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Evidence for the biosynthesis of DHEA from cholesterol by first-trimester human placental tissue: source of androgens.

With a view to establishing whether first-trimester human placentas possess the ability to synthesize DHEA from cholesterol, homogenates of this tissue obtained from two groups of women undergoing elective termination of normally progressing pregnancy between 10 - 12 weeks gestation (n = 5, age 23 - 29 years and n = 5, age 21 - 27 years) were incubated separately with [26-(14)C]cholesterol for the generation of [14C]isocaproic acid + pregnenolone and [7n-3H]pregnenolone for the biosynthesis of [3H]DHEA. Controls consisted of homogenates heated in a boiling water bath for 10 min. Using the reverse-isotope dilution analysis, desmolase efficiency expressed as mean specific activity of [14C]isocaproic acid varied from 282 to 725 dpm/mmol, while that of 17 alpha-hydroxylase and steroid C-17,20-lyase, catalyzed conversion of [7n-3H]pregnenolone to [3H]DHEA varied from 3498 to 26 258 dpm/mmol. The corresponding efficiencies of enzymicconversion varied between 5.8 x 10( -2) and 1.5 x 10( -1) % for [14C]isocaproic acid, but between 5.5 x 10( -2) and 4.1 x 10( -1) % for [3H]DHEA. No such metabolite was evident in the controls of heat-denatured homogenates. These are the first study results to demonstrate that early placentas are capable of converting cholesterol to pregnenolone to DHEA, contrary to the widely held concept of DHEA production by fetal and maternal adrenal glands. This finding has important physiological implications and could provide a new dimension to the concept of fetoplacental steroidogenesis.

Adult↗

Treatment of pouchitis with dehydroepiandrosterone (DHEA) - a case report.

BACKGROUND: Dehydroepiandrosterone (DHEA) inhibits activation of nuclear factor kappa B (NF-kappaB), which is known to be activated in inflammatory lesions of ulcerative colitis, via PPARalpha. In a pilot trial DHEA was effective for the treatment of active ulcerative colitis. Pouchitis is a common complication after proctocolectomy for ulcerative colitis and still a therapeutical challenge. CASE: DHEA 200 mg/d was tested in chronic active pouchitis in a 35-year-old female patient. DHEA was given for eight weeks, and follow up for further eight weeks was performed. The number of stools dropped from 15-18/d to 8/d, the addition of mucus, which was observed initially, was absent during treatment. The consistence of stools improved from liquid/soft to soft/solid. Abdominal pain resolved and endoscopical signs of inflammation improved. Eight weeks after termination of treatment with DHEA, the patient again suffered from 12 to 18 soft to liquid stools per day and mild abdominal pain. CONCLUSION: Therapeutic effects of DHEA in pouchitis should be evaluated systematically.

Adjuvants, Immunologic↗

Suppression of DHEA sulfotransferase (Sult2A1) during the acute-phase response.

The acute-phase response (APR) induces alterations in lipid metabolism, and our data suggest that this is associated with suppression of type II nuclear hormone receptors that are key regulators of fatty acid, cholesterol, and bile acid metabolism. Recently, the farnesoid X receptor (FXR), constitutive androstane receptor (CAR), and pregnane X receptor (PXR) were found to regulate DHEA sulfotransferase (Sult2A1), which plays an important role in DHEA sulfation and detoxification of bile acids. Because FXR, PXR, and CAR are suppressed during the APR, we hypothesized that Sult2A1 is downregulated during the APR. To induce the APR, mice were treated with LPS, which will then trigger the release of various cytokines, and the mRNA levels of Sult2A1 and the sulfate donor 3'-phosphoadenosine 5'-phosphosulfate synthase 2 (PAPSS2), as well as the enzyme activity of Sult2A1, were determined in the liver. We found that mRNA levels of Sult2A1 decrease in a time- and dose-dependent manner during the LPS-induced APR. Similar changes were observed in the mRNA levels of PAPSS2, the major synthase of PAPS in the liver. Moreover, hepatic Sult2A1 activity and serum levels of DHEA-sulfate (DHEA-S) were significantly decreased in LPS-treated animals. These results suggest that decreased levels or activities of FXR, PXR, and CAR during the APR could contribute to decreases in Sult2A1, resulting in decreased sulfation of DHEA and lower circulating level of DHEA-S. Finally, we found that both TNF and IL-1 caused a significant decrease in the mRNA level of Sult2A1 in Hep3B human hepatoma cells, suggesting that the proinflammatory cytokines TNF and IL-1 mediate the inhibitory effect of LPS on Sult2A1 mRNA level. Our study provides a possible mechanism by which infection and inflammation are associated with altered steroid metabolism and cholestasis.

Acute-Phase Reaction↗

Vitamin E attenuates myocardial oxidative stress induced by DHEA in rested and exercised rats.

Sixty-four male Sprague-Dawley rats were randomly assigned to one of eight treatment groups to determine whether vitamin E (VitE) could help protect the heart from oxidative stress induced by either dehydroepiandrosterone (DHEA) or exercise. Oxidative stress was indicated by lipid peroxidation [i.e., thiobarbituric acid-reactive substances (TBARS)] and two scavenger enzymes. VitE supplementation (250 IU VitE/kg of diet) was given to one-half of the rats. DHEA acetate (0.35 mol/kg body wt) was injected intraperitoneally to one-half of the animals while the others were injected with corn oil vehicle. All treatments lasted for 5 wk. Next, 32 rats were randomly assigned to run for 1 h on a motorized rodent treadmill at 21 m/min up a 12% grade and then were killed. The remaining rats were killed at rest. Exercise increased TBARS in heart independent of treatment (1.94 +/- 0.12 vs. 2.43 +/- 0.11 nmol/mg protein). VitE attenuated the amount of TBARS in heart when DHEA was given. DHEA significantly increased TBARS in heart. Total and selenium-dependent glutathione peroxidase activities in heart were unaffected by any treatment. DHEA increased catalase activity at rest. Exercise increased catalase activity (71.5 +/- 7.9 vs. 97.4 +/- 9.5 mu mol x min-1 x mg protein-1); however, when VitE was given, the response to exercise was attenuated (74.1 +/- 8.4 vs. 80.9 +/- 9.9 mu mol center dot min-1 x mg protein-1). These results suggest that aerobic exercise and DHEA are mild oxidative stressors on the heart and that VitE supplementation can be beneficial in attenuating these combined stressors on the heart.

Animals↗

The effects of moderate alcohol supplementation on estrone sulfate and DHEAS in postmenopausal women in a controlled feeding study.

BACKGROUND: We have demonstrated that moderate alcohol consumption (15 g/d, 30 g/d) for 8 weeks resulted in significantly increased levels of serum estrone sulfate and DHEAS in 51 postmenopausal women in a randomized, placebo-controlled trial. We now report on the relationships between serum estrone sulfate and dehydroepiandrosterone sulfate (DHEAS) levels after 4 weeks of moderate alcohol supplementation, and compare the results to the 8 weeks data to elucidate time-to-effect differences. METHODS: Postmenopausal women (n = 51) consumed 0 (placebo), 15 (1 drink), and 30 (2 drinks) g alcohol (ethanol)/ day for 8 weeks as part of a controlled diet in a randomized crossover design. Blood samples were drawn at baseline, at 4 weeks and at 8 weeks. Changes in estrone sulfate and DHEAS levels from placebo to 15 g and 30 g alcohol per day were estimated using linear mixed models. RESULTS AND DISCUSSION: At week 4, compared to the placebo, estrone sulfate increased an average 6.9% (P = 0.24) when the women consumed 15 g of alcohol per day, and 22.2% (P = 0.0006) when they consumed 30 g alcohol per day. DHEAS concentrations also increased significantly by an average of 8.0% (P < 0.0001) on 15 g of alcohol per day and 9.2% (P < 0.0001) when 30 g alcohol was consumed per day. Trend tests across doses for both estrone sulfate (P = 0.0006) and DHEAS (P < 0.0001) were significant. We found no significant differences between the absolute levels of serum estrone sulfate at week 4 versus week 8 (P = 0.32) across all doses. However, absolute DHEAS levels increased from week 4 to week 8 (P < 0.0001) at all three dose levels. CONCLUSIONS: These data indicate that the hormonal effects due to moderate alcohol consumption are seen early, within 4 weeks of initiation of ingestion.

Clinical Trial↗

Disproportionate suppression of dehydroepiandrosterone sulfate (DHEAS) in treated patients with congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

Serum concentrations of dehydroepiandrosterone sulfate (DHEAS) were measured in 28 patients (18 females, 10 males) with congenital adrenal hyperplasia due to 21-hydroxylase deficiency who were treated with oral hydrocortisone (non-salt losers) or hydrocortisone and 9-alpha-fluorohydrocortisone (salt-losers). Adequacy of therapy was assessed by clinical findings, determination of bone age, urinary excretion of 17-ketosteroids, and serum concentration of 17-hydroxyprogesterone. These allowed the separation of patients into three groups: poorly controlled, adequately controlled and overtreated. Individual values for serum levels of DHEAS were compared to mean normal values for age. In the adequately controlled and overtreated patients, mean serum concentrations of DHEAS were significantly lower than normal values for age (P less than 0.05). In the poorly treated patients, the mean serum concentration of DHEAS was not significantly different from normal values for age (P = 0.50). These data indicate that the serum concentration of DHEAS is overly suppressed in treated patients with congenital adrenal hyperplasia due to 21-hydroxylase deficiency. This finding suggests that measurement of the serum levels of DHEAS has limited value in assessing the adequacy of therapy in this disease.

Adolescent↗

Changes in bone turnover markers and menstrual function after short-term oral DHEA in young women with anorexia nervosa.

Bone loss is a serious consequence of anorexia nervosa (AN). Subnormal levels of serum dehydroepiandrosterone (DHEA) are seen in patients with AN and may be causally linked to their low bone density. We hypothesized that oral DHEA would decrease markers of bone resorption (urinary N-telopeptides [NTx]), and increase markers of bone formation (serum bone-specific alkaline phosphatase and osteocalcin [OC]). Fifteen young women (age 15-22 years) with AN were enrolled in a 3-month, randomized, double-blinded trial of 50, 100, or 200 mg of daily micronized DHEA. Blood and urinary levels of adrenal and gonadal steroids and bone turnover markers were measured. No adverse clinical side effects of DHEA were noted, and a 50 mg daily dose restored physiologic hormonal levels. At 3 months, NTx levels had decreased significantly in both the 50 mg (p = 0.018) and the 200 mg (p = 0.016) subgroups. OC levels simultaneously increased within treatment groups over time (p = 0.002). Eight out of 15 (53%) subjects had at least one menstrual cycle while on therapy. Short-term DHEA was well-tolerated and appears to normalize bone turnover in young women with AN. Resumption of menses in over half of subjects suggests that DHEA therapy may also lead to estradiol levels sufficient to stimulate the endometrium in this group of patients.

Administration, Oral↗

DHEA and the skeleton (through the ages).

Dehydroepiandrosterone (DHEA) and its sulfate ester, DHEAS, are the most abundant steroids in the human circulation, although their exact biological significance is not completely understood. DHEA(S) levels are high in fetal life, decrease after birth, and show a marked pubertal increase to a maximal level during young adulthood. In healthy adults, DHEAS levels decline to 10-20% of peak levels by age 70 yr. This review summarizes information concerning the role of DHEA in skeletal physiology, including modulation of the skeletal insulin-like growth factor regulatory system, and its effects on secretion of proresorptive cytokines. The pattern of secretion of DHEA throughout the life cycle is discussed, as well as its potential usefulness in specific disease states as an agent with anabolic and antiosteolyic effects on bone.

Adult↗

Plasma levels of 7-hydroxylated dehydroepiandrosterone (DHEA) metabolites and selected amino-thiols as discriminatory tools of Alzheimer's disease and vascular dementia.

OBJECTIVE: The early differential diagnosis of Alzheimer's disease (AD) remains still problematic. We developed a laboratory test enabling us to distinguish patients with AD from those with vascular dementia (VD) and healthy subjects. METHODS: The AD group consisted of 22 women and 18 men. The VD group consisted of 16 women and 8 men. Age-matched controls consisted of 12 women and 9 men. Plasma pregnenolone sulfate (PregS), dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) were determined by radioimmunoassay. 17-Hydroxypregnenolone (17Preg) and 7-hydroxylated metabolites of DHEA (7alphaDHEA, 7betaDHEA) were determined by radioimmunoassay after separation by high performance liquid chromatography (HPLC). Homocysteine (Hcy), cysteine (Cys), cysteinylglycine (Cysgly) and glutathione (GSH) were measured by HPLC. RESULTS: The ANOVA results of significant between-group differences were as follows: The PregS and the 17-Preg and DHEAS levels were independent from the diagnosis. The 7alphaDHEA levels significantly depended on the sex (p < 0.05) and diagnosis (p < 0.01). Amino-thiols were influenced by the diagnosis (p < 0.01, p = 0.0541, p < 0.01 and p = 0.0536 for Cys, Hcy, Cysgly and GSH, respectively). Using a stepwise backward regression analysis, the following parameters were obtained: X = 11.5 + 4.03 x sex +1.09 x Hcy + 0.190 x PregS - 4.76 x DHEAS + 3.00 x DHEA - 34.3 x 77alphaDHEA - 0.885 x Cysgly from which P-value as a discriminator was calculated according to the formula: P = 1/(1 + e(-x)). Then, for P > 0.5, a subject was considered as AD-positive (with 89% correct prediction). DISCUSSION: The opportunity of early differential diagnosis of AD should help physicians to use suitable treatment for retardation of pathological processes.

17-alpha-Hydroxypregnenolone↗

Total testosterone and DHEAS levels as predictors of androgen-secreting neoplasms: a populational study.

Androgen excess affects between 2% and 10% of women. While the majority of these patients suffer from polycystic ovary syndrome, a few present with an androgen-secreting neoplasm. An elevated circulating total testosterone level and dehydroepiandiosterone sulfate (DHEAS) level have been proposed as screening methods for detecting ovarian and adrenal androgen-secreting neoplasms, respectively. To determine the predictive value of these tests for androgen-secreting tumors in a population of consecutive hyperandrogenic patients, we studied 478 consecutive untreated hyperandrogenic patients presenting over a ten-year period (1987-97). All had at least two of the following features: (1) oligomenorrhea (i.e. cycles > 35 days or < 8 cycles/year), (2) hyperandrogenemia (i.e. a total or free testosterone, or DHEAS > 95th percentile of controls), or (3) hirsutism (i.e. a modified Ferriman-Gallwey score > or = 6). None of these patients had a prior diagnosis of an androgen-secreting neoplasm. Basal levels of testosterone and DHEAS were determined in all patients, with transvaginal sonography and an adrenal computed tomography scan in select individuals. Of the 478 patients included, 65% had hirsutism and oligomenorrhea; 20% had hyperandrogenic oligomenorrhea; and 15% had hirsutism and hyperandrogenemia, without overt oligomenorrhea. Overall, 11 (2.3%) patients had a total testosterone > 8.7 nmol/l (250 ng/dl), of which one actually had an androgen-secreting neoplasm (i.e. true-positive). This postmenopausal patient presented with rapidly progressive virilization, and demonstrated an ovarian hilar cell tumor at surgery. The calculated sensitivity of an elevated testosterone level (> 8.67 nmol/l) for a neoplasm was 100% (1/1), the specificity was 98% (467/477), and the negative predictive value was 100% (467/467), but the positive predictive value was only 9% (1/11). Ten subjects had DHEAS levels > 16.3 mumol/l (6000 ng/ml), and none was diagnosed with an adrenocortical tumor. Although the sensitivity and positive predictive value of a high DHEAS for a neoplasm could not be calculated due to the absence of a test case, the specificity was 98% (468/478) and the negative predictive value was 100% (468/468). These data suggest that the measurement of testosterone and DHEAS is not a cost-effective method of screening for these tumors, due to the low frequency of the disorder and the fact that clinical evaluation alone is often sufficient screening.

Adrenal Cortex Neoplasms↗

Morphological and biochemical evaluation of RAW 264.7 macrophages after acute and chronic administration of DHEA and AED.

The effect of adrenal hormones namely dehydroepiandrosterone (DHEA, 10-50 ug/day) and androstenedione (AED, 10-50 ug/day), on RAW 264.7 macrophage survival at 24, 48 and 72 hours after lipopolysaccharide (LPS, 2 micrograms/ml) exposure was investigated in an in vitro environment. RAW cells were obtained from American Type Culture Collection and standard laboratory protocols were followed in cells plating (10(6) cells/well), phase terminating, morphological evaluation, and biochemical marker analysis. From physiologic to supraphysiologic doses of DHEA and AED at 24 hours caused increased levels of cellular proteins and cell number without causing any significant (p < 0.05) change in cellular membrane integrity (Maliondialdehyde, MDA) or viability (morphology). At 48 and 72 hours, cells treated with either AED or DHEA did not sustain the increased cellular proliferation as observed at 24 hours and did not significantly differ (p < 0.05) in cellular protein content. RAW 264.7 cells treated with LPS for 30 minutes prior to AED or DHEA exposure caused slight decrease in cell number and cell protein content. The decrease in both cell number and cell protein content were not attributed to increased cell damage or decreases in cell viability due to the fact that the cellular MDA levels were not statistically higher than the control values (p < 0.05). Morphological Evaluations of cells using Image Pro Software, revealed no significant or adverse changes when compared with cells treated with media alone. Dot blot analysis of pro-inflammatory cytokine (TNF alpha) production after LPS treatment was suppressed by DHEA while AED had a minor influence on the responses. These data imply that LPS mediated activation of RAW 264.7 cells can be inhibited by the addition of pharmacological doses of adrenal hormones such as DHEA.

Adjuvants, Immunologic↗

Dehydroepiandrosterone replacement in healthy men with age-related decline of DHEA-S: effects on fat distribution, insulin sensitivity and lipid metabolism.

Many animal and human studies show that supraphysiological doses of dehydroepiandrosterone (DHEA) can influence body composition and carbohydrate and lipid metabolism. Most studies have concentrated on women and have not been randomized, thus creating controversial results. With this in mind, we designed a cross-over double-blind placebo-controlled study of 12 men aged 59.0 +/- 4.8 years, who received either 50 mg/24 h DHEA or placebo for 3 months to assess the influence of DHEA on the content and distribution of fat tissue and serum insulin, glucose, total cholesterol, low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol levels, as well as testosterone, estradiol, DHEA-sulfate (S), prostate-specific antigen (PSA) concentrations and indexes of insulin sensitivity and resistance. Patients were recruited from university employees attending for periodic health checks, with normal hepatic and renal function with endogenous DHEA-S level < 1500 ng/dl. Our results did not reveal any significant changes in study parameters, apart from a statistically significant increase in DHEA-S levels after therapy with active substance.

Adipose Tissue↗

Low serum levels of DHEAS in untreated polymyalgia rheumatica/giant cell arteritis.

OBJECTIVE: To address a controversy regarding the existence of a relative adrenal hypofunction in patients with untreated polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) we evaluated baseline serum levels of ACTH, cortisol, and DHEAS in a cohort of patients with recent onset PMR/GCA not previously treated with glucocorticoids, in comparison with healthy controls. Possible correlations between baseline DHEAS levels and laboratory measures of disease activity were also explored. METHODS: Basal serum levels of these hormones were prospectively investigated in 25 patients with active untreated disease and compared with those of 25 age- and sex-matched control subjects. RESULTS: Of the 25 patients, 19 had isolated PMR and 6 had biopsy-proven GCA + PMR. Basal levels of cortisol and ACTH in PMR/GCA patients did not differ from control subjects; in relation to inflammatory status, lower than expected basal production of cortisol was observed in active untreated PMR/GCA. Baseline serum DHEAS levels were significantly lower in all patients compared with controls. In these patients, a significant correlation was found between baseline DHEAS values and laboratory measures of disease activity. The percentage of DHEAS reduction and the severity of inflammatory response were higher in women than in men. CONCLUSION: Patients with PMR/GCA with new-onset active disease before steroid treatment have inappropriately normal cortisol levels regarding the ongoing inflammation, and significantly lower levels of DHEAS compared to the age- and sex-matched healthy control subjects. These data support the existence of a relative adrenal hypofunction in PMR and GCA.

Adrenocorticotropic Hormone↗

Plasma levels of estradiol, testosterone, and DHEAS do not predict risk of coronary artery disease in men.

Prior studies have reported men with coronary artery disease (CAD) to have elevated plasma levels of estrogens and reduced concentrations of dehydroepiandrosterone (DHEA) or DHEA-sulfate (DHEAS). We investigated whether gonadal steroids or DHEAS are risk factors for CAD in men, using a prospective design, in a well characterized population studied at regular intervals. We studied 46 men (Cardiac group) who developed CAD and 124 men (Control group) who remained free of CAD (mean follow-up, 9.5 years). We measured testosterone (T), estradiol (E2), and DHEAS, as well as plasma binding of T and E2, in samples stored before the onset of CAD (Cardiac group) or at matched times (Control group). Body mass index, blood pressure, and total serum cholesterol were measured at each visit. Both systolic blood pressure (SBP; P less than 0.001) and cholesterol (P less than 0.001) were increased in the Cardiac group, but no significant differences were found in total or free T or E2, the ratio of E2/T, or DHEAS between the two groups. The difference in cholesterol was significant only in men less than or equal to 65 years old (P less than 0.001), and SBP only in men greater than 65 years old (P less than 0.005). Cholesterol (P less than 0.05) and E2 (P less than 0.001) appeared to decrease with age in the Cardiac, but not the Control, group. Moreover, total (P less than 0.01) and free E2 (P less than 0.05) were lower only in Cardiac men less than or equal to 55 years old.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effects of dehydroepiandrosterone-sulphate (DHEA-S) administration on puerperal lactation and maternal prolactin and estradiol levels.

Effects of dehydroepiandrosterone-sulphate (DHEA-S) on puerperal lactation and maternal serum prolactin and estradiol levels were examined in 111 cases of normal vaginal delivery without any complication. The amount of lactation in the DHEA-S administrated group was significantly decreased on the second day of the puerperium (p less than 0.05). No significant difference could be found after the third day of the puerperium, or in the total amount of lactation up to the seventh day of the puerperium. There was also no significant difference in the changes in neonatal body weight. No significant change was observed in maternal serum prolactin levels following DHEA-S administration. But the maternal serum estradiol levels were significantly higher at 0, 6, 12, 24 and 36 hours after delivery following the administration of DHEA-S (p less than 0.05 approximately 0.005). These facts suggested that the transient inhibition of lactation by DHEA-S may be caused by the effect on mammary glands of estrogens which were converted from DHEA-S in the placenta.

Dehydroepiandrosterone↗

DHEA: a hormone with multiple effects.

Dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEAS) represent the major androgens secreted by the adrenal gland. Various functions including metabolic, immune, and cognitive effects have been attributed to this steroid and are reviewed here. Since the levels of DHEA correlate with general good health, and aging is associated with a decline in the secretion of this steroid, a growing interest in replacement of DHEA in elderly people has developed. The findings from recent studies of replacement of DHEA in elderly people are discussed.

Aged↗

[DHEA: another hormonal modulator of bone blood flow in rats].

Dehydroepiandrosterone (DHEA) is a steroid with important effects on the bone tissue. We tried to check up if it influenced also the bone blood flow (similarly as estradiol and testosterone). We administered DHEA (Sigma) dissolved in dimethylsulphoxide s.c. three times weekly for four weeks in the doses of 15-20 mg per rat on 125 mg/kg body weight to female rats--sham-operated or oophorectomized (OOX). In two experiments (A and B) we ascertained the uptake of 85Sr-microspheres, local blood flow, cardiac output, density and ash weight of the burned tibia, in the third experiment (C) 24 hour incorporation of 45Ca and 3H-proline into the bone. The 85Sr-microsphere uptake in the tibia was elevated after OOX in both experiments A and B; this increase was inhibited completely (and statistically significantly versus the OOX group) by the administration of DHEA. Similar and also significant reactions were found in the microsphere uptake values in the distal end of femur. No significant changes could be demonstrated in the diaphysis of femur and calvaria as well as in the cardiac output, output, blood pressure and heart rate. The incorporation of 45Ca and 3H-proline into the tibia (experiment C) was significantly increased after OOX. The administration of DHEA inhibited this increase significantly in the values of 3H-proline. The density of tibia in both experiments A and B and ash weight of tibia in experiment A, suppressed after OOX, were significantly increased after the administration of DHEA to OOX females. The results show that also DHEA--in the experimental conditions used--has similar effect on the bone blood flow as estradiol and testosterone.

Animals↗

Dehydroepiandrosterone sulfate (DHEA-S) and psychiatric and laboratory measures of frailty in a residential care population.

Previous reports have found low levels of dehydroepiandrosterone sulfate (DHEA-S) in association with frailty in elderly patients. The mechanisms underlying these associations are not known. Therefore, psychiatric symptoms and disorders that are common in frail elderly patients were correlated with DHEA-S levels in a convenience sample selected from a nursing home population. Low DHEA-S levels were associated with high degrees of self-rated disability and insomnia. In women, low DHEA-S levels were also associated with increased numbers of pain sites. However, cognitive impairment was associated with higher DHEA-S levels in women. Thus, in frail elderly patients, there are contradictory relationships between DHEA-S and neuropsychiatric measures of frailty (cognitive impairment, disability, insomnia, and number of pain sites), and there may also be gender differences in these relationships.

Age Factors↗