Sexual dysfunction is a liability associated with many psychotropic medications, and the full scope of this problem is only recently gaining its deserved recognition. When assessing emergence of side effects, most clinical studies rely on spontaneous reporting of adverse experiences. Because most patients do not feel comfortable reporting sexual side effects, it is not surprising that treatment-emergent sexual dysfunction is often underreported in these trials. In one prospective study, specific inquiry about sexual dysfunction with treatment of fluoxetine, paroxetine, sertraline, or fluvoxamine resulted in nearly a threefold increase in reporting of sexual problems, compared with only spontaneous communication (Montejo-Gonzalez et al. 1997).
Typically, data derived from clinical studies estimate sexual disability attributed to SRIs to be less than 20%, whereas in clinical practice the incidence appears to be significantly higher, perhaps as high as 40%. This side effect clearly has an adverse effect on medication adherence, partly because discussion of sexual issues is difficult for patients and clinicians alike. Although all SRIs and venlafaxine have been associated with male and female sexual dysfunction, there is a prevailing view among clinicians that this side effect might be more problematic with paroxetine, although few controlled data are available to address this issue. In a comparison study of 200 subjects treated with paroxetine, fluoxetine, fluvoxamine, or sertraline, paroxetine treatment was associated with higher rates of anorgasmia or difficulty with ejaculation and impotence in both men and women (Montejo-Gonzalez et al. 1997). Significant differences among the four drugs were not noted with respect to decrease in libido, delay in orgasm, or patient attitude toward treatment-induced sexual disability. In a large cross-sectional observational study (N = 6,297) conducted by Clayton et al. (2002), paroxetine was associated with the highest prevalence of overall sexual dysfunction, compared with a wide range of novel antidepressants, including mirtazapine, venlafaxine, sertraline, citalopram, fluoxetine, nefazodone, and bupropion. However, a significant difference between paroxetine and the other agents was observed with only fluoxetine, bupropion, and nefazodone. Waldinger et al. (1998) studied 51 men without depression who had premature ejaculation and noted greater delay in time to ejaculation during paroxetine treatment, compared with treatment with fluoxetine, fluvoxamine, and sertraline.
The above findings have led to the use of paroxetine and other SRIs in the treatment of premature ejaculation (PE) in men (Balon 1996). Head-to-head comparisons between paroxetine and other antidepressants in the treatment of PE currently exist only for dapoxetine and mirtazapine. Safarinejad (2006) used a measure called the Intravaginal Ejaculatory Latency Time (IELT) to test paroxetine's effectiveness in slowing down male climax versus dapoxetine, a short-acting SRI that is currently awaiting FDA approval for the treatment of PE. Male patients taking paroxetine in a randomized, double-blind fashion showed IELT increases from a mean of 31 seconds at baseline to 370 seconds with treatment, whereas subjects taking dapoxetine (38 seconds to 179 seconds) or placebo (34 seconds to 55 seconds) did not fare as well. Ejaculatory latency was likewise compared, using the IELT measure, between paroxetine and mirtazapine. In a 6-week double-blind study, treatment with paroxetine (20 mg/day), but not mirtazapine (30 mg/day), resulted in significant delays in orgasm and ejaculation in men with PE (Waldinger et al. 2003).
Sexual side effects emerge in a dose-dependent fashion and do not appear to diminish with prolonged administration. Strategies to lessen the impact of psychotropic medications on sexual function include using dosage reduction, changing to a different antidepressant with lesser sexual side-effect liability, and adding an agent, such as sildenafil, yohimbine, buspirone, cyproheptadine, amantadine, methylphenidate, or bupropion, to reverse the sexual side effects (Rosen et al. 1999). Controlled studies demonstrating the efficacy of these agents are largely lacking, with one exception. Ephedrine, an a- and ^-adrenergic agonist previously shown to enhance genital blood flow in women, was evaluated in 19 women experiencing SRI-induced sexual dysfunction from paroxetine, sertraline, or fluoxetine (Meston 2004). Although ephedrine (50 mg taken within 1 hour of sexual activity onset)
significantly improved self-reported scores of desire and orgasm intensity compared with baseline, these measures, in addition to sexual arousal and satisfaction, were also similarly enhanced by placebo.
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How to increase your staying power to extend your pleasure-and hers. There are many techniques, exercises and even devices, aids, and drugs to help you last longer in the bedroom. However, in most cases, the main reason most guys don't last long is due to what's going on in their minds, not their bodies.