-315 nm) to make it.

At high latitudes, winter UVB is too weak for much vitamin D production, however long you spend outdoors. In cities such as London, Boston or Berlin, there are several months a year when the skin makes little.

UVB is also a well-established cause of skin cancer, and dermatology groups recommend sun protection. Short periods outdoors in summer, without burning, allow some vitamin D production. How long is safe depends on skin type, location and season; follow your national health service or dermatology guidance. Never let your skin burn.

Who is most likely to be low

Low vitamin D is common. A systematic review (Hilger 2014) covered 195 studies in 44 countries with more than 168,000 participants. In 37 percent of the studies, average blood levels were below 50 nmol/L (20 ng/mL). Levels varied widely; newborns and older people in institutions appeared most at risk.

• Older adults: The skin makes less vitamin D with age, and older people often spend less time outdoors, eat less and absorb less. Care-home residents are at highest risk, and this is also the group most vulnerable to cognitive decline.
• People with darker skin, especially far from the equator: Melanin absorbs UVB, so darker skin needs more sun to make the same amount. In US survey data from 2005–2006 (Forrest and Stuhldreher 2011), 42 percent of adults had levels of 50 nmol/L or below. The figure was 82 percent in Black and 69 percent in Hispanic adults. Food sources matter more for this group.
• People with obesity: Vitamin D is stored in body fat. Wortsman (2000) found that obese and lean people had the same skin capacity to make it. But after whole-body UV exposure, the rise in blood vitamin D3 was 57 percent lower in obese people. People with obesity typically need higher doses to reach the same blood levels.
• People who get little sun: Office and shift workers, people in care homes, people who cover most of their skin for religious or cultural reasons, and anyone in a northern winter. Window glass blocks UVB, and sunscreen and air pollution reduce it.
• People with malabsorption: Celiac disease, inflammatory bowel disease, Crohn’s disease and other conditions that affect fat absorption reduce uptake from food and supplements.
• People on certain medicines: Anticonvulsants (phenytoin, carbamazepine), glucocorticoids and some antiretroviral drugs speed up vitamin D breakdown.

If you are in one of these groups, ask your doctor whether you need a supplement or a test.

What observational studies show

Studies that measure vitamin D and follow people over time fairly consistently link low levels to worse cognitive outcomes. They cannot prove cause.

• Older women: In 6,257 older women in the Study of Osteoporotic Fractures (Slinin 2012), those with very low levels had higher odds of cognitive impairment at the start. Those below 25 nmol/L had a 58 percent higher risk of decline in global cognition over four years than women at 75 nmol/L or higher. Vitamin D was not linked to executive function.
• Older Italians: In 858 adults aged 65 and older followed for six years (Llewellyn 2010), those below 25 nmol/L fared worse than those at 75 nmol/L or more. Their risk of substantial decline on the MMSE, a standard memory and thinking test, was 60 percent higher. Their scores fell by an extra 0.3 points a year.
• European men: In 3,369 men aged 40–79 tested once (Lee 2009), lower vitamin D was linked to lower processing-speed scores after adjustment, but not to other test scores.
• Pooled studies: A systematic review of 37 studies (Balion 2012) found that, in the 8 that could be pooled, people below 50 nmol/L scored about 1.2 MMSE points lower. In 4 studies, people with Alzheimer’s disease had lower vitamin D than controls.
• Dementia risk: Littlejohns (2014) followed 1,658 adults for a mean of 5.6 years. Those below 25 nmol/L had more than double the risk of dementia and Alzheimer’s disease of those at sufficient levels. It was one of the first large studies to track new dementia cases, which supports the order of events (low vitamin D first).
• Supplement users: In 12,388 dementia-free people in a US Alzheimer’s research dataset (Ghahremani 2023), those taking vitamin D supplements had a 40 percent lower rate of dementia. Differences were larger in women, people with normal cognition and people without the APOE4 gene variant. People who choose supplements may differ in other ways, and the trials below found no benefit.

The main problem is confounding. People with low vitamin D are more likely to be older, less active, obese, isolated and chronically ill, and each of these raises dementia risk. The cause may also run backwards: people in the early stages of dementia may go outdoors less and eat worse, lowering their vitamin D.

What the trials show

VITAL-Cog

VITAL enrolled 25,871 US men aged 50 and over and women aged 55 and over (Manson 2019). They took 2000 IU of vitamin D3 a day or a placebo, and omega-3s were tested in the same trial.

The cognitive results (Kang 2021) came from participants aged 60 and over: 3,424 tested by telephone over 2.8 years and 794 tested in person over 2.0 years. Vitamin D made no difference to the rate of decline in global cognition, the main outcome.

Most participants were not deficient: average starting blood level was 30.8 ng/mL (77 nmol/L) (Luttmann-Gibson 2019). Critics argue this made a benefit harder to find. But the cognitive analysis found no difference in effect by starting level. A possible benefit in Black participants (19 percent of the sample) was a subgroup finding the authors said needs confirmation.

DO-HEALTH

DO-HEALTH (Bischoff-Ferrari 2020) enrolled 2,157 generally healthy European adults aged 70 and older. It tested 2000 IU of vitamin D3 a day, 1 g of omega-3s a day and a strength-training program, alone and combined. After three years, none of them changed scores on the Montreal Cognitive Assessment, one of the trial’s main outcomes.

Trials in people with low levels

These are fewer. Jorde (2019) studied 422 Norwegian adults (mean age 52, mean starting level 34 nmol/L). For four months they took a placebo or high-dose vitamin D (100,000 IU once, then 20,000 IU a week).

Cognitive scores did not improve, with no differences in any subgroup, including those with the lowest levels. Four months is short, and these doses are above the upper limit and were given under medical supervision.

The Women’s Health Initiative (Rossom 2012) included 4,143 women aged 65 and older. Calcium (1,000 mg) plus vitamin D (400 IU a day) did not reduce dementia or mild cognitive impairment over 7.8 years. The vitamin D dose was low.

The pattern is consistent: supplements have not measurably improved cognition. Whether long-term correction of deficiency in high-risk groups, such as older adults or people with early cognitive impairment, can slow decline has not been well tested.

Why vitamin D might matter for the brain

The biology gives reasons to expect a link. Eyles (2005) mapped vitamin D receptors and the enzyme that activates vitamin D in human brain tissue. Staining was strongest in the hypothalamus and in large neurons of a dopamine-producing area of the midbrain.

Receptors also sit in the hippocampus, the memory center that is damaged early in Alzheimer’s disease, and in the prefrontal cortex. The brain can activate vitamin D locally, so in some ways it acts like a neurosteroid.

Lab studies suggest several mechanisms. Most come from cells and animals:

• Nerve growth factor: Active vitamin D increased nerve growth factor in cultured embryonic rat hippocampal neurons (Brown 2003). A related growth factor supports dopamine neurons, which has led to research in Parkinson’s disease; that link is not established.
• Inflammation: In lab studies, vitamin D reduces inflammatory signals in the nervous system. A review (Fernandes de Abreu 2009) proposed that calming brain inflammation may link deficiency to neurodegenerative disease.
• Amyloid clearance: Active vitamin D helped immune cells taken from the blood of Alzheimer’s patients clear amyloid beta, the protein that forms plaques, in the lab (Masoumi 2009). This does not show that supplements can prevent or reverse the disease.
• Serotonin: Patrick and Ames (2014) proposed, but did not test in trials, that vitamin D regulates the enzyme that makes serotonin in the brain.

These mechanisms make a causal role plausible. But the null trials, mostly in people who were not deficient, leave open the possibility that confounding and reverse causation explain the observational data. The answer is not known.

Frequently Asked Questions

What is the best vitamin D level for brain health?

No best level for cognition has been established. In the Cardiovascular Health Study (Littlejohns 2014), dementia risk rose markedly below 50 nmol/L (20 ng/mL), the level the IOM considers adequate. There is no evidence that higher levels add cognitive benefit, and the IOM noted possible risks at high levels.

Should I take vitamin D with vitamin K2?

K2 is often suggested with vitamin D to direct calcium into bone. The reasoning is sound, but evidence for cognitive benefit from adding K2 is limited, and there is no strong evidence that people taking usual vitamin D doses need it. Vitamin K interacts with warfarin and similar blood thinners, so talk to your doctor first if you take them.

How long does it take to correct a deficiency?

It depends on how low the level is, body weight, absorption, sun exposure and the treatment a doctor prescribes. Doctors sometimes prescribe doses above the 4,000 IU upper limit for a limited time; take these only under medical supervision. Your doctor will decide whether a repeat test is needed.

Sources

• Eyles, D. W., Smith, S., Kinobe, R., Hewison, M., & McGrath, J. J. (2005). Distribution of the vitamin D receptor and 1-alpha-hydroxylase in human brain. Journal of Chemical Neuroanatomy, 29(1), 21–30. doi:10.1016/j.jchemneu.2004.08.006

• Brown, J., Bianco, J. I., McGrath, J. J., & Eyles, D. W. (2003). 1,25-Dihydroxyvitamin D3 induces nerve growth factor, promotes neurite outgrowth and inhibits mitosis in embryonic rat hippocampal neurons. Neuroscience Letters, 343(2), 139–143. doi:10.1016/s0304-3940(03)00303-3

• Fernandes de Abreu, D. A., Eyles, D., & Féron, F. (2009). Vitamin D, a neuro-immunomodulator: implications for neurodegenerative and autoimmune diseases. Psychoneuroendocrinology, 34(Suppl 1), S265–S277. doi:10.1016/j.psyneuen.2009.05.023

• Masoumi, A., Goldenson, B., Ghirmai, S., Avagyan, H., Zaghi, J., Abel, K., … & Fiala, M. (2009). 1alpha,25-dihydroxyvitamin D3 interacts with curcuminoids to stimulate amyloid-beta clearance by macrophages of Alzheimer’s disease patients. Journal of Alzheimer’s Disease, 17(3), 703–717. doi:10.3233/JAD-2009-1080

• Patrick, R. P., & Ames, B. N. (2014). Vitamin D hormone regulates serotonin synthesis. Part 1: relevance for autism. The FASEB Journal, 28(6), 2398–2413. doi:10.1096/fj.13-246546

• Hilger, J., Friedel, A., Herr, R., Rausch, T., Roos, F., Wahl, D. A., Pierroz, D. D., Weber, P., & Hoffmann, K. (2014). A systematic review of vitamin D status in populations worldwide. British Journal of Nutrition, 111(1), 23–45. doi:10.1017/S0007114513001840

• Forrest, K. Y., & Stuhldreher, W. L. (2011). Prevalence and correlates of vitamin D deficiency in US adults. Nutrition Research, 31(1), 48–54. doi:10.1016/j.nutres.2010.12.001

• Littlejohns, T. J., Henley, W. E., Lang, I. A., Annweiler, C., Beauchet, O., Chaves, P. H., … & Llewellyn, D. J. (2014). Vitamin D and the risk of dementia and Alzheimer disease. Neurology, 83(10), 920–928. doi:10.1212/WNL.0000000000000755

• Llewellyn, D. J., Lang, I. A., Langa, K. M., Muniz-Terrera, G., Phillips, C. L., Cherubini, A., Ferrucci, L., & Melzer, D. (2010). Vitamin D and risk of cognitive decline in elderly persons. Archives of Internal Medicine, 170(13), 1135–1141. doi:10.1001/archinternmed.2010.173

• Lee, D. M., Tajar, A., Ulubaev, A., Pendleton, N., O’Neill, T. W., O’Connor, D. B., … & Wu, F. C. (2009). Association between 25-hydroxyvitamin D levels and cognitive performance in middle-aged and older European men. Journal of Neurology, Neurosurgery & Psychiatry, 80(7), 722–729. doi:10.1136/jnnp.2008.165720

• Balion, C., Griffith, L. E., Strifler, L., Henderson, M., Patterson, C., Heckman, G., Llewellyn, D. J., & Raina, P. (2012). Vitamin D, cognition, and dementia: a systematic review and meta-analysis. Neurology, 79(13), 1397–1405. doi:10.1212/WNL.0b013e31826c197f

• Slinin, Y., Paudel, M., Taylor, B. C., Ishani, A., Rossom, R., Yaffe, K., … & Ensrud, K. E. (2012). Association between serum 25(OH) vitamin D and the risk of cognitive decline in older women. The Journals of Gerontology Series A, 67(10), 1092–1098. doi:10.1093/gerona/gls075

• Ghahremani, M., Smith, E. E., Chen, H. Y., Creese, B., Goodarzi, Z., & Ismail, Z. (2023). Vitamin D supplementation and incident dementia: effects of sex, APOE, and baseline cognitive status. Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring, 15(1), e12404. doi:10.1002/dad2.12404

• Manson, J. E., Cook, N. R., Lee, I. M., Christen, W., Bassuk, S. S., Mora, S., … & Buring, J. E. (2019). Vitamin D supplements and prevention of cancer and cardiovascular disease. The New England Journal of Medicine, 380(1), 33–44. doi:10.1056/NEJMoa1809944

• Kang, J. H., Vyas, C. M., Okereke, O. I., Ogata, S., Albert, M., Lee, I. M., … & Manson, J. E. (2021). Effect of vitamin D on cognitive decline: results from two ancillary studies of the VITAL randomized trial. Scientific Reports, 11(1), 23253. doi:10.1038/s41598-021-02485-8

• Luttmann-Gibson, H., Mora, S., Camargo, C. A., Cook, N. R., Demler, O. V., Ghoshal, A., … & Manson, J. E. (2019). Serum 25-hydroxyvitamin D in the VITamin D and OmegA-3 TriaL (VITAL): clinical and demographic characteristics associated with baseline and change with randomized vitamin D treatment. Contemporary Clinical Trials, 87, 105854. doi:10.1016/j.cct.2019.105854

• Bischoff-Ferrari, H. A., Vellas, B., Rizzoli, R., Kressig, R. W., da Silva, J. A. P., Blauth, M., … & Orav, E. J. (2020). Effect of vitamin D supplementation, omega-3 fatty acid supplementation, or a strength-training exercise program on clinical outcomes in older adults: the DO-HEALTH randomized clinical trial. JAMA, 324(18), 1855–1868. doi:10.1001/jama.2020.16909

• Jorde, R., Kubiak, J., Svartberg, J., Fuskevåg, O. M., Figenschau, Y., Martinaityte, I., & Grimnes, G. (2019). Vitamin D supplementation has no effect on cognitive performance after four months in mid-aged and older subjects. Journal of the Neurological Sciences, 396, 165–171. doi:10.1016/j.jns.2018.11.020

• Rossom, R. C., Espeland, M. A., Manson, J. E., Dysken, M. W., Johnson, K. C., Lane, D. S., … & Margolis, K. L. (2012). Calcium and vitamin D supplementation and cognitive impairment in the Women’s Health Initiative. Journal of the American Geriatrics Society, 60(12), 2197–2205. doi:10.1111/jgs.12032

• Tripkovic, L., Lambert, H., Hart, K., Smith, C. P., Bucca, G., Penson, S., … & Lanham-New, S. (2012). Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis. The American Journal of Clinical Nutrition, 95(6), 1357–1364. doi:10.3945/ajcn.111.031070

• Wortsman, J., Matsuoka, L. Y., Chen, T. C., Lu, Z., & Holick, M. F. (2000). Decreased bioavailability of vitamin D in obesity. The American Journal of Clinical Nutrition, 72(3), 690–693. doi:10.1093/ajcn/72.3.690

• Ross, A. C., Manson, J. E., Abrams, S. A., et al. (2011). The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. Journal of Clinical Endocrinology & Metabolism, 96(1), 53–58. doi:10.1210/jc.2010-2704

• Demay, M. B., Pittas, A. G., Bikle, D. D., et al. (2024). Vitamin D for the prevention of disease: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology & Metabolism, 109(8), 1907–1947. doi:10.1210/clinem/dgae290