Antidepressant-induced Sexual Dysfunction Research Articles

Antidepressant-Induced Sexual Dysfunction: an Updated Review

Antidepressant-induced sexual dysfunction (ADISD) is a common problem and is associated with a significant risk of nonadherence. Serotonergic antidepressants are associated with a substantial risk of ADISD. Bupropion, transdermal selegiline, nefazodone, and moclobemide are associated with a lower risk of ADISD, and early data suggests that this may also be true for vilazodone. Only 10 % of patients show spontaneous improvement in ADISD on waiting and watching. This strategy should be reserved for patients earlier in the course of the adverse effect. When possible, switching to an antidepressant with a lower incidence of ADISD is a recommended strategy. When continuation of the offending antidepressant is essential, addition of an antidote may be tried. While early data were not encouraging, two large randomized, controlled trials have provided strong evidence supporting the use of bupropion as an antidote for ADISD. Phosphodiesterase-5 inhibitors like sildenafil and tadalafil have been shown to be efficacious in a substantial proportion of patients. Attention to ADISD is very important given that it is an important cause of nonadherence to antidepressants.

Psychotropic-induced sexual dysfunction

Psychotropic-induced sexual dysfunction is a common and bothersome side effect of psychotropic medications. The majority of information available on the subject primarily pertains to antidepressants, but antipsychotics can also cause significant sexual dysfunction. The mechanisms behind these adverse events are thought to be primarily due to antidepressants' effects on serotonin and to antipsychotics' anti-dopaminergic activity. Sexual dysfunction can have many causes, not just psychotropic medication, therefore this article aims to examine the etiology of sexual dysfunction, as well as discuss differential diagnoses. Treatment for psychotropic-induced sexual dysfunction will be discussed, with more data available for the treatment of antidepressant-induced sexual dysfunction. The paucity of data for antipsychotic-induced sexual dysfunction does make it more difficult to treat.

Antidepressant-induced sexual dysfunction in men

Most of the available antidepressant medications, including tricyclic antidepressants, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, and dual noradrenergic/serotonergic reuptake inhibitors have been reported to be associated with sexual dysfunction in both sexes. This manuscript reviews evidence concerning the relative incidence of treatment emergent sexual dysfunction in men being treated with antidepressant drugs. Both double-blind controlled trials and large clinical series report a high incidence of sexual dysfunction, especially ejaculatory delay, with serotonergic drugs. The incidence of sexual dysfunction in men appears to be much lower with drugs whose primary mechanism of action involves adrenergic or dopaminergic systems.

Reports of Sexual Disorders Related to Serotonin Reuptake Inhibitors in the French Pharmacovigilance Database: An Example of Underreporting

Depressive disorders and use of antidepressants are associated with adverse effects on sexual function. In pharmacoepidemiological studies, sexual disorders are reported by more than 50% of patients taking serotonin reuptake inhibitors (SRIs). The aim of this study was to determine the reporting rate of sexual disorders in association with SRIs, and to investigate the association between reported cases and the use of SRIs. All cases of adverse drug reactions (ADRs) involving sexual disorders, spontaneously reported to the French Pharmacovigilance Database from 1 January 1985 to December 2009, were reviewed. Cases of sexual disorders in SRI users were described. We calculated the rate of reported sexual disorders as a percentage of the total ADRs reported for each drug. The association between reported cases and the use of SRIs was assessed using reporting odds ratios (ROR) with 95% confidence intervals (CIs). A total of 11,863 ADRs in association with SRIs were collected, of which 98 (0.83%) were spontaneous reports of sexual disorders. Subjects were, on average, 45.0±10.6 years of age and mainly male. Sexual disorders were associated with the use of SRI antidepressants (ROR 4.47; 95% CI 3.61-5.53), milnacipran (ROR 11.72; 95% CI 5.79-23.72), fluvoxamine (ROR 6.91; 95% CI 3.79-12.58), paroxetine (ROR 5.54; 95% CI 3.92-7.83), venlafaxine (ROR 3.50; 95% CI 1.93-6.36), fluoxetine (ROR 3.46; 95% CI 2.26-5.29), citalopram (ROR 2.69; 95% CI 1.28-5.67) and sertraline (ROR 2.49; 95% CI 1.03-6.01). It is likely that there are instances of underreporting, particularly for ADRs that are embarrassing to talk about spontaneously. Despite the likely underreporting of this well-described adverse effect, this case/non-case study performed in a large national pharmacovigilance database confirms the existence of the risk of sexual disorders associated with SRIs, and is an example of the lack of sensitivity of spontaneous notification to measure ADRs. Minimization of antidepressant-induced sexual dysfunction could be an important factor to avoid unsuccessful treatment. Physicians should advise their patients on the possible sexual adverse effects.

Strategies for managing sexual dysfunction induced by antidepressant medication

Sexual dysfunction (including altered sexual desire, orgasmic and ejaculatory dysfunction, erectile and other problems) is a relatively common side effect of antidepressant medication. These sexual side effects may compromise a person's lifestyle and result in a lack of compliance with the prescribed antidepressant to the detriment of the person's mental health. A wide range of management strategies are possible to address this problem, including behavioural, psychological and pharmacological approaches. 1. To determine the effectiveness of management strategies for sexual dysfunction caused by antidepressants.2. To determine the adverse effects and acceptability of the different management strategies. We searched the Cochrane Depression, Anxiety and Neurosis Group's Specialized Register (CCDANCTR, to 1 January 2013), which includes relevant randomised controlled trials from the following bibliographic databases: The Cochrane Library (all years), EMBASE (1974 to date), MEDLINE (1950 to date) and PsycINFO (1967 to date). Additional searches were carried out by the author team on the same biomedical databases (using terms for 'sexual dysfunction' only) together with CINAHL (1982 to Jan 2012). The reference lists of reports of all included studies were screened. We included randomised controlled trials that compared management strategies for antidepressant-induced sexual dysfunction versus placebo or any alternative strategy. Two authors independently extracted data and assessed trial quality. Study authors were contacted for additional information. We included 23 trials involving 1886 people in this updated review. Twenty-two of these trials investigated the addition of medication to treat the identified dysfunction, with most agents studied in only single studies. One study investigated switching to an alternative antidepressant.In men, data for the phosphodiesterase inhibitors sildenafil (three studies, 255 participants) and tadalafil (one study, 54 participants) indicated they led to a greater improvement in erectile function than placebo. Combined data from three sildenafil studies found benefit over placebo on International Index of Erectile Function ratings of ability to achieve (MD 1.04, 95% CI 0.65 to 1.44), and maintain erections (MD 1.18, 95% CI 0.78 to 1.59). A single point improvement on these ratings is equivalent to an improvement in frequency from 'sometimes' to 'most times'. Men receiving tadalafil were more likely to report improved erectile function (RR 11.50, 95% CI 3.03 to 43.67). For women it remains uncertain whether sildenafil is more effective than placebo. Unpublished data could reduce this uncertainty.Data from three studies in men and women of bupropion 150 mg twice daily indicate a benefit over placebo on rating scale scores (SMD 1.60, 95% CI 1.40 to 1.81), but response rates in two studies of bupropion 150 mg once daily demonstrated no statistically significant difference in effect (RR 0.62, 95% CI 0.09 to 4.41).Other augmentation strategies failed to demonstrate significant improvements in sexual dysfunction compared with placebo.One trial involving 75 people with sexual dysfunction due to sertraline assessed the effect of changing antidepressant. Switching to nefazodone was significantly less likely to result in the re-emergence of sexual dysfunction than restarting sertraline (RR 0.34, 95% CI 0.19 to 0.60), however, nefazodone is no longer available for clinical use.There is an absence of randomised trials assessing the effects of switching to currently-available antidepressant agents with lower rates of adverse sexual effects, the role of psychological or mechanical interventions, or of techniques such as drug holidays.We identified no data for any of the strategies included in the trials assessed that indicated that they led to a worsening of psychiatric symptoms. However, the relatively small numbers assessed for many of the interventions studied means that the possibility of such an effect cannot confidently be excluded in all cases.Given the small numbers of studies assessing most of the strategies assessed, the presence of any unpublished trials could have substantial effects on estimates of effect. In some cases, only results from particular items or subscales within ratings scales are available. It is likely that this could act to bias estimates of effect obtained, increasing apparent effectiveness. The evidence currently available is rather limited. For men with antidepressant-induced erectile dysfunction, the addition of sildenafil or tadalafil appears to be an effective strategy. For women with antidepressant-induced sexual dysfunction the addition of bupropion at higher doses appears to be the most promising approach studied so far.

5‐HT2A Receptor ‐1438 G/A Polymorphism and Serotonergic Antidepressant‐Induced Sexual Dysfunction in Male Patients with Major Depressive Disorder: A Prospective Exploratory Study

To date, few studies have specifically investigated the genetic determinants of antidepressant-induced sexual dysfunction (SD). The aim of this prospective study was to examine whether the 5-HT2A receptor -1438 G/A polymorphism has functional consequences on sexual well-being in young adult men presenting with their first episode of major depressive disorder (MDD) after serotonergic antidepressant treatment. Between May 2010 and June 2011, a total of 56 drug-naïve patients presenting with their first episode of MDD were recruited from a psychiatric hospital and received either a selective serotonin reuptake inhibitor or venlafaxine monotherapy; the patients were then genotyped. Over the course of antidepressant treatment, the population was divided into a SD group (N=16) and a non-SD group (N=29) based on the Arizona Sexual Experience Scale (ASEX). Participants who did not achieve a significant improvement, as assessed by the Hamilton Depression Rating Scale (HAMD-17), were excluded from the final data analysis. The primary outcome measures were the differences in the genotype distribution and allele frequencies between groups. In the SD group, the AA genotype was significantly overrepresented (P=0.004), and the mean baseline HAMD-17 score, the mean baseline ASEX score, and the mean end-point ASEX score were significantly higher than those in the non-SD group (P=0.026, P=0.004, and P<0.001, respectively). The mean end-point HAMD-17 score (P=0.115) did not differ significantly between the two groups. These results suggest that the AA genotype may be a genetic trait offering an opportunity to strengthen early detection of serotonergic antidepressant-induced SD in young adult male patients with MDD, whereas the G allele is protective against SD in this population.

Factors influencing fluoxetine-induced sexual dysfunction in female rats

Treatment with selective serotonin reuptake inhibitors, such as fluoxetine, produces sexual side effects with low sexual desire being the most prevalent effect in females. In few studies have preclinical models for such antidepressant-induced sexual dysfunction been fruitful. In the current manuscript, the effects of fluoxetine on multiple measures of female sexual motivation and sexual receptivity were examined. Ovariectomized, Fischer rats were primed with 10μg estradiol benzoate and 500μg progesterone. Partner preference, active investigation of the male, and measures of sexual behavior were examined after injection with 15mg/kg fluoxetine. Factors (pretesting for sexual behavior, size of the test arena, non-contact time with a male) that differ among experiments designed to study antidepressant-induced female rat sexual dysfunction were studied.The male preference ratio was not affected by fluoxetine treatment but active investigation of the male was reduced; lordosis behavior was inhibited and pretesting for sexual receptivity amplified fluoxetine's inhibition; size of the testing arena or non-contact experience with the male had no effect. Regardless of test condition, when given the opportunity to escape from the male, fluoxetine-treated females displayed escape behavior. Measures of male preference and active investigation, but not lordosis behavior, appeared to be affected by fluoxetine's impact on activity. The collective data provided a behavioral profile of fluoxetine-induced sexual dysfunction. These findings reinforce the value of multiple measures when attempting to model antidepressant-induced female sexual dysfunction.

Agomelatine: a review for general practitioners

AbstractAgomelatine is a novel melatonergic antidepressant that restores disrupted biological rhythms, essentially by resetting the circadian clock. Two different, non-monoaminergic, and possibly synergistic pathways, appear to be involved in its mechanism of action. Agomelatine is a melatonin 1 (MT1) and melatonin 2 (MT2) receptor agonist and serotonin (5-hydroxytryptamine) 2C (5-HT2C) receptor antagonist. It is effective in treating moderate-to-severe depression, alleviating the symptoms of anxiety, and restoring the disrupted sleep patterns that often result from this potentially devastating disease. Agomelatine is generally well tolerated with little, if any, propensity for antidepressant-induced sexual dysfunction, weight gain, or discontinuation reactions. However, it has the potential to cause temporary hepatotoxicity, and liver functions need to be monitored as a result. Clinically, meaningful drug interactions are unlikely, with the exception of co-administered potent cytochrome P 1A2 (CYP1A2) en...

SAMe and sexual functioning

BackgroundSexual dysfunction is a known side effect of antidepressant treatment (ADT), affecting up to 58–73% of those who receive ADT, potentially affecting antidepressant adherence. Consequently, it is vital to develop novel treatments that target antidepressant-induced sexual dysfunction. MethodsWe examined whether adjunctive S-adenosyl-l-methionine (SAMe) is associated with greater improvement in sexual functioning than adjunctive placebo by measuring changes in sexual functioning using the Massachusetts General Hospital–Sexual Functioning Questionnaire (MGH-SFQ) during a 6-week, single-center, randomized, double-blind trial of SAMe augmentation for SSRI/SNRI- nonresponders. ResultsControlling for the degree of arousal dysfunction at baseline as well as the degree of change in HDRS-17 scale scores during the course of the study, men treated with adjunctive SAMe demonstrated significantly lower arousal dysfunction at endpoint than those treated with adjunctive placebo. In addition, controlling for the degree of erectile dysfunction at baseline as well as the degree of change in HDRS-17 scale scores, men treated with adjunctive SAMe demonstrated significantly lower erectile dysfunction at endpoint than those treated with adjunctive placebo. ConclusionsIn the present study, we have observed that adjunctive SAMe can have positive benefit on male arousal and erectile dysfunction, independent of improvement in depressive symptoms. These findings are preliminary, and warrant replication. Clinical trials.gov identifierNCT00093847; titled ‘Optimizing the Effectiveness of Selective Serotonin Reuptake Inhibitors (SSRIs) in Treatment-Resistant Depression’, accessible at: http://clinicaltrials.gov/ct2/show/NCT00093847.

Agomelatine in the Treatment of Major Depressive Disorder

To demonstrate the clinical effectiveness of an antidepressant drug requires evidence beyond short- and long-term efficacy, including a favourable adverse-effect profile and sustained treatment adherence. Under these conditions, patients should experience enhanced social and functional outcomes. The novel antidepressant agomelatine, a melatonergic MT(1)/MT(2) receptor agonist with serotonin 5-HT(2C) receptor antagonist activity, displays antidepressant efficacy with a favourable adverse-effect profile that is associated with good patient adherence. Specifically, agomelatine has demonstrated significant short-term (6-8 weeks) and sustained (6 months) antidepressant efficacy relative to placebo, as well as evidence of relapse prevention (up to 10 months). In head-to-head comparative studies with venlafaxine and sertraline, there was evidence of early (at 1-2 weeks) and sustained (at 6 months) advantages for agomelatine. In addition to evidence of early efficacy, agomelatine also restored disturbed sleep-wake patterns early in treatment. There was no evidence of antidepressant-induced sexual dysfunction, weight gain or discontinuation-emergent symptoms. Agomelatine has demonstrated a range of properties that suggest it could offer advantages over current treatments for major depressive disorder, although further comparative trials are still required, as is evidence from real-world clinical practice.

Antidepressant-Induced Sexual Dysfunction among Newer Antidepressants in a Naturalistic Setting

ObjectiveAntidepressants used to treat depression are frequently associated with sexual dysfunction. Sexual side effects affect the patient's quality of life and, in long-term treatment, can lead to non-compliance and relapse. However, studies covering many antidepressants with differing mechanisms of action were scarce. The present study assessed and compared the incidence of sexual dysfunction among different antidepressants in a naturalistic setting.MethodsParticipants were married patients diagnosed with depression, per DSM-IV diagnostic criteria, who had been taking antidepressants for more than 1 month. We assessed the participants via the Arizona Sexual Experiences Scale (ASEX), Beck Depression Inventory (BDI), and State-Trait Anxiety Inventory (STAI), and assessed their demographic variables, types and dosages of antidepressants, and duration of antidepressant use via their medical records.ResultsOne hundred and one patients (46 male, 55 female, age 42.2±7 years) completed the instruments. Thirteen were taking fluoxetine (mean dose 21.3±8.5 mg/day), 24 were taking paroxetine (mean dose 20.4±7.2 mg/day), 20 taking citalopram (mean dose 22.1±6.5 mg/day), 22, venlafaxine (mean dose 115.7±53.2 mg/day) and 22, mirtazapine (mean dose 18±8.7 mg/day). Mean ages, sex ratios, and BDI and STAI scores did not differ significantly across antidepressants. A substantial number of participants (46.5%, n=47) experienced sexual dysfunction. The prevalence of sexual dysfunction differed across drugs: citalopram 60% (n=12), venlafaxine 54.5% (n=12), paroxetine 54.2% (n=13), fluoxetine 46.2% (n=6), and mirtazapine 18.2% (n=4). Regression analyses revealed the significant factors for sexual dysfunction were being female, total scores on the BDI and SAI, and type of antidepressant (F=4.92, p<0.0001). Of the antidepressants, the mirtarzapine group's total ASEX score was significantly lower than the scores of the citalopram, fluoxetine, and paroxetine groups.ConclusionThe incidence of sexual dysfunction was substantially high during antidepressant treatment. The incidence of sexual dysfunction differed among antidepressants having different mechanisms of action. Our study suggests the need for clinicians to consider the impact of pharmacotherapy on patients' sexual functioning in the course of treatment with antidepressants.

CS05-02 - The involvement of dopamine in human sexuality

Studies in humans and animals have suggested that the central dopaminergic system is involved in all components of male and female sexual behavior: desire, erection, orgasm and satisfaction. Copulating activity enhances DA release in the nucleus accumbens as measured by microdialysis in male rats. This rise in DA release lasts until ejaculation and then declines during the refractory period.Dopaminergic agonists such as L-dopa, apomorphine, amantadine, bupropion, amphetamines and cocaine have been reported to arouse sexual behavior. Short term use of cocaine and other drugs that increase dopaminergic activity (Marijuana, MDMA) facilitate sexual desire and erection and delay ejaculation. These effects are reversed in chronic abuse when brain DA is depleted.Central dopaminergic blockers, like first generation antipsychotics suppress sexual functioning via the D2 receptors blockade and the corresponding elevation in plasma prolactin levels. Due to their weak antagonistic activity at D2 receptors, second generation antipsychotics are associated with fewer sexual side effects and thus provide an option in the treatment of patients with schizophrenia.Enhancement of dopaminergic activity by the addition of the DA agonists or bupropion, a norepinephrine-dopamine reuptake inhibitor, has been reported as an effective approach in the management of antidepressant-induced sexual dysfunction. The significant facilitating role of the DA system on sexual function should not be viewed independently. The dopaminergic system interacts with other systems like gonadal hormones, Nitric Oxide and serotonine in the complex neurobiology of sexual function.

Antidepressant-induced sexual dysfunction

AbstractDepression and sexual dysfunction are both common in the general population. When they co-exist they have the potential to impact negatively on each other in a bidirectional manner. Medication used to treat depression may cause additional problems with the sexual response cycle; although no drug is completely innocent, serotonergic agents such as selective serotonin reuptake inhibitors (SSRIs) and serotonin and noradrenaline reuptake inhibitors (SNRIs) are most frequently implicated in antidepressant-induced sexual dysfunction. Adherence to long-term treatment may be compromised, which may have serious consequences. Various psychological and pharmacological strategies, including the ad hoc use of sildenafil, may offer some respite.

Sildenafil as Treatment for Antidepressant-Induced Sexual Dysfunction—Reply

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Sildenafil as Treatment for Antidepressant-Induced Sexual Dysfunction

Sildenafil as Treatment for Antidepressant-Induced Sexual Dysfunction

Sildenafil as Treatment for Antidepressant-Induced Sexual Dysfunction

Sildenafil as Treatment for Antidepressant-Induced Sexual Dysfunction

Viagra for Women?: Drug May Help Women with Sexual Side Effects of Antidepressants

Antidepressant-induced sexual dysfunction adversely affects the quality of life of antidepressant users and reduces compliance with treatment. Animal models provide an instructive approach for examining potential sexual side effects of novel drugs. This review discusses the stability and reproducibility of our standardized test procedure that assesses the acute, subchronic and chronic effects of psychoactive compounds in a 30 minute mating test. In addition, we present an overview of the effects of several different (putative) antidepressants on male rat sexual behavior, as tested in our standardized test procedure. By comparing the effects of these mechanistically distinct antidepressants (paroxetine, venlafaxine, bupropion, buspirone, DOV 216,303 and S32006), this review discusses the putative mechanism underlying sexual side effects of antidepressants and their normalization.This review shows that sexual behavior is mainly inhibited by antidepressants that increase serotonin neurotransmission via blockade of serotonin transporters, while those that mainly increase the levels of dopamine and noradrenaline are devoid of sexual side effects. Those sexual disturbances cannot be normalized by simultaneously increasing noradrenaline neurotransmission, but are normalized by increasing both noradrenaline and dopamine neurotransmission. Therefore, it is hypothesized that the sexual side effects of selective serotonin reuptake inhibitors may be mediated by their inhibitory effects on dopamine signaling in sex brain circuits. Clinical development of novel antidepressants should therefore focus on compounds that simultaneously increase both serotonin and dopamine signaling.

Combining Mirtazapine and Duloxetine in Treatment-Resistant Depression Improves Outcomes and Sexual Function

To the Editors:One frequently underestimated reason for antidepressant drug discontinuation is sexual dysfunction. Although 50% of untreated depressed patients report difficulties with sexual function,1 antidepressant-induced sexual dysfunction has been reported in up to 70% of patients treated with

A novel approach for predicting antidepressant-induced sexual dysfunction in rats

Sexual dysfunction is associated with antidepressant discontinuation. Therefore, there is a need for models that predict antidepressant-induced sexual dysfunction. To develop a predictive method for evaluating antidepressant-induced sexual dysfunction. Male Sprague-Dawley rats were allowed access to sexually receptive females during a single overnight mating session and then treated with antidepressants known to produce differing levels of sexual dysfunction in the clinic. Two to three weeks later, following either acute, subchronic (7-day), or chronic (14-day) antidepressant treatment, rats were observed for penile erections (PE) in the presence of sexually receptive females that were not accessible for contact but served as visual, auditory, and olfactory stimuli in the testing area. Chronic treatment of fluoxetine (10 mg/kg), desipramine (10 mg/kg), and bupropion (20 mg/kg) reduced the number of PE 71, 53, and 8%, respectively, relative to vehicle-treated rats. This rank order of the compounds' propensity for reducing PE is comparable to the rank order of the compounds' ability to produce sexual dysfunction during antidepressant treatment in the clinic. Additionally, drugs used to treat antidepressant-induced sexual dysfunction in the clinic, such as sildenafil, yohimbine, and dopamine agonists, were also effective in attenuating the deficits in the number of noncontact PE produced by chronic fluoxetine treatment. Taken together, this model represents a novel approach for predicting antidepressant-induced sexual dysfunction in rats, which parallels the pattern of reports of sexual dysfunction in the clinic associated with different antidepressant treatments and the ability of adjunct treatment to reverse the sexual impairments produced by antidepressants.

A Review of the Assessment of Antidepressant-Induced Sexual Dysfunction used In Randomized, Controlled Clinical Trials

Sexual dysfunction is a well-known side effect of many antidepressants. Obtaining accurate data on sexual dysfunction from clinical trials is difficult because of methodological problems. This paper reviews the assessment and reporting of sexual dysfunction in clinical trials. 79 randomized double-blind studies comparing efficacy and tolerability of new antidepressants in major depressive disorder were included. Papers were searched for the methodology of adverse event assessment and for any information on treatment-emergent sexual dysfunction. 74.7% of the reviewed studies relied on spontaneous reports, 17.7% on non-specific side-effect checklists and only 7.6% on specific assessment instruments. 31.6% of the reviewed studies reported sexual dysfunction as a side effect of antidepressant treatment. Detailed information on the kind of sexual dysfunction based on DSM-IV terminology was provided by only 10.1% of the papers. More recent studies published in 2000 or later reported sexual dysfunction more often (48.6%) than studies published before the year 2000 (18.2%). The specific assessment of sexual dysfunction should be adopted as a part of the safety and tolerability assessment in clinical trials. Future research is needed to elaborate the advantages and disadvantages of the available instruments for the assessment of sexual dysfunction.