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Background In laboratory studies, exercise immediately before sexual stimuli improved sexual arousal of women taking antidepressants [1]. We evaluated if exercise improves sexual desire, orgasm, and global sexual functioning in women experiencing antidepressant‐induced sexual side effects. Methods Fifty‐two women who were reporting antidepressant sexual side effects were followed for 3 weeks of sexual activity only. They were randomized to complete either three weeks of exercise immediately before sexual activity (3×/week) or 3 weeks of exercise separate from sexual activity (3×/week). At the end of the first exercise arm, participants crossed to the other. We measured sexual functioning, sexual satisfaction, depression, and physical health. Results Exercise immediately prior to sexual activity significantly improved sexual desire and, for women with sexual dysfunction at baseline, global sexual function. Scheduling regular sexual activity significantly improved orgasm function; exercise did not increase this benefit. Neither regular sexual activity nor exercise significantly changed sexual satisfaction. Conclusions Scheduling regular sexual activity and exercise may be an effective tool for the behavioral management of sexual side effects of antidepressants.

Sexual dysfunction is a common side effect of selective serotonin reuptake inhibitors (SSRIs) like paroxetine in the treatment of depression, imposing a considerable risk on medication adherence and hence therapeutic success. Bupropion, a norepinephrine and dopamine reuptake inhibitor, is recommended as an alternative treatment without adverse effects concerning sexual arousal and libido. We investigated the neural bases of paroxetine-related subjective sexual dysfunction when compared with bupropion and placebo. We scanned 18 healthy, heterosexual males in a randomized, double-blind, within-subject design while watching video clips of erotic and nonerotic content under steady-state conditions after taking 20 mg of paroxetine, 150 mg of bupropion, and placebo for 7 days each. Under paroxetine, ratings of subjective sexual dysfunction increased compared with placebo or bupropion. Activation along the anterior cingulate cortex (ACC), including subgenual, pregenual, and midcingulate cortices, in the ventral striatum and midbrain was decreased when compared with placebo. In contrast, bupropion let subjective ratings and ACC activations unchanged and increased activity of brain regions including posterior midcingulate cortex, mediodorsal thalamus, and extended amygdala relative to placebo and paroxetine. Brain regions that have been related to the processing of motivational (ventral striatum), emotional, and autonomic components of erotic stimulation (anterior cingulate) in previous studies showed reduced responsiveness under paroxetine in our study. Drug effects on these regions may be part of the mechanism underlying SSRI-related sexual dysfunction. Increased activation under bupropion may point to an opposite effect that may relate to the lack of impaired sexual functioning.

Methadone is largely recognized as an effective treatment for opiate-dependent patients; however, it causes reduced brain dopaminergic action resulting in significant sexual dysfunction. Bupropion is a dopamine reuptake inhibitor which can potentially improve erectile function among male patients on methadone (MMT). This is a phase II, randomized, double-blind, parallel-group, placebo-controlled trial, involving 80 MMT male patients (73.4%) with mean age of 42.83 years ±9.68. These MMT male patients were randomly assigned into two groups to receive bupropion and placebo, respectively. The primary efficacy outcome measure was the difference between the two groups in end-point mean improvement scores using the measurement of Clinical Global Impression Scale adapted for Sexual Function (CGI-SF) at baseline (week 0) and at weeks 2, 4, and 6. Malay version of the sexual desire inventory-2 (SDI-2-BM) and Malay version of International Index of Erectile Function 15 (Mal-IIEF-15) domain scores were evaluated as secondary parameters. Improvement of the end-point mean from baseline were seen across the scores of SDI-2-BM (mean difference = 11.77 ± 2.90, 95% confidence interval (CI) [3.89, 19.54], p < .001) and Mal-IIEF-15 (mean difference = 8.37 ± 2.71, 95% CI [15.75, 0.99], p = .02), and the total plasma testosterone level (mean difference = 4.03, 95% CI [0.90, 7.15], p = .01). A categorical improvement of “much/very much improved” (CGI-SF score = 2) was reported by 58.3% (n = 21/36) of bupropion SR-assigned versus 27.7% (n = 10/36) placebo-assigned patient. Bupropion was well tolerated with no serious adverse events reported other than insomnia (17.7%). Six weeks of bupropion SR treatment reported significant improvement in key aspects of sexual function among male opiate-dependent patients on methadone maintenance treatment with emergent sexual dysfunction.

Understanding individual differences in susceptibility to antidepressant therapy side-effects is essential to optimize the treatment of depression. We performed genome-wide association studies (GWAS) to search for genetic variation affecting the susceptibility to side-effects. The analysis sample consisted of 1439 depression patients, successfully genotyped for 421K single nucleotide polymorphisms (SNPs), from the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study. Outcomes included four indicators of side-effects: general side-effect burden, sexual side-effects, dizziness and vision/hearing-related side-effects. Our criterion for genome-wide significance was a prespecified threshold ensuring that, on average, only 10% of the significant findings are false discoveries. Thirty-four SNPs satisfied this criterion. The top finding indicated that 10 SNPs in SACM1L mediated the effects of bupropion on sexual side-effects (p = 4.98 × 10(-7), q = 0.023). Suggestive findings were also found for SNPs in MAGI2, DTWD1, WDFY4 and CHL1. Although our findings require replication and functional validation, this study demonstrates the potential of GWAS to discover genes and pathways that could mediate adverse effects of antidepressant medication.

Background Attention-deficit hyperactivity disorder (ADHD) is a neuropsychiatric disorder that begins in childhood. Atomoxetine is a selective inhibitor of the presynaptic norepinephrine transporter. Several studies have demonstrated the safety and efficacy of atomoxetine in the treatment of ADHD. Objective The objective of this analysis was to provide additional information on the frequency, time to onset and time to resolution of sexual and genitourinary (GU) treatment-emergent adverse events (TEAEs) reported during atomoxetine treatment in clinical trials. Methods Data from all adult atomoxetine placebo-controlled ADHD trials were pooled for this analysis, for a total of 3,314 patients (atomoxetine, n  = 1,738; placebo, n  = 1,576). Additionally, data from all adolescent patients (baseline age ≥13 to <18 years) within all ADHD placebo-controlled trials were pooled for analysis, for a total of 538 patients (atomoxetine, n  = 329; placebo, n  = 209). Rates of sexual and GU TEAEs were summarized by sex for each age group. Time to onset and resolution of sexual and GU TEAEs were summarized and compared using Kaplan–Meier methods. Results Overall, the baseline characteristics of randomized patients in the atomoxetine and placebo groups were similar. Profiles of sexual and GU TEAEs for atomoxetine appeared clinically similar to placebo in female patients and in adolescent male patients. Adult male patients reported relatively more sexual and GU TEAEs when taking atomoxetine compared with placebo, with libido decreased (4.6 vs. 3.0 %), dysuria (3.7 vs. 1.5 %), urinary hesitation (6.9 vs. 2.4 %), urine flow decreased (2.5 vs. 0.6 %), ejaculation disorder (2.8 vs. 1.1 %) and erectile dysfunction (8.0 vs. 1.9 %) being the most common. The time to onset of the most common TEAEs in adult male patients tended to occur relatively early in dosing: within the first 2 weeks for GU TEAEs, and during the second and third week of dosing for erectile and ejaculation issues. The median time to resolution for these events ranged from around 3–8 weeks after event onset, depending on the event. While the common sexual and GU TEAEs showed numerically higher percentages of discontinuations in atomoxetine-treated patients compared with placebo, most incidences of the sexual and GU TEAEs were not considered severe. Conclusions The sexual and GU TEAE profiles of patients taking atomoxetine were generally similar to those of patients taking placebo in the female and adolescent male populations, with greater frequency of TEAEs reported in adult males taking atomoxetine compared with placebo. The time to onset of the TEAEs tended to be shorter, and time to resolution tended to be longer in adult male patients treated with atomoxetine compared with those receiving placebo. The conclusions must be interpreted with caution because the TEAEs were likely underreported.

Objective: The primary objective was to evaluate sexual function (SF) separately in men and women with major depressive disorder (MDD) before and during treatment with bupropion sustained release (SR) or paroxetine. The secondary objectives involved a comparative evaluation of the Sex Effects Scale (Sex FX) and the Investigator-Rated Sexual Desire and Functioning Scale (IRSD-F), as well as a comparison of antidepressant outcomes and an examination of the relation between level of depression and SF over time. Method: There were 141 patients (68 women and 73 men) who met DSM-IV criteria for a current major depressive episode. They were randomly assigned to receive bupropion SR (150 to 300 mg daily) or paroxetine (20 to 40 mg daily) under double-blind trial conditions. Patients were assessed at baseline and at 2, 4, 6, and 8 weeks with the 17-item Hamilton Depression Rating Scale (HDRS17), Sex FX, and IRSD-F. Results: Prior to treatment, women reported significantly lower SF on both the Sex FX and IRSD-F scales, compared with men. During treatment, there were no significant drug differences on measures of SF over time for women; however, men who were treated with paroxetine reported a worsening of SF, whereas bupropion SR did not significantly alter SF. Both bupropion SR and paroxetine produced clinically and statistically significant reductions in HDRS17 scores as well as comparable rates of response and remission. There was a statistically significant correlation between the 2 measures of SF at all visits. There was also a significant inverse relation between depression and SF in women, but not in men, irrespective of drug. Conclusion: According to the Sex FX scale, a significant difference in antidepressant-related sexual dysfunction was detected in men, but not women, during treatment with bupropion SR or paroxetine.

While sexual dysfunction is a well-known side effect of taking selective serotonin reuptake inhibitors (SSRIs), in an undetermined number of patients, sexual function does not return to pre-drug baseline after stopping SSRIs. The condition is known as post-SSRI sexual dysfunction (PSSD) and is characterised most commonly by genital numbness, pleasureless or weak orgasm, loss of libido and erectile dysfunction. This article provides a commentary on the incidence and prevalence of PSSD based on a combination of academic literature as well as clinical and research experience. A number of obstacles to quantifying the occurrence of PSSD are outlined including difficulty in designing a suitable study method. Other contextual obstacles include patient embarrassment at raising sexual concerns, the response of healthcare professionals, inability to stop an antidepressant due to withdrawal issues in a proportion of patients and patient unawareness that their sexual difficulties are linked to prior medication compounded by variability of online information and a lack of information aimed at public education. A definition of PSSD with diagnostic criteria has been published. A MedDRA code for PSSD has also been introduced, but this is yet to be adopted by regulators.

Background Antidepressant treatment is related to various sexual dysfunctions. This may cause discontinuation of the medication. This study aims to evaluate the level of sexual dysfunction of antidepressant users and the possible factors linked. Methods Demographic variables and sexual dysfunction level of 452 people in total (291 males and 161 females) were assessed by demographic data form and Psychotropic-related Sexual Dysfunction Questionnaire (PreSEXDQ). Results Sexual dysfunction was highly prevalent among both females (88.7%) and males (84.5%). Among females, significant differences were observed based on antidepressant type, with those using bupropion experiencing lower levels of sexual dysfunction compared to those on SSRIs, SNRIs, or vortioxetine. In contrast, no significant differences were found for males. Conclusions This highlights the importance of considering gender and medication type when addressing and managing psychotropic-related sexual dysfunction. Furthermore, additional studies are needed to determine whether a causal relationship exists between psychiatric medication-related sexual dysfunction and treatment discontinuation.

Abstract Background Second-generation antipsychotics (SGAs) are widely prescribed for psychiatric disorders but frequently cause sexual dysfunction, particularly in women—a side effect often underrecognized. This study assessed the association between SGAs and female sexual dysfunction using the US Food and Drug Administration Adverse Event Reporting System (FAERS). Study Methods We analyzed FAERS data from Q1 2004 to Q4 2023, identifying female sexual dysfunction cases using predefined MedDRA Preferred Terms. Nine SGAs were included: aripiprazole, quetiapine, olanzapine, risperidone, paliperidone, lurasidone, brexpiprazole, asenapine, and ziprasidone. Disproportionality analyses were conducted using frequentist (ROR, PRR) and Bayesian (BCPNN, MGPS) methods. Results were stratified by symptom type and prolactin-related drug effects. Study Results A total of 11 786 reports were identified, peaking in 2017. Women aged 19-41 years accounted for the largest subgroup (n = 4787, 40.6%). Antipsychotics accounted for 9 of the top 50 drugs linked to sexual dysfunction, with aripiprazole, quetiapine, and olanzapine most frequently reported. Aripiprazole was strongly associated with compulsive sexual behavior (ROR: 296.23) and hypersexuality. Risperidone and paliperidone were linked to decreased libido and anorgasmia. Prolactin-elevating drugs were associated with older age, intramuscular use, and more serious outcomes. Conclusion This pharmacovigilance study highlights significant associations between specific SGAs and female sexual dysfunction. Disproportionality signals vary by drug, symptom type, and prolactin-related mechanisms. Clinicians should consider sexual side effects in treatment decisions and monitor patients accordingly. Further prospective studies are warranted.

Background Sexual dysfunction is a social challenge that devastates many people, including cancer patients. However, among the numerous reported side effects of chemotherapy sexual dysfunction is the least studied and reported. The chemotherapeutics used among cancer patients are potential risk factors for the development of sexual dysfunction, and such an understanding of these risk factors can lead to numerous interventions to bypass their effects on sexual activity. Objective The goal of this study was to determine the prevalence, classification and factors associated with sexual dysfunction among cancer patients receiving chemotherapy. Methods A cross-sectional study was conducted among 214 cancer patients at the Mbarara Regional Referral Hospital in southwestern Uganda for a period of 3 months from August to October 2023. A systematic sampling technique was employed in the study; a questionnaire was used to collect patient data. The standardized female sexual function index and international index of erectile function tools were used to classify types of sexual dysfunctions among women and men, respectively. Sexual dysfunction-associated factors were analyzed by logistic regression using Stata version 17. Results A total of 127 males and 87 females with a median age of 50 years were enrolled. Overall (42.1%) of the patients, (54.3%) males and (24.1%) females experienced sexual dysfunction. (33.9%) of male reported overall sexual dissatisfaction, while among female (18.4%) patients reported decreased sexual desire. while others reported reduced arousal and vaginal pain. Multivariate logistic regression revealed the following independent risk factors for sexual dysfunctions: male sex (AOR 3.99, 95% CI 1.93–8.25; p value = 0.001), gastrointestinal cancer (AOR 3.46, 95% CI 1.34–8.93; p value = 0.010) and anthracyclines use (AOR 4.26, 95% CI 1.02, 17.76; p value = 0.047). Conclusions Our findings suggest that there is a high prevalence of sexual dysfunction among cancer patients at the Mbarara Regional Referral Hospital. In male patients, overall sexual dissatisfaction is the most prevalent, while decreased sexual desire is prevalent in females. Routine screening of sexual functions should be encouraged for all patients receiving chemotherapies. Males patients, those diagnosed with gastrointestinal cancers and those receiving regimens containing anthracyclines should be more closely monitored for sexual dysfunction.