Monoamines and Neurosteroids in Sexual Function During Induced Hypogonadism in Healthy Men

Bloch, Miki; Rubinow, David R.; Berlin, Kate; Kevala, Karl; Kim, Hee Yong; Schmidt, Peter J.

doi:10.1001/archpsyc.63.4.450

Cited by 14 publications

(7 citation statements)

References 72 publications

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“…Indeed, androsterone levels are implicated in the reduced libido observed in this trial. In a subsample of these men in whom lumbar punctures were performed, we observed that CSF androsterone levels but not CSF measures of T or DHT correlated with the symptom of decreased sexual function (Bloch et al, 2006).…”

Section: Discussionmentioning

confidence: 61%

Pharmacologically Induced Hypogonadism and Sexual Function in Healthy Young Women and Men

Schmidt

Steinberg

Negro

et al. 2008

Neuropsychopharmacol

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Studies fail to find uniform effects of age-related or induced hypogonadism on human sexual function. We examined the effects of induced hypogonadism on sexual function in healthy men and women and attempted to identify predictors of the sexual response to induced hypogonadism or hormone addback. The study design used was a double-blind, controlled, crossover (self-as-own control). The study setting was an ambulatory care clinic in a research hospital, and the participants were 20 men (average ± SD age ¼ 28.5 ± 6.2 years) and 20 women (average ± SD age ¼ 33.5 ± 8.7 years), all healthy and with no history of psychiatric illness. A multidimensional scale assessing several domains of sexual function was the main outcome measure. Participants of the study received depot leuprolide acetate (Lupron) every 4 weeks for 3 months (men) or 5 months (women). After the first month of Lupron alone, men received (in addition to Lupron) testosterone enanthate (200 mg intramuscularly) or placebo every 2 weeks for 1 month each. Women received Lupron alone for 2 months, and then, in addition to Lupron, they received estradiol and progesterone for 5 weeks each. The results of the study: in women, hypogonadism resulted in a significant decrease in global measures of sexual functioning, principally reflecting a significant decrease in the reported quality of orgasm. In men, hypogonadism resulted in significant reductions in all measured domains of sexual function. Testosterone restored sexual functioning scores in men to those seen at baseline, whereas neither estradiol nor progesterone significantly improved the reduced sexual functioning associated with hypogonadism in women. Induced hypogonadism decreased sexual function in a similar number of men and women. No predictors of response were identified except for levels of sexual function at baseline. In conclusion, our data do not support a simple deficiency model for the role of gonadal steroids in human sexual function; moreover, while variable, the role of testosterone in sexual function in men is more apparent than that of estradiol or progesterone in women.

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Section: Discussionmentioning

confidence: 61%

Pharmacologically Induced Hypogonadism and Sexual Function in Healthy Young Women and Men

Schmidt

Steinberg

Negro

et al. 2008

Neuropsychopharmacol

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“…Androsterone is a metabolite of DHEA which potently modulates GABA(A) receptors. Owing to its GABAergic activity, androsterone induction represents a potential mechanism for DHEA's moodenhancing effects (Bloch et al, 2006). Increases in rACC activity suggest that DHEA administration may lead to increases in cognitive regulation as well as suppression of negative emotional reactivity.…”

Section: Discussionmentioning

confidence: 99%

DHEA Enhances Emotion Regulation Neurocircuits and Modulates Memory for Emotional Stimuli

Sripada

Marx

King

et al. 2013

Neuropsychopharmacol

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Dehydroepiandrosterone (DHEA) is a neurosteroid with anxiolytic, antidepressant, and antiglucocorticoid properties. It is endogenously released in response to stress, and may reduce negative affect when administered exogenously. Although there have been multiple reports of DHEA's antidepressant and anxiolytic effects, no research to date has examined the neural pathways involved. In particular, brain imaging has not been used to link neurosteroid effects to emotion neurocircuitry. To investigate the brain basis of DHEA's impact on emotion modulation, patients were administered 400 mg of DHEA (N=14) or placebo (N=15) and underwent 3T fMRI while performing the shifted-attention emotion appraisal task (SEAT), a test of emotional processing and regulation. Compared with placebo, DHEA reduced activity in the amygdala and hippocampus, enhanced connectivity between the amygdala and hippocampus, and enhanced activity in the rACC. These activation changes were associated with reduced negative affect. DHEA reduced memory accuracy for emotional stimuli, and also reduced activity in regions associated with conjunctive memory encoding. These results demonstrate that DHEA reduces activity in regions associated with generation of negative emotion and enhances activity in regions linked to regulatory processes. Considering that activity in these regions is altered in mood and anxiety disorders, our results provide initial neuroimaging evidence that DHEA may be useful as a pharmacological intervention for these conditions and invite further investigation into the brain basis of neurosteroid emotion regulatory effects.

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“…In this study, Bloch et al (2006) observed that changes in CSF levels of ADT (but not of testosterone (T) or other neurosteroids) were correlated with changes in sexual functioning, both during hypogonadism and T replacement. In rodents, DHEA treatment increases levels of allopregnanolone in both plasma as well as in the hippocampus and hypothalamus (Bernardi et al 2005).…”

Section: Introductionmentioning

confidence: 98%

“…A potential role for the neurosteroid androsterone (ADT) in the mediation of DHEA’s therapeutic effects was suggested by Bloch et al (2006) in his investigation of men in whom hypogonadism was induced with GnRH agonist. In this study, Bloch et al (2006) observed that changes in CSF levels of ADT (but not of testosterone (T) or other neurosteroids) were correlated with changes in sexual functioning, both during hypogonadism and T replacement. In rodents, DHEA treatment increases levels of allopregnanolone in both plasma as well as in the hippocampus and hypothalamus (Bernardi et al 2005).…”

Section: Introductionmentioning

confidence: 99%

DHEA metabolism to the neurosteroid androsterone: a possible mechanism of DHEA’s antidepressant action

et al. 2015

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Monoamines and Neurosteroids in Sexual Function During Induced Hypogonadism in Healthy Men

Abstract: These data suggest that the neurosteroid androsterone contributes to the regulation of sexual function in men.

Cited by 14 publications

References 72 publications

Pharmacologically Induced Hypogonadism and Sexual Function in Healthy Young Women and Men

Pharmacologically Induced Hypogonadism and Sexual Function in Healthy Young Women and Men

DHEA Enhances Emotion Regulation Neurocircuits and Modulates Memory for Emotional Stimuli

DHEA metabolism to the neurosteroid androsterone: a possible mechanism of DHEA’s antidepressant action

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