Antidepressant-induced Sexual Dysfunction Research Articles

Management strategies for antidepressant-related sexual dysfunction

Antidepressant-related sexual dysfunction is one of the most frequently met adverse effects for individuals suffering from major depressive disorder. When primary prevention by non-pharmacological measures fails, empirical coping strategies might be proposed. In this article, we present a brief overview of pharmacological strategies for antidepressant-related sexual dysfunction, considering antidepressants and conceivable corrective medications. We suggest dividing these strategies into three groups: (1) tapering (dose reduction, therapeutic window or short-term treatment interruption); (2) maintenance (focusing on spontaneous remission); (3) optimizing treatment (substitution for another antidepressant or addition of treatments to correct sexual side effects). Whichever strategy is selected, we encourage the clinician to propose the most adequate therapeutic option for the patient, while considering the efficacy and overall tolerance of the current antidepressant strategy, the affected phase of sexuality and patient preferences and gender. This summary is limited to antidepressant treatments and correctors marketed in France and aimed at a clinician reading to help manage patients suffering from antidepressant-induced sexual dysfunction.

What are effective strategies for treating antidepressant-induced sexual dysfunction in women?

What are effective strategies for treating antidepressant-induced sexual dysfunction in women?

Bupropion - an antidepressant drug with broad therapeutic potential

Introduction: Bupropion is currently mainly used as an atypical antidepressant due to its psychotropic effects. In addition, it shows high potential in reducing withdrawal cravings in addicts, which is also used in the treatment of nicotinism. However, studies in recent years have shown that it may also be useful in other conditions.Aim of the study: Our aim was to review the known usage of bupropion in the fields of psychiatry, neurology and internal medicine, and to identify potential directions for further research. Methods and materials: We reviewed the literature available in the PubMed database, using the key words: "bupropion"; "depression"; "smoking cessation"; "obesity"; "ADHD".Results: Bupropion- an antidepressant drug belonging to the group of selective norepinephrine and dopamine reuptake inhibitors. Bupropion is approved by the FDA(Food and Drug Administration) for the treatment of depression, seasonal affective disorder and nicotinism. The literature shows that it is also effective in off-label indications - treatment of antidepressant-induced sexual dysfunction, attention deficit hyperactivity disorder (ADHD), depression in bipolar disorder, obesity, neuropathic pain and cancer-related fatigue syndrome.Conclusion: Due to the specific effects of bupropion, there are many more usage for the drug than the primary indications for which it is usually used. The usage of the drug described in the literature require additional studies on a larger group of patients.

Ginkgo Biloba: A Famous Living Fossil Tree and an Ancient Herbal Traditional Chinese Medicine

Background: Ginkgo (Ginkgo biloba) is a living fossil and a deciduous tree, having extracts with antidiabetic, antioxidant, anticancer, antihypertensive, immunostimulating, hepatoprotective, and antimicrobial activities, memory enhancement efficiency, and beneficial effects against neurodegenerative disease. Objective: This study aimed at evaluating the medicinal values and natural benefits of Ginkgo. Methods: This review investigated publication in MEDLINE/PubMed database and Google Scholar. The keywords used for an electronic search were Ginkgo biloba, living fossil, bioactive components, and traditional Chinese medicine. Results: The main active constituents of Ginkgo biloba are flavone glycosides such as kaempferol, quercetin, and isorhamnetin, terpene lactones, alkylphenols, proanthocyanidins, rhamnose, glucose, D-glucaric acid, ginkgolic acid, organic acids such as hydroxykinurenic, kynurenic, protocatechic, shikimic, and vanillic. Ginkgo kernels have been used as medicine or eaten as nuts in traditional medicinal science. The most notable pharmaceutical applications of Ginkgo are observed in cardiovascular disease, Alzheimer's disease, impaired cerebral performance, vascular insufficiency, antidepressant-induced sexual dysfunction, premenstrual syndrome, liver fibrosis, vascular disease, tinnitus, macular degeneration, memory, and vertigo. Conclusion: The development of modern drugs from Ginkgo by considering the importance of traditional medicinal Asian science with further research works should be emphasized.

Pharmacologic interventions for antidepressant-induced sexual dysfunction: a systematic review and network meta-analysis of trials using the Arizona sexual experience scale.

Despite the prevalence of antidepressant-related sexual side effects, comparisons of treatments for these problematic side effects are lacking. To address this, we performed a systematic review and Bayesian network meta-analysis to compare interventions for antidepressant-induced sexual dysfunction in adults. Using PubMed and clinicaltrials.gov, we identified published and unpublished prospective treatment trials from 1985 to September 2020 (primary outcome: the Arizona sexual experience scale [ASEX] score). The quality of evidence was assessed using the Grading of Recommendations Assessment, Development, and Evaluation framework. We identified 57 citations (27 randomized controlled trials, 66 treatment arms, 27 open-label trials, and 3 crossover trials) that evaluated 33 interventions (3108 patients). In the systematic review, 44% (25/57) of trials reported successful interventions; this was more common in open-label (70%, 19/27) compared to placebo-controlled studies (22%, 6/27). In the meta-analysis of placebo-controlled studies that used the ASEX (N=8), pycnogenol was superior to placebo (standardized mean difference: -1.8, 95% credible interval [CrI]: [-3.7 to 0.0]) and there was evidence that, at a 6% threshold, sildenafil improved sexual dysfunction (standardized mean difference: -1.2, 95% CrI [-2.5 to 0.1]). In the meta-analysis including single-arm studies (15 studies), treatment response was more common with sildenafil, tianeptine, maca, tiagabine, and mirtazapine compared to placebo, but these differences failed to reach statistical significance. While heterogeneity across randomized controlled trials complicates identifying the single best intervention, multiple trials suggest that sildenafil ameliorates antidepressant-induced sexual dysfunction. More randomized controlled trials are needed to examine the putative efficacy of other interventions.

Antidepressant-induced sexual dysfunction: A naturalistic study comparing sexual dysfunction among patients taking escitalopram, desvenlafaxine, and mirtazapine

Background: Antidepressant drugs are frequently associated with sexual dysfunction. Sexual side effects affect the patients' quality of life and in the long term and can lead to noncompliance and relapse. However, studies covering many antidepressants with different mechanisms of action are scarce. Aims: The aim of this study is to compare the rates of sexual dysfunction among patients taking escitalopram, desvenlafaxine, and mirtazapine. Settings and Design: Cross-sectional study. Materials and Methods: Arizona Sexual Experience Scale (ASEX), Hamilton Rating Scale for Depression (21 items), and State and Trait Anxiety Inventory. Statistical Analysis Used: Fisher's exact t-test, Chi-square test, and analysis of variance depending on the type of variable. Results: Eighty-four participants (42 males and 42 females) completed all instruments. Of these, 28 were taking escitalopram (13.93 ± 5.15), 28 were taking desvenlafaxine (76.79 ± 25.39), and 28 were taking mirtazapine (16.88 ± 3.88). A substantial number of patients (40.5%, n = 34) had sexual dysfunction. The prevalence of sexual dysfunction varied across the drugs; escitalopram (60.7%), desvenlafaxine (35.7%), and mirtazapine (25%). Regression analysis revealed that the significant factor for sexual dysfunction was the type of antidepressant used. The mirtazapine group's total ASEX score was significantly lower than the scores for escitalopram and desvenlafaxine (χ2 = 7.807, P = 0.020). Conclusion: The incidence of sexual dysfunction is substantially high during antidepressant treatment. The rates of sexual dysfunction differed among antidepressants having different mechanisms of action. Mirtazapine-induced lesser sexual dysfunction compared to desvenlafaxine and escitalopram.

PS-1-5 How to Manage Antidepressant-Induced Sexual Dysfunction

PS-1-5 How to Manage Antidepressant-Induced Sexual Dysfunction

Antidepressant‐induced sexual dysfunction

Sexual dysfunction is a frequent, potentially distressing, adverse effect of antidepressants and a leading cause of medication non-adherence. Sexual function should be actively assessed at baseline, at regular intervals during treatment, and after treatment cessation. Trials comparing the risk of sexual dysfunction with individual antidepressants are inadequate, but it is reasonable to conclude that the risk is greatest with selective serotonin reuptake inhibitors (SSRIs) and serotonin and noradrenaline reuptake inhibitors (SNRIs), less with tricyclic antidepressants (except clomipramine) and mirtazapine, and least with moclobemide, agomelatine, reboxetine and bupropion. Management of antidepressant-induced sexual dysfunction requires an individualised approach (eg, considering other causes, dose reduction, addition of medication to treat the adverse effect, switching to a different antidepressant). Post-SSRI sexual dysfunction has been recently identified as a potential, although rare, adverse effect of SSRIs and SNRIs. Consider the possibility of post-SSRI sexual dysfunction in patients in whom sexual dysfunction was absent before starting antidepressants but develops during or soon after antidepressant treatment and still persists after remission from depression and discontinuation of the drug.

Prevalence of antidepressant-induced sexual dysfunction among psychiatric outpatients attending a tertiary care hospital.

Objectives:To measure the prevalence of sexual dysfunction in psychiatric outpatients treated with fluoxetine, paroxetine, venlafaxine or mirtazapine.Methods:This is a retrospective cross-sectional study conducted in Sultan Qaboos University Hospital, Muscat, Oman. All patients above 18 years of age, attending psychiatric clinic and taking fluoxetine, paroxetiene, venlafaxine or mirtazapine for various indications were invited to participate in the study. A data collection sheet was designed to document the patients’ demographic features, psychiatric diagnosis, type, dose and duration of antidepressant treatment. Sexual side effects’ part of Toronto Side Effect Scale (TSES) was used to assess the presence of sexual dysfunction.Results:A total of 137 patients (Male: 51%, Female: 49%) were included in the study. The mean age for the participants was 38 years (range: 19-72 years). The number of patients for each antidepressant was as follows: paroxetine (52 patients), fluoxetine (36), mirtazapine (36 patients) and venlafaxine (17 patients). The average duration of the antidepressant use was 3.9 years. The overall prevalence of sexual dysfunction was 39%. Paroxetine was the most common antidepressant associated with sexual dysfunction especially for decreased libido (59.6%) and delayed ejaculation (34.4%). In contrary, mirtazapine was the lowest among antidepressants to cause sexual dysfunction.Conclusion:Sexual dysfunction is common among patients treated with antidepressants particularly selective serotonin reuptake inhibitors (SSRIs). Addressing this side effects early in treatment can improve compliance to treatment and prevent relapse.

Pycnogenol supplementation as an adjunct treatment for antidepressant-induced sexual dysfunction.

Major depressive disorder is a serious mental disorder in which treatment with antidepressant medication is associated with incidence of adverse events, such as constipation, diarrhea, dry mouth, headache, insomnia, and sexual dysfunction (SDys). Escitalopram (ESC), an effective and safe selective serotonin reuptake inhibitor with good tolerability, was used in this study. In this study, we investigated the prospective effect of Pycnogenol (PYC), an antioxidant, anti-inflammatory, and vasodilator agent, on ESC-induced SDys. This was a randomized, parallel, open-label study. Seventy-two outpatients of both genders with depression were randomized into two groups as follows: 37 patients from the ESC + PYC group took 50mg of PYC per day for 4 months in ESC co-treatment, and 35 subjects from the ESC group took ESC only. Five patients dropped out and were excluded from the analysis. The participants were examined every month (visits 1-4). ESC use led to improvement of depressive symptoms and severity scored by standardized psychiatric tests. PYC co-treatment resulted in attenuation of SDys beginning at 1 month of treatment and continuing for two consecutive months. Furthermore, an increase in heart rate in the PYC group was registered. We propose that PYC-mediated SDys attenuation is based on its ability to improve endothelial functions by its antioxidant, anti-inflammatory, vasodilatory, and anticoagulant action. We assume that the action of PYC on heart rate is in accordance with the aforementioned vasodilatory action of PYC and consequent baroreflex-mediated heart rate response. PYC co-treatment reduced ESC-induced SDys and elevated heart rate.

Effect of In-Class vs Online Education on Sexual Health Communication Skills in First-Year Medical Students: a Pilot Study.

Online education is effective for knowledge acquisition, but its effect on clinical skill development is not well characterized. We aimed to compare communication skills of 50 first-year medical students who learned to assess and treat patients through an online learning module vs an in-class lecture. Twenty-six students were randomized to learn about antidepressant-induced sexual dysfunction in class and 24 learned the same content through an online module. Students were individually observed conducting an interview with a standardized patient with antidepressant-induced sexual dysfunction. Students were assessed by faculty raters blinded to the student's learning mode. Standardized patients were asked about their willingness to have the student as their physician. More students who learned in class vs online demonstrated appropriate verbal empathy (18 [69%] vs 8 [33%]; P = 0.01), defined as completing each task in the "verbal empathy" assessment domain, as measured by a faculty rater. Other assessed variables were not significantly different. Standardized patients' willingness (vs unwillingness; P = 0.01) to have the student as their physician was associated with the demonstration (by faculty appraisal) of a number of basic skills: using open-ended questions, asking one question at a time, using gender-neutral terminology when asking about the patient's relationship, and using appropriate sexual-health terminology. This study, although limited by a single-site design and the small number of participants, offers preliminary evidence that, if confirmed, may suggest that in-class learning from a psychiatrist (vs from an online module) is associated with greater verbal empathy in the assessment of SSRI-related sexual dysfunction.

Antidepressant-Induced Sexual Side Effects: Incidence, Assessment, Clinical Implications, and Management

Antidepressant medications can cause numerous types of sexual dysfunction. It is important to screen for and treat antidepressant-induced sexual dysfunction, which is often under-reported and may exacerbate mood symptoms and negatively affect relationships and medication adherence. Management strategies include watchful waiting, reducing the antidepressant dose, adding a different type of antidepressant or a medication for erectile dysfunction, switching to another antidepressant, drug holidays, and timing of sexual relations with respect to antidepressant dose. [ Psychiatr Ann . 2017;47(3):154–160.]

Comparing the Efficacy of Bupropion and Amantadine on Sexual Dysfunction Induced by a Selective Serotonin Reuptake Inhibitor.

Background:Antidepressant-induced sexual dysfunction (SD) is a common problem, associated with a significant risk of non-adherence. Selective Serotonin Reuptake Inhibitors (SSRIs) are associated with a substantial risk of SD. Only 10 % of patients show spontaneous improvement during follow up period.Objectives:This study aimed to compare two proposed medication (bupropion vs. amantadine) in alleviating SD in patients treated with SSRIs.Patients and Methods:In a randomized, single-blinded, clinical trial in Iran, 46 patients were recruited based on DSM-IV-TR criteria and semi-structured interview. Then, they were randomized into two treatment groups using table of random numbers. Eight patients were excluded and finally 38 patients completed the study which lasted for 4 weeks. Twenty patients were given bupropion, 18 patients were randomly assigned to another group, and given amantadine. Patients were assessed with the Arizona sexual experience scale (ASEX) at baseline and 4 weeks after the treatment.Results:A total of 38 patients completed the study (18 patients in amantadine vs. 20 patients in bupropion).The mean ASEX scores gradually declined in both study groups during the trial. The reduction of ASEX score in bupropion group was more than that of amantadine group that was statistically significant. So, the addition of bupropion at higher doses appears to be more effective approach in comparison with amantadine.Conclusions:These results provide empirical support for conducting a further study on comparing different add-on strategies for treating drug-induced SD.

Use of an operant paradigm for the study of antidepressant-induced sexual dysfunction

These studies were designed to develop a paradigm for the detection of antidepressant-induced sexual dysfunction in female rats. Ovariectomized, Fischer rats were conditioned to nose poke to open a guillotine door to gain access to a sexually active male. To develop the procedure, we examined the acquisition and stability of the response with a 15-s fixed interval, compared rats treated with 10 μg estradiol benzoate and 500 μg progesterone with those that received only estradiol benzoate, and carried out a preliminary analysis of the effects of 5, 10, and 15 mg/kg fluoxetine. We then more fully evaluated the effects of 5 mg/kg fluoxetine. Fluoxetine reduced sexual motivation, as assessed by the number of nose pokes, the number of nose poke episodes, and the latency to approach the male. In addition, changes in the females' sexual motivation were examined before and after ejaculation during the final conditioning trials. The number of nose pokes was reduced and the latency to initiate a new nose poke episode was increased following ejaculation. The robustness of the antidepressant-induced decline in sexual motivation is in marked contrast to the findings with several other animal models for sexual dysfunction and illustrates the usefulness of the operant procedure.

A Systematic Review Of The Use Of Bupropion For Hypoactive Sexual Desire Disorder In Premenopausal Women.

Objective: To assess the efficacy of bupropion therapy for hypoactive sexual desire disorder (HSDD) in women. Methods: A systematic review was performed utilizing the standard databases. Data were abstracted for study quality, characteristics, and outcomes. Due to the small number of studies and lack of consistently reported outcomes, a meta-analysis was not performed. Results: Two studies (289 women) met inclusion criteria. While one study had low risk of bias, the other had areas of high risk of bias. Both trials reported improvement in sexual function domains with treatment ranging from 12 weeks to 112 days. Conclusions: Despite two trials demonstrating benefit with bupropion treatment for premenopausal women with HSDD, the evidence is limited and not of adequate quality to recommend the therapy. More trials are needed in this area. Corresponding author: David M. Haas, MD, MS Dept. of OB/GYN, 550 N University Blvd, UH 2440, Indianapolis, IN 46202 (317)880-3959 (office), dahaas@iupui.edu DOI : 10.14302/issn.2381-862X.jwrh-14-546 Freely Available Online www.openaccesspub.org | JWRH CC-license DOI : 10.14302/issn.2381-862X.jwrh-14-546 Vol-1 Issue 1 Pg. no.15 INTRODUCTION Female sexual dysfunction is a prevalent problem worldwide with reported rates of 10-30% . Hypoactive sexual desire disorder (HSDD) is a common form of sexual dysfunction affecting females more often than males at rates of 30% and 15%, respectively 2, . HSDD is defined in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) as “the persistent or recurrent deficiency or absence of sexual fantasies/thought, and/or desire for sexual activity that causes personal distress or interpersonal difficulties”. It is not uncommon for women with HSDD to also have concomitant sexual arousal and/or orgasmic disorders . Additionally, HSDD and low sexual desire in general are believed to be underestimated by health care providers and are associated with decreased relationship satisfaction and distress for many women and their partners 1, . Furthermore, impaired sexual desire has been shown to be associated with depressed mood. While studies have shown improvement in sexual function with relief of depressive symptoms, additional investigation into the psychological and physiological effects of antidepressants has provided evidence of antidepressant-induced sexual dysfunction as an adverse effect of many of these medications . Despite ongoing research into female sexual dysfunction and HSDD, the exact etiology of these disorders is yet to be determined. There have been many trials conducted to determine the efficacy of various therapies in the treatment of HSDD. Decreased androgen levels have been shown to be associated with a decline in libido. Testosterone therapy (oral, transdermal patch, or topical) has been investigated through randomized controlled trials (RCTs) indicating statistically significant improvement in sexual desire . Testosterone transdermal patches have been approved for HSDD treatment in Europe. However, the U.S. Food and Drug Administration did not approve testosterone therapy for the treatment of HSDD due to the unknown long term adverse events (Moynihan 2004). In addition to testosterone therapies, investigations of genital vasodilators, dopaminergic therapies, estrogen therapies, and melanocortin receptor-acting bremelanotide have been conducted 1, . However, despite these investigations, there continues to be no FDA approved treatment for HSDD in the United States. Bupropion is a centrally-acting medication that is currently approved for use in the treatment of major depressive disorder, seasonal affective disorder, and smoking cessation (Bupriopion package insert 2014). The exact mechanism of action of bupropion has yet to be determined, however, it is believed to act centrally on both dopaminergic and norepinephrine systems with no serotonergic action . In addition to its role in mood improvement, bupropion has been shown to be effective in the reversal of SSRI-induced sexual dysfunction when supplemented to current therapy as well as a (Continued on page 16) Freely Available Online www.openaccesspub.org | JWRH CC-license DOI : 10.14302/issn.2381-862X.jwrh-14-546 Vol-1 Issue 1 Pg. no.16 substitution therapy . In addition to treatment of iatrogenic sexual dysfunction, study results indicate prosexual effects through the use of bupropion 12, . The objective of this study was to systematically review the data regarding bupropion treatment for HSDD treatment and to perform a meta-analysis to synthesize the trial results to determine if bupropion is effective

Comparing the Efficacy of Bupropion and Amantadine On Sexual Dysfunction Induced by a Selective Serotonin Reuptake Inhibitor

Antidepressant-induced sexual dysfunction (SD) is a common problem, associated with a significant risk of non-adherence. Selective Serotonin Reuptake Inhibitors (SSRIs) are associated with a substantial risk of SD. Only 10 % of patients show spontaneous improvement during follow up period. The aim is to compare two proposed medication (bupropion vs.amantadine) in alleviating SD of patients treated with SSRIs. The study was a single-blind,4-week trial SSRI treated outpatients, in remission for more than 8weeks and have SD, were randomly allocated to two parallel groups. Twenty patients were given bupropion Eighteen patients were randomly assigned to another group, given amantadine. Patients were assessed with the Arizona Sexual Experience Scale (ASEX) at baseline and 4 weeks after the treatment.38 patients completed the study (18 patients in amantadine vs.20 patients in bupropion). The mean ASEX scores gradually declined in both study groups during the trial. The reduction of ASEX score of bupropion is greater than the amantadine that was statistically significant. SoThe addition of bupropion at higher doses appears to be more effective approach in comparison with amantadine. These results provide empirical support for conducting a further study on comparing different add-on strategies for treating drug induced SD.

A Double-Blind Placebo-Controlled Trial of Maca Root as Treatment for Antidepressant-Induced Sexual Dysfunction in Women

Objective. We sought to demonstrate that maca root may be an effective treatment for antidepressant-induced sexual dysfunction (AISD) in women. Method. We conducted a 12-week, double-blind, placebo-controlled trial of maca root (3.0 g/day) in 45 female outpatients (mean age of 41.5 ± 12.5 years) with SSRI/SNRI-induced sexual dysfunction whose depression remitted. Endpoints were improvement in sexual functioning as per the Arizona Sexual Experience Scale (ASEX) and the Massachusetts General Hospital Sexual Function Questionnaire (MGH-SFQ). Results. 45 of 57 consented females were randomized, and 42 (30 premenopausal and 12 postmenopausal women) were eligible for a modified intent-to-treat analysis based on having had at least one postmedication visit. Remission rates by the end of treatment were higher for the maca than the placebo group, based on attainment of an ASEX total score ≤ 10 (9.5% for maca versus 4.8% for placebo), attaining an MGH-SFQ score ≤ 12 (30.0% for maca versus 20.0% for placebo) and reaching an MGH-SFQ score ≤ 8 (9.5% for maca versus 5.0% for placebo). Higher remission rates for the maca versus placebo group were associated with postmenopausal status. Maca was well tolerated. Conclusion. Maca root may alleviate SSRI-induced sexual dysfunction in postmenopausal women. This trial is registered with NCT00568126.

Antidepressant-induced sexual dysfunction during treatment with fluoxetine, sertraline and trazodone; a randomized controlled trial

BackgroundSelective serotonin reuptake inhibitors (SSRIs) are common treatments for patients with major depressive disorder (MDD). However, adverse effects of SSRIs on sexual function are common in the treatment of patients with MDD. There is a discrepancy in the reported frequency of SSRI-induced sexual dysfunction. On the other hand, there is also less evidence about sexual dysfunction with serotonin receptor antagonists and reuptake inhibitors (SARIs). Therefore, we aimed to assess sexual dysfunction in MDD patients who received fluoxetine, sertraline and trazodone. MethodIn a single-blind, randomized, controlled trial in Kermanshah, Iran, during 2009–2010, 195 patients who met the DSMIV-IR criteria for MDD were enrolled. The patients completed the Hamilton Depression Rating Scale (HAM-D) and the sexual function questionnaire (SFQ). Eligible patients were allocated in three treatment groups (receiving fluoxetine, sertraline or trazodone) for 14 weeks randomly. Measurement of HAMD was repeated in 4-week interval. Analysis for comparing sexual dysfunction among three groups and men and women was performed. ResultsThere were 102 men and 93 women in the three groups receiving fluoxetine (n=64), sertraline (n=67) and trazodone (n=64). There was no significant difference in the sexual dysfunction of the patients in the three groups at baseline (P>.05). After treatment, both men and women who had received fluoxetine had the most impairment in desire/drive items (43%–51% and 44%–50%, respectively), while patients receiving trazodone had the least impairment in these items (12%–18% and 23%–24%, respectively). Trazodone was also induced with a lower rate of impairment in arousal/orgasm items in men (9%–15%) compared with the other two drugs. Compared with fluoxetine and trazodone, sertraline was associated with intermediate impairment in sexual function (39%–42% in desire/drive items and 32%–39% in arousal/orgasm items) that was lower than that with fluoxetine and more than that with trazodone. ConclusionThere were different rates of sexual dysfunction with different antidepressants drugs in under treated patients. Compared with fluoxetine, and sertraline, trazodone was associated with the fewest sexual dysfunction. Fluoxetine was also associated with more sexual dysfunction than sertraline. Further research to better identify the differences among antidepressant drugs is recommended.

Management of antidepressant-induced sexual dysfunction.

Antidepressant-induced sexual dysfunction is a common, troublesome complication of antidepressant treatment that patients often fail to report, which can have major consequences, including non-adherence to treatment with resultant relapse of depressive illness. The aim of this paper is to review the extent, causation and evidence-based management of antidepressant-induced sexual dysfunction to inform clinical practice. The preponderance of evidence suggests that antidepressant s can be divided into high risk (selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants, monoamine oxidase inhibitors) and low risk (agomelatine, bupropion, moclobemide and reboxetine) categories with regard to propensity for antidepressant-induced sexual dysfunction, although there is disagreement, particularly about mirtazapine, and methodological issues militate against definitive findings. Antidepressant-induced sexual dysfunction is dose-dependent to an extent, but patient vulnerability factors are also relevant. There are significant differences in antidepressant-induced sexual dysfunction between men and women. It is important to ask antidepressant -treated patients about sexual dysfunction as few self-report; this may well contribute to antidepressant non-adherence. Consider using an antidepressant with low risk of antidepressant-induced sexual dysfunction for initial treatment. When antidepressant-induced sexual dysfunction has developed, try to persuade the patient to wait in case tolerance develops. Then consider changing to a lower risk or use of high/low risk antidepressant combinations but pharmacological expertise is required. Adjunctive sildenafil can help in both sexes.

P.2.a.021 Genome-wide association study of antidepressant-induced sexual dysfunction in depressed males

The feeding and running activities of rats were used to characterize the stressful effects of footshock. A 12-hour light/dark cycle was continuously in effect. During the preshock stage, all rats lived in individual cages where they could drink water, press a lever once for each 45 mg food pellet or run in an attached running wheel. During the shock stage, rats were moved to cages where they could drink and eat, but not run. Five s of light followed by 5 s of a light + tone compound preceded five progressively more intense shock levels. Rats in group AE were trained to pull a ceiling chain to avoid/escape from footshocks that were scheduled 24 hours per day. In group YS, the frequency, intensity and pattern of shocks for a rat were yoked to a rat in group AE. Rats in group CN were not shocked. During recovery, rats were allowed to resume running. During the dark, but not the light of the first day of shock, the intake of groups AE and YS was less than the intake of group CN. By the third day of shock, the food intake of group AE recovered and was no longer different from the intake of group CN. Intake of group YS remained less than the intakes of groups AE and CN during the remainder of the shock stage. When shock was terminated, the intake of the YS group recovered, but neither running nor food intake differed among groups. These results suggest that although inescapable shock disrupts food intake more than escapable shock, this disruption is specific to the duration of the shock stage and depends on rat's circadian pattern of intake.