Supplements

DHEA

Updated · 26 sources · Editorial policy

DHEA (dehydroepiandrosterone, drug name prasterone) is a steroid made mainly by the adrenal glands. It has little hormonal action of its own. Instead, tissues convert it into androgens such as testosterone and into estrogens. Blood levels peak in early adulthood and fall steadily with age, which is why oral DHEA is sold as an “anti-aging” and testosterone-boosting supplement.

There are two very different products. Oral DHEA is sold over the counter in the US as a dietary supplement and is not an FDA-approved drug. The only FDA-approved DHEA product is Intrarosa, a 6.5 mg vaginal insert approved in 2016 for painful intercourse caused by menopause. Large trials of oral DHEA in older adults found no meaningful benefit for muscle, strength, body composition or quality of life, and WADA prohibits DHEA at all times as an anabolic steroid.

This page summarizes what the Intrarosa label, clinical trials, guidelines and regulators report. It is for education only and is not medical advice.

Property Detail
Class Endogenous adrenal steroid; precursor of androgens and estrogens
Chemistry 3β-hydroxyandrost-5-en-17-one, C₁₉H₂₈O₂, 288.4 g/mol
Main circulating form DHEA sulfate (DHEAS), made in the adrenal zona reticularis
Approved product Intrarosa (prasterone) 6.5 mg vaginal insert, once daily; FDA 2016, EU 2018
Oral form Dietary supplement in the US; not FDA-approved
Oral doses in cited trials 25–150 mg/day; 50 mg/day in the 1-year DHEAge trial
Half-life Apparent terminal half-life over 20 h after oral dosing in older adults, because DHEAS is converted back to DHEA
US schedule Not a controlled substance; excluded by name from the federal definition of “anabolic steroid”
WADA status Prohibited at all times (S1.1, anabolic androgenic steroids); non-Specified

What it is

DHEA is made from cholesterol through pregnenolone. In the innermost layer of the adrenal cortex, the zona reticularis, the enzyme P450c17 converts pregnenolone to 17α-hydroxypregnenolone and then to DHEA. The enzyme SULT2A1 then adds a sulfate group, and DHEAS is released into the blood (Miller and Auchus, Endocr Rev 2011). The adrenal makes very little testosterone directly. Instead, DHEA is turned into active hormones in other tissues, by enzymes including 3β-hydroxysteroid dehydrogenases, 5α-reductases and aromatase (Intrarosa label).

DHEA levels change markedly with age. A study of 981 men and 481 women aged 11–89 measured serum DHEAS (Orentreich et al., JCEM 1984):

Group Peak age Mean DHEAS at peak Mean DHEAS over age 70
Men 20–24 years 3,470 ng/mL 670 ng/mL
Women 15–19 years 2,470 ng/mL 450 ng/mL

Logarithmic means. Levels were significantly higher in men than in women between ages 20 and 69.

This decline is the basis for marketing DHEA as a replacement hormone for aging. A fall in a hormone level does not by itself show that restoring it brings benefits, and the trials below tested that idea directly.

DHEA is also the parent of 7-keto-DHEA, a metabolite sold as a separate supplement. Unlike DHEA, 7-keto-DHEA is not converted into testosterone or estrogen.

Pharmacokinetics

Oral DHEA

A pharmacokinetic study gave 25 mg or 50 mg DHEA, or placebo, daily for 8 days to 24 healthy men and women with a mean age of 67.8 (Legrain et al., JCEM 2000). Key findings:

  • Blood DHEA had an apparent terminal half-life of more than 20 hours, similar to DHEAS. The authors explained this by the large amount of DHEAS formed after an oral dose, which is slowly converted back to DHEA.
  • Women converted DHEAS back to DHEA to a significantly greater extent than men.
  • No steroid accumulated over 8 days of dosing.

In the 2-year Mayo Clinic trial, DHEA raised median DHEAS by 3.4 µg/mL in older men and 3.8 µg/mL in older women compared with placebo (Nair et al., NEJM 2006). In the 1-year French DHEAge trial, 50 mg/day restored DHEAS to the range of young adults, with a small rise in testosterone and estradiol, mainly in women (Baulieu et al., PNAS 2000).

Vaginal prasterone (Intrarosa)

The vaginal insert is designed to act locally, but some drug and its products reach the blood. In postmenopausal women, the label reports these day-7 values (Intrarosa label):

Measure (day 7, mean) Placebo Intrarosa 6.5 mg/day
Prasterone peak 1.60 ng/mL 4.42 ng/mL
Prasterone AUC 0–24 h 24.82 ng·h/mL 56.17 ng·h/mL
Testosterone peak 0.12 ng/mL 0.15 ng/mL
Estradiol peak 3.33 pg/mL 5.04 pg/mL

Over 12 weeks in the two main trials, trough levels of prasterone, testosterone and estradiol rose by 47%, 21% and 19% from baseline. The label notes that trough values may underestimate the total increase in exposure.

Approved medical use: vaginal prasterone (Intrarosa)

FDA approved Intrarosa (NDA 208470, submitted by EndoCeutics) on November 16, 2016 (FDA approval letter). It is approved only for moderate to severe dyspareunia (pain during intercourse), a symptom of vulvar and vaginal atrophy, due to menopause. The labeled dose is one 6.5 mg vaginal insert once daily at bedtime (Intrarosa label).

The European Commission authorized Intrarosa on January 8, 2018, for vulvar and vaginal atrophy in postmenopausal women with moderate to severe symptoms (EMA EPAR).

This approval does not extend to oral DHEA. Intrarosa is a low, locally acting vaginal dose with its own trial program, and its results say nothing about oral supplements taken for other reasons.

Pivotal trials

Two 12-week randomized, double-blind, placebo-controlled trials supported approval. Each had four co-primary endpoints: dyspareunia severity, the percentage of superficial and parabasal vaginal cells (markers of a mature vs thinned vaginal lining), and vaginal pH (Intrarosa label; Labrie et al., Menopause 2016):

Outcome at week 12 (difference vs placebo) Trial 1 (n = 81 vs 77) Trial 2 (n = 325 vs 157)
Dyspareunia severity score −0.40 (p = 0.0132) −0.35 (p = 0.0002)
Superficial cells +4.71 percentage points +8.46 percentage points
Parabasal cells −45.77 percentage points −29.53 percentage points
Vaginal pH −0.83 −0.67

Intent-to-treat populations. The cell and pH results had p under 0.0001 in both trials. Trial 1 randomized 255 women, including an active-comparator arm; Trial 2 randomized 558 women 2:1.

The dyspareunia score fell substantially on placebo too: in Trial 2, by 1.06 points on placebo vs 1.42 on prasterone. In Trial 2, moderate to severe vaginal dryness also improved by 0.27 points more than placebo (p = 0.004) (Labrie et al., 2016).

A 2026 meta-analysis of 5 unique randomized trials (1,611 women) confirmed improvements over placebo in dyspareunia (mean difference −0.40, 95% CI −0.66 to −0.15) and vaginal dryness (−0.23, 95% CI −0.35 to −0.11) (Lemos et al., Menopause 2026).

Regulatory status of oral DHEA

  • Dietary supplement, not a drug. No oral DHEA product is FDA-approved. Endocrine Society guideline authors have noted that DHEA is readily available over the counter and through internet orders, which reduces commercial interest in long-term trials (Bornstein et al., JCEM 2016).
  • Not a controlled substance. The Anabolic Steroid Control Act of 2004 defines “anabolic steroid” as a substance chemically and pharmacologically related to testosterone, other than estrogens, progestins, corticosteroids and dehydroepiandrosterone (Public Law 108-358). DHEA is not listed in Schedule III (21 CFR 1308.13).
  • Sport. WADA lists prasterone (DHEA) by name under S1.1, anabolic androgenic steroids, when administered exogenously. It is prohibited in and out of competition and is a non-Specified substance. The listing does not exempt any route of administration, so prasterone medicines such as Intrarosa are also covered (WADA 2026 Prohibited List).

What the research shows

All of the following trials used oral DHEA unless stated otherwise.

Muscle, strength and body composition in older adults

Two long, well-designed trials tested whether restoring youthful DHEA levels improves the body in older people:

Trial Participants Dose and duration Main findings
Nair et al., NEJM 2006 87 men with low DHEAS and bioavailable testosterone; 57 women with low DHEAS 2 years; DHEA vs placebo (men also had a testosterone arm) No significant effect on body composition, VO₂ peak, muscle strength, insulin sensitivity or quality of life. BMD rose at the ultradistal radius in women and the femoral neck in men
Percheron et al., Arch Intern Med 2003 (DHEAge) 280 healthy men and women aged 60–80 50 mg/day for 1 year DHEAS restored to young-adult levels; no effect on handgrip, knee strength or thigh muscle and fat area

The Nair authors concluded that DHEA had no physiologically relevant benefit on body composition, physical performance, insulin sensitivity or quality of life.

A 2020 meta-analysis of randomized trials found no change in body weight (−0.16 kg, 95% CI −1.02 to 0.70) or BMI. It did find a small rise in lean body mass of 0.45 kg (95% CI 0.15–0.75) and a change in fat mass of −0.85% (95% CI −1.18 to −0.51). The authors noted that the clinical relevance of these changes is debated (Wang et al., Steroids 2020).

Testosterone and training in young men

DHEA is often marketed to men as a testosterone booster. The evidence:

  • Small average rise. A 2020 meta-analysis of 42 publications found that DHEA raised testosterone by 28.0 ng/dL on average (95% CI 21.4–34.6). The rise was larger in women than men (31.0 vs 21.4 ng/dL) and with doses over 50 mg/day than lower doses (58.0 vs 19.4 ng/dL) (Li et al., Exp Gerontol 2020).
  • No training benefit. In young men, a single 50 mg dose raised androstenedione by 150% within an hour but did not change testosterone or estrogens. In a second 8-week resistance-training study, 9 men took 150 mg/day and 10 took placebo. Free and total testosterone, estrogens, lipids and liver enzymes did not change, and strength and lean mass rose similarly in both groups (Brown et al., J Appl Physiol 1999).

Sexual function and menopause symptoms

A 2014 Mayo Clinic meta-analysis pooled 23 randomized trials of systemic DHEA in 1,188 postmenopausal women with normal adrenal function. DHEA did not significantly improve libido or sexual function (standardized mean difference 0.35, 95% CI −0.02 to 0.73). It also had no significant effect on lipids, glucose, weight, BMI or bone density. The confidence in these results was rated low (Elraiyah et al., JCEM 2014).

The Endocrine Society’s guideline on androgens in women, written with ACOG, ASRM, the European Society of Endocrinology and the International Menopause Society, recommends against the routine use of DHEA. It cites limited data on effectiveness and safety in normal women and in women with adrenal insufficiency (Wierman et al., JCEM 2014).

In the 1-year DHEAge trial, women over 70 showed improved libido scores and bone turnover, and women showed changes in skin hydration, thickness and sebum production (Baulieu et al., 2000). These were secondary findings from one trial.

Adrenal insufficiency in women

Women whose adrenal glands do not work lose most of their DHEA and androgen production. This is the setting with the best case for DHEA:

  • Early trial. In a crossover trial in 24 women with adrenal insufficiency, 50 mg each morning for 4 months improved overall well-being, depression and anxiety scores, and several measures of sexual interest and satisfaction compared with placebo (Arlt et al., NEJM 1999).
  • Meta-analysis. Pooling 10 trials, DHEA produced a small improvement in health-related quality of life (effect size 0.21, 95% CI 0.08–0.33) and a small benefit on depression. Effects on anxiety and sexual well-being were not significant. The authors judged the effect “small and perhaps trivial” (Alkatib et al., JCEM 2009).
  • Guideline. The 2016 Endocrine Society guideline on primary adrenal insufficiency suggests a trial of DHEA in women with low libido, depressive symptoms or low energy despite optimized glucocorticoid and mineralocorticoid replacement. It describes a dose of 25–50 mg once each morning in premenopausal women, stopping after 6 months if there is no sustained benefit, and monitoring with morning DHEAS aimed at the mid-normal range. This is a weak recommendation based on low-quality evidence (Bornstein et al., JCEM 2016).

Depression

A 2020 meta-analysis of 12 randomized trials (742 participants) found that DHEA improved depressive symptoms compared with placebo (standardized mean difference −0.28, 95% CI −0.45 to −0.11). The quality of evidence was rated very low (Peixoto et al., J Neurosci Res 2020).

Memory and cognition

A Cochrane review found only three usable trials in people over 50 without dementia. It concluded that the evidence does not support a benefit of DHEA on cognitive function (Grimley Evans et al., Cochrane 2006).

IVF in poor responders

DHEA has been used before IVF in women whose ovaries respond poorly to stimulation. A 2024 Cochrane review of 28 randomized trials found that DHEA pre-treatment likely makes little or no difference to live birth or ongoing pregnancy (OR 1.30, 95% CI 0.95–1.76; 9 trials, 1,433 women) or clinical pregnancy (OR 1.18, 95% CI 0.93–1.49; 13 trials, 1,886 women). Evidence certainty was moderate (Naik et al., Cochrane 2024).

Side effects and risks

Androgenic and skin effects

In postmenopausal-women trials, the most frequently reported adverse effects were dermatological or androgenic symptoms. Data were sparse and too inconsistent to pool (Elraiyah et al., 2014). The depression meta-analysis likewise found side effects to be uncommon, mild and transient, and mostly androgen-related (Peixoto et al., 2020). DHEA raises testosterone more in women than in men (Li et al., 2020), so women are more likely to notice androgenic effects.

Lipids

A 2020 meta-analysis of 23 trials found no change in total cholesterol, LDL or triglycerides. HDL cholesterol fell by 3.1 mg/dL (95% CI 1.3–4.9). The fall was seen in women (−5.1 mg/dL) but not men (+0.13 mg/dL) (Qin et al., Nutr Metab Cardiovasc Dis 2020). In the adrenal insufficiency trial, total and HDL cholesterol both decreased significantly (Arlt et al., 1999).

Hormone-sensitive conditions

DHEA is converted to estrogens and androgens. The Intrarosa label warns that estrogen is a prasterone metabolite and that estrogen use is contraindicated in women with known or suspected breast cancer. Intrarosa has not been studied in women with a history of breast cancer (Intrarosa label). The label also notes that two DHEA metabolites, testosterone and estradiol, are carcinogenic in animals, and that no long-term animal carcinogenicity studies of prasterone have been done.

Intrarosa: label safety data

From the Intrarosa label (Intrarosa label):

Finding Intrarosa Placebo
Vaginal discharge, four 12-week trials 5.71% (38 of 665) 3.66% (17 of 464)
Vaginal discharge, 52-week open-label trial 14.2% (74 of 521) No placebo group
Abnormal Pap smear at 52 weeks 2.1% (11 of 521) No placebo group

The 11 abnormal Pap smears were 10 cases of atypical cells of undetermined significance and 1 low-grade lesion. The trial investigators attributed the discharge to the insert’s fat base melting at body temperature (Labrie et al., 2016).

The only contraindication is undiagnosed abnormal genital bleeding, which must be evaluated first. Intrarosa is indicated only for postmenopausal women and has not been studied in pregnancy, breastfeeding, children, or kidney or liver impairment.

Long-term safety is unknown

The longest placebo-controlled trials of oral DHEA lasted 1–2 years and did not find major adverse effects (Nair et al., 2006; Baulieu et al., 2000). The Endocrine Society notes that there are no long-term studies of risk (Wierman et al., 2014) and that long-term outcome data in women with adrenal insufficiency are lacking (Bornstein et al., 2016).

Drug testing in sport

Because prasterone is listed by name, athletes subject to WADA rules face an anti-doping violation whether it comes from a supplement or a prescription vaginal insert (WADA 2026 Prohibited List).

Key takeaways

  • A hormone precursor, not a hormone. DHEA is made in the adrenal glands from pregnenolone and converted in tissues into testosterone and estrogens. Levels peak in the late teens to early 20s and fall to a fraction of that after 70.
  • Two separate products. Oral DHEA is an unapproved dietary supplement. The only FDA-approved form is Intrarosa, a 6.5 mg daily vaginal insert approved in 2016 for menopausal dyspareunia.
  • Intrarosa works modestly for its indication. In two 12-week trials it reduced dyspareunia scores by 0.35–0.40 points more than placebo and clearly improved vaginal cell and pH markers. Vaginal discharge was the main side effect.
  • Oral DHEA does not build muscle. Trials of 1–2 years in older adults found no meaningful gains in strength, muscle or quality of life, and 150 mg/day did not improve training results in young men.
  • Benefits elsewhere are small or unproven. Small effects were seen in women with adrenal insufficiency and in depression, while sexual function after menopause, cognition and IVF outcomes showed no clear benefit. HDL cholesterol fell in women.
  • Banned in sport. WADA lists prasterone under S1.1, prohibited at all times, regardless of route.

Sources

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  25. 21 CFR 1308.13, Schedule III. eCFR.
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