There are two forms of Vitamin D found in food and supplements: Vitamin D2, which is found in mushrooms, and Vitamin D3, which is found in animal foods. Vitamin D2 is not as bioavailable as D3, which means your body cannot use it as readily; however, it can still raise your vitamin D levels.^[65] Most D3 supplements are derived from lanolin, a waxy substance secreted by the skin glands of wooly animals. Sheep are sheared, then the lanolin coating is squeezed off the wool. Since the sheep are not killed in the process, this source of D3 will be acceptable to some vegetarians. For vegans, the only acceptable D3 supplements will be the ones explicitly labeled as vegan, which derive their vitamin D3 from lichen extracts.

Dietary sources of vitamin D include the following foods:^[8]

• fatty fish (such as tuna or salmon)
• fish liver oil
• beef liver
• egg yolks
• mushrooms (vitamin D2), especially mushrooms that have been exposed to UV light^[66]

Most foods are not natural sources of vitamin D, but many in the U.S. are fortified with vitamin D. Some common vitamin-D-fortified foods include the following:

• milk and other dairy products such as yogurt
• soy, almond, and oat milk
• orange juice
• breakfast cereals

Most animal-based foods have some vitamin D in the form of the vitamin D metabolite 25-hydroxyvitamin D (25(OH)D), along with small amounts of vitamin D3. The impact of dietary 25(OH)D on vitamin D status is an ongoing area of research, but it is worth noting that if the 25(OH)D content in foods such as beef, chicken, pork, turkey and eggs were taken into account, the amount of vitamin D present in these foods would be 2-18 times higher than the amount of the parent vitamin alone.^[67]

Potentially. Vitamin D status was associated with androgen levels in men in an observational study,^[68] and a randomized controlled trial found that Vitamin D supplementation (around 3000 IU/day or 75 μg/day) increased testosterone levels in healthy overweight men.^[69] It is important to note that vitamin D supplementation has not been shown to increase testosterone to supraphysiological levels, nor is there any evidence that supraphysiological vitamin D intake will further enhance testosterone levels beyond moderate-level supplementation. More research is needed to determine the effects of vitamin D supplementation on testosterone levels in different populations.

Low vitamin D levels may be linked to increased all-cause mortality, particularly in older adults. Observational studies have shown a general trend for associations between low vitamin D levels and all-cause mortality in general^[76] and elderly^[77] populations.

The link between increased all-cause mortality and low vitamin D levels in elderly participants has been confirmed by clinical trials showing decreased mortality with vitamin D3 supplementation.^[78]

Although associations between low vitamin D levels and increased all-cause mortality in the general population have been reported in observational studies,^[76] randomized controlled trials with adult participants 18 years or older have failed to confirm this, finding no evidence for an association between vitamin D supplementation and all-cause mortality compared to a placebo.^[79]

More research is needed to better understand the influence of vitamin D supplementation on all-cause mortality and longevity in different populations.

Multiple sclerosis (MS) is an autoimmune disease that affects the myelin sheath of neurons, which can be thought of as more or less analogous to the insulation on electrical wires. Degradation of the myelin sheath degrades the ability of neurons to propagate signals back and forth between the body and brain, resulting in MS. There are associations between residing in latitudes further away from the equator and increased risk of MS,^[80] and more sun exposure during childhood is associated with reduced risk of MS during adulthood.^[81]

Vitamin D has been shown to have a therapeutic effect in mice with experimental autoimmune encephalomyelitis, an animal model for MS. However, human trials to date have not found evidence in support of a role for vitamin D supplementation in the treatment of MS.^[82] More research is needed to better understand whether vitamin D supplementation may benefit any particular populations of people with MS.

It is also important to note that some of the side effects of toxicity from high-dose vitamin D supplementation, such as fatigue, muscle weakness and urinary dysfunction, mimic the course of MS disease progression,^[83] underscoring the importance of consulting with a physician before considering aggressive vitamin D supplementation for MS.

Numerous studies have been published suggesting that vitamin D may help to ameliorate some factors associated with the etiology of Alzheimer’s disease, prompting some scientists to suggest that it may be helpful for treating or preventing the disease.^[84] In support of this idea, Vitamin D treatment has been shown to have neuroprotective effects in in vivo animal studies, and human observational studies have found associations between low vitamin D levels and an increased risk of Alzheimer’s. Additionally, an in vitro study of immune cells cultured from the blood of people with Alzheimer’s found that treatment of these cells with vitamin D can increase their breakdown of amyloid-β protein aggregates, which accumulate in the brains of people with Alzheimer’s disease and may be associated with disease pathogenesis.^[85]

However, clinical randomized controlled trials (RCTs) are the only true test of whether or not any given supplement is useful to treat a disease, and the RCTs to date on vitamin D supplementation and Alzheimer’s have reported mixed results. Although one study found that 800 IU (20 μg) of vitamin D taken daily for 12 months significantly improved cognitive function in people with Alzheimer’s disease,^[86] many other trials of vitamin D supplementation in people with Alzheimer’s disease have not found significant effects.^[87] Although vitamin D deficiencies may increase Alzheimer’s disease risk, evidence for a therapeutic effect in Alzheimer’s patients is mostly lacking.

Preclinical studies on vitamin D have indicated that it may interact with and interfere with various signaling pathways associated with other neurodegenerative diseases, such as Parkinson’s disease, multiple sclerosis, and vascular dementia. Unfortunately, as with Alzheimer’s disease, the results of clinical trials of vitamin D in people with these neurodegenerative diseases have overall been mixed, although some trials have reported positive effects on disease pathology. More large-scale, multicenter clinical trials are needed to better understand when, or if, vitamin D supplementation might be indicated as part of treatment strategies for neurodegenerative disease.^[17]

Research suggests that there may be a link between low vitamin D levels and the risk of developing erectile dysfunction (ED), but there is not yet a known dose for treating it. Further research is needed to determine whether supplementation with vitamin D can be beneficial for people suffering from ED.^[90]

Many people get depressed during the winter months, when we produce less vitamin D. So, can supplemental vitamin D cure seasonal depression, and maybe other types of depression? No, alas — but it may help.

Vitamin D is the “sunshine vitamin”,^[50] and sunshine is implicated in mood. So it makes sense that researchers have intently explored vitamin D supplementation for depression. But depression is complex, and the mechanisms at work are not well-understood. However, careful analysis of the trials testing the effects of vitamin D on depression and mood-related pathways will help provide some insight into whether, or if, vitamin D may be helpful for depression in different contexts or populations.

Two reviews of observational studies and intervention trials reached the same conclusions: When parsing the observational data, both reviews found a correlation between depression and low levels of vitamin D (≤20 ng/mL). When parsing the trial data, both reviews found benefits from supplementation, but also assessed some of the included studies as having low methodological quality and high risk of bias.^[91][92]

Those two reviews were published in 2017 and 2016, so shortly after a 2015 meta-analysis of randomized controlled trials (RCTs) reported finding no significant reduction in depression after vitamin D supplementation. Its authors, however, mentioned that “most of the studies focused on individuals with low levels of depression and sufficient serum vitamin D at baseline”.^[93] In other words, they didn’t rule out the possibility that in people with higher levels of depression or lower levels of vitamin D, supplementation might be more effective.

This hypothesis lines up with the conclusions of a 2014 meta-analysis, which found that, if one considered only the studies whose subjects had low levels of vitamin D at baseline (≤20 ng/mL) and were then given enough vitamin D to achieve sufficiency over the course of the trial, then supplemental vitamin D was about as effective as antidepressant medication.^[94] However, this meta-analysis did not account for publication bias.

A 2018 meta-analysis focused on major depression and found a moderate benefit from vitamin D. However, it stresses the low number of qualifying studies (four trials) and, like the 2017 and 2016 reviews, deplores the low methodological quality of some of the studies.^[95] Additionally, a 2016 randomized controlled trial of vitamin D supplementation in people with major depressive disorder purportedly saw an antidepressant effect,^[96] but this study was retracted in 2021 due to concerns over the validity of the participant data.^[97]

Finally, let’s mention a 2016 RCT that found that pregnant women who took a daily dose of 2,000 IU (50 μg) of vitamin D3 during late pregnancy had lower scores on a postpartum depression screening scale than those who did not supplement.^[98] However, this study only addressed postpartum depression in healthy women with a low-to-moderate pre-partum risk of depression; it may not have wider applicability, and further research is needed.

Vitamin D insufficiency (≤20 ng/mL) has been associated with depression. If your depression is severe, you are more likely to benefit from correcting an insufficiency. If your levels of vitamin D are sufficient, however, then whether your depression is severe or not, supplementation isn’t likely to help. (Due to the poor overall methodological quality of the studies, those conclusions are at best preliminary.)

In support of this, a number of observational studies have found that people with depression are more likely to have low vitamin D levels.^[99] However, randomized controlled trials don’t consistently find beneficial effects of vitamin D supplementation on depression.^[100][101] One reason for this could be that benefits only occur if a person has sufficiently severe depression symptoms. In support of this, two meta-analyses of randomized controlled trials found that vitamin D supplementation reduced the severity of depression symptoms in people with depression but had no effect on depression symptoms in people without depression.^[102][103]

Vitamin D receptors can be found pretty much everywhere in the human body, so the ways in which vitamin D might affect your mood are innumerable. One of those mechanisms could be hormonal, since vitamin D helps regulate testosterone levels,^[69][68] and since low testosterone can impair the mood of both men^{[104][105][106][107]} and women.^[108]

We should remember, however, that correlation is not causation. As stated above, the observational data suggests a correlation between depression and low levels of vitamin D, but that doesn’t mean that low levels of vitamin D cause the depression. It might be that depressed people go outside less, thus getting less sunlight, thus producing less vitamin D: the depression would then be the cause of the low vitamin D levels, rather than its consequence.

Even if depression is a consequence, not a cause, it doesn’t mean that low levels of vitamin D aren’t also a consequence. People who go outside less get less sunlight, but also probably less exercise — and we know that exercise benefits mood,^[109] both directly and by promoting better sleep.

And of course, a consequence can have more than one cause. For instance, a decrease in vitamin D production during the winter months is a possible factor in seasonal affective disorder (SAD),^[110] but so is a decrease in illumination,^[111] since one meta-analysis^[112] and a more recent RCT^[113] found that light therapy (using visible light, free of the UVB rays that allow your skin to produce vitamin D) can improve SAD symptoms, often as much as can pharmaceuticals. It should be noted, however, that a few trials with small sample sizes make for rather weak evidence, especially since the meta-analysis didn’t account for publication bias.

The findings on vitamin D are less consistent. One study found an association between depression and seasonal changes in vitamin D,^[114] but another study found no effect of supplemental vitamin D on SAD.^[115] And compounding the uncertainty, the researchers of both studies stressed that potential confounders were numerous.

To summarize:

• Low levels of vitamin D have been associated with depression, but it doesn’t follow that low levels of vitamin D are the cause of the depression. They’re probably one of the factors at play in seasonal depression, but so is the decrease in illumination.
• If your vitamin D levels are not low, supplementation isn’t likely to benefit your mood. If they are low, supplementation is more likely to help if you suffer from major depression.
• If you suspect your vitamin D levels are low, you can have them assessed through a 25-hydroxyvitamin D blood test. Assessing your vitamin D levels twice in a year — in midsummer and midwinter, when there is the most and least sunlight — is an efficient way of estimating what your levels are around the year.

Vitamin D supplements have the potential for interactions with certain medications. Some examples of medications are included below. Since the following is not a comprehensive list, it is important to discuss vitamin D supplementation with your healthcare provider when taking any prescription medications.^[70]

Orlistat (also known as Xenical and Alli). These weight loss drugs may reduce vitamin D absorption from the diet and supplements.^[71]

Statins. Statin drugs reduce cholesterol synthesis in the body. High levels of vitamin D supplementation can potentially reduce the cholesterol-lowering ability of statin drugs by binding to and competing with a common statin-binding enzyme.^[72]

Corticosteroid medications, such as prednisone. Corticosteroids reduce vitamin D metabolism, and vitamin D deficiencies were reported to occur with 2x higher frequency in people taking oral corticosteroids compared to non-users.^[73]

Thiazide diuretics. Diuretics are drugs that promote water loss in the body. Because thiazides decrease calcium loss through urine, and vitamin D increases calcium absorption, taking vitamin D supplements alongside thiazides can potentially lead to dangerously high calcium levels (hypercalcemia).^[74][75]

A moderate amount of fat appears to lead to better vitamin D absorption.

Fat-soluble vitamins 101:

• There are four fat-soluble vitamins that humans need: vitamins A, D, E, and K. All the other vitamins are water-soluble.
• Fat solubility affects two primary things: how well the vitamin is absorbed with fat-containing meals, and how long it’s stored in your body.

Being fat-soluble is a double-edged sword. On the one hand, you can store those vitamins in your body fat and liver, which means you don’t necessarily need daily intake. A sunny vacation can provide you with enough stored vitamin D to last you weeks or even months.^[24]

On the other hand, you can accidentally overdose on these vitamins more easily. Case studies of vitamin A overdose are actually not that uncommon. Eating the livers of some large fish, seals, or polar bears can easily cause vitamin A poisoning.^[25][26][27]

But most of us don’t eat shark liver or polar bear liver, and vitamin D overdose^[28] is less common than vitamin A overdose. In the context of vitamin D intake solely from dietary sources (and not supplements), our problem is less likely to be overdosing on fat-soluble vitamins than it is to be getting enough of them. Let’s take a look at how to get enough vitamin D by taking it with the right amount of fat.

Some people take a vitamin-D-containing multivitamin in the morning, either with coffee or on an empty stomach. Others take a multivitamin with three eggs and buttered coffee. Whether or not either of these is ideal is an open question.

It is commonly assumed that vitamin D is better absorbed when taken with a low to moderate amount of fat, as compared to no fat or lots of fat, based on an often-noted study. Specifically, researchers have shown that in people given a single, large dose of vitamin D, taking it with 11 grams of fat leads to higher levels of vitamin D in the bloodstream, compared to taking it with either 35 grams or 0 grams — absorption was 16% higher and 20% higher, respectively.^[3] An important caveat to this work is that these apparent differences in absorption were only noted by measuring plasma vitamin D levels 12 hours after taking a single large dose of 50,000 IU (1,250 μg). When plasma vitamin D levels were assessed one month and three months after this large dose, the groups didn’t significantly differ in their levels of circulating vitamin D. One alternative interpretation of this work is therefore that vitamin D may be well-absorbed regardless of the amount of fat it is taken with, or on an empty stomach. Changes in plasma vitamin D levels 12 hours postdose with respect to dietary fat content may simply reflect altered rates of absorption into the bloodstream, rather than increased or decreased absolute absorption, as is commonly inferred from the data. Examining plasma vitamin D levels after a single dose at earlier (<12 hours) and later times (>12 hours) might have shed more light on this. Another possibility, given that participants in the above study had the same blood vitamin D levels regardless of whether they took it with some additional fat, is that the limiting factor for achieving long-term steady state vitamin D levels in the blood is more dependent on absorption of vitamin D into the tissues over time, and less on achieving maximal acute vitamin D levels in the blood after a single dose. The ability of fat to acutely enhance blood vitamin D suggests that fat may enhance intestinal absorption. However, it’s not clear that this ultimately matters in terms of achieving stable, steady-state blood vitamin D levels over a longer period of time. In other words, simply taking vitamin D may be more important than what it is taken with.

The same researchers did a later study that showed 32% higher plasma vitamin D levels when people took a large dose with a meal containing 30 grams of fat, compared to a fat-free meal. But again, they used a single large dose of 50,000 IU of vitamin D.^[29] Although they tested blood vitamin D levels at additional acute time-points (10, 12, and 14 hours), testing at additional timepoints beyond 14 hours (ideally, 24-48 hours, while the vitamin D meal was still present in the intestines) would have been necessary to see whether or not the plasma levels of the people who ate the fat-free meal ever reached those of those who ate the fatty meal, as one would expect if the effect of a fatty meal is to expedite the intestinal uptake of vitamin D. Unfortunately, the study authors failed to perform any longer-term followup.

More research is therefore needed to better understand interactions between meal fat content and vitamin D absorption. Taking the evidence all together, it is safe to say that vitamin D is absorbed well enough no matter which type of meal (or no meal) it is taken with. Since vitamin D is stored in body fat, the apparent effects of meal fat content relative to changes in acute absorption may ultimately be less important than regular consumption to support optimal steady-state levels.

Your body can produce vitamin D when the skin is exposed to ultraviolet B (UVB) rays.^[30] Yet it is these rays that sunscreens are designed to primarily block.^[31] So will using sunscreen tank your vitamin D levels?

Sunscreen and vitamin D production

Sunscreen can decrease vitamin D production under both controlled laboratory testing and real-world conditions.^[32][33] This decrease is most notable if sunscreen is used consistently and properly (i.e., when using a broad-spectrum sunscreen, the right sun protection factor (SPF), amount, and reapplication schedule).^[34][35][36]

Yet, the amount to which sunscreen decreases vitamin D production appears to be small — a counterintuitive finding.^[37] How could this be? Two factors have been proposed as possible explanations:^[37]

1. People may not be appropriately using sunscreen during periods of sun exposure (i.e., incorrect type, amount, SPF, or application frequency). If not used correctly, UVB rays could easily reach areas of your skin where sunscreen is absent or where coverage is not sufficient enough.

2. While sunscreen does a good job of blocking most UVB rays, it doesn’t entirely block them. A high amount of exposure to UVB rays is not required to kickstart vitamin D production in the skin. So, it’s possible that low amounts of UVB radiation could get past the sunscreen to initiate vitamin D creation.

One important caveat — studies to date have generally been conducted on people with less skin pigmentation (i.e., those with Fitzpatrick skin types 1–3). A different result may be seen in those with Fitzpatrick skin types 4–6.

Generally speaking, 5 to 30 minutes of unprotected sun exposure to the hands, face, and arms at least three times a week between 11 a.m. and 3 p.m. is considered enough to keep blood vitamin D levels out of the deficient range (<30 nmol/L or <12 ng/mL).^[38][39]

When determining how much sunlight you might need, there are two basic factors to consider:

• The UV index (a measure of UV radiation intensity, from 0 to 11+)
• Your Fitzpatrick skin type (a measure of how your skin responds to UV rays, from 1 to 6)

When the UV index forecast in your area is 3 or higher, people with Fitzpatrick skin types 1 or 2 should keep unprotected sun exposure to less than 10 minutes; skin types 3 or 4, less than 15 minutes; and skin types 5 or 6, less than 30 minutes.^[40][41]

Fitzpatrick skin type scale

Keep in mind that longer periods of unprotected sun exposure don’t necessarily lead to higher vitamin D production, as the UVB rays will eventually cause the vitamin D in your skin to degrade to an inactive state.^[42] This is a safety mechanism that helps protect your body against vitamin D toxicity.

Don’t stop using sunscreen just to get your vitamin D levels up — a balance can be struck here. In addition to an appropriate dose of sun exposure, you can increase vitamin D through diet and supplementation. Diet and supplementation strategies will be particularly important for those who live in areas of low sun exposure or at latitudes where the sun’s rays may not be as potent for vitamin D production (greater than 37 degrees north and south of the equator).

To summarize: Depending on the UV index and your skin type, 5–30 minutes of unprotected sun exposure to the hands, face, and arms at least three times a week between 11 a.m. and 3 p.m. should be enough to keep your vitamin D levels out of the deficient range. However, for people who live in northerly locations, have darker Fitzpatrick skin types, and/or lack sun exposure, supplementation may be required to maintain adequate vitamin D levels, as dietary sources of vitamin D tend to be inadequate.^[47]

Supplementation is required to prevent a vitamin D deficiency for most people, since dietary sources of vitamin D tend to be inadequate,^[47] and the amount of vitamin D produced in the skin through sun exposure can vary with geographical location^[48] and individual skin pigmentation.^[49]

Vitamin D insufficiency, defined as blood levels less than or equal to 20 ng/mL, may affect as much as 50% of the population worldwide,^[50][51] including 41.6% of Americans. Unsurprisingly, low levels are especially common in Americans with darker skin; Vitamin D insufficiency affects 82.1% of the African American/Black population, and 69.2% of the Hispanic population.^[52]

More surprisingly, it appears that even people who live in countries with sunlight year round often don’t produce enough vitamin D.^[53] This is probably due, at least in part, to most people now working indoors, leaving little skin exposed when venturing outside, and sometimes also using sunscreen.

However, the only way to know for sure if your vitamin D levels are sufficient is to undergo a 25-hydroxyvitamin D blood test. Assessing your vitamin D levels twice in a year — in midsummer and midwinter, when there is the most and least sunlight — is an efficient way of estimating what your levels are around the year.

In Canada and the United States, the Recommended Daily Allowance (RDA) for vitamin D falls between 400 and 800 IU (10–20 μg) (International Units).^[39] These amounts, which some researchers criticize as inadequate,^[54][55] can be obtained naturally from only a few food sources, notably fatty fish (such as salmon, tuna, and sardines). However, in Canada and the United States, milk is often fortified with vitamin D.

Since few foods are rich in vitamin D, supplementation is a valid option. Should your blood test show that your vitamin D levels are low, start supplementing with 2,000 IU (50 μg) a day (a number that, based on the available evidence, should provide the best balance of efficacy and safety), then get tested again after a couple of months.

To summarize: It is estimated that as much as half the world, including more than 40% of Americans, have low levels of vitamin D (≤20 ng/mL). People with darker skin and people who seldom go unprotected under the sun are especially at risk. The only sure way to test for vitamin D deficiency is a 25-hydroxyvitamin D blood test; if levels are low, supplement.

Adequate vitamin D levels are defined as having blood levels of vitamin D (25(OH)D) in the range of 50-125 nmol/L (12-20 ng/mL).^[56] The only way to determine vitamin D status is through a blood test.

Where you live may influence your risk of Vitamin D deficiency. Vitamin D synthesis rates tend to vary with geographical location, which influences the amount of UVB exposure from the sun. People further away from the equator have lower rates of vitamin D synthesis,^[57] and weather patterns associated with more cloud cover and darkness also can also reduce how much vitamin D is made through sun exposure.^[58]

Breastfeeding^[59] - see “Should vitamin D supplements be given to infants and children?” below.

Medical conditions that limit the absorption of dietary fats.^[60] As a fat-soluble vitamin, the absorption of vitamin D is dependent on the ability of the gut to absorb fats from the diet.^[61]

Dark skin pigmentation. Darker skin color reduces absorption of UVB, limiting production of vitamin D by the skin during sunlight exposure.^[56]

Obesity. People with obesity (defined as a BMI of 30 or more) tend to have lower vitamin D levels compared to people without obesity, which is thought to be caused by an increased sequestration of vitamin D in subcutaneous fat stores.^[56]

Gastric bypass surgery. During gastric bypass surgery, parts of the gastrointestinal tract that absorb vitamin D are bypassed, limiting absorption and potentially causing a deficiency.^[62][63]

Aging. The ability to make vitamin D in the skin during sun exposure decreases with age, by an amount of 13% per decade, according to one study comparing vitamin D synthesis after a single incidence of sun exposure in younger and older adults.^[64]

The American Academy of Pediatrics (AAP) recommends that exclusively breastfed infants receive 400 IU (10 μg) a day of vitamin D for the first year of life and that toddlers and older children receive 600 IU (15 μg) a day. This is to prevent the consequences of vitamin D deficiency (particularly rickets), since human milk and most foods are inadequate sources of vitamin D, and the majority of infants and children do not get enough sun exposure to produce all the vitamin D that they need.^[59]

There are two important exceptions to this vitamin D supplementation recommendation. First, formula-fed infants that consume at least 32 oz of formula per day usually do not require supplementation, since most formulas are fortified with vitamin D. Second, if a lactating parent is supplementing with 6400 IU (160 μg) a day of vitamin D, studies find that enough vitamin D passes into the breastmilk to negate the need for direct infant supplementation.^[88]

Vitamin D toxicity in children is rare, but not impossible. The estimated tolerable upper limits set by the AAP are 1000 IU (25 μg) a day for children 0–1 years old, 2500 IU (62.5 μg) a day for children 1–3 years old, 3000 IU (75 μg) a day for children 4–8 years old, and 4000 IU (100 μg) a day for children nine years and older. Toxicity usually occurs with accidental ingestion of large doses of supplemental vitamin D, as found in a case series of 7 children who consumed between 266,000 and 800,000 IU (6650–20000 μg) a day due to erroneously manufactured supplements.^[89]

Vitamin D supplementation in infants and children should be discussed with a clinician, especially if there are concerns about vitamin D serum levels. A clinician can order blood work to better guide any supplement decisions.