There is no evidence that DHEA  improves quality of life but there is some evidence that it is associated with and rogenic side effects .
There is uncertainty whether DHEA decreases menopausal symptoms , but DHEA may slightly improve sexual function compared with placebo
BACKGROUND During menopause a decreasing ovarian follicular response generally causes a fluctuation and eventual decrease in estrogen levels .
This can lead to the development of various perimenopausal and postmenopausal symptoms ( for example hot flushes , night sweats , vaginal dryness ) .
Dehydroepi and rosterone ( DHEA ) is one of the main precursors of and rogens , which in turn are converted to testosterone and estrogens .
It is possible that the administration of DHEA may increase estrogen and testosterone levels in peri- and postmenopausal women to alleviate their symptoms and improve general wellbeing and sexual function ( for example libido , dyspareunia , satisfaction ) .
Treatment with DHEA is controversial as there is uncertainty about its effectiveness and safety .
This review should clearly outline the evidence for DHEA in the treatment of menopausal symptoms and evaluate its effectiveness and safety by combining the results of r and omised controlled trials .
OBJECTIVES To assess the effectiveness and safety of administering DHEA to women with menopausal symptoms in the peri- or postmenopausal phase .
Endocrine, neuroendocrine and behavioral effects of oral dehydroepiandrosterone sulfate supplementation in postmenopausal women.
Aging in women and men is characterized by a progressive decline of circulating dehydroepi and rosterone ( DHEA ) levels and its sulfate ester ( DHEAS ) . The improvement of wellbeing described in postmenopausal women treated with DHEA  suggests that this steroid may exert specific actions on the central nervous system ( CNS ) . The postmenopausal period is associated with several neuroendocrine modifications . The decrease of circulating levels of beta-endorphin is considered a hormonal marker of those changes . The aim of the present study was to investigate neuroendocrine and behavioral effects of three months of DHEAS supplementation in postmenopausal women . Postmenopausal women ( n = 22 ) were divided in three groups : the first group was treated with oral DHEAS ( n = 8) ( 50 mg/day ) , the second treated with the same dose of oral DHEAS + transdermal estradiol ( n = 8) ( DHEAS ) 50 mg/day , estradiol 50 micrograms/patch ) and the third with transdermal estradiol alone ( n = 6 ) ( 50 micrograms/day ) . Before and after 1 , 2 and 3 months of therapy , the following circulating steroid and protein hormone levels were evaluated : DHEA , DHEAS , and rostenedione , testosterone , estrone , estradiol , 17-hydroxyprogesterone , sex hormone-binding globulin ( SHBG ) , follicle-stimulating hormone ( FSH ) , luteinizing hormone ( LH ) , beta-endorphin , growth hormone ( GH ) and cortisol , and a Kupperman score was performed . Before and after treatments , plasma beta-endorphin levels were evaluated in response to three neuroendocrine tests : ( a ) clonidine , an alpha 2-presynaptic adrenergic agonist ( 1.25 mg i.v . ) ( b ) naloxone , an opioid receptor antagonist ( 4 mg i.v . ) and ( c ) fluoxetine , a serotonin selective reuptake inhibitor ( 30 mg p.o . ) . In both groups of women treated with  DHEAS  , mean basal serum DHEA , DHEAS , and rostenedione , and testosterone levels significantly increased after treatment , while no changes were shown in the group receiving estradiol alone . Serum estradiol , estrone , GH and plasma beta-endorphin levels significantly increased progressively for the three months of treatment , with higher levels for estrone and estradiol in subjects receiving estradiol alone or plus DHEAS . Serum SHBG , cortisol , and 17-hydroxyprogesterone did not show significant variations under any treatment . Serum LH and FSH levels showed a significant decrease in groups treated with estradiol alone or plus DHEAS at the second and third months . The Kupperman score showed that all treatments were associated with similar and progressive improvement . Before therapy clonidine , naloxone and fluoxetine stimuli failed to modify circulating beta-endorphin levels . After each of the treatments , the beta-endorphin response was completely restored and was similar , independent of the kind of therapy . Restoration of the beta-endorphin response to specific stimuli suggests that DHEAS and /or its active metabolites modulates the neuroendocrine control of pituitary beta-endorphin secretion , which may support the therapeutic efficacy of the DHEAS on behavioral symptoms
There is no evidence that DHEA  improves quality of life but there is some evidence that it is associated with and rogenic side effects .
There is uncertainty whether DHEA decreases menopausal symptoms , but DHEA may slightly improve sexual function compared with placebo
BACKGROUND During menopause a decreasing ovarian follicular response generally causes a fluctuation and eventual decrease in estrogen levels .
This can lead to the development of various perimenopausal and postmenopausal symptoms ( for example hot flushes , night sweats , vaginal dryness ) .
Dehydroepi and rosterone ( DHEA ) is one of the main precursors of and rogens , which in turn are converted to testosterone and estrogens .
It is possible that the administration of DHEA may increase estrogen and testosterone levels in peri- and postmenopausal women to alleviate their symptoms and improve general wellbeing and sexual function ( for example libido , dyspareunia , satisfaction ) .
Treatment with DHEA is controversial as there is uncertainty about its effectiveness and safety .
This review should clearly outline the evidence for DHEA in the treatment of menopausal symptoms and evaluate its effectiveness and safety by combining the results of r and omised controlled trials .
OBJECTIVES To assess the effectiveness and safety of administering DHEA to women with menopausal symptoms in the peri- or postmenopausal phase .