SEARCH · PubMed Health

Results for “DHEAS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources

PubMed1981

Serum levels of DHEAS in gynecologic endocrinopathy and infertility.

Serum dehydroepiandrosterone sulfate (DHEAS) was measured in 32 infertility patients who were found to be ovulatory, in 37 women with oligomenorrhea, and in 52 hirsute patients under basal conditions. It was also measured in conjunction with adrenocorticotropic hormone (ACTH) stimulation and dexamethasone suppression in 10 of the hirsute women. Serum DHEAS levels were elevated in only 19% of the infertile women with regular ovulation, in 34% of the oligomenorrheic patients, and in 60% of the hirsute women. Of the C-19 steroids (androgens) measured in the 52 hirsute women, ie, total and unbound serum testosterone (T), androstenedione (A), and DHEAS, unbound serum T was most frequently elevated. Eighty-two percent of the hirsute women had either an elevated serum DHEAS level or an increased unbound T level, suggesting 1) that elevations in unbound serum T may be associated with or result from increased serum DHEAS levels and 2) that only a minority of women with so-called idiopathic hirsutism do not have demonstrable androgen excess. Three of 10 hirsute women with elevated serum DHEAS levels had an increased ACTH-induced rise in DHEAS. Dexamethasone given as a single daily dose of 0.5 mg at bedtime resulted in a marked decrease in serum DHEAS in all of the 10 hirsute patients tested within 2 weeks of therapy. Thus, serum DHEAS is a clinically useful indication of adrenal C-19 steroid secretion. When combined with clinical and other hormonal evaluations, its measurement adds an important dimension to the study of gynecologic endocrinology and infertility.

17-Ketosteroids↗

PubMed2006

Rapid column-switching liquid chromatography/mass spectrometric assay for DHEA-sulfate in the plasma of patients with Alzheimer's disease.

A simple and highly sensitive method for the quantification of dehydroepiandrosterone-3-sulfate (DHEAS) in human plasma was developed. DHEAS was directly determined in plasma using column-switching liquid chromatography/mass spectrometry (LC-MS). The plasma was filtered with a membrane filter. The filtrate was injected onto a pre-column without further sample preparation such as extraction or derivatization. The pre-column was washed with an aqueous solution to remove interference and the analyte was eluted into a reversed-phase C(18) analytical column for separation and detection using a column-switching valve. The calibration range of DHEAS was 0.01-10 micromol/L, and the linearity of the method was 0.999. The limit of detection (LOD) at a signal-to-noise (S/N) ratio of 3 was 5 nmol/L. The accuracy and precision (%CV) were less than 10% in within-day and day-to-day variations. To explore the relationship between Alzheimer's disease and the DHEAS level in human plasma, the concentrations of DHEAS in female patients with Alzheimer's disease (n = 20) and in normal female subjects (n = 20) were measured. The level of DHEAS was significantly decreased in the plasma of patients with Alzheimer's disease (p < 0.0002) compared with that in normal subjects. From the results, we concluded that our method is sufficiently sensitivity and reliability for the quantification of DHEAS in clinical samples. Plasma DHEAS concentration could be an important marker to understand the pathogenesis of Alzheimer's disease.

Aged↗

PubMed2006

Dehydroepiandrosterone sulfate (DHEA-S) and Alzheimer's dementia in older subjects.

OBJECTIVES AND METHODS: We investigated the association of serum dehydroepiandrosterone sulfate (DHEA-S) levels with dementia of Alzheimer's type (DAT) and impairment in selected cognitive domains (memory, language, attention and working memory) in 158 patients (75.5+/-6.7 years, 46 men) with first-diagnosed probable DAT and in 158 age- and sex-matched controls. As secondary goal, we evaluated whether DHEA-S baseline levels were associated with cumulative 6-year mortality. RESULTS: A negative correlation between DHEA-S levels and age was observed (R=-0.25, p<0.001). Age-stratified analysis did not show significant differences of DHEA-S levels between DAT patients and controls. No significant association was found between DHEA-S levels and impairment in selected cognitive domains. Cox regression analysis showed that baseline DHEA-S levels were not associated with cumulative 6-year mortality. CONCLUSIONS: In a sample of newly-diagnosed DAT patients, we did not find significant association between presence of DAT or impairment in cognitive domains and DHEA-S levels; baseline DHEA-S levels are not associated with cumulative mortality in patients and controls.

Age Factors↗

PubMed2002

Dehydroepiandrosterone (DHEA) metabolism in Saccharomyces cerevisiae expressing mammalian steroid hydroxylase CYP7B: Ayr1p and Fox2p display 17beta-hydroxysteroid dehydrogenase activity.

We have engineered recombinant yeast to perform stereospecific hydroxylation of dehydroepiandrosterone (DHEA). This mammalian pro-hormone promotes brain and immune function; hydroxylation at the 7alpha position by P450 CYP7B is the major pathway of metabolic activation. We have sought to activate DHEA via yeast expression of rat CYP7B enzyme. Saccharomyces cerevisiae was found to metabolize DHEA by 3beta-acetylation; this was abolished by mutation at atf2. DHEA was also toxic, blocking tryptophan (trp) uptake: prototrophic strains were DHEA-resistant. In TRP(+) atf2 strains DHEA was then converted to androstene-3beta,17beta-diol (A/enediol) by an endogenous 17beta-hydroxysteroid dehydrogenase (17betaHSD). Seven yeast polypeptides similar to human 17betaHSDs were identified: when expressed in yeast, only AYR1 (1-acyl dihydroxyacetone phosphate reductase) increased A/enediol accumulation, while the hydroxyacyl-CoA dehydrogenase Fox2p, highly homologous to human 17betaHSD4, oxidized A/enediol to DHEA. The presence of endogenous yeast enzymes metabolizing steroids may relate to fungal pathogenesis. Disruption of AYR1 eliminated reductive 17betaHSD activity, and expression of CYP7B on the combination background (atf2, ayr1, TRP(+)) permitted efficient (>98%) bioconversion of DHEA to 7alpha-hydroxyDHEA, a product of potential medical utility.

17-Hydroxysteroid Dehydrogenases↗

PubMed1996

Antioxidant activity of dioscorea and dehydroepiandrosterone (DHEA) in older humans.

Dioscorea is a yam steroid extract used in commercial steroid synthesis and consumed by people. DHEA is a steroid which declines with age, but without known activity. This study was designed to determine whether dioscorea supplementation could increase serum dehydroepiandrosterone sulfate (DHEAS) in humans and modulate lipid levels in older people. The subjects were selected volunteers aged 65-82 years. The serum DHEAS level, lipid peroxidation and lipid profile were assessed. Three weeks of dioscorea supplementation had no affect on serum DHEAS level. However DHEA intake of 85 mg/day increased serum DHEA levels 100.3%. DHEA and dioscorea significantly reduced serum lipid peroxidation, lowered serum triglycerides, phospholipid and increased HDL levels. Both DHEA and the steroid yam extract, dioscorea, have significant activities as antioxidant to modify serum lipid levels.

Aged↗

PubMed2006

Dehydroepiandrosterone sulfate (DHEAS) and risk for mortality among older Taiwanese.

PURPOSE: Studies based on Western populations showed a negative relationship between dehydroepiandrosterone sulfate (DHEAS) level and mortality, but no study examined this relationship in a non-Western country. We use data from a large, nationally representative sample (n = 963) of older Taiwanese to investigate whether serum DHEAS, predicts subsequent mortality during a 3-year period (2000 to 2003) and whether an effect remains after controlling for baseline health status. METHODS: Baseline data collection included an individual interview, physical examination, and blood sample. A logit model is used to test the relationship between DHEAS level and risk for mortality, controlling for age, sex, and smoking status. RESULTS: Results show a marginally significant inverse relationship between DHEAS level and 3-year mortality risk. Participants with low DHEAS levels (<54.5 microg/dL) have 64% greater odds of dying than those with higher DHEAS levels (p < 0.06). After adjusting for various indicators of health status in 2000, the odds ratio (OR) for low DHEAS level remains substantial (OR = 1.41), but not statistically significant. CONCLUSIONS: Although the analysis is limited by the short follow-up and small number of deaths, results are consistent with the notion that DHEAS level has a sizeable effect on mortality.

Aged↗

PubMed2005

Alterations in DHEA metabolism in schizophrenia: two-month case-control study.

OBJECTIVE: The goals of this study were to determine whether alterations in serum dehydroepiandrosterone (DHEA), its sulfated conjugate (DHEAS), androstenedione, testosterone, and progesterone concentrations occur in schizophrenia patients compared with healthy controls over two months, and their associations with psychopathology, emotional distress, and antipsychotic treatment. METHOD: Serum hormones were repeatedly determined for 21 antipsychotic-treated male DSM-IV schizophrenia patients and 14 healthy controls. Observations were at four time points: upon entry into the study, and after 2, 4 and 8 weeks. RESULTS: In schizophrenia patients compared with healthy controls serum concentration of DHEA and androstenedione found increased, but that of DHEAS decreased, while progesterone and testosterone showed normal levels. Schizophrenia patients were also characterized by elevated androstenedione/DHEAS molar ratios, and reduced DHEAS/DHEA and testosterone/androstenedione molar ratios compared with healthy controls. Concentrations and molar ratios of serum hormones did not significantly change during the study either among schizophrenia patients, or healthy controls. Among patients alterations in DHEA, DHEAS and androstenedione were associated with emotional distress, anxiety, dysphoric mood, positive and activation symptoms, serum prolactin levels, but were not related to age, antipsychotic agents, and extrapyramidal side effects. CONCLUSIONS: Alterations in DHEA metabolism in schizophrenia are attributed to the distress, anxiety, severity of symptoms, prolactin levels, and may represent a marker for impaired hormonal responses to stress. These findings should be considered when evaluating the discrepancies in DHEA studies in schizophrenia.

Adult↗

PubMed2006

DHEAS deficiency during consumption of sustained-action prescribed opioids: evidence for opioid-induced inhibition of adrenal androgen production.

UNLABELLED: Dehydroepandrosterone (DHEA)-dehydroepiandrosterone sulfate (DHEAS) deficiency often produces fatigue, depression, weakness, and sexual dysfunction, which improve during replacement therapy. DHEAS deficiency is a sensitive marker for generalized adrenal insufficiency, but it has not been related to opioid ingestion. DHEAS values were determined in 34 male and 32 female opioid-consuming outpatients aged 35-78 years, in stable health, and in 33 male and 53 female nonopioid-consuming control subjects. No subjects used anticonvulsants or corticosteriod medications, and none had malignant, collagen-vascular, or endocrine disease other than menopause or opioid-induced androgen deficiency. Adrenocorticotropic hormone (ACTH) values were measured in 94 of 152 subjects. DHEAS levels were lower in opioid consumers than in control subjects in a dose-related pattern (P < .01), were below age-specific norms in 67% of opioid consumers and 8% of controls (P < .001), and were below our laboratory's lowest detection limit (15 mug/dL) in 29% of opioid users and 1% of controls (P < .001). DHEAS values were also lower in opioid-consuming nonsmokers than in smokers (P < .05) and were unrelated to body mass index or concurrent hormonal replacement therapy. ACTH levels were normal and unrelated to opioid use. The combination of subnormal DHEAS levels in the presence of normal ACTH values in most opioid-consuming patients suggests that these low levels result from factors other than diminished adrenal ACTH stimulation. PERSPECTIVE: The study documents a dose-related DHEAS deficiency in a majority of nonhospitalized adults who are chronically consuming sustained-action oral or transdermal opioids for control of nonmalignant pain. This deficiency in these patients has not previously been recognized and is probably symptomatic. Evaluation of replacement therapy should receive high priority.

Adrenal Glands↗

PubMed2006

Differential effect of DHEA on mitogen-induced proliferation of T and B lymphocytes.

Dehydroepiandrosterone (DHEA) is the predominant steroid hormone secreted by adrenal gland, and it has been proposed in recent years that DHEA has significant effects on immune function. We investigated the effect of DHEA (1 x 10(-5) - 1 x 10(-8)M) on proliferation of human T cells and B cells and on immunoglobulin production, a representative function of B cells. High doses of DHEA (1 x 10(-5)) significantly inhibited proliferation of peripheral blood mononuclear cells (PBMCs) and T cells induced by T cell mitogens hemagglutinin (PHA) and concanavalin A (Con A). Proliferation of PBMCs induced by B cell mitogens pokeweed mitogen (PWM) was increased by 1 x 10(-7) - 1 x 10(-6)M DHEA. Proliferation of PBMCs and B cells induced by Staphylococcus aureus Cowan strain I (SAC) was not significantly changed at any concentrations of DHEA. However, a concentration of 1 x 10(-7)M DHEA tended to potentiate their proliferation. This study suggested that DHEA acted on T and B lymphocytes differentially in immune system.

Adult↗

PubMed2006

Difference in pre- and post-treatment plasma DHEA levels were significantly and positively correlated with difference in pre- and post-treatment Hamilton depression scores following successful therapy for major depression.

OBJECTIVE: Clinical studies of endogenous concentrations of dehydroepiandrosterone (DHEA) and its relation to depression are limited. This study examined whether pre- and post-treatment changes in plasma DHEA levels are correlated with pre- and post-treatment differences in Hamilton depression scores following successful antidepressant therapy for major depression with venlafaxine XR. METHOD: Thirty-four medication-free major depressive outpatients (Hamilton Rating Scale for Depression 17, HAM-D 17 score > or = 17) were treated with antidepressants. At baseline, plasma DHEA levels of all subjects were measured but only those who remitted (HAM-D 17 score < or = 7) before the end of this study had their plasma DHEA levels measured at remission-onset. Blood from subjects was drawn at 0900-1100 h. Depression severity was assessed with the HAM-D 17 scale at baseline, and on day 7, 14, 28, 56 and 84. Subjects were administered at minimum 75 mg/day venlafaxine XR until remission onset. RESULTS: Fifteen patients remitted before the end of this study. Plasma DHEA levels decreased from baseline to remission was significant (P=0.017). After controlling for age and gender, pre- and post-treatment difference in Hamilton depression scores and the pre- and post-treatment difference in DHEA concentrations were significantly correlated (P=0.044). CONCLUSION: This preliminary study provides the first clinical evidence identifying that difference in pre- and post-treatment plasma DHEA levels were significantly and positively correlated with difference in pre- and post-treatment Hamilton depression scores following successful therapy with venlafaxine XR for major depression in remitters; but non-remitters were not examined. It is not known if DHEA levels would show similar or dissimilar changes in non-remitters.

Adolescent↗

PubMed2007

Analysis of clinical symptomatology, extrapyramidal symptoms and neurocognitive dysfunction following dehydroepiandrosterone (DHEA) administration in olanzapine treated schizophrenia patients: a randomized, double-blind placebo controlled trial.

Several studies have demonstrated the effective use of dehydroepiandrosterone (DHEA) in the management of mood, however studies of its use in psychosis remain limited. The aim of this study was to investigate for the first time efficacy of DHEA augmentation with standardized antipsychotic medication (olanzapine) and to explore effects of DHEA augmentation on side-effect profiles including weight gain, glucose tolerance, aggression, quality of life and neurocognitive function. Finally, we aimed to analyze any relationship between plasma levels and clinical response to DHEA administration. Forty patients with chronic schizophrenia stabilized on olanzapine were randomized in double-blind fashion to receive either DHEA (titrated up to 150mg) or placebo augmentation for a period of 12-weeks. Blood samples were collected at baseline, mid-study and study completion. Results indicated improvement of negative symptoms (SANS scale) even when baseline scores were controlled as a covariate. Some improvement in Parkinsonism and akathisia compared to baseline was seen in patients receiving DHEA. No change in psychosis as reflected by the PANSS was noted. Patients receiving DHEA appeared to demonstrate relatively stable glucose levels compared to controls at the end of the study. An improvement in cognitive performance (most notably memory), which did not reach significance due to low sample number, was observed following DHEA administration. Results further suggest preliminary evidence of involvement of the neurosteroid system in schizophrenia pathophysiology, and confirm initial "cautious" findings identifying an agent capable of improving negative symptoms and certain features of extrapyramidal side effects.

Adolescent↗

PubMed1988

Physicochemical characterization of [3H] DHEA binding in rat liver.

Dehydroepiandrosterone (DHEA), the native clinical steroid and steroid precursor, may have a targeted physiologic role. A high affinity (Kd 2.3nM) and steroid specific [3H] DHEA binding macromolecule in male Sprague-Dawley rat hepatic cytosol suggests that DHEA may have receptor mediated physiologic action. 3[H] DHEA binding was highest in the liver followed by kidney and testis cytosols. Sulfhydryl reagents such as N-ethylmalemide and iodoacetamide inhibited the binding of [3H]DHEA by up to 60-70%. The DHEA-macromolecular complex was stable at 35 degrees C. and addition of 5mM molybdate or 0.3M KCl increased stability. Interestingly, rat liver cytosol, specific binding at 4 degrees C increased by almost 40-50% with addition of 0.1M NaSCN or 0.3M KCl. Sucrose gradient analyses showed a 7-8 S macromolecular complex in the low salt and 3-4 S complex under high salt conditions. The [3H] DHEA- macromolecular complex shows minimal temperature dependent activation in vitro at 25 degrees C as judged by binding to DNA-cellulose. The results suggest a specific high affinity macromolecule for DHEA in rat liver cytosol with unique physicochemical properties.

Animals↗

PubMed2001

Dehydroepiandrosterone (DHEA) reduces neuronal injury in a rat model of global cerebral ischemia.

INTRODUCTION: Many studies report an inverse correlation between levels of DHEA and neurological diseases. Exogenous DHEA protects hippocampal neurons against excitatory amino acid induced neurotoxicity. The purpose of this experiment is to evaluate the effect of DHEA in an animal model of transient but severe forebrain ischemia. METHODS: At thirteen days prior to induction of ischemia, male Wistar rats were implanted with various doses of DHEA-placebo, 25 mg, 50 mg or 100 mg. Forebrain ischemia was induced for 10 min using a modified four-vessel occlusion technique, with hippocampal neuronal injury assessed at 7 days post-ischemically and expressed as a percentage of total cells. RESULTS: Both normal and necrotic hippocampal CA(1) cells were counted. Percentages of hippocampal injury observed were 88+/-13% in animals treated with placebo, 84+/-8% in the 25 mg DHEA group, and 60+/-7% in the 50 mg DHEA group. Animals treated with 100 mg DHEA displayed a significant (P<0.05) reduction of hippocampal CA(1) cell injury at 60+/-7% CONCLUSION: Treatment with a high dose, but not a low or moderate dose, of DHEA implantation reduces hippocampal CA(1) neuronal injury following severe but transient forebrain ischemia.

Animals↗

PubMed2001

Reduction in DNA damage in brain and peripheral blood lymphocytes of elderly dogs after treatment with dehydroepiandrosterone (DHEA).

Steady state levels of DNA damage are substantial in vertebrate animals as a consequence of exposure to endogenous and environmental mutagens. DNA damage may contribute to organismal senescence and an increased risk for specific age-related diseases. In this study, we determined if treatment with the neuroactive adrenal steroid, dehydroepiandrosterone (DHEA), which exhibits antioxidant and anticarcinogenic properties in rodents, would reduce DNA damage in the brain and peripheral blood lymphocytes (PBLs) of elderly dogs. Elderly male dogs, physiologically equivalent to 59-69-year-old men, were randomly assigned to receive no treatment (n=9 dogs) or DHEA at 100mg/kg PO daily (n=8 dogs). Extent of DNA damage in brain cells and PBLs was measured using alkaline comet assay. The effect of DHEA treatment on the susceptibility of PBLs to H(2)O(2)-induced DNA damage was also measured. We found that elderly male dogs receiving daily DHEA treatment for 7 months had significantly less DNA damage detectable in their brain compared to age-matched control dogs. After 7 months treatment, DHEA-treated dogs also had a significant reduction in DNA damage in PBLs compared to pre-treatment levels. We also found that PBLs of dogs treated with DHEA were more resistant to H(2)O(2)-induced DNA damage than PBLs of untreated dogs. Our results did not show that basal DNA damage in PBLs was strongly correlated with DNA damage within the brain. The results of this study suggest that DHEA supplementation can significantly reduce steady state levels of DNA damage in the mammalian brain. Further evaluation of DHEA as a neuroactive agent and its effects on DNA damage and gene expression in other tissues and species is warranted.

Administration, Oral↗

PubMed2000

The effect of 7-oxo-DHEA acetate on memory in young and old C57BL/6 mice.

7-Oxo-dehydroepiandrosterone, which can be formed from dehydroepiandrosterone (DHEA) by several mammalian tissues, is more effective than its parent steroid as an inducer of thermogenic enzymes when administered to rats. Using the Morris water maze procedure, we tested DHEA and its 7-oxo-derivative for their ability to reverse the memory abolition induced by scopolamine in young C57BL/6 mice, and for their effect on memory in old mice. A single dose of 7-oxo-DHEA-acetate at 24 mg/kg b.w. completely reversed the impairment caused by 1 mg of scopolamine per kg b.w. (P < 0.001). DHEA (20 mg/kg) was also effective (P < 0.01). In old mice given the same single doses followed by feeding 0.05% of the respective steroid in the diet, memory of the water maze training was retained through a four week test period in mice receiving 7-oxo-DHEA-acetate (P < 0.05) but not in the control or DHEA-treated groups. When old mice were not tested until five weeks after being trained 7-oxo-DHEA exerted a slight, but statistically insignificant, improvement in memory retention. The possible effect of 7-oxo-DHEA in human memory problems deserves investigation.

Aging↗

PubMed1998

Dehydroepiandrosterone (DHEA) and systemic lupus erythematosus.

OBJECTIVE: This study was performed to evaluate in vivo and in vitro data on the effects of the adrenal steroid dehydroepiandrosterone (DHEA) with emphasis on its potential use in the treatment of systemic lupus erythematosus (SLE). METHODS: The literature dealing with DHEA was reviewed. RESULTS: Initially, research on DHEA focused on effects of DHEA in relation to obesity. Over the past decade, research stimulated by associations between the physiological decline in DHEA and aging, cardiovascular disease, changes in metabolism, brain function, and immune senescence have generated insight into the many effects that DHEA or its metabolites may have. In SLE a role for sex hormones in both the etiopathogenesis and disease activity is recognized. In SLE, as in aging, low DHEA levels are frequently found, especially with corticosteroid treatment. CONCLUSIONS: Research data in the elderly, on both hormonal and immunologic effects, suggest that DHEA may become an adjunctive treatment for SLE patients.

Aged↗

PubMedDate not supplied

Dehydroepiandrosterone (DHEA) and aging.

Dehydroepiandrosterone sulfate (DHEAS) is the most abundant circulating steroid hormone in humans and can readily be converted to its parent steroid DHEA by tissue sulfatases. Yet, a biologic function for these steroids has not been defined. The link between DHEA and aging has been raised by: (1) its well documented age-related decline, and (2) a preventive effect of DHEA on numerous age-related illnesses: ischemic heart-disease, cognitive impairment, immunodeficiency, malignancies, osteoporosis. These effects have been suggested by epidemiological studies in humans. Animal studies support a protective effect of DHEA on these age-related diseases. However, it remains unknown whether these results in animals can be transposed in humans, because adrenal secretion of DHEA seems to be particular to primates. In humans, only a few studies have been performed. The effects of oral supplementation with DHEA have, so far, focused on the possible metabolic effects of DHEA. A few studies have shown: the absence of any side-effects; no change in body-weight; conflicting results on body-composition and lipids and no effect on insulin-tolerance. The latest study showed a beneficial effect on well-being but these results need to be confirmed.

Journal Article↗

PubMed2006

DHEA, a neurosteroid, decreases cocaine self-administration and reinstatement of cocaine-seeking behavior in rats.

Dehydroepiandrosterone (DHEA), which can act as a potential antidepressant in both animals and humans, appears to lower distress involved with cocaine withdrawal. In fact, a role for neurosteroids in modulation of substance-seeking behavior is becoming increasingly clear. Therefore, we tested the effects of DHEA on the self-administration of cocaine (1 mg/kg/infusion) by rats. At maintenance, a relatively low dose of exogenous DHEA (2 mg/kg; i.p.) attenuated cocaine self-administration after several days of chronic treatment. More than 2 weeks (19 days) of daily DHEA injections were required to decrease the cocaine-seeking behavior of rats to less than 20% of their maintenance levels. DHEA does not seem to decrease cocaine self-administration by increasing the reinforcing properties of the drug, as indicated by a cocaine dose-response determination. After being subjected to extinction conditions in the presence of DHEA, rats demonstrated a minimal response to acute exposure to cocaine (10 mg/kg), which indicated a protective effect of DHEA on relapse to cocaine usage. Our results suggest a potential role for the neurosteroid DHEA in controlling cocaine-seeking behavior, by reducing both the desire for cocaine usage and the incidence of relapse.

Adjuvants, Immunologic↗