Introduction Previous research has indicated that serotonergic genes may influence ejaculatory function. Attempts to investigate effects of polymorphisms in serotonergic genes have been carried out, but so far, no study has conducted exploratory genotype analyses regarding the serotonin receptor 1A, 1B, and 2C subtypes, which have been hypothesized to mediate the inhibitory effects of serotonin on ejaculation in rodents. Aim The aim of the present study was to investigate effects of a total of six single nucleotide polymorphisms (SNPs) located in genes encoding serotonin receptor subtypes 1A, 1B, and 2C on self-reported ejaculation latency time. Methods A retrospective self-report measure of ejaculation latency time was used to investigate ejaculatory function in a population-based sample of 1,399 male twins. DNA was collected using self-administered saliva sampling. Main Outcome Measure Calculations of allelic effects were conducted using the Generalized Estimating Equations module of PASW 18.0, which appropriately controls for between-subjects dependence. Results Out of six investigated polymorphisms, two SNPs (both serotonin receptor 5-HT1B linked) had a significant main effect on ejaculation latency time. Of these, one (rs11568817) remained significant after Bonferroni correction for multiple testing, indicating that individuals homozygous for the G allele had significantly shorter ejaculation latencies. Conclusions The results of this study support the hypothesis that serotonergic genes play a role in ejaculatory function in the general population. Replication of the results of the present study is warranted.

Erectile dysfunction (ED) has been extensively studied in the past few decades, and significant advances have been made in understanding its etiology. Most cases of this type of dysfunction have an organic etiology, and ED occurs primarily in older men. However, relatively little is known about erectile problems in young men or about the interconnection between psychiatric symptoms and ED etiology. In this study, the authors investigated ED symptoms in a large, population-based sample of 18-48-year-old men. Participants reported ED symptoms from their first intercourse experience as well as those occurring at present. The authors assessed the association between reported ED symptoms during early partnered sexual experiences and present ED symptoms. Furthermore, the authors investigated associations between age, symptoms of anxiety and depression, and erectile problems. Results indicated that age was a significant predictor of ED problems already in young age groups. ED problems were prevalent to a much higher extent during early sexual intercourse experiences and appeared to pass with time for most men. Anxiety and depression were significant predictors of present erectile problems. Implications of the results and potential limitations were discussed.

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IntroductionRecently, testosterone (T) has been shown to be associated with premature ejaculation (PE) symptoms in the literature. Furthermore, studies suggest that the etiology of PE is partly under genetic control.AimThe aim of this study was to reassess findings suggesting an association between testosterone (T) and a key symptom of PE, ejaculation latency time (ELT), as well as exploratively investigating associations between six androgen-related genetic polymorphisms and ELT.Materials and MethodsStatistical analyses were performed on a population-based sample of 1,429 Finnish men aged 18–45 years (M = 26.9, SD = 4.7). Genotype information was available for 1,345–1,429 of these (depending on the polymorphism), and salivary T samples were available from 384 men. Two androgen receptor gene-linked, two 5-alpha-reductase type 2-gene-linked, and two sex hormone-binding globuline gene-linked polymorphisms were genotyped.Main Outcome MeasuresEjaculatory function was assessed using self-reported ELT.ResultsWe found no association between salivary T levels and ELT. We found a nominally significant association between a 5-alpha-reductase type 2-gene-linked polymorphism (rs2208532) and ELT, but this association did not remain significant after correction for multiple testing. One single nucleotide polymorphism in the sex hormone-binding globulin gene (rs1799941) moderated (significantly after correction for multiple testing) the association between salivary T and ELT, so that A:A genotype carriers had significantly lower salivary T levels as a function of increasing ELT compared with other genotype groups.ConclusionsWe were unable to find support for the hypothesis suggesting an association between T levels and ELT, possibly because of the low number of phenotypically extreme cases (the sample used in the present study was population based). Our results concerning genetic associations should be interpreted with caution until replication studies have been conducted. Jern P, Westberg L, Ankarberg-Lindgren C, Johansson A, Gunst A, Sandnabba NK, and Santtila P. Associations between salivary testosterone levels, androgen-related genetic polymorphisms, and self-estimated ejaculation latency time. Sex Med 2014;2:107–114.

Introduction The etiology of sexual preference disorders (paraphilias) in general and pedophilia in particular remains unknown. There are some indications of biological factors related to pedophilic interest and pedophilic disorder. Aim To examine single-nucleotide polymorphisms (SNPs) potentially associated with pedophilic sexual interest. Methods The sample consisted of 1,672 men 18 to 45 years old from the Genetics of Sex and Aggression sample who had submitted saliva samples. Fifty-four SNPs were genotyped and relevant SNPs were analyzed. Main Outcome Measures A self-report questionnaire designed specifically for the Genetics of Sex and Aggression sample was used to measure sexual interest in and sexual behavior toward children and adolescents. DNA extraction and genotyping were used to measure possible associations between male pedophilia and SNPs. Results Before controlling for multiple testing, statistically significant associations were found for SNPs linked to androgen, estrogen, prolactin, corticotrophin, serotonin, and oxytocin. No associations remained significant after controlling for multiple testing. Conclusion The results of the present study suggest a complex biological mechanism affecting adult sexual interest in children. Very small effect sizes characterized the findings, and several polymorphisms related to different hormonal functioning were initially related to the phenotype.

Introduction Female sexual desire and arousal problems have been shown to have a heritable component of moderate size. Previous molecular genetic studies on sexual desire have mainly focused on genes associated with neurotransmitters such as dopamine and serotonin. Nevertheless, there is reason to believe that hormones with more specific functions concerning sexuality could have an impact on sexual desire and arousal. Aim The aim of the present study was to investigate the possible effects of 17 single nucleotide polymorphisms (SNPs) located in estrogen receptor genes on female sexual desire and subjective and genital arousal (lubrication). Based on previous research, we hypothesized that ESR1 and ESR2 are relevant genes that contribute to female sexual desire and arousal. Main Outcome Measures The desire, arousal, and lubrication subdomains of the Female Sexual Function Index self-report questionnaire were used. Methods The present study involved 2,448 female twins and their sisters aged 18–49 who had submitted saliva samples for genotyping. The participants were a subset from a large-scale, population-based sample. Results We found nominally significant main effects on sexual desire for three ESR2-linked SNPs when controlled for anxiety, suggesting that individuals homozygous for the G allele of the rs1271572 SNP, and the A allele of the rs4986938 and rs928554 SNPs had lower levels of sexual desire. The rs4986938 SNP also had a nominally significant effect on lubrication. No effects for any of the SNPs on subjective arousal could be detected. Conclusions The number of nominally significant results for SNPs in the ESR2 gene before correcting for multiple testing suggests that further studies on the possible influence of this gene on interindividual variation in female sexual functioning are warranted. In contrast, no support for an involvement of ESR1 was obtained. Our results should be interpreted with caution until replicated in independent, large samples.

The aim of the present study was to investigate how women's tendency to pretend orgasm during intercourse is associated with orgasm function and intercourse-related pain, using a longitudinal design where temporal stability and possible causal relationships could be modeled. The study sample consisted of 1421 Finnish women who had participated in large-scale population-based data collections conducted at two time points 7 years apart. Pretending orgasm was assessed for the past 4 weeks, and orgasm function and pain were assessed using the Female Sexual Function Index for the past 4 weeks. Associations were also computed separately in three groups of women based on relationship status. Pretending orgasm was considerably variable over time, with 34% of the women having pretended orgasm a few times or more at least at one time point, and 11% having done so at both time points. Initial bivariate correlations revealed associations between pretending orgasm and orgasm problems within and across time, whereas associations with pain were more ambiguous. However, we found no support in the path model for the leading hypotheses that pretending orgasms would predict pain or orgasm problems over a long period of time, or that pain or orgasm problems would predict pretending orgasm. The strongest predictor of future pretending in our model was previous pretending (R = .14). Relationship status did not seem to affect pretending orgasm in any major way.

FSFs varied considerably over 7 years and relationship status was of importance when assessing temporal stability and cross-domain effects. Our results advocate tailored psychobehavioural treatment interventions for female sexual dysfunctions that take partner-specific factors into account.