Use of paroxetine (Paxil) appears to put healthy men at greater risk of sperm DNA fragmentation, according to data from a small study.
In a study of 35 healthy male volunteers, SSRI treatment was significantly correlated with increased DNA fragmentation (odds ratio 11.12, P = 0.0003) on multivariate logistic regression, after correcting for age and body mass index.
“Healthy volunteers demonstrated a dramatic increase in DNA fragmentation within just a few weeks of paroxetine treatment, without an apparent impact on standard semen parameters. This negative impact on sperm DNA fragmentation may affect reproductive outcomes, even with [intracytoplasmic sperm injection],” study investigator Dr. Cigdem Tanrikut said in an interview.
“Certainly, one should query male patients about SSRI use. However, based on these preliminary findings, it would be premature to suggest a patient come off of SSRIs altogether or change to an alternate therapy given the lack of data regarding other newer antidepressants,” said Dr. Tanrikut, Director of Male Reproductive Medicine at Massachusetts General Hospital's Fertility Center in Boston.
Men in the study ranged in age from 18 to 65 years. Intake assessment included physical exam, semen analysis, and the Brief Sexual Function Inventory (BSFI). Repeat semen analysis was obtained before SSRI initiation.
Paroxetine was given for 5 weeks: 10 mg daily during week 1; 20 mg daily during week 2; 30 mg daily during weeks 3–4; and 20 mg daily during week 5. Semen analysis was performed at weeks 2 and 4. One month after cessation of the SSRI, a final semen analysis was then performed. The BSFI was completed at week 4 and at the final semen collection.
The unadjusted odds ratio of having abnormal DNA fragmentation while on paroxetine was 9.33. In addition, BSFI revealed significant sexual dysfunction on paroxetine as compared with baseline. Up to 35% of men noted significant changes in erectile function, and up to 47% of subjects reported ejaculatory difficulties while on paroxetine. At least partial recovery of sexual function was noted within 1 month after stopping treatment.
The study was supported by the Frederick J. and Theresa Dow Wallace Fund of the New York Community Trust and Brady Urology Foundation.