Endogenous Dehydroepiandrosterone Research Articles

Endogenous dehydroepiandrosterone and depression in postmenopausal women: a systematic review of observational studies.

The associations between endogenous dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS), and depression in older women are uncertain. However, DHEA supplements are widely available over the counter in some countries, and some people may be taking DHEA with the hope of positive mood effects. This systematic review aimed to investigate the association between endogenous DHEA/DHEAS blood concentrations and depression/depressive symptoms in community-dwelling postmenopausal women.Evidence Review: Searches were conducted in Ovid MEDLINE, EMBASE, PsycINFO, and Web of Science databases for observational studies with at least 100 community-dwelling participants until March 9, 2022. The bibliographies of retrieved articles were manually searched. The studies published in English and meeting the inclusion criteria were included in the review. The risk of bias was assessed with the modified Hoy tool for cross-sectional designs and the Joanna Briggs Institute modified critical appraisal checklist for cohort studies. Of the 30 articles retrieved for full-text review, 14 met the criteria for inclusion. Seven studies were cross-sectional, six were longitudinal, and one had both cross-sectional and longitudinal data. Five of eight cross-sectional studies found no association between DHEAS and depression, whereas three studies reported an inverse association. Similarly, most of the studies (n = 4) with longitudinal data reported no association, whereas two studies reported either an inverse association or mixed results for DHEAS and depression severity. No association between DHEA and depression was found irrespective of the study design. Heterogeneity of design was a barrier to meta-analysis and between study comparison. The majority of studies were limited by high risk of bias in at least one assessed domain. This systematic review does not support an association between endogenous DHEA/DHEAS and depression in postmenopausal women.

Impacts of adrenarcheal DHEA levels on spontaneous cortical activity during development

Dehydroepiandrosterone (DHEA) production is closely associated with the first pubertal hormonal event, adrenarche. Few studies have documented the relationships between DHEA and functional brain development, with even fewer examining the associations between DHEA and spontaneous cortical activity during the resting-state. Thus, whether DHEA levels are associated with the known developmental shifts in the brain’s idling cortical rhythms remains poorly understood. Herein, we examined spontaneous cortical activity in 71 typically-developing youth (9–16 years; 32 male) using magnetoencephalography (MEG). MEG data were source imaged and the power within five canonical frequency bands (delta, theta, alpha, beta, gamma) was computed to identify spatially- and spectrally-specific effects of salivary DHEA and DHEA-by-sex interactions using vertex-wise ANCOVAs. Our results indicated robust increases in power with increasing DHEA within parieto-occipital cortices in all frequency bands except alpha, which decreased with increasing DHEA. In the delta band, DHEA and sex interacted within frontal and temporal cortices such that with increasing DHEA, males exhibited increasing power while females showed decreasing power. These data suggest that spontaneous cortical activity changes with endogenous DHEA levels during the transition from childhood to adolescence, particularly in sensory and attentional processing regions. Sexually-divergent trajectories were only observed in later-developing frontal cortical areas.

Endogenous DHEAS Is Causally Linked With Lumbar Spine Bone Mineral Density and Forearm Fractures in Women.

ContextA recent pooled analysis of four clinical trials demonstrated that treatment with dehydroepiandrosterone (DHEA) increases lumbar spine bone mineral density (LS-BMD) in women. The causal effect of endogenous adrenal-derived DHEA sulphate (DHEAS) on LS-BMD and fracture risk in women is unknown.ObjectiveTo determine whether circulating DHEAS is causally associated with LS-BMD and fracture risk in women.MethodsA 2-sample Mendelian randomization study using genetic predictors of serum DHEAS derived from the largest available female-specific genome wide association study (GWAS) meta-analysis (n = 8565). Genetic associations with dual-energy X-ray absorptiometry–derived BMD (n = 22 900) were obtained from female-specific GWAS summary statistics available from the Genetic Factors for Osteoporosis consortium while individual-level data of 238 565 women of white ancestry from the UK Biobank were used for associations with fractures (11 564 forearm fractures, 2604 hip fractures) and estimated heel BMD by ultrasound (eBMD).ResultsA 1 SD genetically instrumented increase in log serum DHEAS levels was associated with a 0.21 SD increase in LS-BMD (P = 0.01) and a 0.08 SD increase in eBMD (P < 0.001). Genetically predicted DHEAS decreased forearm fracture risk (odds ratio 0.70, 95% CI 0.55-0.88 per SD increase in DHEAS) while no significant causal association with hip fractures was observed.ConclusionsGenetically predicted serum DHEAS increases LS-BMD and decreases forearm fracture risk in women. Based on the results of the present study and previous randomized controlled trials of DHEA treatment, we propose that both endogenous adrenal-derived DHEA(S) and pharmacological DHEA treatment improve bone health in women.

Association of endogenous DHEA/DHEAS with coronary heart disease: A systematic review and meta-analysis.

The clinical significance of dehydroepiandrosterone (DHEA) and its sulphate (DHEAS) in coronary heart disease (CHD) has not been thoroughly elucidated to date. We performed a meta-analysis to clarify the correlations between endogenous DHEA(S) and CHD. We performed a literature search without language restriction up to August 10, 2017, and retrieved records from EMBase, PubMed, Web of Science, CNKI and WanFang databases to identify eligible cohort studies focused on the relation between DHEA(S) and CHD. A total of 26 studies were included in the systematic review and 14 case-control studies were included in the meta-analysis,which was performed using RevMan 5.1 and STATA 12. Subgroup analyses were used to discover possible sources of heterogeneity. Quality assessment was carried out using the Newcastle-Ottawa Scale. Odds ratios with 95% confidence intervals were calculated. Heterogeneity analyses were performed using meta-regression and tests for publication bias were performed. The overall average DHEAS diffusivity of CHD cases was significantly lower than that of controls with a summarized standard (std) mean difference of -0.23(95% CI, -0.45 to -0.01, P=.04). There was no association between DHEA concentration and CHD with a summarized mean difference of -0.07 (95% CI, -0.32 to 0.18, P=.59). No association was found between DHEAS concentration and arteriosclerosis patients with a summarized standard (std) mean difference of -0.46(95% CI, -0.96 to 0.04, P=.07). All of the results had a high degree of heterogeneity. The present study suggested that decreased DHEAS may be associated with coronary heart disease risk but not with arteriosclerosis. We did not find a significant association between DHEA and CHD risk.

Do dehydroepiandrosterone, progesterone, and testosterone influence women’s depression and anxiety levels? Evidence from hair-based hormonal measures of 2105 rural Indian women

Depressive and anxiety disorders substantially contribute to the global burden of disease, particularly in poor countries. Higher prevalence rates for both disorders among women indicate sex hormones may be integrated in the pathophysiology of these disorders. The Kshetriya Gramin Financial Services study surveyed a random sample of 4160 households across 876 villages in rural Tamil Nadu, India. An interviewer-administered questionnaire was conducted to quantify depressive (K6-D) and anxiety (K6-A) symptoms. Alongside, hair samples for sex hormone profiling were collected from a subsample of 2105 women aged 18–85 years. Importantly, 5.9%, 14.8%, and 46.3% of samples contained non-detectable hormone levels for dehydroepiandrosterone, progesterone, and testosterone, respectively. Our primary analysis imputes values for the non-detectable sample and we check robustness of results when non-detectable values are dropped. In this cohort of women from rural India, higher depressive symptomatology is associated with lower levels of dehydroepiandrosterone and higher depressive and anxiety symptoms are associated with higher levels of testosterone. Progesterone shows no clear association with either depressive or anxiety symptoms. These results support a potential protective effect of higher endogenous dehydroepiandrosterone levels. An important caveat on the potential negative effect of hair testosterone levels on women’s mental health is that the testosterone analysis is sensitive to how non-detectable values are treated.

Endogenous dehydroepiandrosterone levels and its derivatives modifies the association between total estradiol and type 2 diabetes risk in postmenopausal women: The Rotterdam Study

Endogenous dehydroepiandrosterone levels and its derivatives modifies the association between total estradiol and type 2 diabetes risk in postmenopausal women: The Rotterdam Study

Progress in research of sodium prasterone sulfate in vaginal atrophy

Sodium prasterone sulfate (DHEAS) and dehydroepiandrosterone (DHEA) are endogenous steroid compounds, which are synthesized and secreted by adrenal gland. They are the precursors of steroid hormones,including sex hormone. Based on intracrine theory,the majority of postmenopausal women will have vaginal atrophy,which is caused by the absence of endogenous hormones,DHEAS or DHEA. Moderate supplementation of DHEAS can relieve the associated symptoms of vaginal atrophy.Many clinical researches have demonstrated that DHEAS can efficiently alleviate the related symptoms of vaginal atrophy.The concentration of androgen and estrogen in patients with long term use of DHEAS are still in the normal intracrine physiological range. Therefore,DHEAS may become the first drug for the treatment of vaginal atrophy in the future.

Sex-specific effects of dehydroepiandrosterone (DHEA) on glucose metabolism in the CNS

DHEA is a neuroactive steroid, due to its modulatory actions on the central nervous system (CNS). DHEA is able to regulate neurogenesis, neurotransmitter receptors and neuronal excitability, function, survival and metabolism. The levels of DHEA decrease gradually with advancing age, and this decline has been associated with age related neuronal dysfunction and degeneration, suggesting a neuroprotective effect of endogenous DHEA. There are significant sex differences in the pathophysiology, epidemiology and clinical manifestations of many neurological diseases. The aim of this study was to determine whether DHEA can alter glucose metabolism in different structures of the CNS from male and female rats, and if this effect is sex-specific. The results showed that DHEA decreased glucose uptake in some structures (cerebral cortex and olfactory bulb) in males, but did not affect glucose uptake in females. When compared, glucose uptake in males was higher than females. DHEA enhanced the glucose oxidation in both males (cerebral cortex, olfactory bulb, hippocampus and hypothalamus) and females (cerebral cortex and olfactory bulb), in a sex-dependent manner. In males, DHEA did not affect synthesis of glycogen, however, glycogen content was increased in the cerebral cortex and olfactory bulb. DHEA modulates glucose metabolism in a tissue-, dose- and sex-dependent manner to increase glucose oxidation, which could explain the previously described neuroprotective role of this hormone in some neurodegenerative diseases.

Dehydroepiandrosterone and Muscle Strength during a Menstrual Cycle in Female Athletes

Dehydroepiandrosterone (DHEA) is the common precursor of several reproductive hormones. DHEA-sulfate (DHEA-S) declines during adult aging and has been considered as a strong predictor for human longevity. The purpose of the study was to track the evolution of serum DHEA-S concentration and muscle strength during a menstrual cycle for young athletes. Ten female athletes (21 years of age) were enrolled in this longitudinal observation with hormonal and muscle strength assessments for every 7 days since the first day of menses, including Menses (M), Ovulatory (O), Luteal 1 (L1) and Luteal 2 (L2) periods. Despite total mood disturbance was not changed, muscle strength and serum DHEA-S concentrations were declined simultaneously during L2 period with a significant increase of serum estradiol and progesterone concentrations. Furthermore, during L2 period, sympathetic power mirrored by low-frequency heart rate variability (LF-HRV) and body temperature were relatively greater than the rest of the phases. We conclude that physical but not mental capabilities were compromised during premenstrual period for young female athletes. These findings suggest that circumventing athletic event during premenstrual period may be important to maximize the competition outcome for female athletes. This is probably because of increased consumption of endogenous DHEA for the biosynthesis of reproductive hormones during premenstrual phase.

Allosteric modulation of sigma-1 receptors by SKF83959 inhibits microglia-mediated inflammation.

Recent studies have shown that sigma-1 receptor orthodox agonists can inhibit neuroinflammation. SKF83959 (3-methyl-6-chloro-7,8-hydroxy-1-[3-methylphenyl]-2,3,4,5-tetrahydro-1H-3-benzazepine), an atypical dopamine receptor-1 agonist, has been recently identified as a potent allosteric modulator of sigma-1 receptor. Here, we investigated the anti-inflammatory effects of SKF83959 in lipopolysaccharide (LPS)-stimulated BV2 microglia. Our results indicated that SKF83959 significantly suppressed the expression/release of the pro-inflammatory mediators, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS), and inhibited the generation of reactive oxygen species. All of these responses were blocked by selective sigma-1 receptor antagonists (BD1047 or BD1063) and by ketoconazole (an inhibitor of enzyme cytochrome c17 to inhibit the synthesis of endogenous dehydroepiandrosterone, DHEA). Additionally, we found that SKF83959 promoted the binding activity of DHEA with sigma-1 receptors, and enhanced the inhibitory effects of DHEA on LPS-induced microglia activation in a synergic manner. Furthermore, in a microglia-conditioned media system, SKF83959 inhibited the cytotoxicity of conditioned medium generated by LPS-activated microglia toward HT-22 neuroblastoma cells. Taken together, our study provides the first evidence that allosteric modulation of sigma-1 receptors by SKF83959 inhibits microglia-mediated inflammation. SKF83959 is a potent allosteric modulator of sigma-1 receptor. Our results indicated that SKF83959 enhanced the activity of endogenous dehydroepiandrosterone (DHEA) in a synergic manner, and inhibited the activation of BV2 microglia and the expression/release of the pro-inflammatory mediators, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS).

The Metabolic Change of Serum Dehydroepiandrosterone Sulfate, Free Fatty Acids and Desaturase Activity in Isolated Post-Challenge Hyperglycemia

The aim of this study is to investigate the association between endogenous dehydroepiandrosterone sulfate (DHEA-S) and fatty acid, desaturase in isolated post-challenge hyperglycemia (IPH) subjects. 241 IPH subjects aged 35 to 70 years participated. Serum DHEA-S concentration was measured using the enzyme-linked immunosorbent assays. Fatty acid profiles were detected by gas chromatography-mass spectrometry, and desaturase activities were expressed by fatty acid product-to-precursor ratios. Relationships were assessed using multiple regression. The results suggested that DHEA-S concentration was negatively associated with palmitic acid (P < 0.001), and positively with γ-linolenic acid and eicosatetraenoic acid in men (P = 0.002 and P = 0.001, respectively), and negatively with palmitic acid (P = 0.037) and positively with docosapentaenoic acid, docosahexaenoic acid (P = 0.018 and P < 0.001, respectively) in women. In addition, a positive association was observed between DHEA-S and delta-9-desaturase (D9D-18, P = 0.031) in men, and also delta-6-desaturase (D6D, P = 0.034) in women. In Conclusions, there is different DHEA-S, fatty acid profile and the desaturase activities in both genders with the IPH subjects.

Clinical review: The benefits and harms of systemic dehydroepiandrosterone (DHEA) in postmenopausal women with normal adrenal function: a systematic review and meta-analysis.

Exogenous dehydroepiandrosterone (DHEA) therapy has been proposed to replenish the depletion of endogenous DHEA and its sulfate form, which occurs with advancing age and is thought to be associated with loss of libido and menopausal symptoms. We conducted a systematic review and meta-analysis to summarize the evidence supporting the use of systemic DHEA in postmenopausal women with normal adrenal function. We searched MEDLINE, EMBASE, PsycInfo, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, and Scopus through January 2014. Pairs of reviewers, working independently, selected studies and extracted data from eligible randomized controlled trials (RCTs). We used the random-effects model to pool across studies and evaluated heterogeneity using the I(2) statistic. We included 23 RCTs with moderate to high risk of bias enrolling 1188 women. DHEA use was not associated with significant improvement in libido or sexual function (standardized mean difference, 0.35; 95% confidence interval, -0.02 to 0.73; P value = .06; I(2) = 62%). There was also no significant effect of DHEA on serious adverse effects, serum lipids, serum glucose, weight, body mass index, or bone mineral density. This evidence warranted low confidence in the results, mostly due to imprecision, risk of bias, and inconsistency across RCTs. Evidence warranting low confidence suggests that DHEA administration does not significantly impact sexual symptoms or selected metabolic markers in postmenopausal women with normal adrenal function.

Neuroprotective–neurotrophic effect of endogenous dehydroepiandrosterone sulfate during intense stress exposure

Recent reports demonstrate neurotrophic properties of dehydroepiandrosterone sulfate (DHEAS) in men at rest, as well as profound neurotrophic responses to stress in both men and women. Little is known of neuroprotective–neurotrophic effects of DHEAS during stress exposure, either in men or women. This translational study was designed to examine neuroprotective–neurotrophic effects of DHEAS throughout intense stress exposure in healthy men and women. The study took place within a stressful 12-day military survival course. Utilizing a longitudinal cross-sectional repeated measures design, One hundred sixteen healthy active-duty military personnel (80% male) were studied before, during, and 24h after the course. The dependent variable was the neurotrophin salivary nerve growth factor (sNGF). In terms of total hormone output, the effect of DHEAS on sNGF was mediated by testosterone. Unlike testosterone or cortisol, DHEAS reliably predicted sNGF at each time point, and change in DHEAS predicted change in sNGF across time points. Baseline DHEAS predicted total sNGF output across the stress trajectory. Consistent with preclinical as well as cross-sectional human research, this study demonstrates neuroprotective–neurotrophic effects of DHEAS in healthy men and women exposed to intense stress. Results are evaluated in relation to established criteria for causation.

Endogenous sex hormones, blood pressure change, and risk of hypertension in postmenopausal women: The Multi-Ethnic Study of Atherosclerosis

ObjectiveSex steroid hormones have been postulated to involve in blood pressure (BP) regulation. We examine the association of endogenous sex hormone levels with longitudinal change of BP and risk of developing hypertension in initially normotensive postmenopausal women. MethodsWe conducted prospective analysis among 619 postmenopausal women free of hypertension at baseline in the Multi-Ethnic Study of Atherosclerosis (MESA). Change of BP and development of incident hypertension were assessed during a mean of 4.8 years follow-up. ResultsAfter adjusting for age, race/ethnicity, and lifestyle factors, baseline serum estradiol (E2), total and bioavailable testosterone (T), dehydroepiandrosterone (DHEA) were each positively associated and sex-hormone binding globulin (SHBG) was inversely associated with risk of hypertension. Additional adjustment for body mass index eliminated the associations for E2 and T but only attenuated the associations for DHEA and SHBG. The corresponding multivariable hazard ratios (95% CIs) in the highest quartile were 1.28 (0.83–1.97) for E2, 1.38 (0.89–2.14) for total T, 1.42 (0.90–2.23) for bioavailable T, 1.54 (1.02–2.31) for DHEA, and 0.48 (0.30–0.76) for SHBG. Adjustment for fasting glucose, insulin, and C-reactive protein further attenuated the association for DHEA but not for SHBG. Associations of sex hormones with longitudinal BP change were similar. ConclusionIn postmenopausal women, higher endogenous E2, T, and DHEA and lower SHBG were associated with higher incidence of hypertension and greater longitudinal rise in BP. The associations for E2, T, and DHEA were mostly explained by adiposity, while the association for SHBG was independent of measures of adiposity, insulin resistance, and systemic inflammation.

Elevated serum dehydroepiandrosterone sulphate level correlates with increased risk for metabolic syndrome in the elderly men

The previous studies regarding the association between endogenous dehydroepiandrosterone (DHEA) sulphate level and metabolic syndrome are inconsistent. This study aimed to investigate such relationship in elderly Taiwanese men. Five hundred and eighty-five elderly Taiwanese men (mean age 68.7 +/- 8.3 years) were enrolled as the baseline cohort population in 2000. In addition to a questionnaire, body mass index (BMI), blood pressure, fasting blood glucose, lipids, albumin and serum DHEA-S levels were measured for each participant. Metabolic syndrome was based on the definition by the America Heart Association/National Heart Lung Blood Institute. The prevalence of metabolic syndrome was 33.3%. Using multivariate logistic regression analyses with adjustments for age, smoking, alcohol, physical activities, albumin and BMI, there was a positive relationship between serum DHEA-S level and metabolic syndrome. The highest DHEA-S quartile group had increased risk for metabolic syndrome (odds ratio = 2.68, 95% confidence interval: 1.44-5.01, P < 0.01) compared with the lowest quartile group. The mean serum DHEA-S level increased with increasing number of metabolic syndrome components. The prevalence of metabolic syndrome increases with elevated DHEA-S levels among elderly Taiwanese men. Thus, elevated serum DHEA-S level should be treated as an important risk factor for metabolic syndrome in elderly men.

Several Candidates in Running as Anxiety-Disorder Biomarker

Several Candidates in Running as Anxiety-Disorder Biomarker

Dehydroepiandrosterone and age-related cognitive decline

In humans the circulating concentrations of dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS) decrease markedly during aging, and have been implicated in age-associated cognitive decline. This has led to the hypothesis that DHEA supplementation during aging may improve memory. In rodents, a cognitive anti-aging effect of DHEA and DHEAS has been observed but it is unclear whether this effect is mediated indirectly through conversion of these steroids to estradiol. Moreover, despite the demonstration of correlations between endogenous DHEA concentrations and cognitive ability in certain human patient populations, such correlations have yet to be convincingly demonstrated during normal human aging. This review highlights important differences between rodents and primates in terms of their circulating DHEA and DHEAS concentrations, and suggests that age-related changes within the human DHEA metabolic pathway may contribute to the relative inefficacy of DHEA replacement therapies in humans. The review also highlights the value of using nonhuman primates as a pragmatic animal model for testing the therapeutic potential of DHEA for age-associate cognitive decline in humans.

The neurosteroid dehydroepiandrosterone (DHEA) and its metabolites alter 5-HT neuronal activity via modulation of GABAA receptors

Dehydroepiandrosterone (DHEA) and its metabolites, DHEA-sulphate (DHEA-S) and androsterone, have neurosteroid activity. In this study, we examined whether DHEA, DHEA-S and androsterone, can influence serotonin (5-HT) neuronal firing activity via modulation of γ-aminobutryic acid (GABA(A)) receptors. The firing of presumed 5-HT neurones in a slice preparation containing rat dorsal raphe nucleus was inhibited by the GABA(A) receptor agonists 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridinyl-3-ol (THIP) (25 μM) and GABA (100 μM). DHEA (100 and 300 μM) and DHEA-S (1, 10 and 100 μM) caused a rapid and reversible attenuation of the response to THIP. DHEA (100 μM) and DHEA-S (100 μM) also attenuated the effect of GABA. Androsterone (10 and 30 μM) markedly enhanced the inhibitory response to THIP (25 μM). The effect was apparent during androsterone administration but persisted and even increased in magnitude after drug wash-out. The data indicate that GABA(A) receptor-mediated regulation of 5-HT neuronal firing is sensitive to negative modulation by DHEA and its metabolite DHEA-S is sensitive to positive modulation by the metabolite androsterone. The effects of these neurosteroids on GABA(A) receptor-mediated regulation of 5-HT firing may underlie some of the reported behavioural and psychological effects of endogenous and exogenous DHEA.

Biochemical and functional evidence for the control of pain mechanisms by dehydroepiandrosterone endogenously synthesized in the spinal cord

We investigated the role and mechanism of action of dehydroepiandrosterone (DHEA) produced by the spinal cord (SC) in pain modulation in sciatic-neuropathic and control rats. Real-time polymerase chain reaction (PCR) after reverse transcription revealed cytochrome P450c17 (DHEA-synthesizing enzyme) gene repression in neuropathic rat SC. A combination of pulse-chase experiments, high performance liquid chromatography (HPLC), and flow-scintillation detection showed decreased DHEA biosynthesis from pregnenolone in neuropathic SC slices. Radioimmunoassays demonstrated endogenous DHEA level drop in neuropathic SC. Behavioral analysis showed a rapid pronociceptive and a delayed antinociceptive action of acute DHEA treatment. Inhibition of DHEA biosynthesis in the SC by intrathecally administered ketoconazole (P450c17 inhibitor) induced analgesia in neuropathic rats. BD1047 (sigma-1 receptor antagonist) blocked the transient pronociceptive effect evoked by acute DHEA administration. Chronic DHEA treatment increased and maintained elevated the basal nociceptive thresholds in neuropathic and control rats, suggesting that androgenic metabolites generated from daily administered DHEA exerted analgesic effects while DHEA itself (before being metabolized) induced a rapid pronociceptive action. Indeed, intrathecal administration of testosterone, an androgen deriving from DHEA, caused analgesia in neuropathic rats. Together, these molecular, biochemical, and functional results demonstrate that DHEA synthesized in the SC controls pain mechanisms. Possibilities are opened for pain modulation by drugs regulating P450c17 in nerve cells.

Sex differences in the relationship between DHEAS and health

Dehydroepiandrosterone (DHEA) and its sulfate form (DHEAS) have been the focus of considerable publicity because of their demonstrated associations with a broad range of health outcomes. Yet, knowledge about the effects of endogenous DHEA(S) on health in humans is limited and often inconclusive, largely because few of the studies have been based on prospective surveys of population-representative samples. This analysis uses a national longitudinal survey in Taiwan to investigate whether DHEAS is associated with subsequent changes (2000–2003) in functional limitations, cognitive impairment, depressive symptoms, and global self-rated health. Regression models based on this older Taiwanese sample show that among men, lower levels of DHEAS are related to declines in mobility and self-assessed health status and increases in depressive symptoms, while both low and very high levels of DHEAS are associated with poor cognitive function. There are no significant associations among women. These findings differ from those in a previous cross-sectional analysis based on the Taiwan study and underscore the importance of using prospective data to examine the effects of DHEAS on health. The evidence based on this and other longitudinal studies suggests that endogenous DHEAS is related to health outcomes for men, but not women, in both Western and non-Western populations.