Menopause
Everything in the library studied for it, medical and holistic together. Within each kind, what was shown to help comes first, strongest evidence first. What was tested and not shown to help stays on the list.
Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on
Medication
Hot flashes
Shown to reduce hot flashes in menopausal women by about one a day against placebo, an effect smaller than estrogen.
Compared with placebo [10]
The numbers and sources
- Effect
- Across four trials, clonidine reduced daily hot flashes by 0.95 more than placebo (95% CI -1.44 to -0.47) [10].
- Population
- Menopausal women in 10 clonidine trials, 4 of them pooled for frequency [10].
- Sources
- [10]
- Caveats
- Most trials had methodological deficiencies, and the authors state effects are smaller than for estrogen [10].
Hot flashes
Shown to reduce the frequency and duration of menopausal hot flashes more than placebo on gabapentin, across seven trials.
The numbers and sources
- Effect
- Women on gabapentin reported a greater reduction than placebo in hot flash frequency (SMD 2.99, 95% CI 2.01 to 3.98), duration (SMD 0.89, 95% CI 0.49 to 1.30) and composite score (SMD 2.31, 95% CI 1.50 to 3.11). Dizziness and unsteadiness were more frequent on gabapentin [17].
- Population
- Postmenopausal women in 7 placebo-controlled trials [17].
- Sources
- [17]
- Caveats
- Not an approved use. The evidence is for gabapentin, from one meta-analysis that does not report the change in number of hot flashes a day in its abstract.
Menopausal hot flashes
Shown to reduce moderate and severe hot flashes in postmenopausal women on desvenlafaxine 100 mg, an unapproved use. Venlafaxine lowered hot flash scores in women with breast cancer.
The numbers and sources
- Effect
- In six placebo-controlled trials, desvenlafaxine 100 mg lowered the frequency of moderate and severe hot flashes at week 12 (SMD -0.49, 95% CI -0.91 to -0.07), as did 150 mg (SMD -0.36, 95% CI -0.54 to -0.19) [19]. In women treated for breast cancer, venlafaxine at 75 mg a day or more lowered hot flash scores against non-hormonal comparators (SMD 2.06, 95% CI 0.40 to 3.72) [20].
- Population
- Postmenopausal women with moderate to severe hot flashes in 6 RCTs [19]; women treated for breast cancer in randomized trials of venlafaxine [20].
- Sources
- [19], [20]
- Caveats
- No SNRI label cited here lists hot flashes. The venlafaxine analysis had very high heterogeneity (I² 98.7%) and signs of publication bias, and its comparators were other non-hormonal treatments [20].
Menopausal hot flashes
Shown to reduce hot flash frequency and severity modestly in menopausal women. Paroxetine 7.5 mg is the one SSRI product approved for this use.
The numbers and sources
- Effect
- Against placebo, SSRIs lowered hot flash frequency (difference in means -0.93, 95% CI -1.46 to -0.37) and severity (standardized difference -0.34, 95% CI -0.59 to -0.10) [19]. The label for paroxetine 7.5 mg reports two placebo-controlled trials in which the frequency of moderate to severe hot flashes fell more than on placebo at weeks 4 and 12 [20].
- Population
- 2,069 menopausal and postmenopausal women in 11 RCTs followed 1 to 9 months [19]; 1,174 postmenopausal women with at least 7 to 8 moderate to severe hot flashes a day in two trials of 12 and 24 weeks [20].
- Sources
- [19], [20]
- Caveats
- The pooled analysis ranked escitalopram ahead of other SSRIs by indirect comparison [19]. In one of the two label trials, severity did not differ from placebo at week 12 [20].
Hormone therapy
Sexual function in postmenopausal women
Shown to raise satisfying sexual events, desire, arousal and orgasm, and lower sexual distress, in postmenopausal women. Long-term data are limited.
The numbers and sources
- Effect
- Compared with placebo or a comparator, testosterone raised satisfying sexual event frequency by a mean of 0.85 (95% CI 0.52 to 1.18), desire by an SMD of 0.36 (95% CI 0.22 to 0.50), arousal by 0.28 (95% CI 0.21 to 0.35) and orgasm by 0.25 (95% CI 0.18 to 0.32), and lowered sexual distress by an SMD of -0.27 (95% CI -0.36 to -0.17) [6]. A 2026 systematic review reported improved desire with transdermal testosterone in postmenopausal trials, including one of more than 800 women. In two premenopausal trials of 31 to 261 women, libido, satisfying sexual events and satisfaction improved [7].
- Population
- 36 blinded RCTs with 8,480 participants, at least 12 weeks long, analyzed in postmenopausal women [6]; 33 studies, including 7 RCTs in postmenopausal and 2 in premenopausal women [7].
- Sources
- [6], [7]
- Caveats
- No effects were found on body composition, musculoskeletal measures or cognition, but few women contributed data to those outcomes [6]. The 2026 review was not pooled, and androgen levels and long-term safety were inconsistently reported [7]. Long-term data are limited.
Sexual function in menopause
Shown to improve sexual function slightly in menopausal women overall, though oral DHEA alone did not differ from placebo.
The numbers and sources
- Effect
- Compared with placebo, DHEA improved sexual function by an SMD of 0.31 (95% CI 0.07 to 0.55). Oral DHEA alone showed an SMD of 0.11 (95% CI -0.13 to 0.35), and one intravaginal trial 0.42 (95% CI 0.03 to 0.81) [5].
- Population
- Peri- and postmenopausal women, 5 trials with 261 women in the main analysis [5].
- Sources
- [5]
- Caveats
- The oral-only result did not differ from placebo. The overall evidence was rated moderate to low quality [5].
Painful sex and vaginal dryness after menopause
Shown to lower pain during sex and vaginal dryness in postmenopausal women using intravaginal DHEA. This applies to the vaginal form, not oral DHEA.
The numbers and sources
- Effect
- Pooled against placebo, intravaginal DHEA lowered dyspareunia scores by a mean difference of -0.40 (95% CI -0.66 to -0.15) and vaginal dryness by -0.23 (95% CI -0.35 to -0.11) [6]. In the largest single trial, daily intravaginal DHEA for 12 weeks reduced pain at sexual activity by 0.36 severity units over placebo and vaginal dryness by 0.27 units over placebo. Parabasal cells fell 27.7% and vaginal pH 0.66 units over placebo. Serum steroids stayed within normal postmenopausal values [7]. In an open-label trial against vaginal estradiol, 92% on DHEA and 82% on estradiol improved by at least 1 point in dyspareunia at 12 weeks (OR 2.87, 95% CI 1.00 to 8.25, p = 0.051). Vaginal pH, maturity index and clinical signs of atrophy improved more on estradiol [8].
- Population
- 1,611 postmenopausal women with vulvovaginal atrophy in 5 unique RCTs [6]; 482 postmenopausal women (325 on DHEA, 157 on placebo) in one phase 3 RCT [7]; 172 postmenopausal women, mean age 62.4, in the estradiol comparison [8].
- Sources
- [6], [7], [8]
- Caveats
- The phase 3 trial was run by the drug's developer, EndoCeutics. The estradiol comparison was open label. This is a local vaginal treatment and does not describe oral DHEA.
Testosterone and estradiol levels in postmenopausal women
Shown to raise testosterone by about 24 ng/dL and estradiol by about 8 pg/mL in postmenopausal women.
The numbers and sources
- Effect
- DHEA raised serum testosterone by 24.31 ng/dL (95% CI 15.22 to 33.40) and estradiol by 7.86 pg/mL (95% CI 6.33 to 9.40). Trials using 50 mg a day or more showed larger rises in testosterone (29.65 ng/dL) [10].
- Population
- Postmenopausal women in 21 RCTs [10].
- Sources
- [10]
- Caveats
- These are blood levels, not symptoms or outcomes. Subgroup confidence intervals overlapped [10].
Hot flashes and night sweats
Shown to cut hot flash frequency about 75% relative to placebo in menopausal women, though placebo alone cut them about 58%.
The numbers and sources
- Effect
- Oral hormone therapy reduced weekly hot flash frequency by a weighted mean difference of -17.92 against placebo (95% CI -22.86 to -12.99), a 75% reduction relative to placebo (95% CI 64.3 to 82.3). Severity fell with an OR of 0.13 (95% CI 0.07 to 0.23). Women on placebo also had a 57.7% reduction from baseline [1].
- Population
- 24 double-blind RCTs with 3,329 women, lasting 3 months to 3 years [1].
- Sources
- [1]
- Caveats
- The large placebo response means unblinded comparisons overstate the effect. The search ran to 2002, and the trials used fixed oral doses [1].
Menopause symptom scores and quality of life
Shown to lower menopause symptom scores and improve menopause quality of life against controls, with larger effects from estradiol-containing therapy.
The numbers and sources
- Effect
- Against controls, hormone therapy lowered the Kupperman menopause index more, by an SMD of -1.21 (95% CI -1.43 to -0.98) in estradiol-containing subgroups and -0.39 (95% CI -0.67 to -0.10) in others. The menopause-specific quality of life score improved by an SMD of -0.43 (95% CI -0.60 to -0.27). Vaginal pH fell (SMD -0.97, 95% CI -1.08 to -0.87) [2].
- Population
- 5,089 women in 24 RCTs, 3,062 on hormone therapy [2].
- Sources
- [2]
- Caveats
- Controls were not all placebo, and one subgroup used acupuncture as the comparison. Treatment-emergent adverse events did not differ (OR 0.93, 95% CI 0.78 to 1.13) [2].
Depressive symptoms in perimenopause
Shown to lower depressive symptoms slightly in perimenopausal women with depressive symptoms, with no benefit in women not selected for them.
The numbers and sources
- Effect
- In placebo-controlled trials, hormone therapy was associated with a small reduction in depressive symptom severity (SMD -0.23, 95% CI -0.43 to -0.03). No clear difference was seen by route [11].
- Population
- Perimenopausal women with depressive symptoms in 12 RCTs [11].
- Sources
- [11]
- Caveats
- The authors rate certainty as limited [11]. A systematic review of 17 RCTs in younger menopausal women, not selected for depressive symptoms, found no benefit on depression [12].
Quality of life and menopause symptoms
Not shown to improve quality of life in menopausal women or in older adults over 2 years.
The numbers and sources
- Effect
- In menopausal women, DHEA did not improve quality of life (SMD 0.16, 95% CI -0.03 to 0.34, 8 studies, 287 women). Effects on menopausal symptoms were unclear because trials measured them in ways that could not be pooled [5]. In older men and women over 2 years, quality of life did not change [3].
- Population
- Peri- and postmenopausal women in 28 trials (1,273 women) [5]; 144 elderly adults [3].
- Sources
- [3], [5]
- Caveats
- Quality of life evidence was rated moderate quality [5].
Supplements
Bone density after menopause
Shown to keep bone density steady over 2 years in postmenopausal women with low bone density, on a blend with soy isoflavones, while it fell on placebo.
The numbers and sources
- Effect
- In 100 late postmenopausal women with low bone density, a daily blend of 60 mg icariin, 15 mg daidzein and 3 mg genistein held bone density steady over 24 months. With placebo, lumbar spine density fell 2.4% and femoral neck density 1.8%. The groups differed at the lumbar spine at 12 and 24 months and at the femoral neck at 24 months. Both groups took 300 mg of calcium a day, and endometrial thickness showed no detectable hyperplasia [1]. A meta-analysis of 12 RCTs with 1,017 patients found higher bone density when Epimedium was added to conventional osteoporosis drugs (p = 0.03) or used in place of them (p = 0.009) [2]. In 58 postmenopausal women, 740 mg a day of Epimedium prenylflavonoids for 6 weeks raised the bone formation marker BSAP [3]. A 2025 meta-analysis of 10 RCTs (890 patients with primary osteoporosis) found higher lumbar spine bone density with Epimedium as an add-on or alternative to conventional drugs (SMD 1.15, 95% CI 0.61 to 1.70) [4].
- Population
- 100 postmenopausal women [1]; patients with osteoporosis in 12 RCTs [2] and 10 RCTs [4]; healthy postmenopausal women [3].
- Sources
- [1], [2], [3], [4]
- Caveats
- The blend in [1] also contained soy isoflavones. The trials in [2] and [4] compared Epimedium with conventional drugs, not placebo, and the abstract of [2] gives p-values without effect sizes. Review [4] searched Chinese databases.
Menopausal symptoms
Limited evidence: four small trials reported lower menopausal symptom scores in perimenopausal and postmenopausal women.
The numbers and sources
- Effect
- All 4 RCTs in a systematic review reported favorable effects on Kupperman and Greene climacteric scores in perimenopausal and postmenopausal women [5].
- Population
- Healthy perimenopausal, early and late postmenopausal women [5].
- Sources
- [5]
- Caveats
- Few rigorous trials, and the authors state safety had not been established [5].
Memory in postmenopausal women
One trial without placebo found memory scores rose from baseline over 6 months in postmenopausal women with mild cognitive impairment in India.
The numbers and sources
- Effect
- Over 6 months, scores on the Montreal Cognitive Assessment rose from baseline on 25 mg of pyridoxine a day (p = 0.0323), and homocysteine fell. The abstract reports change from baseline, not a comparison with the untreated group [7].
- Population
- 180 postmenopausal women with mild cognitive impairment in India, randomized to pyridoxine, 100 mg of vitamin C, or no treatment [7].
- Sources
- [7]
- Caveats
- One trial with no placebo. Menopause quality of life scores did not change overall [7].
Therapies
Hot flashes in menopause
Mixed results: hot flash frequency did not differ from sham acupuncture, fell compared with no treatment, and was higher than with hormone therapy.
Compared with sham acupuncture [15]; waiting list or no intervention [15]; hormone therapy [15]; relaxation [15]
The numbers and sources
- Effect
- Against sham, hot flash frequency did not differ (-1.13 flushes a day, 95% CI -2.55 to 0.29, 8 trials, 414 women) and severity was slightly lower (SMD -0.45, 95% CI -0.84 to -0.05), a difference that disappeared once trials in women with breast cancer were removed. Against no treatment, frequency fell (SMD -0.50, 95% CI -0.69 to -0.31, 3 trials, 463 women). Women on hormone therapy had 3.18 fewer flushes a day than women given acupuncture [15].
- Population
- 16 trials with 1,155 perimenopausal or postmenopausal women [15].
- Sources
- [15]
- Caveats
- Evidence was low or very low in quality, and adverse effect data were lacking [15].
Anxiety and mood, compared with plain foot massage
Limited evidence: two trials in women found anxiety and depression fell as much with plain foot massage or lay foot manipulation as with reflexology.
Compared with nonspecific foot massage [7]; lay foot manipulation, and conventional care [6]
The numbers and sources
- Effect
- In 76 women with menopausal symptoms, anxiety scores fell from 0.43 to 0.22 with reflexology and from 0.37 to 0.27 with foot massage, and depression scores fell from 0.37 to 0.20 and from 0.36 to 0.20, with no difference between groups. Hot flushes and night sweats changed similarly [7]. In 385 women with advanced breast cancer, state anxiety and depressive symptoms did not differ between groups [6].
- Population
- 76 women aged 45 to 60 [7]. 385 women with advanced breast cancer [6].
- Sources
- [7], [6]
- Caveats
- In the menopause trial, 14 of 37 women given foot massage believed they had not received true reflexology [7].
Food and drink
Hot flashes in menopause
Mixed results: two reviews found soy isoflavones, mostly as extracts, cut hot flashes by about 20% or one a day, while a Cochrane review found no conclusive evidence in women.
Compared with placebo [6][8]; placebo or control groups in randomized trials [7]
The numbers and sources
- Effect
- Extracted or synthesized soy isoflavones (median 54 mg a day) for 6 weeks to 12 months reduced hot flash frequency by 20.6% (95% CI -28.38 to -12.86) and severity by 26.2% against placebo, with high heterogeneity [6]. Dietary and supplemental soy isoflavones were linked to fewer daily hot flashes (mean difference -0.79, 95% CI -1.35 to -0.23) and less vaginal dryness [7]. A Cochrane review of 43 trials found no conclusive evidence that phytoestrogens reduce hot flashes or night sweats, noted a placebo response of 1% to 59%, and found extracts high in genistein (over 30 mg a day) consistently reduced hot flashes in four trials [8].
- Population
- Perimenopausal and postmenopausal women in 17 trials [6], 62 studies of 6,653 women [7] and 43 trials of 4,364 women [8].
- Sources
- [6], [7], [8]
- Caveats
- Most trials tested extracts or supplements, not soy foods, and dietary soy trials could not be pooled [8]. In one review 74% of trials had a high risk of bias in three or more areas [7].
Lab markers
Age at menopause
Linked to earlier menopause at lower AMH for a woman's age, though AMH alone did not predict the age at menopause with precision.
The numbers and sources
- Effect
- A systematic review found that studies generally showed lower age-specific AMH associated with an earlier age at menopause. AMH alone could not predict the age at menopause with precision: in women under 40, estimates and confidence intervals ranged from 2 to 12 years. Its predictive value rose with age, as the time to menopause shortened [16]. In one cohort enrolled from 1992 to 2001 and followed to 2013, AMH was the only ovarian reserve test that independently predicted time to menopause (hazard ratio 0.70, 95% CI 0.56 to 0.86), and it narrowed the spread around the predicted age from 20 to 10.1 years without predicting the earliest or latest ages [17].
- Population
- 41 studies with 28,858 women, 27 of them on the onset of menopause [16]. 155 women with regular cycles aged 21 to 46 at entry, 81 of whom became postmenopausal [17].
- Sources
- [16], [17], [3], [18], [19]
- Caveats
- Observational. The American College of Obstetricians and Gynecologists states that more data are needed on AMH as a predictor of time to menopause [3]. The 2024 guideline on premature ovarian insufficiency states that AMH is not the primary diagnostic test for that condition and does not support routine AMH testing to predict it [18]. The 2012 workshop on staging reproductive aging set no AMH figure, citing the lack of standardized assays [19].
Breast cancer after menopause
Linked to more breast cancer in postmenopausal women at higher levels, with twice the risk in the top fifth of estradiol against the bottom fifth.
The numbers and sources
- Effect
- In pooled individual data from nine prospective studies, the relative risks of breast cancer for the second to fifth fifths of estradiol, against the lowest fifth, were 1.42 (95% CI 1.04 to 1.95), 1.21 (0.89 to 1.66), 1.80 (1.33 to 2.43) and 2.00 (1.47 to 2.71). For free estradiol the top fifth had a relative risk of 2.58 (1.76 to 3.78). The increases remained after women diagnosed within 2 years of blood collection were excluded [7].
- Population
- 663 postmenopausal women who developed breast cancer and 1,765 who did not, none taking sex hormones when blood was drawn [7].
- Sources
- [7], [4]
- Caveats
- Observational. The Endocrine Society notes that median estradiol in the control women of such studies ran from 5.9 to 27.5 pg/mL from one study to the next, a spread it attributes largely to assay differences, so the fifths are not fixed levels [4]. In a trial of estrogen given alone, breast cancer did not rise (see the trial block below).
Fractures in older women and men
Linked to more fractures at low levels: 2.5 times the hip fracture risk in older women with undetectable estradiol, and more fractures in older men below 16 pg/mL.
The numbers and sources
- Effect
- Among women aged 65 or older, those with undetectable estradiol (below 5 pg/mL) had a relative risk of 2.5 for hip fracture (95% CI 1.4 to 4.6) and 2.5 for vertebral fracture (1.4 to 4.2) against women with detectable levels [8]. In older Swedish men measured by mass spectrometry, each standard deviation lower estradiol had a hazard ratio for fracture of 1.34 (1.22 to 1.49). The relation was nonlinear and strong below 16 pg/mL [9].
- Population
- 133 women with later hip fracture and 138 with later vertebral fracture, compared with randomly selected women from the same cohort, estrogen users excluded [8]. 2,639 men with a mean age of 75, followed for 3.3 years on average [9].
- Sources
- [8], [9]
- Caveats
- Observational. The women's results were adjusted for age and weight only [8]. Many routine assays cannot quantify levels this low [4].
Bone loss across the menopausal transition
One cohort found FSH levels and their change over 4 years predicted spine and hip bone loss through the menopausal transition, while estradiol changes did not.
The numbers and sources
- Effect
- Over 4 years, lumbar spine bone density fell 5.6% in women who reached natural postmenopause and 3.2% in late perimenopause. Baseline FSH, later FSH and their interaction predicted the loss. With a baseline FSH below 25 mIU/mL, a follow-up FSH above 70 predicted a 4-year spine loss of 0.05 g/cm2. Estradiol below 35 pg/mL went with lower bone density, but yearly estradiol changes did not predict loss [12].
- Population
- 2,311 premenopausal or early perimenopausal women at five sites of the Study of Women's Health Across the Nation, examined yearly for five visits [12].
- Sources
- [12]
- Caveats
- Observational, from one cohort. FSH rises as ovarian function declines, so it may mark the stage of the transition and not act on bone itself.
Fractures, stroke and breast cancer in trials of estrogen therapy after menopause
Mixed results: in one large trial estrogen alone cut fractures by 27% and raised strokes by 33% in postmenopausal women, with little or no difference in breast cancer.
The numbers and sources
- Effect
- A Cochrane review drew its main results from the Women's Health Initiative. Among 10,739 women who had had a hysterectomy, oral conjugated equine estrogen for an average of 7 years, against placebo, gave relative risks of 0.73 for all clinical fractures (95% CI 0.65 to 0.80), 1.33 for stroke (1.06 to 1.67), 1.78 for gallbladder disease requiring surgery (1.42 to 2.24), 0.94 for coronary events (0.78 to 1.13), 1.32 for venous clots (1.00 to 1.74) and 0.79 for breast cancer (0.61 to 1.01). Among 16,608 women with a uterus, estrogen with a progestin for 5.6 years gave 0.78 for fractures (0.71 to 0.86), 1.39 for stroke (1.09 to 2.09), 2.03 for venous clots (1.55 to 6.64) and 1.27 for breast cancer (1.03 to 1.56) [10].
- Population
- 24 randomized trials with 45,660 women, most of them postmenopausal American women with a mean age over 60 [10].
- Sources
- [10], [7]
- Caveats
- A marker that tracks an outcome is not always one whose correction changes it. Higher estradiol went with more breast cancer in cohorts [7], and estrogen given alone did not raise it in this trial. The trials set a dose and did not target a blood level. The review's authors caution that the results rest on one study of oral therapy, and that only about 30% of the women were aged 50 to 59 [10].
Breast cancer
Shown in a genetic study to go with 6% less breast cancer overall per 25 nmol/L higher SHBG, and with more estrogen receptor negative disease.
The numbers and sources
- Effect
- In a Mendelian randomization analysis, each 25 nmol/L of genetically higher SHBG had an odds ratio of 0.94 for breast cancer overall (95% CI 0.90 to 0.98), 0.92 for estrogen receptor positive disease (0.87 to 0.97) and 1.09 for estrogen receptor negative disease (1.00 to 1.18) [11]. In pooled prospective studies of postmenopausal women, higher SHBG was associated with a decrease in breast cancer risk (P for trend 0.041) [12].
- Population
- 122,977 breast cancer cases and 105,974 controls in genome-wide data [11]. 663 postmenopausal women who developed breast cancer and 1,765 who did not [12].
- Sources
- [11], [12]
- Caveats
- The genetic study's authors describe the finding for estrogen receptor negative disease as new and in need of further investigation [11]. Genetic estimates describe lifelong differences.
Sexual function in women
Mixed results: women's testosterone levels did not track sexual function in one survey, while testosterone treatment improved sexual function in trials of postmenopausal women.
The numbers and sources
- Effect
- In a community survey of 1,021 Australian women aged 18 to 75, no clinically significant relationship was found between a low score in any domain of sexual function and a low total or free testosterone, and the authors concluded that no single androgen level predicts low sexual function [25]. In a meta-analysis of 36 randomized trials, testosterone treatment in postmenopausal women increased satisfactory sexual events (mean difference 0.85, 95% CI 0.52 to 1.18) and sexual desire (standardized mean difference 0.36, 0.22 to 0.50). Acne and hair growth were more likely, and oral testosterone raised LDL cholesterol [26].
- Population
- 1,021 women drawn at random from the electoral roll in Victoria, Australia [25]. 8,480 participants in 36 trials of at least 12 weeks [26].
- Sources
- [25], [26]
- Caveats
- The survey is cross-sectional. The trials tested treatment in women with low sexual desire, not a blood level, and the authors call for study of long-term effects [26].
Body composition, physical performance and quality of life in trials that raised DHEA-S
Not shown to change body composition, physical performance, sexual function or quality of life in a meaningful way when DHEA-S was raised with DHEA in older adults.
The numbers and sources
- Effect
- In a 2-year trial in older adults with low DHEA-S, DHEA raised the level by a median of 3.4 µg/mL in men and 3.8 µg/mL in women, which is 340 and 380 µg/dL. It had no significant effect on body composition, and did not change peak oxygen consumption, muscle strength, insulin sensitivity or quality of life. Bone density rose at the femoral neck in men and at the ultradistal radius in women [8]. Across 25 trials in older men, DHEA reduced fat mass slightly (standardized mean difference -0.35, 95% CI -0.65 to -0.05), an effect that disappeared after adjusting for the rise in testosterone and estradiol, with no effect on blood lipids, blood sugar, bone, sexual function or quality of life [9]. A review of 8 trials called the effect on muscle strength and physical function inconclusive [10]. In postmenopausal women, 23 trials found no significant improvement in libido or sexual function (0.35, -0.02 to 0.73) and no significant effect on lipids, glucose, weight or bone density [11]. A Cochrane review found no improvement in quality of life (0.16, -0.03 to 0.34) and more androgenic side effects, mainly acne (odds ratio 3.77, 1.36 to 10.4) [12].
- Population
- 87 older men and 57 older women with low DHEA-S, treated for 2 years [8]. 1,353 older men in 25 trials, mean follow-up 36 weeks [9]. 661 adults aged 50 or older in 8 trials [10]. 1,188 postmenopausal women in 23 trials [11]. 1,273 women in 28 trials [12].
- Sources
- [8], [9], [10], [11], [12]
- Caveats
- A marker that tracks an outcome is not always one whose correction changes it. Low DHEA-S went with more deaths in cohorts. The trials measured body composition, function and quality of life, not deaths. The reviewers of the trials in women rated confidence in the evidence as low [11].