Links between Aggressive Sexual Fantasies and Sexual Coercion: A Replication and Extension of a Multifactorial Model.

Current research indicates that aggressive sexual fantasies (ASF) are related to sexual aggression, above and beyond other risk factors for this behavior. There have, however, rarely been explicitly considered in multifactor models aiming to explain sexual aggression. One exception is the multifactorial Revised Confluence Model of Sexual Aggression that was replicated in two samples of male individuals who were convicted of sexual offenses and a small sample of men from the general population and evidenced a high relevance of ASF, respectively. There were, however, no further attempts to replicate the model in larger samples from the general population. We, therefore, used a subsample from the Finnish Genetics of Sexuality and Aggression project including 3269 men (age: M = 26.17 years, SD = 4.76) to do so. Cross-sectional latent structural equation models corroborated previous research and the assumption that ASF are a central component in multifactor models that aim to explain sexual aggression: ASF and antisocial behavior/aggression were equally important associates of sexual coercion when also considering adverse childhood experiences, hypersexuality, and callous-unemotional traits. Additionally, ASF mediated the links between hypersexuality, callous-unemotional traits, as well as childhood sexual abuse and sexual coercion. These links held stable when entering further risk factors, that is, distorted perceptions, rape-supportive attitudes, and violent pornography consumption into the model. Contrasting assumptions, alcohol consumption and antisocial behavior/aggression did not interact. These results illustrate the potential importance of ASF for sexual aggression. They indicate that ASF require consideration by research on sexual aggression as well as in the treatment and risk assessment of sexual perpetrators.

Elucidating the role of negative parenting in the genetic v. environmental influences on adult psychopathic traits.

BACKGROUND: Psychopathic traits involve interpersonal manipulation, callous affect, erratic lifestyle, and antisocial behavior. Though adult psychopathic traits emerge from both genetic and environmental risk, no studies have examined etiologic associations between adult psychopathic traits and experiences of parenting in childhood, or the extent to which parenting practices may impact the heritability of adult psychopathic traits using a genetically-informed design. METHODS: In total, 1842 adult twins from the community reported their current psychopathic traits and experiences of negative parenting during childhood. We fit bivariate genetic models to the data, decomposing the variance within, and the covariance between, psychopathic traits and perceived negative parenting into their genetic and environmental components. We then fit a genotype × environment interaction model to evaluate whether negative parenting moderated the etiology of psychopathic traits. RESULTS: Psychopathic traits were moderately heritable with substantial non-shared environmental influences. There were significant associations between perceived negative parenting and three of four psychopathy facets (interpersonal manipulation, erratic lifestyle, antisocial tendencies, but not callous affect). These associations were attributable to a common non-shared environmental pathway and not to overlapping genetic effects. Additionally, we found that primarily shared environmental influences were stronger on psychopathic traits for individuals with a history of greater negative parenting. CONCLUSIONS: Utilizing a genetically-informed design, we found that both genetic and non-shared environmental factors contribute to the emergence of psychopathic traits. Moreover, perceptions of negative parenting emerged as a clear environmental influence on the development of interpersonal, lifestyle, and antisocial features of psychopathy.

Uncovering the genetic architecture of broad antisocial behavior through a genome-wide association study meta-analysis.

Despite the substantial heritability of antisocial behavior (ASB), specific genetic variants robustly associated with the trait have not been identified. The present study by the Broad Antisocial Behavior Consortium (BroadABC) meta-analyzed data from 28 discovery samples (N = 85,359) and five independent replication samples (N = 8058) with genotypic data and broad measures of ASB. We identified the first significant genetic associations with broad ASB, involving common intronic variants in the forkhead box protein P2 (FOXP2) gene (lead SNP rs12536335, p = 6.32 × 10-10). Furthermore, we observed intronic variation in Foxp2 and one of its targets (Cntnap2) distinguishing a mouse model of pathological aggression (BALB/cJ strain) from controls (BALB/cByJ strain). Polygenic risk score (PRS) analyses in independent samples revealed that the genetic risk for ASB was associated with several antisocial outcomes across the lifespan, including diagnosis of conduct disorder, official criminal convictions, and trajectories of antisocial development. We found substantial genetic correlations of ASB with mental health (depression rg = 0.63, insomnia rg = 0.47), physical health (overweight rg = 0.19, waist-to-hip ratio rg = 0.32), smoking (rg = 0.54), cognitive ability (intelligence rg = -0.40), educational attainment (years of schooling rg = -0.46) and reproductive traits (age at first birth rg = -0.58, father's age at death rg = -0.54). Our findings provide a starting point toward identifying critical biosocial risk mechanisms for the development of ASB.

Causal Influences of Same-Sex Attraction on Psychological Distress and Risky Sexual Behaviors: Evidence for Bidirectional Effects.

Although health disparities among same-sex attracted compared to heterosexual individuals are typically explained by minority stress, there is limited evidence for a causal effect. This study investigated whether same-sex attraction was causally associated with psychological distress and risky sexual behavior using sociosexual behavior as a proxy. The sample comprised monozygotic and dizygotic twins and their non-twin siblings (n = 2036, 3780 and 2356, respectively) genotyped and assessed for same-sex attraction, psychological distress (anxiety and depressive symptoms), and risky sexual behavior. Causal influences were investigated with same-sex attraction as the predictor and psychological distress and risky sexual behavior as the outcomes in two separate Mendelian Randomization-Direction of Causation (MRDoC) models using OpenMx in R. The MRDoC model improves on the Mendelian Randomization and Direction of Causation twin models by allowing analyses of variables with similar genetic architectures, incorporating polygenic scores as instrumental variables and specifying pleiotropy and residual covariance. There were significant causal influences flowing from same-sex attraction to psychological distress and risky sexual behavior (standardized coefficients = 0.13 and 0.16; 95% CIs 0.03-0.23 and 0.08-0.25, respectively). Further analyses also demonstrated causal influences flowing from psychological distress and risky sexual behavior toward same-sex attraction. Causal influences from same-sex attraction to psychological distress and risky sexual behavior may reflect minority stress, which reinforces ongoing measures to minimize social disparities. Causal influences flowing in the opposite direction may reflect rejection sensitivity, stigma-inducing outcomes of risky sexual behavior, and recall bias; however, further research is required to specifically investigate these processes.

Heritability of Bullying and Victimization in Children and Adolescents: Moderation by the KiVa Antibullying Program.

OBJECTIVE: Bullying affects approximately a quarter of schoolchildren and is associated with numerous adverse outcomes. Although distinct risk factors for bullying and victimization have been identified, few studies have investigated the genetic and environmental underpinnings of bullying and victimization. The aims of this study were twofold: first, to examine the contributions of genetic and environmental factors to bullying and victimization, and second, to analyze whether the KiVa antibullying program moderated the magnitude of these contributions by comparing estimates derived from the KiVa versus control groups. METHOD: The sample comprised students from schools that participated in the evaluation of the KiVa antibullying program in Finland during 2007-2009. Bullying and victimization were measured using peer nominations by classmates. The sample for the twin analyses comprised of 447 twins (107 monozygotic and 340 dizygotic twins) aged 7-15. RESULTS: Genetic contributions accounted for 62% and 77% of the variance in bullying and in victimization at pre-intervention, respectively. There was a post-intervention difference in the overall role of genetic and environmental contributions between the intervention and the control group for bullying and victimization, with non-shared environmental effects playing a lesser role (and genes a larger role) in the intervention than in the control group context. CONCLUSIONS: This study replicates previous findings on the genetic underpinnings of both bullying and victimization, and indicates that a school-based antibullying program reduces the role of non-shared environmental factors in bullying and victimization. The results indicate that prevention and intervention efforts need to target both environmental and (heritable) individual level factors to maximize effectiveness.

Erectile Dysfunction in Young Men: Testosterone, Androgenic Polymorphisms, and Comorbidity With Premature Ejaculation Symptoms.

BACKGROUND: The association between erectile dysfunction (ED), free testosterone (T), and androgenic genetic polymorphisms is still unclear. As most studies in the field have focused on older (>40 y.o.) men, data from young men is scarce. In addition, the clinically observed comorbidity between ED and premature ejaculation (PE) has not been explained. AIM: The aim of the present study was 3-fold: to assess in a sample of young men (1) the association between ED and T; (2) the role of androgenic genetic polymorphisms in the aforementioned association; and (3) comorbidity between ED and PE symptoms. METHODS: Statistical analyses were performed on a population-based sample of 2,302 Finnish men, (Mage = 26.8 years). Hormone samples were available from 317 men, and genotype information was available from a minimum of 1,144 men depending on genetic locus. For twin analyses, the sample contained 533 male individuals from opposite-sex fraternal twin pairs, 491 identical male individuals (110 complete pairs), 493 male individuals from male fraternal twin pairs (92 complete pairs), and 658 siblings of twins. OUTCOMES: The main outcome measure includes association between levels of salivary T and ED, main effects of the androgen-related genetic polymorphisms on ED scores. Bivariate twin models of PE and ED were fitted to elucidate possible shared etiology. RESULTS: We found no significant association between T levels and ED and no significant main effects of the androgenic genetic polymorphisms on ED. We found no evidence suggesting that any of the genetic polymorphisms would moderate the association between T and ED symptoms. We found shared unique environmental influences between PE and ED (rE = .28). CLINICAL TRANSLATION: Obtained data suggest that ED has T-independent causes and that any comorbidity between PE and ED is not explained by a set of genes affecting both phenotypes. STRENGTHS & LIMITATIONS: First, the sample size for both parts of the study was relatively small, which may make some statistical analyses underpowered. Furthermore, as the sample was a population-based sample of relatively young men, the number of clinically relevant ED cases was low. Second, some concerns about T derived from saliva exist because saliva sampling comes with increased risks of error particularly because saliva samples are more vulnerable to contamination. CONCLUSION: We found no significant association between free T levels, androgenic genetic polymorphisms, and ED in the younger age cohort. Twin analysis suggested a common nonshared environmental component in PE and ED. Zhuravleva1 ZD, Johansson A, Jern P. Erectile Dysfunction in Young Men: Testosterone, Androgenic Polymorphisms, and Comorbidity With Premature Ejaculation Symptoms. J Sex Med 2021;18:265-274.

Is the association between childhood maltreatment and aggressive behavior mediated by hostile attribution bias in women? A discordant twin and sibling study.

Understanding the mechanisms behind aggressive behavior (AGG) is vital so that effective prevention and intervention strategies can be developed. Maltreated children are hypothesized to be prone to social information processing biases, such as hostile attribution bias (HAB), which, in turn, may increase the likelihood of behaving aggressively. The first aim of the present study was to replicate findings regarding associations between childhood maltreatment (CM), HAB, and aggression in a population-based sample of Finnish female twins and their sisters (N = 2,167). However, these associations might not be causal but instead confounded by familial factors, shared between the variables. The second aim was, thus, to test the associations when potential confounding by familial (genetic or common environmental) effects were controlled for using a multilevel discordant twin and sibling design within (a) 379 pairs of twins (npairs = 239) or siblings (npairs = 140), and (b) within the 131 monozygotic (MZ) twin pairs. Consistent with previous studies, HAB mediated the association between CM and AGG when familial confounding was uncontrolled. No support was found for the mediation when controlling for familial confounding. Between-pair associations were found between CM and AGG, and between CM and HAB. In addition, within-pair associations were found between HAB and AGG, and between CM and AGG, however, these were nonsignificant in the discordant MZ analysis, offering the most stringent control of familial confounding. The results indicate the necessity of taking familial confounding into account when investigating the development of AGG.

Preliminary Evidence for an Association Between Variants of the Catechol-O-Methyltransferase (COMT) Gene and Premature Ejaculation.

BACKGROUND: Studies have suggested that dopamine plays a role in the neurobiological mechanism that triggers ejaculation, leading scientists to hypothesize that dopamine-related genetic polymorphisms could contribute to symptoms of premature ejaculation (PE). AIM: To investigate associations between dopamine receptor and catechol-O-methyltransferase (COMT; an enzyme involved in the catabolism of dopamine) gene-linked polymorphisms and PE. METHODS: PE status in patient groups was determined by clinical diagnosis performed by a physician specializing in sexual medicine. Self-reported PE symptoms from a validated questionnaire also were reported. Saliva samples were collected from 149 patients with PE and 1,022 controls from a population-based sample. In total, we tested associations between PE and 11 single-nucleotide polymorphisms in the dopamine receptor D1, D2, and D3 genes and in the COMT gene. OUTCOMES: We found no associations between dopamine receptor gene polymorphisms and PE, but 2 COMT-linked loci (rs4680 and rs4818) had significant associations after correction for multiple testing. RESULTS: 1 COMT gene-linked locus that was associated with PE symptoms in the present study, rs4680, is a well-documented functional polymorphism that causes a valine-to-methionine substitution. The other polymorphism, rs4818, is in high linkage disequilibrium with the rs4680 locus, indicating that they capture the same effect. Surprisingly, the rs4680 variant that was statistically significantly more prevalent in the PE group (ie, the valine-encoding allele) has been associated with higher enzymatic activity and therefore lower synaptic dopamine levels. CLINICAL TRANSLATION: Drugs targeting the dopaminergic system could affect PE symptoms. STRENGTHS AND LIMITATIONS: No replication sample was available for the present study; thus, our findings should be interpreted with caution. Moreover, a limitation of our study is the small sample in the context of genetic association studies (although it should be mentioned that genetically informative samples with phenotypic information about PE symptoms are scarce, and most previous genetic association studies of PE have used samples of similar or smaller size). However, our results are plausible: we report an association between one of the most extensively studied and understood genetic polymorphisms in psychiatric research and PE, and our results are in line with the long-standing hypothesis that dopamine influences human ejaculatory function. CONCLUSIONS: We report an association between 2 COMT gene-linked loci and PE symptoms, but our results should be treated with caution until independently replicated. Jern P, Johansson A, Strohmaier J, et al. Preliminary Evidence for an Association Between Variants of the Catechol-O-Methyltransferase (COMT) Gene and Premature Ejaculation. J Sex Med 2017;14:1558-1565.

Nausea and Vomiting During Pregnancy is Highly Heritable.

Nausea and vomiting during pregnancy (NVP) affects about 70 % of all expectant mothers and commonly impacts their physical health and psychosocial functioning. The aim of this study was to estimate the heritability of the presence, duration and severity of NVP. The sample consisted of 1723 women (M age = 41.78, SD = 11.67) including twins in both complete and incomplete pairs and their sisters from two cohorts participating in the NVP Genetics Consortium. The sample comprised 159 monozygotic and 140 dizygotic complete twin pairs, and 69 twin-sister pairs. We applied an extended twin design using OpenMx and Mx for secondary analysis. Individual differences in NVP were best explained by additive genetic and unique environmental effects. Heritability estimates were 73 % (95 % CIs = 57-84 %) for presence, 51 % (95 % CIs = 36-63 %) for duration and 53 % (95 % CIs = 38-65 %) for severity of NVP. The genetic correlation between duration and severity was almost perfect. Our results show that genes play an important role in different aspects of NVP and justify the importance of searching for genetic variants.

Paraphilic Sexual Interests and Sexually Coercive Behavior: A Population-Based Twin Study.

Prior research with selected clinical and forensic samples suggests associations between paraphilic sexual interests (e.g., exhibitionism and sexual sadism) and sexually coercive behavior. However, no study to date used a large, representative and genetically informative population sample to address the potential causal nature of this association. We used self-report data on paraphilic and sexually coercive behavior from 5990 18- to 32-year-old male and female twins from a contemporary Finnish population cohort. Logistic regression and co-twin control models were employed to examine if paraphilic behaviors were causally related to coercive behavior or if suggested links were confounded by familial (genetic or common family environment) risk factors. Results indicated that associations between four out of five tested paraphilic behaviors (exhibitionism, masochism, sadism, and voyeurism, respectively) and sexually coercive behavior were moderate to strong. Transvestic fetishism was not independently associated with sexual coercion. Comparisons of twins reporting paraphilic behavior with their paraphilic behavior-discordant twin further suggested that associations were largely independent of shared genetic and environmental confounds, consistent with a causal association. In conclusion, similar to previously reported predictive effects of paraphilias on sexual crime recidivism, paraphilic behavior among young adults in the general population increases sexual offending risk. Further, early identification of paraphilic interest and preventive interventions with at-risk individuals might also reduce perpetration of first-time sexual violence.

Genetic variation of the growth hormone secretagogue receptor gene is associated with alcohol use disorders identification test scores and smoking.

The multifaceted gut-brain peptide ghrelin and its receptor (GHSR-1a) are implicated in mechanisms regulating not only the energy balance but also the reward circuitry. In our pre-clinical models, we have shown that ghrelin increases whereas GHSR-1a antagonists decrease alcohol consumption and the motivation to consume alcohol in rodents. Moreover, ghrelin signaling is required for the rewarding properties of addictive drugs including alcohol and nicotine in rodents. Given the hereditary component underlying addictive behaviors and disorders, we sought to investigate whether single nucleotide polymorphisms (SNPs) located in the pre-proghrelin gene (GHRL) and GHSR-1a gene (GHSR) are associated with alcohol use, measured by the alcohol use disorders identification test (AUDIT) and smoking. Two SNPs located in GHRL, rs4684677 (Gln90Leu) and rs696217 (Leu72Met), and one in GHSR, rs2948694, were genotyped in a subset (n = 4161) of a Finnish population-based cohort, the Genetics of Sexuality and Aggression project. The effect of these SNPs on AUDIT scores and smoking was investigated using linear and logistic regressions, respectively. We found that the minor allele of the rs2948694 SNP was nominally associated with higher AUDIT scores (P = 0.0204, recessive model) and smoking (P = 0.0002, dominant model). Furthermore, post hoc analyses showed that this risk allele was also associated with increased likelihood of having high level of alcohol problems as determined by AUDIT scores ≥ 16 (P = 0.0043, recessive model). These convergent findings lend further support for the hypothesized involvement of ghrelin signaling in addictive disorders.

Rigorous tests of gene-environment interactions in a lab study of the oxytocin receptor gene (OXTR), alcohol exposure, and aggression.

Naturalistic studies of gene-environment interactions (G X E) have been plagued by several limitations, including difficulty isolating specific environmental risk factors from other correlated aspects of the environment, gene-environment correlation (rGE ), and the use of a single genetic variant to represent the influence of a gene. We present results from 235 Finnish young men in two lab studies of aggression and alcohol challenge that attempt to redress these limitations of the extant G X E literature. Specifically, we use a latent variable modeling approach in an attempt to more fully account for genetic variation across the oxytocin receptor gene (OXTR) and to robustly test its main effects on aggression and its interaction with alcohol exposure. We also modeled aggression as a latent variable comprising various indices, including the average and maximum levels of aggression, the earliest trial on which aggression was expressed, and the proportion of trials on which the minimum and maximum levels of aggression were expressed. The best fitting model for the genetic variation across OXTR included six factors derived from an exploratory factor analysis, roughly corresponding to six haplotype blocks. Aggression levels were higher on trials in which participants were administered alcohol, won, or were provoked. There was a significant main effect of OXTR on aggression across studies after controlling for covariates. The interaction of OXTR and alcohol was also significant across studies, such that OXTR had stronger effects on aggression in the alcohol administration condition. © 2015 Wiley Periodicals, Inc.

A study of possible associations between single nucleotide polymorphisms in the estrogen receptor 2 gene and female sexual desire.

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.

Sexually coercive behavior following childhood maltreatment.

Child maltreatment is associated with adult sexually coercive behavior. The association may be causal or confounders that increase the risk of both childhood victimization and sexually coercive behavior might explain the observed links. We examined if childhood maltreatment was related to sexual coercion independently of familial (genetic or common family environment) risk factors, thereby addressing potential causality. Participants were 6,255 18 to 33-year-old twins from the Finnish population-based study "Genetics of Sex and Aggression" who responded to self-report questionnaires of child maltreatment and sexually coercive behavior. We used generalized estimating equations to elucidate risk of sexual coercion in maltreated compared to unrelated, non-maltreated individuals. To adjust for unmeasured familial factors, we used the co-twin control method and compared sexual coercion risk within maltreatment-discordant twin pairs. Further, we examined possible differential effects of maltreatment subtypes and compared mean differences in maltreatment summary scores between sexually coercive individuals and controls. Sexual coercion was moderately more common among individuals maltreated as children versus unrelated controls (38.3 vs. 22.8 %; age- and gender-adjusted odds ratio, aOR = 2.31, 95 % CI 1.75-3.05) and the risk increase remained similar within maltreatment-discordant twins (OR = 2.82, 95 % CI 1.42-5.61). Moreover, different maltreatment subtypes predicted sexual coercion equally well and effect sizes remained similar within discordant twin pairs. We conclude that associations between child maltreatment and sexual coercion are largely independent of shared familial confounds, consistent with a causal inference. Importantly, detection and targeted interventions for maltreated children should remain a priority to reduce societal sexually coercive behavior.

The Genetics of Sexuality and Aggression (GSA) twin samples in Finland.

The Genetics of Sexuality and Aggression (GSA) project was launched at the Abo Akademi University in Turku, Finland in 2005 and has so far undertaken two major population-based data collections involving twins and siblings of twins. To date, it consists of about 14,000 individuals (including 1,147 informative monozygotic twin pairs, 1,042 informative same-sex dizygotic twin pairs, 741 informative opposite-sex dizygotic twin pairs). Participants have been recruited through the Central Population Registry of Finland and were 18-49 years of age at the time of the data collections. Saliva samples for DNA genotyping (n = 4,278) and testosterone analyses (n = 1,168) were collected in 2006. The primary focus of the data collections has been on sexuality (both sexual functioning and sexual behavior) and aggressive behavior. This paper provides an overview of the data collections as well as an outline of the phenotypes and biological data assembled within the project. A detailed overview of publications can be found at the project's Web site: http://www.cebg.fi/.

The Prevalence of BDSM in Finland and the Association between BDSM Interest and Personality Traits.

According to previous research, interest in BDSM (Bondage-Discipline, Dominance-Submission and Sadomasochism) activities is high in several European countries and various BDSM practices are not uncommon. There is a limited amount of research on the personalities of BDSM practitioners, but in previous research practitioners have been found to have better overall well-being and to be more educated than the general population. The current study explored the prevalence of BDSM interest and practice in a Finnish sample (n = 8,137, age range 18-60, M = 30.14, SD = 8.08) and investigated the association between BDSM interest and personality measured with the six-factor personality measure HEXACO. A total of 38% of the sample was interested in BDSM sex and non-heterosexual individuals displayed almost twice as much interest and at most 83% more participation in BDSM than heterosexual individuals. Younger participants (18-28 years old) displayed almost three times as much interest than older participants. There were some associations between BDSM interest and personality factors, but the effect sizes of these associations were modest. The study shows that BDSM interest is quite common among the Finnish population.

Are single nucleotide polymorphisms in the oxytocin and vasopressin 1A/1B receptor genes likely candidates for variation in ejaculatory function?

UNLABELLED: What's known on the subject? and What does the study add? There is also evidence that the etiology of premature ejaculation is partially genetic. So far, all molecular genetic studies of premature ejaculation have focused on serotonergic and dopaminergic genes. Serotonergic and dopaminergic neurotransmission aside, studies on both animals and humans have shown that both oxytocin and vasopressin are also involved in ejaculatory function. The present study is, to our knowledge, the first to investigate effects of polymorphisms in oxytocin and vasopressin receptor genes on ejaculatory function. Although a large sample (1517 men) was available for the present study, we could not detect any clear-cut effects of any gene variant on ejaculatory function. We detected a heterozygote effect of one polymorphism (rs75775) in the oxytocin receptor gene. Rare variants of the vasopressin receptor 1A gene may theoretically have a stronger impact on ejaculatory function, but would need a very large sample in order to be established. Based on our results, we conclude that the oxytocin and vasopressin receptor genes are unlikely targets for successful pharmacogenetic interventions. OBJECTIVES: • To investigate associations between single nucleotide polymorphisms (SNPs) linked to the oxytocin, and arginine vasopressin 1A and 1B receptor genes and ejaculatory function. • To investigate these associations in a large, population-based sample. PATIENTS AND METHODS: • In all, 1517 male twins and non-twin brothers of twins aged 18-45 years (mean = 26.43; sd = 4.87) provided questionnaire data regarding ejaculatory function and relevant covariates and saliva samples for genotyping. • A Bayesian linear mixed-effects model, which appropriately controls for between-subjects dependence, was used to estimate genotype associations. • We corrected for multiple testing using a linkage disequilibrium correlation measure. RESULTS: • We found a heterozygote effect on one SNP in the oxytocin receptor gene (rs75775), so that individuals heterozygous for this SNP had significantly elevated risk for premature ejaculation symptoms compared with carriers of either homozygote. • Several SNPs in the arginine vasopressin receptor genes had rare or very rare genotypes. This study may be underpowered to detect potential effects of rare genotypic variants in arginine vasopressin receptor genes. CONCLUSIONS: • Our results regarding the oxytocin receptor polymorphisms support previous studies that indicate a complex relationship between oxytocin and ejaculatory function. • Oxytocin receptor genes are, for example, unlikely suitable targets for pharmacogenetic intervention studies. • Rare variants in arginine vasopressin receptor genes may have significant effects on premature ejaculation, but would need larger sample sizes or case-control designs to be detected.

A study of possible associations between single nucleotide polymorphisms in the serotonin receptor 1A, 1B, and 2C genes and self-reported ejaculation latency time.

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-HT(1B) 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.

Controlling anger in self-reported sober and alcohol intoxicated states: moderating effects of trait anger and alcohol consumption.

Controlling anger in self-reported sober and alcohol intoxicated states: Moderating effects of trait anger and alcohol consumption. Scandinavian Journal of Psychology 52, 382-388. Retrospective self-reports about prior sober and alcohol intoxicated states were explored to reveal moderating effects of trait anger and alcohol consumption on anger control. The analyses were based on self-reports of trait anger and alcohol consumption as well as self-reports of the participants' typical levels of anger control in sober and alcohol intoxicated states in a population based sample of Finnish twins and their siblings (N = 4,852). The reported levels of anger control were lower regarding prior alcohol intoxicated states than sober states. A three-way interaction between alcohol consumption, trait anger and anger control was found. Whereas no interaction between alcohol consumption and trait anger was found in the self-reported sober state, there was an interactive effect of trait anger and alcohol consumption on anger control in the intoxicated state, indicating that the difference in anger control between those with high levels of alcohol consumption and those with low levels, was greater at higher levels of trait anger. Women had lower levels of anger control than men, but the relationship between trait anger, alcohol consumption and anger control was similar for both genders. In conclusion, the results showed that those with high levels of trait anger and alcohol consumption showed the lowest levels of anger control in self-reported alcohol intoxicated states, and indicate the importance of separating between anger control when sober and intoxicated since anger control seems to be differently related to at least trait anger and alcohol consumption in these states.

Testing causal models of the relationship between childhood gender atypical behaviour and parent-child relationship.

An association between childhood gender atypical behaviour (GAB) and a negative parent-child relationship has been demonstrated in several studies, yet the causal relationship of this association is not fully understood. In the present study, different models of causation between childhood GAB and parent-child relationships were tested. Direction of causation modelling was applied to twin data from a population-based sample (n= 2,565) of Finnish 33- to 43-year-old twins. Participants completed retrospective self-report questionnaires. Five different models of causation were then fitted to the data: GAB → parent-child relationship, parent-child relationship → GAB, reciprocal causation, a bivariate genetic model, and a model assuming no correlation. It was found that a model in which GAB and quality of mother-child, and father-child relationship reciprocally affect each other best fitted the data. The findings are discussed in light of how we should understand, including causality, the association between GAB and parent-child relationship.