Evaluation of endocrine profile and hypothalamic-pituitary-testis axis in selective serotonin reuptake inhibitor-induced male sexual dysfunction.
Abstract
PURPOSE: To evaluate endocrine profile and hypothalamic-pituitary-testis (HPT) axis in male depressed patients with selective serotonin reuptake inhibitor (SSRI)-induced sexual dysfunction (SDF).
MATERIALS AND METHODS: Eighty-six fertile depressed male patients with SSRI-induced SDF, aged 18 to 50 years, were enrolled in the study (group 1). Sixty-two age-matched depressed fertile patients who currently receive one of the SSRIs but without SDF (group 2), and 68 age-matched healthy fertile men who had never received a psychiatric diagnosis (group 3) served as controls.
Pretreatment evaluation included history and physical examination and International Index of Erectile Function. Two blood samples were drawn from each subject at 20-minute intervals for the determination of the resting levels of the following hormones: luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, prolactin, and estradiol. The HPT axis was also assessed using the gonadotropin-releasing hormone test.
RESULTS: The prevalence of hormonal abnormalities in groups 1, 2, and 3 were 83.7% (72), 51.6% (32), and 11.8% (7), respectively (P = 0.001 vs group 1 and 0.007 vs group 2). Compared with normal controls, the subjects taking SSRIs had significantly lower serum levels of LH, FSH, and testosterone. In addition, there were significantly decreased LH and FSH responses to gonadotropin-releasing hormone test in groups 1 and 2 compared with normal controls. Of patients in groups 1 and 2, 68 (79.1%) and 27 (43.5%) had elevated serum levels of prolactin (P = 0.0001 vs group 1 and 0.001 vs group 2).
CONCLUSIONS: Most depressed subjects taking SSRIs with and without SDF had diminished HPT axis function.
What are your thoughts on this study? Should those on SSRI’s come off?
My first thought is that it looks like a chicken-and-egg problem. Chronic low T leads to depression, and generally speaking it’s exactly the kind of not-too-dysfunctional blah-dysthymia depression that your average primary care doc is likely to throw an SSRI at without much further thought. How many of the guys on SSRIs in this study had low T before they got put on meds in the first place?
Yes, Docs treat the symptoms of hypogonadism with SSRIs, which is mal-practice and common.
Otherwise, SSRI’s increase E2. The SSRI competes with E2 for clearance by rate limited liver pathways. Many other meds [Rx, OTC] can do this too. Which can confound studies like the one above. Increased E2 lowers LH/FSH and T.
One should try to find alternatives to SSRI’s or get off of AD meds completely. Too many side effects.
“not-too-dysfunctional blah-dysthymia depression” what great medical terminology!
The impaired gonadotropin release is new data. More E2, increased feedback to the HPTA from E2, and gonadotropin-releasing hormone resistance. That is a double impact.
Ok, I see your guy’s points. This study only suggests a relationship but does not suggest causality. To determine if SSRI’s induce hypogonadism, the researchers should have performed baseline testosterone panel tests prior to the use of SSRI’s and compare it with post results.
What is this talk about prolactin though? What role does that play in all of this? I asked my endocrinologist if the Lexapro I was taking could have caused the low testosterone results and said that since my prolactin levels were normal, he doesn’t suspect this to be the reason.
[quote]KSman wrote:
Endo is probably clueless.[/quote]
I don’t know too much about what role prolactin plays in all of this but it is also referenced in the article I posted above. So what role does prolactin play? If my prolactin levels were normal, does that suggest my hypogonadism wasn’t triggered from the Lexapro?