Vibrator-Assisted Start-Stop Exercises Improve Premature Ejaculation Symptoms: A Randomized Controlled Trial.

Premature ejaculation (PE) is associated with decreased quality of life, lower confidence and self-esteem, and higher levels of depression, anxiety, and interpersonal difficulties. Here we investigated the effectiveness of vibrator-assisted start-stop exercises for treatment of PE, and whether the treatment effect could be enhanced by an additional psychobehavioral intervention. Fifty participants with a mean age of 41.7 years were included and randomized into two treatment groups and a waiting list control group. Participants were instructed to perform start-stop exercises while stimulating the penis with a purpose-made vibrator, 3 times a week for 6 weeks. Additionally, participants in one of the treatment groups received additional psychoeducation and performed mindfulness meditation-based body scan exercises three times a week. Data were gathered through online questionnaires before and after treatment, as well as 3 and 6 months after treatment. The interventions reduced PE symptoms with large effect sizes (partial η2 = .20 across the three groups, d [95% CI] = 1.05 [.27, 1.82] and 1.07 [.32, 1.82] for treatment groups compared to waiting list control group). The additional psychobehavioral intervention did not further reduce PE symptoms, but did decrease PE-associated negative symptoms such as levels of sexual distress, anxiety, and depression. No side effects were reported. Vibrator-assisted start-stop exercises can be offered as an adequate treatment option for PE.

HPA-axis dysregulation is not associated with accelerated epigenetic aging in patients with hypersexual disorder.

BACKGROUND: Hypersexual disorder (HD) - a nonparaphilic sexual desire disorder with impulsivity component - was evaluated for inclusion as a diagnosis in the DSM-5 and the diagnosis compulsive sexual behavior disorder is included as an impulse control disorder in the ICD-11. Hypothalamic-pituitary-adrenal (HPA)-axis hyperactivity is believed to affect cellular senescence and has been implicated in HD. No previous study investigated HD or HPA-axis dysregulation in relation to measures of epigenetic age (EA) acceleration. METHODS: This study reports on a case-control study set-up from a well-characterized cohort, contrasting EA predictors in relation to 60 HD patients and 33 healthy volunteers (HV) and 19 mixed HD/HV exhibiting dexamethasone suppression test (DST) non-suppression to 73 mixed HD/HV DST controls. The genome-wide methylation pattern was measured in whole blood from 94 subjects using the Illumina Infinium Methylation EPIC BeadChip and preprocessed according to specialized protocols suitable for epigenetic age estimation. The online DNAm Age Calculator (https://dnamage. GENETICS: ucla.edu/) was implemented to retrieve various EA predictors, which were compared between the in-silico generated subgroups. RESULTS: Quality control analyses indicated strong correlations between the EA measure DNA methylation GrimAge (DNAm GrimAge - the EA clock most reliably associated with mortality risk) and chronological age in all sub-groups. The study was adequately powered to detect differences of 2.5 and 3.0 years in DNAm GrimAge minus age in relation to both HD and HPA-axis dysregulation, respectively. Baseline DNAm GrimAge exceeded chronological age by 2.8 years on average across all samples. No EA acceleration marker was associated with HD or DST suppression status (p > 0.05). CONCLUSION: EA acceleration markers shown to be strongly predictive of physiological dysregulation and mortality-risk, are not related to HD or DST non-suppression status (measured after 0.5 mg dexamethasone). The independency of HPA-axis dysregulation to EA acceleration does not support the biological relevance of this dosage-regimen when applied to patients with HD. These findings do not support the notion of accelerated cellular senescence in HD. Studies stratifying DST non-suppressors according to established dosage-regimens in somatic settings are needed to fully elucidate the putative contribution of HPA-axis dysregulation to EA.