These data indicate that correction of severe vitamin D deficiency might improve bone density, but not when given to vitamin D-replete people. Similarly, Finnish children below the age of 2 years who received 1, IU of vitamin D per day for ~2 years did not have better bone density measured by peripheral quantitative CT pQCT compared with children receiving the standard dose of IU per day The Calgary study was designed to evaluate the effect of long-term high-dose vitamin D on bone mass and quality.

A daily dose of IU, 4, IU or 10, IU of vitamin D for 3 years in Canadian adults did not increase BMD, but rather slightly decreased BMD, as measured by the best available methodology high-resolution pQCT Indeed, BMD at the radius and tibia significantly decreased by 3.

Moreover, very high doses might even have negative effects, as a small percentage of participants developed hypercalciuria or hypercalcaemia, which quickly resolved after adjustment of dosing. Of course, this finding might imply that regular follow-up is desirable when using such dosages 19 , Many Mendelian randomization studies showed no causal effect of vitamin D status on a variety of bone traits in populations of European and non-European ancestry.

An early Mendelian randomization study 63 found that genetically predicted one standard deviation increase in 25OHD was not associated with increased femoral neck BMD, lumbar spine BMD or estimated BMD change.

Similar results were observed in relation to total body BMD A more powered Mendelian randomization analysis 65 37, patients with fracture and , control individuals also did not support a causal effect of 25OHD on fracture risk.

However, a Mendelian randomization study in children 66 showed that haplotypes associating with low 25OHD were associated with low pQCT parameters BMD, cross-sectional area and cortical density in 2-year-old children.

Finally, evidence from Mendelian randomization studies 67 refutes causal associations between predicted serum 25OHD concentrations and either BMD or bone metabolism markers found in 1, postmenopausal Chinese women Supplementary Box 6.

In mice, total deletion of VDR generates structural and functional consequences for skeletal and cardiac muscle 9. Furthermore, humans with congenital CYP27B1 mutations or patients with severe combined deficiency of 25OHD and 1,25 OH 2 D due to chronic renal failure develop severe muscle weakness that rapidly improves after treatment with 1,25 OH 2 D 9.

Several meta-analyses have come to different conclusions regarding the consequences of vitamin D supplementation on muscle strength, with both positive 68 and null effects In addition, ample literature is available supporting a link between poor vitamin D status and increased risk of falls, but hesitance remains regarding causality High boluses of vitamin D, however, might transiently increase the risk of falls in older women However, the large ViDA trial showed that monthly , IU doses of vitamin D did not reduce or increase the risk of falls.

The hazard ratio for falls was 0. The VITAL trial also looked at the effects of daily vitamin D supplementation on physical disability and falls in the SRURDY study 75 and found a non-significant OR 0. In further exploratory analysis, the same conclusion was reached when the baseline serum concentration of 25OHD was taken into account.

To our knowledge, no Mendelian randomization studies so far have examined the causal association between genetically estimated 25OHD levels and muscle traits or falls. The role of vitamin D in the skeleton of adults and older adults is more disputed.

The — megatrials were not designed to primarily evaluate the effect of vitamin D supplementation on fracture risk in older adults. These trials 15 , 16 recruited mostly vitamin D-replete adults with a fairly low risk of fracture.

Even the DO-HEALTH trial in older, less vitamin D-replete, adults compared with the other megatrials did not find an effect on non-vertebral fractures By contrast, the — megatrials demonstrate that vitamin D supplementation in vitamin D-replete adults does not improve bone mass, density or quality Taken together, the findings indicate that supplementation with vitamin D only does not have a beneficial effect on fracture risk in vitamin D-replete, mostly white adults.

Of note, the Calgary study demonstrated that high daily doses of vitamin D 4, and especially 10, IU per day might decrease BMD and bone quality 19 , Therefore, the optimal dose in vitamin D-deficient older adults should be at least IU per day but not more than 4, IU per day.

Meta-analyses of older studies suggested a modest decrease in the risk of falls in older, mostly vitamin D-deficient, adults However, the ViDA trial did not confirm this finding as vitamin D supplementation did not change the risk of falls. The New Zealand population was younger and had a better vitamin D status than the participants in the older studies.

There might also be a U-shaped relationship as very high vitamin status, especially due to high bolus doses, might increase the risk of falls 72 , 73 , The lung is increasingly recognized as an important target tissue for vitamin D.

Observational data link poor vitamin D status with several inflammatory lung diseases or impaired lung function 80 , 81 , The most recent analysis published in ref. The number needed to treat for benefit was Subgroup analysis revealed that intermittent monthly or less frequent doses of vitamin D did not generate protection, whereas daily or weekly vitamin D supplementation was more effective for preventing acute respiratory infections OR 0.

In the ViDA trial, however, no effects of vitamin D supplementation were found on acute respiratory infections in older adults In addition, the European DO-HEALTH trial did not show an effect on infections in general nor on upper respiratory infections A substudy of the ViDA trial, however, evaluated the effects of monthly vitamin D supplementation 86 in adults treated for 1.

Overall, in the ITT analysis, no significant effects were observed on FEV1. However, subgroup analysis revealed some beneficial effects, especially in subjects with existing lung problems such as asthma, COPD or a history of smoking Table 2. To date, no Mendelian randomization studies have been performed that examined 25OHD levels, COPD and lung function.

In view of the enormous health implications of the coronavirus disease 19 COVID pandemic caused by the worldwide spread of severe acute respiratory syndrome coronavirus 2, a possible link with poor vitamin D status and the risk or severity of COVID has received great attention.

Seven studies so far compared serum 25OHD concentrations in patients with COVID compared with individuals without COVID ref. In addition, these studies were unable to control for confounding factors, a major problem due to the large number of similarities in the risk factors for vitamin D deficiency and COVID About 31 studies looked at a possible link between vitamin D status and severity of the outcome of COVID Lower serum concentrations of 25OHD were associated with greater mortality, greater need for intensive care treatment or increased severity of illness in general compared with better vitamin D status.

However, this finding was based on observational studies. However, one pilot study which was not placebo-controlled showed a marked reduction in the need for intensive care treatment in patients hospitalized for COVID and treated with a high dose of 25OHD calcifediol at the time of admission Therefore, the link between vitamin D status and COVID is unsettled so far, but many trials are ongoing that might clarify this question.

In , a Mendelian randomization study assessed the causal role of serum 25OHD levels on COVID susceptibility and disease severity Using data from 11, patients with COVID and , control individuals from the Host Genetics Initiative, and six vitamin D SNPs that explain 2.

These results were confirmed in a separate Mendelian randomization study using 81 25OHD SNPs that explain 4. Research investigating the potential effects of vitamin D status on asthma has largely focused on a possible link between prenatal or maternal vitamin D status and wheezing or asthma in the offspring.

A meta-analysis of four prospective studies and three RCTs concluded that vitamin D intake ~ IU per day by women during pregnancy is inversely related to wheezing or asthma in their offspring during up to 3 years of follow-up However, a longer follow-up did not confirm this conclusion: vitamin D supplementation during the prenatal period alone did not influence the 6-year incidence of asthma and recurrent wheeze among children who were at risk of asthma Two Mendelian randomization studies have investigated the causal association between vitamin D and asthma.

These findings suggest that vitamin D levels probably do not have clinically relevant effects on the risk of asthma. The vitamin D endocrine system influences all cells and most cytokines of the immune system 9.

The innate immune system is stimulated by 1,25 OH 2 D and this is in line with a decreased risk of upper respiratory infections with vitamin D supplementation in individuals with vitamin D deficiency Meta-analysis of intervention studies suggested a benefit of vitamin D supplementation of participants with severe vitamin D deficiency and COPD, asthma, or similar lung diseases, and on reducing the risk of acute upper respiratory infections in severely deficient individuals However, where tested, these findings have not been supported by Mendelian randomization studies According to the results of the LUNG-ViDA trial, vitamin D supplementation might modestly improve expiratory lung function If confirmed, such data would imply that the lung is a clinically relevant target issue for vitamin D.

Of note, currently there are insufficient RCTs to evaluate the potential benefit of vitamin D or calcifediol supplementation on the risk or severity of COVID Observational studies have, in line with preclinical data, made a link between poor vitamin D status and increased risk of infection or risk of autoimmune diseases such as multiple sclerosis MS , inflammatory bowel diseases or type 1 diabetes mellitus RCTs in humans dealing with infections have mainly focused on upper respiratory infections and an overview is presented in the previous section.

Unfortunately, no major RCTs have addressed the possible primary or secondary prevention of the major human autoimmune diseases. So far, the — megatrials Table 1 have not shown results related to autoimmune diseases.

Currently, strong evidence exists that supports a causal association between genetically low serum 25OHD levels and increased risk of MS 96 , 97 , 98 , The most recent Mendelian randomization study from evaluated data from The International Multiple Sclerosis Genetics Consortium discovery phase GWAS 14, MS and 26, controls from the USA, Europe, Australia and some Asian countries 97 using six SNPs associated with serum levels of 25OHD and found that each genetically determined unit increase in log-transformed 25 OH D 3 was associated with an odds ratio for MS of 0.

This effect applies to adult-onset and childhood-onset MS. Earlier Mendelian randomization evidence did not support causality of predicted serum 25OHD levels in systemic lupus erythematosus or rheumatoid arthritis.

Consistent null effects on rheumatoid arthritis were found in a Mendelian randomization study in participants from the UK Biobank, using ~ vitamin D-associated SNPs as instruments Similarly, no effect on ulcerative colitis was found in participants from the UK Biobank The UK Biobank study also did not support a causal role of vitamin D on allergic rhinitis.

Finally, Mendelian randomization 94 does not support causal effects of 25OHD on atopic dermatitis. A Mendelian randomization study on type 1 diabetes mellitus did not support causal effects of genetically lowered 25OHD levels on the risk of this disease In summary, the adaptive immune system is downregulated by 1,25 OH 2 D and therefore vitamin D deficiency might predispose to autoimmune diseases 9.

Observational studies have suggested this effect might apply to humans, but too few intervention studies have been conducted to evaluate this statement. Four independent Mendelian randomization studies agree, however, that individuals with genetically driven lower serum 25OHD concentrations have an increased risk of developing MS, either during adolescence or adulthood Table 4.

Intervention studies as summarized in a Cochrane review from ref. An update of these data largely confirmed these observations. To date only one Mendelian randomization study has examined the causal effect of predicted serum 25OHD levels on gestational hypertension and pre-eclampsia.

Overall, the evidence was weak supporting a causal effect of vitamin D status on gestational hypertension OR 0. In summary, pregnant women more frequently have a poor vitamin D status than non-pregnant women of the same age but the absolute and relative values vary from country to country.

Several meta-analyses have suggested that vitamin D supplementation might modestly decrease maternal morbidity and improve the health of their offspring , However, a large RCT in Bangladeshi women with severe vitamin D deficiency did not confirm this observation Therefore, the effects of poor vitamin D status during pregnancy on pregnancy outcomes for mother and infant remains unsettled.

Patients with severe acute illness requiring intensive care frequently have low serum concentrations of 25OHD and this poor vitamin D status is linked with increased morbidity and mortality , Two major RCTs so far in patients in intensive care units ICU have generated conflicting results.

Length of stay in the ICU or hospital, mortality in the ICU, in-hospital mortality and mortality at 6 months did not improve with the intervention. The primary end point day mortality and other non-fatal outcomes were similar in the two groups.

In all vitamin D supplementation RCTs, some safety end points have been reported in addition to mortality see next section. No effects were found on serum calcium or calciuria unless very high doses were used, such as 4,—10, IU per day in the Calgary study.

Even in these circumstances, hypercalcaemia was infrequent and occurred transiently after changes in treatment modality 19 , A modestly increased risk of kidney stones was observed in the WHI trial , but this effect was not seen in the more recent — megatrials that is, ViDA, VITAL and D2d; Table 1.

Furthermore, no changes in kidney function were found in these large trials. Skeletal consequences were either null effects, slight beneficial increases in BMD in subgroups with poor vitamin D status at baseline, or a modest but significant decrease in BMD during high-dose 10, IU per day therapy in the Calgary study An increased risk of fractures in patients receiving high intermittent bolus doses has been reported 71 , Similarly, an increased risk of falls has been reported when either high intermittent doses 71 or high continuous doses were used 72 , Importantly, the — megatrials that is, ViDA, VITAL and D2d , with detailed evaluation of about 30, participants for 2—5 years, did not discover notable adverse effects.

These findings indicate that a daily dose or dose equivalent of 2,—4, IU can be considered as safe in an adult even vitamin D-replete population. High-dose vitamin D also did not modify arterial calcifications during a 3-year follow up in the Calgary study Observational data have repeatedly linked poor vitamin D status with increased mortality.

This effect was extensively documented in several NHANES studies based on representative samples of the US population and confirmed after validation of serum 25OHD concentrations according to standards generated by the US National Institute of Standards and Technology To decrease the possible effect of reverse causation, people who died within the first 3 years after 25OHD measurements were excluded from the analysis; however, the same association between poor vitamin D status and increased mortality remained Using a combination of several European prospective studies, mortality was also higher in the population with the poorest vitamin D status compared with the vitamin D-replete population As nearly all long-term vitamin D supplementation trials include data on mortality, several meta-analyses have shown the effects of vitamin D supplementation on mortality.

A Cochrane analysis 29 evaluated 56 RCTs including 95, participants mostly healthy women older than 70 years with a mean follow-up of 4. Vitamin D supplementation significantly reduced all-cause mortality RR 0. This finding implies that vitamin D supplementation of women for 5 years prevented one additional death.

Vitamin D supplementation also decreased cancer mortality RR 0. In the — megatrials that is, VITAL, ViDA and D2d , overall mortality was much lower than shown in the previous meta-analyses 29 , 36 and did not show an effect of vitamin D supplementation on overall mortality A new meta-analysis of 52 RCTs including a total of 75, participants concluded that vitamin D either vitamin D 3 or D 2 supplementation did not change mortality RR 0.

A subanalysis, however, found that vitamin D 3 instead of D 2 supplementation trials tended to reduce mortality RR 0. These new findings conflict with the reports The difference could be partly because the meta-analysis did not include ten RCTs including ~50, participants using a combination of vitamin D and calcium supplementation.

However, the meta-analysis did include two megatrials VITAL and ViDA that evaluated the effects of vitamin D supplementation in a younger population of mostly vitamin D-replete participants In a large-scale population Mendelian randomization study 10, deaths in 95, total participants , the odds ratios for a genetically determined lower 25OHD concentration was 1.

Nevertheless, both studies may have been underpowered to detect existing causal associations. Finally, evidence from Mendelian randomization did not support an association between 25OHD concentrations and cancer mortality in a sample of 6, deaths from cancer.

These data provide some evidence that genetically lowered vitamin D levels might increase overall mortality risks, but the results have not been consistent across studies, or across causes of mortality.

If vitamin D supplementation exerts beneficial effects on extra-skeletal health outcomes and major diseases, then it is likely to have some effects on mortality, especially in older adults with poor vitamin D status. Preclinical data are mostly in line with the very large number of observational studies linking very poor vitamin D status with skeletal and extra-skeletal health effects Fig.

However, Mendelian randomization studies and the majority of RCTs do not confirm the causality of these associations. Several possible reasons exist for this discrepancy. Most importantly, serum 25OHD levels are a highly confounded variable.

Specifically, serum 25OHD levels are affected by a host of health behaviours, the presence of obesity, socioeconomic status and education levels.

Although most observational studies have attempted to control for such confounding through multivariable adjustment, such approaches depend upon the degree of accuracy of measurement of the confounders, knowledge that such confounding takes place, and most often that the nature of the confounding relationship linear versus nonlinear is known.

Furthermore, statistical adjustment for confounding variables can only be accomplished if the confounding variables are known. The concordance between 25OHD Mendelian randomization studies and RCTs is striking and suggests that Mendelian randomization might be a more relevant way to begin to understand the effect of 25OHD levels on risk of disease than observational studies.

Perhaps the vitamin D endocrine system only has a role in these extra-skeletal effects in people with prolonged and very severe vitamin D deficiency. Studies in countries or population groups with severe vitamin D deficiency who need improved vitamin D status anyway might be the ideal approach to better understand the effect of vitamin D supplementation in individuals with severe vitamin D deficiency.

Most RCTs and Mendelian randomization studies have been undertaken in individuals from the general population in which the rates of severe vitamin D deficiency are low. However, this low degree of variance would affect the statistical power of a study but not introduce bias. New techniques will soon enable us to use a much larger number of SNPs than used in current studies usually based on less than six SNPs , thereby allowing much larger variations in serum 25OHD concentrations to be predicted.

Most RCTs did not last longer than 3—5 years. In such short-term scenarios, answering the question of causality is extremely difficult. This fact implies that only very long-term improvements in vitamin D status might generate beneficial effects.

However, Mendelian randomization studies provide estimates of the effect of a lifetime of genetically lowered vitamin D levels and such Mendelian randomization studies have generally produced null findings. Reverse causality remains a valid rationale to explain the discordance between observational and intervention studies.

The most plausible hypothesis states that individuals with any health problems are less likely to regularly engage in outdoor activity and less exposure to sunlight results in lower vitamin D status. Another mechanism of reverse causality might be that the activity of hepatic hydroxylase is decreased in many major diseases and this decrease could cause low serum 25OHD concentrations.

Indeed, data in mice demonstrate that diet-induced obesity, type 1 diabetes mellitus or T2DM, fasting and exposure to glucocorticoids substantially decrease the gene and protein expression of CYP2R1, thereby decreasing the overall hydroxylase activity , , This finding implies that decreased 25OHD concentrations are the consequence of disease, rather than involved in the origin of these metabolic diseases.

Of course, these data from mice need confirmation in humans. Finally, many diseases other than those described in this Review including brain-related diseases are linked with poor vitamin D status; however, causality is doubtful without adequate Mendelian randomization studies or RCTs.

Improved understanding of the genetic determinants of 25OHD has helped re-assess the role of vitamin D in the aetiology of complex diseases through Mendelian randomization. Taken together, the evidence from over 60 Mendelian randomization studies published to date assessing the role vitamin D does not support a causal role for the large majority of studied outcomes.

Despite this null data, in the few cases where the evidence from Mendelian randomization supported a causal role of vitamin D status, such as in the example of MS, these results had important clinical implications. For instance, clinical care guidelines for the use of vitamin D in preventing MS in those at risk were published by the MS Society of Canada The earlier Mendelian randomization studies used, as instruments for 25OHD levels, SNPs within the four genes related to 25OHD synthesis and metabolism DHCR7 , CYP2R1 , GC and CYP24A1 , which together explained 2.

Later Mendelian randomization studies combined the aforementioned four SNPs with two SNPs in SEC23A and AMDHD1 both genes without clear role in the vitamin D metabolic pathway , and thereby explained ~5. The identification of over 25OHD-associated genetic variants in , which explain a considerable portion of the variance in 25OHD levels ~ These newly identified SNPs will probably enable improved instrumentation of vitamin D in Mendelian randomization studies.

Moreover, with the emergence of large-scale GWAS in densely phenotyped biobanks, we anticipate that more powerful vitamin D Mendelian randomization studies will be published that utilize the optimized set of genetic instruments. Such new studies should revisit previously studied diseases and investigate new disease outcomes, to further aid causal effect estimation.

Therefore, no reason exists at present to recommend vitamin D supplementation of already vitamin D-replete individuals. These data do not contradict the causal link between severe vitamin D deficiency and rickets, or the need to correct severe deficiency at any age. Similarly, the — trials do not contradict the probable beneficial effects of combined supplementation of calcium and vitamin D in older adults with poor vitamin D and calcium status on their risks of fracture or falls.

A few hints have emerged that vitamin D supplementation might have some extra-skeletal benefits, especially in people with severe vitamin D deficiency such as reduced progression to T2DM, decreased numbers of infections, increased lung function and decreased cancer or overall mortality Tables 2 , 3.

These suggestions are largely based on subgroup or post hoc analyses and thus should not result in the systematic recommendation of vitamin D supplements in such populations but might guide the correct design of future studies. The same is true for intermittent high-dose boluses of vitamin D.

Over the past few decades, vitamin D has been a hot topic for scientists and lay people alike, who frequently suggest that vitamin D supplementation might generate a wide variety of health benefits.

The data discussed in the present Review might well dampen such enthusiasm. However, a large number of intervention studies and most probably Mendelian randomization studies are still ongoing, and these might help provide a better understanding of who would benefit from vitamin D supplementation.

However, many vitamin D-replete people take vitamin D supplements without clear benefits. In addition, a small percentage of the population takes higher doses than the upper limit of safe intake. Munns, C. et al. Global consensus recommendations on prevention and management of nutritional rickets.

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Learn more about vitamin D and sunlight for your baby. For more information on vitamin D, check out the American Academy of Pediatrics Vitamin D Recommendation external icon.

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All children need vitamin D beginning shortly after birth. Children younger than 12 months old need IU alert icon of vitamin D each day. Children 12 to 24 months old need IU of vitamin D each day.

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How Well Do You Sleep? Health Conditions Discover Plan Connect. Nutrition Evidence Based How Much Vitamin D Should You Take For Optimal Health? Medically reviewed by Jerlyn Jones, MS MPA RDN LD CLT , Nutrition — By Adda Bjarnadottir, MS, RDN Ice — Updated on June 23, What is vitamin D? How much do you need?

Optimal blood levels Deficiency Sources Can we get enough from the sun? Supplements video Too much FAQ Summary Vitamin D is essential for bone health and immune function. How much vitamin D do you need?

Age Amount male or female 0—12 months 10 micrograms mcg IU 1—70 years 15 mcg IU 71 years and over 20 mcg IU.

What are the optimal blood levels of vitamin D? How common is vitamin D deficiency? What are the main sources of vitamin D? Can we get enough vitamin D from the sun alone? About vitamin D supplements. How much is too much? Frequently asked questions. How we reviewed this article: Sources.

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Jun 23, Written By Adda Bjarnadottir, MS, RDN Ice. Medically Reviewed By Jerlyn Jones, MS MPA RDN LD CLT. Jul 12, Written By Adda Bjarnadottir, MS, RDN Ice. Medically Reviewed By Jared Meacham, Ph. Share this article.

Read this next. Vitamin D — A Detailed Beginner's Guide. By Kris Gunnars, BSc. Sunscreen: Does SPF Matter and Which One Should I Choose? Medically reviewed by Cynthia Cobb, DNP, APRN, WHNP-BC, FAANP.

How Much Vitamin D Is Too Much? The Surprising Truth. By Adda Bjarnadottir, MS, RDN Ice. Malanga Health Benefits and More.

Medically reviewed by Natalie Olsen, R. Who needs testing for vitamin D? See "Patient education: Bone density testing Beyond the Basics " and "Patient education: Osteoporosis prevention and treatment Beyond the Basics ".

Vitamin D supplements — Many types of vitamin D preparations are available for the treatment of vitamin D deficiency or insufficiency. The two commonly available forms of vitamin D supplements are ergocalciferol vitamin D2 and cholecalciferol vitamin D3. We suggest vitamin D3 when possible, rather than vitamin D2, because vitamin D3 may raise vitamin D levels more effectively.

Dosing — The recommended dose of vitamin D depends upon the nature and severity of the vitamin D deficiency. However, some people may need higher doses. The "ideal" dose of vitamin D is determined by testing the individual's 25 OH D level and increasing the vitamin D dose if the level is not within normal limits.

Once a normal level is achieved, continued therapy with international units 20 micrograms of vitamin D per day is usually recommended. Children with rickets softening of the bones, which can be seen on an X-ray may need higher doses of vitamin D and should have medical follow-up to ensure that the rickets resolves.

In people who have diseases or conditions that prevent them from absorbing vitamin D normally, the recommended dose of vitamin D is determined on an individual basis. Do I need other vitamins or minerals? Calcium can be found in food sources table 1 or dietary supplements table 2.

See "Patient education: Calcium and vitamin D for bone health Beyond the Basics ". Monitoring — In adults being treated for vitamin D deficiency, a blood test is recommended to monitor blood levels of 25 OH D three months after beginning treatment.

The dose of vitamin D may need to be adjusted based on these results and subsequent blood levels of 25 OH D obtained to assure that normal levels result from the adjusted dose. However, it is important to follow dosing instructions closely and to avoid taking multiple products that contain vitamin D eg, multivitamin and vitamin D.

If 25 OH D levels do become very elevated, complications such as high blood calcium levels or kidney stones can develop. The amount of vitamin D you need per day to maintain a normal level of hydroxyvitamin D 25[OH]D depends on the pigmentation in your skin, sun exposure, diet, and underlying medical conditions.

In general, adults are advised to take a supplement containing international units 20 micrograms of vitamin D per day to maintain a normal vitamin D level. Older people who are confined indoors may have vitamin D deficiency even at this intake level. See 'Vitamin D supplements' above.

All infants and children are advised to take a vitamin D supplement containing international units 10 micrograms of vitamin D, starting within days of birth. For infants and children, vitamin D is included in most nonprescription infant multivitamin drops.

In some countries, infant drops are available that contain only vitamin D. See "Patient education: Breastfeeding guide Beyond the Basics " and "Patient education: Starting solid foods with babies Beyond the Basics ".

Exposure to the sun or tanning beds is not recommended as a source of vitamin D. This can lead to skin damage and increase the risk of skin cancer. Your health care provider is the best source of information for questions and concerns related to your medical problem.

This article will be updated as needed on our website www. Related topics for patients, as well as selected articles written for health care professionals, are also available.

Some of the most relevant are listed below. Patient level information — UpToDate offers two types of patient education materials. The Basics — The Basics patient education pieces answer the four or five key questions a patient might have about a given condition.

These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Patient education: Vitamin D deficiency The Basics Patient education: Osteoporosis The Basics Patient education: Calcium and vitamin D for bone health The Basics Patient education: Vitamin supplements The Basics Patient education: Vitamin D for babies and children The Basics.

Beyond the Basics — Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are best for patients who want in-depth information and are comfortable with some medical jargon.

Patient education: Sunburn Beyond the Basics Patient education: Weight loss surgery and procedures Beyond the Basics Patient education: Bone density testing Beyond the Basics Patient education: Osteoporosis prevention and treatment Beyond the Basics Patient education: Calcium and vitamin D for bone health Beyond the Basics Patient education: Breastfeeding guide Beyond the Basics Patient education: Starting solid foods with babies Beyond the Basics.

Professional level information — Professional level articles are designed to keep doctors and other health professionals up-to-date on the latest medical findings.

This is consistent with the important concept that taking additional vitamin D may not benefit those who already have adequate blood levels, but those with initially low blood levels may benefit. Multiple Sclerosis The rate of multiple sclerosis MS is increasing in both developed and developing countries, with an unclear cause.

Type 1 Diabetes Type 1 diabetes T1D is another disease that varies with geography—a child in Finland is about times more likely to develop T1D than a child in Venezuela. More research is needed in this area. Flu and the Common Cold The flu virus wreaks the most havoc in the winter, abating in the summer months.

A randomized controlled trial in Japanese school children tested whether taking daily vitamin D supplements would prevent seasonal flu. Half of the study participants received pills that contained 1, IU of vitamin D; the other half received placebo pills.

Although randomized controlled trials exploring the potential of vitamin D to prevent other acute respiratory infections have yielded mixed results, a large meta-analysis of individual participant data indicated that daily or weekly vitamin D supplementation lowers risk of acute respiratory infections.

The findings from this large meta-analysis have raised the possibility that low vitamin D levels may also increase risk of or severity of novel coronavirus COVID infection. Although there is no direct evidence on this issue because this such a new disease, avoiding low levels of vitamin D makes sense for this and other reasons.

Thus, if there is reason to believe that levels might be low, such as having darker skin or limited sun exposure, taking a supplement of or IU per day is reasonable.

This amount is now part of many standard multiple vitamin supplements and inexpensive. More research is needed before we can definitively say that vitamin D protects against the flu and other acute respiratory infections. And when it comes to limiting risk of COVID, it is important to practice careful social distancing and hand washing.

Tuberculosis Before the advent of antibiotics, sunlight and sun lamps were part of the standard treatment for tuberculosis TB. Several case-control studies, when analyzed together, suggest that people diagnosed with tuberculosis have lower vitamin D levels than healthy people of similar age and other characteristics.

There are also genetic differences in the receptor that binds vitamin D, and these differences may influence TB risk. The authors recommended additional trials to test the effectiveness of these supplements in younger populations and those at high risk of developing autoimmune diseases.

Few foods are naturally rich in vitamin D3. The best sources are the flesh of fatty fish and fish liver oils. Smaller amounts are found in egg yolks, cheese, and beef liver.

Certain mushrooms contain some vitamin D2; in addition some commercially sold mushrooms contain higher amounts of D2 due to intentionally being exposed to high amounts of ultraviolet light. Many foods and supplements are fortified with vitamin D like dairy products and cereals. The amount of the vitamin absorbed can vary widely.

The following are conditions that decrease exposure to UVB light and therefore lessen vitamin D absorption:. Note that because ultraviolet rays can cause skin cancer, it is important to avoid excessive sun exposure and in general, tanning beds should not be used.

Vitamin D deficiency may occur from a lack in the diet, poor absorption, or having a metabolic need for higher amounts. If one is not eating enough vitamin D and does not receive enough ultraviolet sun exposure over an extended period see section above , a deficiency may arise.

People who cannot tolerate or do not eat milk, eggs, and fish, such as those with a lactose intolerance or who follow a vegan diet, are at higher risk for a deficiency. Other people at high risk of vitamin D deficiency include:. Vitamin D toxicity most often occurs from taking supplements.

The low amounts of the vitamin found in food are unlikely to reach a toxic level, and a high amount of sun exposure does not lead to toxicity because excess heat on the skin prevents D3 from forming. It is advised to not take daily vitamin D supplements containing more than 4, IU unless monitored under the supervision of your doctor.

The contents of this website are for educational purposes and are not intended to offer personal medical advice. You should seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.

The Nutrition Source does not recommend or endorse any products. Skip to content The Nutrition Source. The Nutrition Source Menu. Search for:. Home Nutrition News What Should I Eat? Recommended Amounts The Recommended Dietary Allowance for vitamin D provides the daily amount needed to maintain healthy bones and normal calcium metabolism in healthy people.

Vitamin D and Health The role of vitamin D in disease prevention is a popular area of research, but clear answers about the benefit of taking amounts beyond the RDA are not conclusive. Learn more about the research on vitamin D and specific health conditions and diseases: Bone health and muscle strength Several studies link low vitamin D blood levels with an increased risk of fractures in older adults.

It included 53 clinical trials with 91, participants who lived independently or in a nursing home or hospital. It did not find a strong association between vitamin D supplements alone and prevention of fractures of any type.

However, it did find a small protective effect from all types of fractures when vitamin D was taken with calcium.

All of the trials used vitamin D supplements containing IU or less. Vitamin D did not lower the incidence of total bone fractures or fractures of the hip or spine. Cancer Nearly 30 years ago, researchers noticed an intriguing relationship between colon cancer deaths and geographic location: People who lived at higher latitudes, such as in the northern U.

Heart disease The heart is basically a large muscle, and like skeletal muscle, it has receptors for vitamin D. Type 2 diabetes Vitamin D deficiency may negatively affect the biochemical pathways that lead to the development of Type 2 diabetes T2DM , including impairment of beta cell function in the pancreas, insulin resistance, and inflammation.

Keep in mind that this analysis has several limitations, chief among them the fact that the studies it included were not designed to explore mortality in general, or explore specific causes of death.

A recent meta-analysis suggests that this reduction in mortality is driven mostly by a reduction in cancer mortality. Although the numbers of non-White participants were small, the findings were similar in this group.

The study used Mendelian randomization, which measured genetic variations to confirm these findings. This confirmation is important because it documents that the adverse health outcomes among people with low levels of vitamin D represent a causal relationship between vitamin D deficiency and premature death.

Specifically, this method removed potential confounding by factors such as obesity, smoking, and alcohol intake. Is There a Difference Between Vitamin D3 and Vitamin D2 Supplements? If you purchase vitamin D supplements, you may see two different forms: vitamin D2 and vitamin D3.

Vitamin D2 is made from plants and is found in fortified foods and some supplements. Vitamin D3 is naturally produced in the human body and is found in animal foods. A meta-analysis of randomized controlled trials that compared the effects of vitamin D2 and D3 supplements on blood levels found that D3 supplements tended to raise blood concentrations of the vitamin more and sustained those levels longer than D2.

References Institute of Medicine. Dietary Reference Intakes for Calcium and Vitamin D. Washington, D. Vitamin D deficiency. New England Journal of Medicine. Gordon CM, DePeter KC, Feldman HA, Grace E, Emans SJ. Prevalence of vitamin D deficiency among healthy adolescents. Lips PT. Worldwide status of vitamin D nutrition.

The Journal of steroid biochemistry and molecular biology. Robinson PD, Högler W, Craig ME, Verge CF, Walker JL, Piper AC, Woodhead HJ, Cowell CT, Ambler GR. The re-emerging burden of rickets: a decade of experience from Sydney.

Archives of Disease in Childhood. Kreiter SR, Schwartz RP, Kirkman Jr HN, Charlton PA, Calikoglu AS, Davenport ML. Nutritional rickets in African American breast-fed infants. The Journal of pediatrics. Misra M, Pacaud D, Petryk A, Collett-Solberg PF, Kappy M.

Vitamin D deficiency in children and its management: review of current knowledge and recommendations. Boonen S, Lips P, Bouillon R, Bischoff-Ferrari HA, Vanderschueren D, Haentjens P.

Need for additional calcium to reduce the risk of hip fracture with vitamin D supplementation: evidence from a comparative metaanalysis of randomized controlled trials. Bischoff-Ferrari HA, Willett WC, Wong JB, Giovannucci E, Dietrich T, Dawson-Hughes B. Fracture prevention with vitamin D supplementation: a meta-analysis of randomized controlled trials.

Cauley JA, LaCroix AZ, Wu L, Horwitz M, Danielson ME, Bauer DC, Lee JS, Jackson RD, Robbins JA, Wu C, Stanczyk FZ. Serum hydroxyvitamin D concentrations and risk for hip fractures. Annals of internal medicine. Cauley JA, Parimi N, Ensrud KE, Bauer DC, Cawthon PM, Cummings SR, Hoffman AR, Shikany JM, Barrett-Connor E, Orwoll E.

Serum hydroxyvitamin D and the risk of hip and nonspine fractures in older men. Journal of Bone and Mineral Research. Bischoff-Ferrari HA, Willett WC, Wong JB, Stuck AE, Staehelin HB, Orav EJ, Thoma A, Kiel DP, Henschkowski J.

Prevention of nonvertebral fractures with oral vitamin D and dose dependency: a meta-analysis of randomized controlled trials. Archives of internal medicine. Vitamin D and vitamin D analogues for preventing fractures in post-menopausal women and older men. Cochrane Database of Systematic Reviews.

Bischoff-Ferrari HA, Dawson-Hughes B, Willett WC, Staehelin HB, Bazemore MG, Zee RY, Wong JB. Effect of vitamin D on falls: a meta-analysis. Broe KE, Chen TC, Weinberg J, Bischoff-Ferrari HA, Holick MF, Kiel DP.