botanical
Ashwagandha
Also known as Withania somniferaModeled ingredients
No ingredient relationship is modeled in this pilot.
Modeled forms
No form relationship is modeled in this pilot.
Evidence-grounded comparison · non-production preview
Review two canonical supplement records topic by topic, with evidence availability, source boundaries, and limitations kept explicit—without rankings or recommendations.
This comparison organizes two separately sourced supplement records. It describes evidence structure and availability without ranking supplements or recommending use.
Reference counts are descriptive. More references do not necessarily mean better or stronger evidence.
Identity boundaries
botanical
No ingredient relationship is modeled in this pilot.
No form relationship is modeled in this pilot.
vitamin
Source boundaries
Ashwagandha: Is it helpful for stress, anxiety, or sleep? — Fact Sheet for Health Professionals
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Vitamin D — Fact Sheet for Health Professionals
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Structural orientation
29 structural observations are available. Topic states remain visible in the aligned comparison below.
Topic-by-topic evidence
Evidence topic
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Mandlik Ingawale DS, Namdeo AG. Pharmacological evaluation of Ashwagandha highlighting its healthcare claims, safety, and toxicity aspects. J Diet Suppl 2021;18:183-226 [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedPanossian AG, Efferth T, Shikov AN, Pozharitskaya ON, Kuchta K, et al. Evolution of the adaptogenic concept from traditional use to medical systems: Pharmacology of stress- and aging-related diseases. Med Res Rev 2021;41:630-703. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedGerontakos SE, Casteleijn D, Shikov AN, Wardle J. A Critical Review to Identify the Domains Used to Measure the Effect and Outcome of Adaptogenic Herbal Medicines. Yale J Biol Med 2020;93:327-46. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedMinistry of Ayush, Government of India. Safety of Ashwagandha, Withania somnifera. Report of the Expert Committee. 2024.
Study type could not be determined · Population basis: unknown · Directness: not assessedLangade D, Thakare V, Kanchi S, Kelgane S. Clinical evaluation of the pharmacological impact of ashwagandha root extract on sleep in healthy volunteers and insomnia patients: A double-blind, randomized, parallel-group, placebo-controlled study. J Ethnopharmacol 2021;264:113276. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedHolvoet H, Long DM, Law A, McClure C, Choi J, et al. Withania somnifera Extracts Promote Resilience against Age-Related and Stress-Induced Behavioral Phenotypes in Drosophila melanogaster; a Possible Role of Other Compounds besides Withanolides. Nutrients 2022;14. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSpeers AB, Cabey KA, Soumyanath A, Wright KM. Effects of Withania somnifera (Ashwagandha) on Stress and the Stress- Related Neuropsychiatric Disorders Anxiety, Depression, and Insomnia. Curr Neuropharmacol 2021;19:1468-95. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedLopresti AL, Smith SJ. Ashwagandha (Withania somnifera) for the treatment and enhancement of mental and physical conditions: A systematic review of human trials. Journal of Herbal Medicine 2021;28:100434.
Systematic review · Population basis: human · Directness: not assessedWithania somnifera (L.) Dunal is an evergreen shrub cultivated in tropical and subtropical areas of Asia, Africa, and Europe. It is commonly called by the Sanskrit name, ashwagandha, because the plant’s roots are said to smell like a wet horse (“ashwa” for horse and “gandha” for smell) [1]. Ashwagandha is also sometimes known as winter cherry or Indian ginseng, although it does not belong to the ginseng family. Ashwagandha root has been used in the traditional Ayurvedic and Unani medicine systems of India as an adaptogen, which is loosely defined as a compound or product that increases the ability of a person to resist, adapt, or become resilient in nonspecific ways to biological, physical, or chemical stressors [2,3]. The chemical composition of ashwagandha root and leaf differ [4]. Most commercial ashwagandha supplements contain extracts from the plant’s root, although some contain extracts from both the root and leaf.
The species name somnifera comes from the Latin word for sleep-inducing, signifying another purported property of this botanical [5]. In addition to sleep, ashwagandha is commonly promoted for stress and anxiety reduction.
Ashwagandha is rich in phytochemicals, including steroidal lactones (known as withanolides) and alkaloids. While withanolides are believed to be responsible for many of ashwagandha’s proposed effects, evidence from preclinical studies suggests that other, non-withanolide components may also be involved [6-8].
Ashwagandha: Is it helpful for stress, anxiety, or sleep? — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessedNorman AW, Henry HH. Vitamin D. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition, 10th ed. Washington DC: Wiley-Blackwell, 2012.
Study type could not be determined · Population basis: unknown · Directness: not assessedJones G. Vitamin D. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease, 11th ed. Philadelphia: Lippincott Williams & Wilkins, 2014.
Study type could not be determined · Population basis: unknown · Directness: not assessedSilva MC, Furlanetto TW. Intestinal absorption of vitamin D: A systematic review. Nutr Rev 2018;76:60-76. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedVitamin D (also referred to as calciferol) is a fat-soluble vitamin that is naturally present in a few foods, added to others, and available as a dietary supplement. It is also produced endogenously when ultraviolet (UV) rays from sunlight strike the skin and trigger vitamin D synthesis.
Vitamin D obtained from sun exposure, foods, and supplements is biologically inert and must undergo two hydroxylations in the body for activation. The first hydroxylation, which occurs in the liver, converts vitamin D to 25-hydroxyvitamin D [25(OH)D], also known as calcidiol. The second hydroxylation occurs primarily in the kidney and forms the physiologically active 1,25-dihydroxyvitamin D [1,25(OH)2D], also known as calcitriol [1].
Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal bone mineralization and to prevent hypocalcemic tetany (involuntary contraction of muscles, leading to cramps and spasms). It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts [1-3]. Without sufficient vitamin D, bones can become thin, brittle, or misshapen. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults. Together with calcium, vitamin D also helps protect older adults from osteoporosis.
Vitamin D has other roles in the body, including reduction of inflammation as well as modulation of such processes as cell growth, neuromuscular and immune function, and glucose metabolism [1-3]. Many genes encoding proteins that regulate cell proliferation, differentiation, and apoptosis are modulated in part by vitamin D. Many tissues have vitamin D receptors, and some convert 25(OH)D to 1,25(OH)2D.
In foods and dietary supplements, vitamin D has two main forms, D2 (ergocalciferol) and D3 (cholecalciferol), that differ chemically only in their side-chain structures. Both forms are well absorbed in the small intestine. Absorption occurs by simple passive diffusion and by a mechanism that involves intestinal membrane carrier proteins [4]. The concurrent presence of fat in the gut enhances vitamin D absorption, but some vitamin D is absorbed even without dietary fat. Neither aging nor obesity alters vitamin D absorption from the gut [4].
Vitamin D — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
A daily dose of 300 to 600 mg ashwagandha root extract (standardized to 5% withanolides) is provisionally recommended for the treatment of generalized anxiety disorder by an international taskforce created by the World Federation of Societies of Biological Psychiatry (WFSBP) and the Canadian Network for Mood and Anxiety Treatments (CANMAT) [18]. The taskforce issued this recommendation in 2022, and they noted that more research is needed to support a stronger recommendation.
Evidence from a small number of studies suggests that taking ashwagandha extract may improve several aspects of sleep, including sleep quality, sleep efficiency, total sleep time, and sleep latency. These benefits tend to be more pronounced among people with insomnia.
Research is limited, but the results from a few clinical trials suggest that ashwagandha extracts may help with sleep. For example, at one study center in India, 150 healthy men and women age 18 to 65 years with self-reported sleep problems characterized by insomnia and lack of restful sleep were randomized to take an ashwagandha root and leaf extract (Shoden) or placebo for 6 weeks [19]. The extract was standardized to contain 21 mg of withanolide glycosides per 60-mg capsule, and participants took two capsules each day. Both groups reported improvements in sleep quality as measured by a validated rating scale, but the improvements were greater in the ashwagandha group (72%) than in the placebo group (29%). In addition, participants who took ashwagandha extract showed improvements in sleep efficiency (time in bed spent in sleep), total sleep time, sleep latency (time taken to fall asleep), and awakening after sleep onset as assessed by actigraphy, which involves wearing a watch monitor on the wrist to measure body motion. They also reported improvements in quality of life.
Langade D, Thakare V, Kanchi S, Kelgane S. Clinical evaluation of the pharmacological impact of ashwagandha root extract on sleep in healthy volunteers and insomnia patients: A double-blind, randomized, parallel-group, placebo-controlled study. J Ethnopharmacol 2021;264:113276. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedLopresti AL, Smith SJ. Ashwagandha (Withania somnifera) for the treatment and enhancement of mental and physical conditions: A systematic review of human trials. Journal of Herbal Medicine 2021;28:100434.
Systematic review · Population basis: human · Directness: not assessedRemenapp A, Coyle K, Orange T, Lynch T, Hooper D, et al. Efficacy of Withania somnifera supplementation on adult's cognition and mood. J Ayurveda Integr Med 2022;13:100510. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedGopukumar K, Thanawala S, Somepalli V, Rao TSS, Thamatam VB, et al. Efficacy and Safety of Ashwagandha Root Extract on Cognitive Functions in Healthy, Stressed Adults: A Randomized, Double-Blind, Placebo-Controlled Study. Evid Based Complement Alternat Med 2021;2021:8254344. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedBaker C, Kirby JB, O'Connor J, Lindsay KG, Hutchins A, et al. The Perceived Impact of Ashwagandha on Stress, Sleep Quality, Energy, and Mental Clarity for College Students: Qualitative Analysis of a Double-Blind Randomized Control Trial. J Med Food 2022;25:1095-101. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessedClinicalTrials.gov. The impact of ashwagandha on perceived stress, sleep and food cravings in college students 2022.
Study type could not be determined · Population basis: unknown · Directness: not assessedFuladi S, Emami SA, Mohammadpour AH, Karimani A, Manteghi AA, et al. Assessment of the Efficacy of Withania somnifera Root Extract in Patients with Generalized Anxiety Disorder: A Randomized Double-blind Placebo- Controlled Trial. Curr Rev Clin Exp Pharmacol 2021;16:191-6. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedMajeed M, Nagabhushanam K, Mundkur L. A standardized Ashwagandha root extract alleviates stress, anxiety, and improves quality of life in healthy adults by modulating stress hormones: Results from a randomized, double-blind, placebo-controlled study. Medicine (Baltimore) 2023;102:e35521. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedMajeed M, Nagabhushanam K, Murali A, Vishwanathan DT, Mamidala RV, et al. A Standardized Withania somnifera (Linn.) Root Extract with Piperine Alleviates the Symptoms of Anxiety and Depression by Increasing Serotonin Levels: A Double-Blind, Randomized, Placebo-Controlled Study. J Integr Complement Med 2024;30:459-68. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessedPandit S, Srivastav AK, Sur TK, Chaudhuri S, Wang Y, et al. Effects of Withania somnifera Extract in Chronically Stressed Adults: A Randomized Controlled Trial. Nutrients 2024;16. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedSmith SJ, Lopresti AL, Fairchild TJ. Exploring the efficacy and safety of a novel standardized ashwagandha (Withania somnifera) root extract (Witholytin®) in adults experiencing high stress and fatigue in a randomized, double-blind, placebo-controlled trial. J Psychopharmacol 2023;37:1091-104. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedSarris J, Ravindran A, Yatham LN, Marx W, Rucklidge JJ, et al. Clinician guidelines for the treatment of psychiatric disorders with nutraceuticals and phytoceuticals: The World Federation of Societies of Biological Psychiatry (WFSBP) and Canadian Network for Mood and Anxiety Treatments (CANMAT) Taskforce. The World Journal of Biological Psychiatry 2022;23:424-55. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedDeshpande A, Irani N, Balkrishnan R, Benny IR. A randomized, double blind, placebo controlled study to evaluate the effects of ashwagandha (Withania somnifera) extract on sleep quality in healthy adults. Sleep Med 2020;72:28-36. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedCheah KL, Norhayati MN, Husniati Yaacob L, Abdul Rahman R. Effect of Ashwagandha (Withania somnifera) extract on sleep: A systematic review and meta-analysis. PLoS One 2021;16:e0257843. [PubMed abstract]
Meta-analysis · Population basis: unknown · Directness: not assessedResearch suggests that ashwagandha extracts may lower stress, anxiety, and cortisol levels. A taskforce created by the World Federation of Societies of Biological Psychiatry and the Canadian Network for Mood and Anxiety Treatments provisionally recommends specific daily doses of ashwagandha root extract for the treatment of generalized anxiety disorder, but they also note that they cannot provide a stronger recommendation without more data.
Results from several clinical trials suggest that ashwagandha extracts may help reduce stress and anxiety. A 2021 systematic review identified seven studies that investigated the use of ashwagandha to treat stress and anxiety [8]. A total of 491 adults, all from India, with either self-reported high stress and anxiety or a diagnosed anxiety disorder, were randomized to take ashwagandha or placebo for 6 to 8 weeks. Six of the studies used extracts made from ashwagandha root alone (three studies, KSM-66), root and leaf (two studies, Sensoril or Shoden), or unspecified parts (one study), while the seventh study used dried root powder made into granules. The ashwagandha dose varied from 240 to 1,250 mg/day of extract or 12,000 mg/day of whole root granules, which is equivalent to 6,000 mg of root powder. Overall, the studies found that ashwagandha significantly reduced stress and anxiety levels (subjectively measured by validated rating scales), reduced sleeplessness and fatigue, and reduced serum cortisol levels (a stress hormone) when compared with placebo. In several studies, the benefits appeared to be greater with doses of 500 to 600 mg/day than with lower doses.
Results from most of the studies published after this 2021 review also suggest that ashwagandha has a beneficial impact on perceived stress [9-17]. For example, one clinical trial conducted in Florida included 60 men and women (mean age 34 years) who reported experiencing stress. Participants took capsules that contained 225 mg/day or 400 mg/day of a proprietary ashwagandha root and leaf extract (NooGandha) or placebo for 30 days [9]. Compared with participants in the placebo group, those in both ashwagandha groups reported positive effects on stress, anxiety, depression, and food cravings as measured by validated rating scales. In addition, participants who took the 225-mg dose had lower saliva cortisol levels than those in the placebo group.
At two health centers in India, 130 healthy men and women age 20 to 55 years with self-reported stress were randomized to take a sustained-released ashwagandha root extract (Prolanza) or placebo for 90 days [10]. The extract was standardized to contain 15 mg withanolides per 300-mg capsule, and participants took one capsule daily. Compared with those who received placebo, participants who took ashwagandha extract reported improvements in stress levels and sleep quality as measured by validated rating scales. They also had lower serum cortisol levels. In addition, participants reported improvements in psychological well-being, memory, and focus. Another study in India randomized 54 participants with mild to moderate stress and anxiety to receive either ashwagandha root extract (Shagandha) or placebo [14]. The participants in the ashwagandha group were given tablets that were standardized to contain 2.5% withanolides; each tablet included 500 mg of the root extract and 5 mg of piperine. At day 60, participants in the ashwagandha group had significantly lower scores for stress and anxiety on two validated rating scales than those in the placebo group. In addition, the quality of life scores increased significantly for people in the ashwagandha group between baseline and day 60, and the researchers noted improvements in multitasking and concentration among the participants in this group.
At the University of Colorado, Colorado Springs, 60 students (age 18–50 years) were randomized to take an ashwagandha root extract (Gaia Herbs) or placebo for 30 days in a double-blind trial [11,12]. The extract contained 2.5 mg withanolides per 350-mg capsule, and participants took two capsules daily. The investigators gathered qualitative, subjective information from participants during daily check-ins and focus groups. Participants who took ashwagandha root extract reported increased well-being, including a sense of calm; improved energy levels; heightened mental clarity; and enhanced sleep quality. While the descriptions of stress were comparable in both groups, participants who took ashwagandha were more likely to describe their stress as manageable compared with those taking placebo.
Another randomized clinical trial included 120 healthy men and women (mean age 54–55 years) who were overweight or mildly obese and experiencing low energy and fatigue [17]. Participants took an ashwagandha root extract (Witholytin, which contains 200 mg hydroalcoholic extract of ashwagandha root standardized to 1.5% withanolides) or placebo twice daily for 12 weeks. Compared with placebo, ashwagandha did not reduce perceived stress, but it did reduce fatigue.
A daily dose of 300 to 600 mg ashwagandha root extract (standardized to 5% withanolides) is provisionally recommended for the treatment of generalized anxiety disorder by an international taskforce created by the World Federation of Societies of Biological Psychiatry (WFSBP) and the Canadian Network for Mood and Anxiety Treatments (CANMAT) [18]. The taskforce issued this recommendation in 2022, and they noted that more research is needed to support a stronger recommendation.
Evidence from a small number of studies suggests that taking ashwagandha extract may improve several aspects of sleep, including sleep quality, sleep efficiency, total sleep time, and sleep latency. These benefits tend to be more pronounced among people with insomnia.
Research is limited, but the results from a few clinical trials suggest that ashwagandha extracts may help with sleep. For example, at one study center in India, 150 healthy men and women age 18 to 65 years with self-reported sleep problems characterized by insomnia and lack of restful sleep were randomized to take an ashwagandha root and leaf extract (Shoden) or placebo for 6 weeks [19]. The extract was standardized to contain 21 mg of withanolide glycosides per 60-mg capsule, and participants took two capsules each day. Both groups reported improvements in sleep quality as measured by a validated rating scale, but the improvements were greater in the ashwagandha group (72%) than in the placebo group (29%). In addition, participants who took ashwagandha extract showed improvements in sleep efficiency (time in bed spent in sleep), total sleep time, sleep latency (time taken to fall asleep), and awakening after sleep onset as assessed by actigraphy, which involves wearing a watch monitor on the wrist to measure body motion. They also reported improvements in quality of life.
In another trial conducted in India, 80 healthy men and women age 18 to 50 years, half of them with insomnia, were randomized to take an ashwagandha root extract (KSM-66) or placebo for 8 weeks [5]. The extract was standardized to a withanolide content of more than 5% per 300-mg capsule, and participants took two capsules each day. Participants with insomnia who took ashwagandha extract showed improvements in sleep quality, sleep onset latency, mental alertness on rising, and perceived anxiety symptoms compared with those taking placebo, as measured by actigraphy and validated rating scales. Participants without insomnia who took ashwagandha also reported that ashwagandha improved their sleep but not their perceived anxiety symptoms or their mental alertness on awakening.
A 2021 systematic review and meta-analysis included five studies (including the two described above) that investigated using ashwagandha to promote sleep [20]. All the studies were conducted in India. A total of 372 adults, either self-described as healthy or with insomnia, took ashwagandha or placebo for 6 to 12 weeks. The dose of the ashwagandha supplement used in these studies ranged from 250 to 600 mg/day as a root extract (KSM-66) or, in one study, 120 mg/day of a root and leaf extract (Shoden). Overall, the studies found that ashwagandha extract had a small but significant effect on improving sleep compared with placebo. The benefits were more prominent when the dose was 600 mg/day and when the treatment duration was at least 8 weeks. Benefits were also more prominent in participants with insomnia.
Ashwagandha: Is it helpful for stress, anxiety, or sleep? — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Lopresti AL, Smith SJ. Ashwagandha (Withania somnifera) for the treatment and enhancement of mental and physical conditions: A systematic review of human trials. Journal of Herbal Medicine 2021;28:100434.
Systematic review · Population basis: human · Directness: not assessedSmith SJ, Lopresti AL, Fairchild TJ. Exploring the efficacy and safety of a novel standardized ashwagandha (Withania somnifera) root extract (Witholytin®) in adults experiencing high stress and fatigue in a randomized, double-blind, placebo-controlled trial. J Psychopharmacol 2023;37:1091-104. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedTandon N, Yadav SS. Safety and clinical effectiveness of Withania Somnifera (Linn.) Dunal root in human ailments. J Ethnopharmacol 2020;255:112768. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedLiverTox. Ashwagandha. In: LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2019. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedInagaki K, Mori N, Honda Y, Takaki S, Tsuji K, et al. A case of drug-induced liver injury with prolonged severe intrahepatic cholestasis induced by Ashwagandha. Kanzo 2017;58:448-54.
Study type could not be determined · Population basis: unknown · Directness: not assessedWeber S, Gerbes AL. Ashwagandha-Induced Liver Injury: Self-Reports on Commercial Websites as Useful Adjunct Tools for Causality Assessment. Am J Gastroenterol 2021;116:2151-2. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedBjornsson HK, Bjornsson ES, Avula B, Khan IA, Jonasson JG, et al. Ashwagandha-induced liver injury: A case series from Iceland and the US Drug-Induced Liver Injury Network. Liver Int 2020;40:825-9. [PubMed abstract]
Case series · Population basis: unknown · Directness: not assessedLubarska M, Hałasiński P, Hryhorowicz S, Mahadea DS, Łykowska-Szuber L, et al. Liver Dangers of Herbal Products: A Case Report of Ashwagandha-Induced Liver Injury. Int J Environ Res Public Health 2023;20. [PubMed abstract]
Case report · Population basis: unknown · Directness: not assessedIreland PJ, Hardy T, Burt AD, Donnelly MC. Drug-induced hepatocellular injury due to herbal supplement ashwagandha. J R Coll Physicians Edinb 2021;51:363-5. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedPhilips CA, Valsan A, Theruvath AH, Ravindran R, Oommen TT, et al. Ashwagandha-induced liver injury-A case series from India and literature review. Hepatol Commun 2023;7. [PubMed abstract]
Case series · Population basis: unknown · Directness: not assessedGannon JM, Forrest PE, Roy Chengappa KN. Subtle changes in thyroid indices during a placebo-controlled study of an extract of Withania somnifera in persons with bipolar disorder. J Ayurveda Integr Med 2014;5:241-5. [PubMed abstract]
Controlled clinical trial · Population basis: unknown · Directness: not assessedSharma AK, Basu I, Singh S. Efficacy and Safety of Ashwagandha Root Extract in Subclinical Hypothyroid Patients: A Double-Blind, Randomized Placebo-Controlled Trial. J Altern Complement Med 2018;24:243-8. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedChittiboyina AG, Khan IA. Current issues in phytomedicine research - Conundrum on the chemistry of ashwagandha and its biological effects. J Ethnopharmacol 2024;325:117871. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedCurry KM, McNeil LE, Flores A, Fuks J. Thyrotoxicosis with Ashwagandha: A Case Report. SSRN 2019.
Case report · Population basis: unknown · Directness: not assessedNatMed. Ashwagandha. 2023.
Study type could not be determined · Population basis: unknown · Directness: not assessedAmerican Herbal Products Association. American Herbal Products Association’s Botanical Safety Handbook, 2nd edition. Boca Raton, FL: CRC Press LLC; 2013.
Study type could not be determined · Population basis: unknown · Directness: not assessedEngels G, Brinckmann J. HerbalGram, The Journal of the American Botanical Council. Ashwagandha. 2013; Issue 99.
Study type could not be determined · Population basis: unknown · Directness: not assessedNational Center for Complementary and Integrative Health. Ashwagandha. 2023.
Study type could not be determined · Population basis: unknown · Directness: not assessedMikulska P, Malinowska M, Ignacyk M, Szustowski P, Nowak J, et al. Ashwagandha (Withania somnifera)-Current Research on the Health-Promoting Activities: A Narrative Review. Pharmaceutics 2023;15. [PubMed abstract]
Narrative review · Population basis: unknown · Directness: not assessedAmerican Herbal Pharmacopoeia. Ashwagandha Root, Withania somnifera - Analytical, Quality Control, and Therapeutic Monograph. Santa Cruz, CA; 2000.
Study type could not be determined · Population basis: unknown · Directness: not assessedPhilips CA, Theruvath AH. A comprehensive review on the hepatotoxicity of herbs used in the Indian (Ayush) systems of alternative medicine. Medicine (Baltimore) 2024;103:e37903. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedMcKeown M. Why did Denmark ban Ashwagandha? McGill University, Office for Science and Society, 2023.
Study type could not be determined · Population basis: unknown · Directness: not assessedANSES. AVIS de l’Agence nationale de sécurité sanitaire de l’alimentation, de l’environnement et du travail relatif aux risques liés à l'utilisation des préparations de Withania somnifera (L.) Dunal dans les compléments alimentaires. 2024.
Study type could not be determined · Population basis: unknown · Directness: not assessedAmerican Herbal Pharmacopoeia. AHP Responds to Claims of Ashwagandha Abortifacient Effects. 2024.
Study type could not be determined · Population basis: unknown · Directness: not assessedSmith SJ, Lopresti AL, Teo SYM, Fairchild TJ. Examining the Effects of Herbs on Testosterone Concentrations in Men: A Systematic Review. Adv Nutr 2021;12:744-65. [PubMed abstract]
Systematic review · Population basis: human · Directness: not assessedLopresti AL, Drummond PD, Smith SJ. A Randomized, Double-Blind, Placebo-Controlled, Crossover Study Examining the Hormonal and Vitality Effects of Ashwagandha ( Withania somnifera) in Aging, Overweight Males. Am J Mens Health 2019;13:1557988319835985. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessedAshwagandha appears to be well tolerated for up to about 3 months of use, but its long-term safety is not known. Common side effects (e.g., loose stools, nausea, drowsiness) are usually mild. However, there are a few reports of more serious side effects, including adverse effects on liver function. Ashwagandha might also affect thyroid function and interact with some medications. Some experts advise against the use of ashwagandha by women who are pregnant and by men with hormone-sensitive prostate cancer.
In the studies described above and in many other clinical trials, ashwagandha has been well tolerated by participants for up to about 3 months of use. Common side effects are mild and include stomach upset, loose stools, nausea, and drowsiness [8,21]. Increased heart rate variability has also been reported [17]. Evidence on the safety of using ashwagandha over many months or years is lacking.
There are a few reports of more serious side effects associated with ashwagandha use, including adverse effects on liver function [22]. In a 2017 report of liver injury that was associated with ashwagandha use, a 20-year-old man in Japan developed liver dysfunction and hyperbilirubinemia after using ashwagandha (plant part and dose not specified) in combination with multiple antianxiety drugs [23]. Since then, the use of ashwagandha has been linked to acute liver injury in other individuals, some of whom had pre-existing liver disease [24-28]. These include five cases of people (three men and two women, age range 21–62 years) who reportedly took supplements that contained 450 to 1,350 mg ashwagandha (plant part not specified) daily over the course of 1 week to 4 months and experienced signs of liver injury, such as jaundice, pruritus, nausea, lethargy, abdominal discomfort, and hyperbilirubinemia [25]. In these cases and others, the conditions of the individuals improved over time after they stopped taking the supplement; some also received medical treatment [23,25-27]. However, the contents of the products that the individuals took were not independently verified in all cases, and some products were combination products that contained ashwagandha and other ingredients.
Some research suggests that ashwagandha might affect thyroid function. In one study, three adult men who took 500 mg/day of a standardized ashwagandha root and leaf extract for 8 weeks had small increases in blood thyroxine (T4) levels [29]. A small clinical trial with 50 participants with subclinical hypothyroidism found that ashwagandha root extract, at a dose of 300 mg twice daily for 8 weeks, lowered serum thyroid-stimulating hormone (TSH) and increased triiodothyronine (T3) and T4 levels compared with placebo [30].
Three case reports have also described thyrotoxicosis in women who were taking ashwagandha extract (age range 32–73 years) [31]. However, the doses of ashwagandha were not specified in two of these case reports, and the third case involved an unusually high dose (1,950 mg/day for more than 2 months) [32]. Discontinuing ashwagandha resolved the symptoms of thyrotoxicosis in all three cases. These findings suggest that ashwagandha might interact with thyroid hormone medications. Ashwagandha might also interact with other medications, including antidiabetes medications, antihypertensives, immunosuppressants, and sedatives [8,33].
Some experts advise against the use of ashwagandha by women who are pregnant because some reports have suggested that it has the potential to cause spontaneous abortion [8,33-38]. A risk assessment released by the Technical University of Denmark in 2020 discussed both this potential abortifacient effect of ashwagandha and potential effects on thyroid and sex hormones; Denmark subsequently banned the use of ashwagandha in 2023 [39,40]. The French Agency for Food, Environmental, and Occupational Health and Safety (ANSES) issued a statement in 2024 that recommended against using ashwagandha in certain populations, including pregnant and breastfeeding women and people with endocrine disorders [41]. One of the sources for this information is a monograph on ashwagandha root published in 2000 by the American Herbal Pharmacopoeia (AHP) [38]; however, AHP has stated that their report has been misrepresented and that there is no evidence that ashwagandha root causes abortions [42]. Ashwagandha use might also increase testosterone levels [8,17,43,44], so according to experts, it might not be safe for men with hormone-sensitive prostate cancer [36,37].
Ashwagandha: Is it helpful for stress, anxiety, or sleep? — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessedGalior K, Grebe S, Singh R. Development of vitamin D toxicity from overcorrection of vitamin D deficiency: A review of case reports. Nutrients 2018, 10, 953. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedAuguste BL, Avila-Casado C, Bargman JM. Use of vitamin D drops leading to kidney failure in a 54-year-old man. CMAJ 2019;191:E390-4. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedVogiatzi MG, Jacobson-Dickman E, DeBoer MD. Vitamin D supplementation and risk of toxicity in pediatrics: A review of current literature. J Clin Endocrinol Metab 2014;99:1132-41. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSingh P, Trivedi N. Tanning beds and hypervitaminosis D: A case report. Ann Intern Med 2014;160:810-1. [PubMed abstract]
Case report · Population basis: unknown · Directness: not assessedLaurent MR, Gielen E, Pauwels S, Vanderschueren D, Bouillon R. Hypervitaminosis D associated with tanning bed use: A case report. Ann Intern Med 2017;166:155-6. [PubMed abstract]
Case report · Population basis: unknown · Directness: not assessedPerez-Castrillon JL, Vega G, Abad L, Sanz A, Chaves J, Hernandez G, Duenas A. Effects of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Am J Cardiol 2007;99:903-5. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedJackson RD, LaCroix AZ, Gass M, Wallace RB, Robbins J, Lewis CE, et al. Calcium plus vitamin D supplementation and the risk of fractures. N Engl J Med 2006;354:669-82. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedMalihi Z, Lawes CMM, Wu Z, Huang Y, Waayer D, Toop L, et al. Monthly high-dose vitamin D supplementation does not increase kidney stone risk or serum calcium: Results from a randomized controlled trial. Am J Clin Nutr 2019;109:1578-87. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessedMalihi Z, Wu Z, Stewart AW, Lawes CMM, Scragg R. Hypercalcemia, hypercalciuria, and kidney stones in long-term studies of vitamin D supplementation: A systematic review and meta-analysis. Am J Clin Nutr 2016;104:1039-51. [PubMed abstract]
Meta-analysis · Population basis: unknown · Directness: not assessedVitamin D toxicity can cause hypercalcemia, hypercalciuria, and high serum 25(OH)D concentrations; in extreme cases, it may lead to renal failure, calcification of soft tissues, cardiac arrhythmias, and death. Vitamin D toxicity is almost always a result of excessive intakes of vitamin D through supplements. Taking calcium supplements in combination with vitamin D supplements may increase the risk of certain adverse effects. The Tolerable Upper Intake Level for vitamin D ranges from 25 to 100 mcg (1,000–4,000 IU), depending on age.
Excess amounts of vitamin D are toxic. Because vitamin D increases calcium absorption in the gastrointestinal tract, vitamin D toxicity results in marked hypercalcemia (total calcium greater than 11.1 mg/dL, beyond the normal range of 8.4–10.2 mg/dL), hypercalciuria, and high serum 25(OH)D levels (typically >375 nmol/l [150 ng/mL]) [158]. Hypercalcemia, in turn, can lead to nausea, vomiting, muscle weakness, neuropsychiatric disturbances, pain, loss of appetite, dehydration, polyuria, excessive thirst, and kidney stones.
In extreme cases, vitamin D toxicity causes renal failure, calcification of soft tissues throughout the body (including in coronary vessels and heart valves), cardiac arrhythmias, and even death. Vitamin D toxicity has been caused by consumption of dietary supplements that contained excessive vitamin D amounts because of manufacturing errors, that were taken inappropriately or in excessive amounts, or that were incorrectly prescribed by physicians, [158-160].
Experts do not believe that excessive sun exposure results in vitamin D toxicity because thermal activation of previtamin D3 in the skin gives rise to various non-vitamin D forms that limit formation of vitamin D3. Some vitamin D3 is also converted to nonactive forms [1]. However, frequent use of tanning beds, which provide artificial UV radiation, can lead to 25(OH)D levels well above 375 to 500 nmol/L (150–200 ng/mL) [161-163].
The combination of high intakes of calcium (about 2,100 mg/day from food and supplements) with moderate amounts of vitamin D (about 19 mcg [765 IU]/day from food and supplements) increased the risk of kidney stones by 17% over 7 years among 36,282 postmenopausal women who were randomly assigned to take 1,000 mg/day calcium and 10 mcg (400 IU)/day vitamin D or a placebo [164]. However, other, shorter (from 24 weeks to 5 years) clinical trials of vitamin D supplementation alone or with calcium in adults found greater risks of hypercalcemia and hypercalciuria, but not of kidney stones [165,166].
The FNB established ULs for vitamin D in 2010 (Table 4) [1]. While acknowledging that signs and symptoms of toxicity are unlikely at daily intakes below 250 mcg (10,000 IU), the FNB noted that even vitamin D intakes lower than the ULs might have adverse health effects over time. The FNB recommended avoiding serum 25(OH)D levels above approximately 125 to 150 nmol/L (50–60 ng/mL), and it found that even lower serum levels (approximately 75–120 nmol/L [30–48 ng/mL]) are associated with increases in rates of all-cause mortality, risk of cancer at some sites (e.g., pancreas), risk of cardiovascular events, and number of falls and fractures among older adults.
| Age | Male | Female | Pregnancy | Lactation |
|---|---|---|---|---|
| 0–6 months | 25 mcg (1,000 IU) | 25 mcg (1,000 IU) | ||
| 7–12 months | 38 mcg (1,500 IU) | 38 mcg (1,500 IU) | ||
| 1–3 years | 63 mcg (2,500 IU) | 63 mcg (2,500 IU) | ||
| 4–8 years | 75 mcg (3,000 IU) | 75 mcg (3,000 IU) | ||
| 9–13 years | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | ||
| 14–18 years | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) |
| 19–50 years | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) |
| 51–70 years | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) | ||
| >70 years | 100 mcg (4,000 IU) | 100 mcg (4,000 IU) |
Vitamin D — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Gotfredsen A, Westergren Hendel H, Andersen T. Influence of orlistat on bone turnover and body composition. Int J Obes Relat Metab Disord 2001;25:1154-60. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedJames WP, Avenell A, Broom J, Whitehead J. A one-year trial to assess the value of orlistat in the management of obesity. Int J Obes Relat Metab Disord 1997;21:S24-30. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedMcDuffie JR, Calis KA, Booth SL, Uwaifo GI, Yanovski JA. Effects of orlistat on fat-soluble vitamins in obese adolescents. Pharmacotherapy 2002;22:814-22. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedRobien K, Oppeneer SJ, Kelly JA, Hamilton-Reeves JM. Drug-vitamin D interactions: A systematic review of the literature. Nutr Clin Pract 2013;28:194-208. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedSchwartz JB. Effects of vitamin D supplementation in atorvastatin-treated patients: A new drug interaction with an unexpected consequence. Clin Pharmacol Ther 2009;85:198-203. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedPerez-Castrillon JL, Vega G, Abad L, Sanz A, Chaves J, Hernandez G, Duenas A. Effects of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Am J Cardiol 2007;99:903-5. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedAloia JF, Li-Ng M, Pollack S. Statins and vitamin D. Am J Cardiol 2007;100:1329. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedBuckley LM, Leib ES, Cartularo KS, Vacek PM, Cooper SM. Calcium and vitamin D3 supplementation prevents bone loss in the spine secondary to low-dose corticosteroids in patients with rheumatoid arthritis. A randomized, double-blind, placebo-controlled trial. Ann Intern Med 1996;125:961-8. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedde Sevaux RGL, Hoitsma AJ, Corstens FHM, Wetzels JFM. Treatment with vitamin D and calcium reduces bone loss after renal transplantation: a randomized study. J Am Soc Nephrol 2002;13:1608-14. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessedLukert BP, Raisz LG. Glucocorticoid-induced osteoporosis: pathogenesis and management. Ann Intern Med 1990;112:352-64. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSkversky AL, Kumar J, Abramowitz MK, Kaskel FJ, Melamed ML. Association of glucocorticoid use and low 25-hydroxyvitamin D levels: Results from the National Health and Nutrition Examination Survey (NHANES): 2001-2006. J Clin Endocrinol Metab 2011;96:3838-45. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedDrinka PJ, Nolten WE. Hazards of treating osteoporosis and hypertension concurrently with calcium, vitamin D, and distal diuretics. J Am Geriatr Soc 1984;32:405-7. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedCrowe M, Wollner L, Griffiths RA. Hypercalcaemia following vitamin D and thiazide therapy in the elderly. Practitioner 1984;228:312-3. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedVitamin D supplements may interact with medications, and some medications may affect vitamin D levels. These medications include orlistat, statins, steroids, and thiazide diuretics.
Vitamin D supplements may interact with several types of medications. A few examples are provided below. Individuals taking these and other medications on a regular basis should discuss their vitamin D intakes and status with their health care providers.
The weight-loss drug orlistat (Xenical and alli), together with a reduced-fat diet, can reduce the absorption of vitamin D from food and supplements, leading to lower 25(OH)D levels [167-170].
Statin medications reduce cholesterol synthesis. Because endogenous vitamin D is derived from cholesterol, statins may also reduce vitamin D synthesis [170]. In addition, high intakes of vitamin D, especially from supplements, might reduce the potency of atorvastatin (Lipitor), lovastatin (Altoprev and Mevacor), and simvastatin (FloLipid and Zocor), because these statins and vitamin D appear to compete for the same metabolizing enzyme [170-173].
Corticosteroid medications, such as prednisone (Deltasone, Rayos, and Sterapred), are often prescribed to reduce inflammation. These medications can reduce calcium absorption and impair vitamin D metabolism [174-176]. In the NHANES 2001–2006 survey, 25(OH)D deficiency (less than 25 nmol/L [10 ng/mL]) was more than twice as common among children and adults who reported oral steroid use (11%) than in nonusers (5%) [177].
Thiazide diuretics (e.g., Hygroton, Lozol, and Microzide) decrease urinary calcium excretion. The combination of these diuretics with vitamin D supplements (which increase intestinal calcium absorption) might lead to hypercalcemia, especially among older adults and individuals with compromised renal function or hyperparathyroidism [170,178,179].
Vitamin D — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Silva MC, Furlanetto TW. Intestinal absorption of vitamin D: A systematic review. Nutr Rev 2018;76:60-76. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedHolick MF. Vitamin D deficiency. N Engl J Med 2007;357:266-81. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedHirsch AL. Industrial Aspects of Vitamin D. In: Feldman D, Pike JW, Adams JS, eds. Vitamin D. 3rd ed. Academic Press; 2011:73-93.
Study type could not be determined · Population basis: unknown · Directness: not assessedNational Institutes of Health. Dietary Supplement Label Database. 2020.
Study type could not be determined · Population basis: unknown · Directness: not assessedTripkovic L, Lambert H, Hart K, Smith CP, Bucca G, Penson S, et al. Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: A systematic review and meta-analysis. Am J Clin Nutr 2012;95:1357-64. [PubMed abstract]
Meta-analysis · Population basis: unknown · Directness: not assessedLehmann U, Hirche F, Stangl GI, Hinz K, Westphal S, Dierkes J. Bioavailability of vitamin D2 and D3 in healthy volunteers, a randomised placebo-controlled trial. J Clin Endocrin Metab 2013;98:4339-45. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedLogan VF, Gray AR, Peddie MC, Harper MJ, Houghton LA. Long-term vitamin D3 supplementation is more effective than vitamin D2 in maintaining serum 25-hydroxyvitamin D status over the winter months. Br J Nutr 2013;109:1082-8. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedTripkovic L, Wilson LR, Hart K, Johnsen S, de Lusignan S, Smith CP, et al. Daily supplementation with 15 µg vitamin D2 compared with vitamin D3 to increase wintertime 25-hydroxyvitamin D status in healthy South Asian and white European women: A 12-wk randomized, placebo-controlled food-fortification trial. Am J Clin Nutr 2017;106:481-90. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessedGraeff-Armas LA, Bendik I, Kunz I, Schoop R, Hull S, Beck M. Supplemental 25-hydroxycholecalciferol is more effective than cholecalciferol in raising serum 25-hydroxyvitamin D concentrations in older adults. J Nutr 2020;150:73-81. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedQuesada-Gomez JM, Bouillon R. Is calcifediol better than cholecalciferol for vitamin D supplementation? Osteoporos Int 2018;29:1697-1711. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedVitamin D is present in dietary supplements as either vitamin D2 or vitamin D3. Both can raise the serum level of 25(OH)D. However, research shows that vitamin D3 increases serum 25(OH)D levels to a greater extent than vitamin D2 and can maintain those higher levels for longer periods of time.
Dietary supplements can contain vitamins D2 or D3. Vitamin D2 is manufactured using UV irradiation of ergosterol in yeast, and vitamin D3 is typically produced with irradiation of 7-dehydrocholesterol from lanolin obtained from the wool of sheep [13,31]. An animal-free version of vitamin D3 sourced from lichen is also available [32]. People who avoid all animal-sourced products can contact dietary supplement manufacturers to ask about their sourcing and processing techniques.
Both vitamins D2 and D3 raise serum 25(OH)D levels, and they seem to have equivalent ability to cure rickets [4]. In addition, most steps in the metabolism and actions of vitamins D2 and D3 are identical. However, most evidence indicates that vitamin D3 increases serum 25(OH)D levels to a greater extent and maintains these higher levels longer than vitamin D2, even though both forms are well absorbed in the gut [33-36].
Some studies have used dietary supplements containing the 25(OH)D3 form of vitamin D. Per equivalent microgram dose, 25(OH)D3 is three to five times as potent as vitamin D3 [37,38]. However, no 25(OH)D3 dietary supplements appear to be available to consumers on the U.S. market at this time [32].
Vitamin D — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessedSempos CT, Binkley N. 25-hydroxyvitamin D assay standardisation and vitamin D guidelines paralysis. Public Health Nutrition 2020;23:1153-64. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedDemay MB, Pittas AG, Bikle DD, Diab DL, Kiely ME, et al. Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1907-1947. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedShah VP, Nayfeh T, Alsawaf Y, Saadi S, Farah M, et al. A Systematic Review Supporting the Endocrine Society Clinical Practice Guidelines on Vitamin D. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1961-1974. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedBouillon R. Comparative analysis of nutritional guidelines for vitamin D. Nat Rev Endocrinol 2017;13:466-79. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedScientific Advisory Committee on Nutrition. Vitamin D and Health. 2016.
Study type could not be determined · Population basis: unknown · Directness: not assessedThe Food and Nutrition Board at the National Academies of Sciences, Engineering, and Medicine has established Recommended Dietary Allowances and Adequate Intakes for vitamin D. These values range from 15 to 20 mcg (600–800 IU) for adults and from 10 to 15 mcg (400–600 IU) for infants, children, and adolescents, depending on age.
Intake recommendations for vitamin D and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by expert committees of NASEM [1]. DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values include the following:
The FNB established RDAs for vitamin D to indicate daily intakes sufficient to maintain bone health and normal calcium metabolism in healthy people. RDAs for vitamin D are listed in both micrograms (mcg) and International Units (IU); 1 mcg vitamin D is equal to 40 IU (Table 2). Even though sunlight is a major source of vitamin D for some people, the FNB based the vitamin D RDAs on the assumption that people receive minimal sun exposure [1]. For infants from birth to 12 months, the FNB developed AIs based on the amount of vitamin D that maintains serum 25(OH)D levels above 20 ng/mL (50 nmol/L) and supports bone development.
| Age | Male | Female | Pregnancy | Lactation |
|---|---|---|---|---|
| 0–6 months* | 10 mcg (400 IU)* | 10 mcg (400 IU)* | ||
| 7–12 months* | 10 mcg (400 IU)* | 10 mcg (400 IU)* | ||
| 1–3 years | 15 mcg (600 IU) | 15 mcg (600 IU) | ||
| 4–8 years | 15 mcg (600 IU) | 15 mcg (600 IU) | ||
| 9–13 years | 15 mcg (600 IU) | 15 mcg (600 IU) | ||
| 14–18 years | 15 mcg (600 IU) | 15 mcg (600 IU) | 15 mcg (600 IU) | 15 mcg (600 IU) |
| 19–50 years | 15 mcg (600 IU) | 15 mcg (600 IU) | 15 mcg (600 IU) | 15 mcg (600 IU) |
| 51–70 years | 15 mcg (600 IU) | 15 mcg (600 IU) | ||
| >70 years | 20 mcg (800 IU) | 20 mcg (800 IU) | ||
| *Adequate Intake (AI) |
Many other countries around the world and some professional societies have somewhat different guidelines for vitamin D intakes [15]. These differences are a result of an incomplete understanding of the biology and clinical implications of vitamin D, different purposes for the guidelines (e.g., for public health in a healthy population or for clinical practice), and/or the use in some guidelines of observational studies in addition to randomized clinical trials to establish recommendations [9,15]. For example, the United Kingdom Scientific Advisory Committee on Nutrition recommends intakes of 10 mcg (400 IU)/day for individuals age 4 years and older [16]. The Endocrine Society recommends routine vitamin D supplementation for children and teens age 1 to 18 years, pregnant women, adults with pre-diabetes, and adults age 75 years and older, but not for healthy adults age 19 to 74 [11,12]. The Endocrine Society does not recommend specific doses but notes that all individuals should adhere to the RDA.
Vitamin D — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessedSilva MC, Furlanetto TW. Intestinal absorption of vitamin D: A systematic review. Nutr Rev 2018;76:60-76. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedBrown LL, Cohen B, Tabor D, Zappala G, Maruvada P, Coates PM. The vitamin D paradox in Black Americans: A systems-based approach to investigating clinical practice, research, and public health—expert panel meeting report. BMC Proceedings, 2018;12(Suppl 6):6. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedPicciano MF. Nutrient composition of human milk. Pediatr Clin North Am 2001;48:53-67. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedWagner CL, Greer FR, American Academy of Pediatrics Section on Breastfeeding, American Academy of Pediatrics Committee on Nutrition. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Pediatrics 2008;122:1142-52. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedDawodu A, Tsang RC. Maternal vitamin D status: Effect on milk vitamin D content and vitamin D status of breastfeeding infants. Adv Nutr 2012;3:353-61. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedDavis CD, Dwyer JT. The 'sunshine vitamin': benefits beyond bone? J Natl Cancer Inst 2007;99:1563-5. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSimon AE, Ahrens KA. Adherence to vitamin D intake guidelines in the United States. Pediatrics 2020;145:e20193574. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedChalcraft JR, Cardinal LM, Wechsler PJ, Hollis BW, Gerow KG, Alexander BM, et al. Vitamin D synthesis following a single bout of sun exposure in older and younger men and women. Nutrients 2020; 12, 2237; doi:10.3390/nu12082237. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedSowah D, Fan X, Dennett L, Hagtvedt R, Straube S. Vitamin D levels and deficiency with different occupations: A systematic review. BMC Public Health 2017;17:519. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedPappa HM, Bern E, Kamin D, Grand RJ. Vitamin D status in gastrointestinal and liver disease. Curr Opin Gastroenterol 2008;24:176-83. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedDrincic A, Fuller E, Heaney RP, Armas LAG. 25-hydroxyvitamin D response to graded vitamin D3 supplementation among obese adults. J Clin Endocrinol Metab 2013;98:4845-51. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedEkwaru JP, Zwicker JD, Holick MF, Giovannucci E, Veugelers PJ. The importance of body weight for the dose response relationship of oral vitamin D supplementation and serum 25-hydroxyvitamin D in healthy volunteers. PLOS ONE 2014;9:e111265. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedChakhtoura M, Rahme M, Fuleihan E-H. Vitamin D metabolism in bariatric surgery. Endocrinol Metab Clin North Am 2017;46:947-82. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedPeterson L, Zeng X, Caufield-Noll CP, Schweitzer MA, Magnuson TH, Steele KE. Vitamin D status and supplementation before and after bariatric surgery: A comprehensive literature review. Surg Obes Relat Dis 2016;12:693-702. [PubMed abstract]
Narrative review · Population basis: unknown · Directness: not assessedChakhtoura MT, Nakhoul N, Akl EA, Mantzoros CS, El Hajj Guleihan GA. Guidelines on vitamin D replacement in bariatric surgery? Identification and systematic appraisal. Metabolism 2016;65:586-97. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedCertain groups of people are more likely than others to have inadequate vitamin D status. These include breastfed infants, older adults, people with limited sun exposure, people with dark skin, people with conditions that limit fat absorption, and people with obesity or those who have undergone gastric bypass surgery.
Obtaining sufficient vitamin D from natural (nonfortified) food sources alone is difficult. For many people, consuming vitamin D-fortified foods and exposing themselves to some sunlight are essential for maintaining a healthy vitamin D status. However, some groups might need dietary supplements to meet their vitamin D requirements. The following groups are among those most likely to have inadequate vitamin D status.
Consumption of human milk alone does not ordinarily enable infants to meet vitamin D requirements, because it provides less than 0.6 to 2.0 mcg/L (25 to 78 IU/L) [1,56,57]. The vitamin D content of human milk is related to the mother’s vitamin D status; studies suggest that the breastmilk of mothers who take daily supplements containing at least 50 mcg (2,000 IU) vitamin D3 have higher levels of the nutrient [57,58].
Although UVB exposure can produce vitamin D in infants, the American Academy of Pediatrics (AAP) advises parents to keep infants younger than 6 months out of direct sunlight, dress them in protective clothing and hats, and apply sunscreen on small areas of exposed skin when sun exposure is unavoidable [59]. The AAP recommends 10 mcg (400 IU)/day vitamin D supplements for exclusively and partially breastfed infants starting shortly after birth and lasting until they are weaned and consume at least 1,000 mL/day vitamin D-fortified formula or whole milk [57]. The AAP also recommends 10 mcg (400 IU)/day supplemental vitamin D for all infants who are not breastfed and ingest less than 1,000 mL/day vitamin D-fortified formula or milk. An analysis of NHANES 2009–2016 data found that only 20.5% of breastfed infants and 31.1% of infants who were not breastfed ingested these recommended amounts of supplements [60].
Older adults are at increased risk of developing vitamin D insufficiency, partly because the skin's ability to synthesize vitamin D declines with age [1,61]. In addition, older adults are likely to spend more time than younger people indoors, and they might have inadequate dietary intakes of the vitamin [1].
Homebound individuals; people who wear long robes, dresses, or head coverings for religious reasons; and people with occupations that limit sun exposure are among the groups that are unlikely to obtain adequate amounts of vitamin D from sunlight [62]. The use of sunscreen also limits vitamin D synthesis from sunlight. However, because the extent and frequency of sunscreen use are unknown, the role that sunscreen may play in reducing vitamin D synthesis is unclear [1].
Greater amounts of the pigment melanin in the epidermal layer of the skin result in darker skin and reduce the skin’s ability to produce vitamin D from sunlight [1]. Black Americans, for example, typically have lower serum 25(OH)D levels than White Americans. However, whether these lower levels in persons with dark skin have significant health consequences is not clear [14]. Those of African American ancestry, for example, have lower rates of bone fracture and osteoporosis than do Whites (see the section below on bone health and osteoporosis).
Because vitamin D is fat soluble, its absorption depends on the gut’s ability to absorb dietary fat [4]. Fat malabsorption is associated with medical conditions that include some forms of liver disease, cystic fibrosis, celiac disease, Crohn’s disease, and ulcerative colitis [1,63]. In addition to having an increased risk of vitamin D deficiency, people with these conditions might not eat certain foods, such as dairy products (many of which are fortified with vitamin D), or eat only small amounts of these foods. Individuals who have difficulty absorbing dietary fat might therefore require vitamin D supplementation [63].
Individuals with a body mass index (BMI) of 30 or more have lower serum 25(OH)D levels than individuals without obesity. Obesity does not affect the skin’s capacity to synthesize vitamin D. However, greater amounts of subcutaneous fat sequester more of the vitamin [1]. People with obesity might need greater intakes of vitamin D to achieve 25(OH)D levels similar to those of people with normal weight [1,64,65].
Individuals with obesity who have undergone gastric bypass surgery can also become vitamin D deficient. In this procedure, part of the upper small intestine, where vitamin D is absorbed, is bypassed, and vitamin D that is mobilized into the bloodstream from fat stores might not raise 25(OH)D to adequate levels over time [66,67]. Various expert groups—including the American Association of Metabolic and Bariatric Surgery, The Obesity Society, and the British Obesity and Metabolic Surgery Society—have developed guidelines on vitamin D screening, monitoring, and replacement before and after bariatric surgery [66,68]
Vitamin D — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessedNorman AW, Henry HH. Vitamin D. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition, 10th ed. Washington DC: Wiley-Blackwell, 2012.
Study type could not be determined · Population basis: unknown · Directness: not assessedJones G. Vitamin D. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease, 11th ed. Philadelphia: Lippincott Williams & Wilkins, 2014.
Study type could not be determined · Population basis: unknown · Directness: not assessedSempos CT, Heijboer AC, Bikle DD, Bollerslev J, Bouillon R, Brannon PM, et al. Vitamin D assays and the definition of hypovitaminosis D. Results from the First International Conference on Controversies in Vitamin D. Br J Clin Pharmacol 2018;84:2194-207. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedLeFevre ML. Screening for vitamin deficiency in adults: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2015;162:133-40. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessedBrooks SPJ, Sempos CT. The importance of 25-hydroxyvitamin D assay standardization and the Vitamin D Standardization Program. Journal of AOAC International 2017;100:1223-4.
Study type could not be determined · Population basis: unknown · Directness: not assessedTaylor CL, Sempos CT, Davis CD, Brannon PM. Vitamin D: moving forward to address emerging science. Nutrients 2017, 9, 1308; doi:10.3390/mu9121308. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSempos CT, Binkley N. 25-hydroxyvitamin D assay standardisation and vitamin D guidelines paralysis. Public Health Nutrition 2020;23:1153-64. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedOffice of Dietary Supplements, National Institutes of Health. Vitamin D Standardization Program (VDSP).
Study type could not be determined · Population basis: unknown · Directness: not assessedDemay MB, Pittas AG, Bikle DD, Diab DL, Kiely ME, et al. Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1907-1947. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessedShah VP, Nayfeh T, Alsawaf Y, Saadi S, Farah M, et al. A Systematic Review Supporting the Endocrine Society Clinical Practice Guidelines on Vitamin D. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1961-1974. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessedHolick MF. Vitamin D deficiency. N Engl J Med 2007;357:266-81. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedBrown LL, Cohen B, Tabor D, Zappala G, Maruvada P, Coates PM. The vitamin D paradox in Black Americans: A systems-based approach to investigating clinical practice, research, and public health—expert panel meeting report. BMC Proceedings, 2018;12(Suppl 6):6. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedSerum concentration of 25(OH)D is the main indicator of vitamin D status. However, the serum concentrations of 25(OH)D that are associated with vitamin D deficiency have not been definitively identified. The Food and Nutrition Board at the National Academies of Sciences, Engineering, and Medicine states that levels of 50 nmol/L (20 ng/mL) or more are sufficient for most people, and that the risk of deficiency increases at serum concentrations of less than 30 nmol/L (12 ng/mL).
Serum concentration of 25(OH)D is currently the main indicator of vitamin D status. It reflects vitamin D produced endogenously and that obtained from foods and supplements [1]. In serum, 25(OH)D has a fairly long circulating half-life of 15 days [1]. Serum concentrations of 25(OH)D are reported in both nanomoles per liter (nmol/L) and nanograms per milliliter (ng/mL). One nmol/L is equal to 0.4 ng/mL, and 1 ng/mL is equal to 2.5 nmol/L.
Assessing vitamin D status by measuring serum 25(OH)D concentrations is complicated by the considerable variability of the available assays (the two most common ones involve antibodies or chromatography) used by laboratories that conduct the analyses [5,6]. As a result, a finding can be falsely low or falsely high, depending on the assay used and the laboratory. The international Vitamin D Standardization Program has developed procedures for standardizing the laboratory measurement of 25(OH)D to improve clinical and public health practice [5,7-10].
In contrast to 25(OH)D, circulating 1,25(OH)2D is generally not a good indicator of vitamin D status because it has a short half-life measured in hours, and serum levels are tightly regulated by parathyroid hormone, calcium, and phosphate [1]. Levels of 1,25(OH)2D do not typically decrease until vitamin D deficiency is severe [2].
Although 25(OH)D functions as a biomarker of exposure, the extent to which 25(OH)D levels also serve as a biomarker of effect on the body (i.e., relating to health status or outcomes) is not clear [1,3].
Researchers have not definitively identified serum concentrations of 25(OH)D associated with deficiency (e.g., rickets), adequacy for bone health, and overall health. After reviewing data on vitamin D needs, an expert committee of the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and Medicine (NASEM) concluded that people are at risk of vitamin D deficiency at serum 25(OH)D concentrations less than 30 nmol/L (12 ng/mL; see Table 1 for definitions of deficiency and inadequacy) [1]. Some people are potentially at risk of inadequacy at 30 to 50 nmol/L (12–20 ng/mL). Levels of 50 nmol/L (20 ng/mL) or more are sufficient for most people. The FNB also noted that serum concentrations greater than 125 nmol/L (50 ng/mL) can be associated with adverse effects [1] (Table 1). The Endocrine Society has not identified 25(OH)D concentrations associated with vitamin D sufficiency, insufficiency, and deficiency and does not recommend routine testing of 25(OH)D concentrations in healthy individuals [11,12].
| nmol/L* | ng/mL* | Health status |
|---|---|---|
| <30 | <12 | Associated with vitamin D deficiency, which can lead to rickets in infants and children and osteomalacia in adults |
| 30 to <50 | 12 to <20 | Generally considered inadequate for bone and overall health in healthy individuals |
| ≥50 | ≥20 | Generally considered adequate for bone and overall health in healthy individuals |
| >125 | >50 | Linked to potential adverse effects, particularly at >150 nmol/L (>60 ng/mL) |
| *Serum concentrations of 25(OH)D are reported in both nanomoles per liter (nmol/L) and nanograms per milliliter (ng/mL). One nmol/L = 0.4 ng/mL, and 1 ng/mL = 2.5 nmol/L. |
Optimal serum concentrations of 25(OH)D for bone and general health have not been established because they are likely to vary by stage of life, by race and ethnicity, and with each physiological measure used [1,13,14]. In addition, although 25(OH)D levels rise in response to increased vitamin D intake, the relationship is nonlinear [1]. The amount of increase varies, for example, by baseline serum levels and duration of supplementation.
Vitamin D — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
Evidence topic
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.Evidence topic
Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.
Structural characterization
Reference counts describe frozen source associations; a larger count does not establish stronger evidence.
No explicit limitation phrase was identified in these imported source blocks.
Speers AB, Cabey KA, Soumyanath A, Wright KM. Effects of Withania somnifera (Ashwagandha) on Stress and the Stress- Related Neuropsychiatric Disorders Anxiety, Depression, and Insomnia. Curr Neuropharmacol 2021;19:1468-95. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedLopresti AL, Smith SJ. Ashwagandha (Withania somnifera) for the treatment and enhancement of mental and physical conditions: A systematic review of human trials. Journal of Herbal Medicine 2021;28:100434.
Systematic review · Population basis: human · Directness: not assessedCheah KL, Norhayati MN, Husniati Yaacob L, Abdul Rahman R. Effect of Ashwagandha (Withania somnifera) extract on sleep: A systematic review and meta-analysis. PLoS One 2021;16:e0257843. [PubMed abstract]
Meta-analysis · Population basis: unknown · Directness: not assessedD'Cruz M, Andrade C. Potential clinical applications of Ashwagandha (Withania somnifera) in medicine and neuropsychiatry. Expert Rev Clin Pharmacol 2022;15:1067-80. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessedLopresti AL, Smith SJ, Malvi H, Kodgule R. An investigation into the stress-relieving and pharmacological actions of an ashwagandha (Withania somnifera) extract: A randomized, double-blind, placebo-controlled study. Medicine (Baltimore) 2019;98:e17186. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessedAshwagandha extracts may help reduce anxiety and stress and improve sleep. However, it is challenging to develop recommendations for using ashwagandha, because the studies that have evaluated it have used various preparations and doses. Ashwagandha appears to be well tolerated during short-term use, but the long-term safety of ashwagandha is not known. In addition, ashwagandha may not be safe for certain people.
Several randomized, placebo-controlled clinical trials, most of them fairly small in size and of short duration, have found that ashwagandha may reduce perceived stress and anxiety and improve the quality and duration of sleep [7,8,20,45]. Because studies have used various ashwagandha preparations (with different extraction and standardization processes) and doses, it is difficult to identify specific extracts or recommended amounts [7,46]. In addition, most studies have been conducted as part of a traditional medical system, so the potential effects of ashwagandha when used as a dietary supplement outside of that approach remain unclear.
Ashwagandha appears to be well tolerated for up to 3 months of use. However, the efficacy and safety of long-term ashwagandha use over months or years for stress, anxiety, or sleep is not known. In addition, ashwagandha may have potential adverse effects on the liver and thyroid and might not be safe for men with prostate cancer or women who are pregnant or breastfeeding.
Ashwagandha: Is it helpful for stress, anxiety, or sleep? — Fact Sheet for Health Professionals
NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.
Source attribution does not imply NIH or ODS endorsement of MEDucated.
No source-backed evidence is currently available for this topic in MEDucated.
The attached ODS revision does not provide an imported source section for this topic.