ABSTRACT
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.
Subject(s)
Aggression , Rape , Humans , Male , Adult , Aggression/psychology , Coercion , Fantasy , Cross-Sectional Studies , Rape/psychology , Sexual Behavior/psychologyABSTRACT
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.
Subject(s)
Parenting , Twins , Adult , Humans , Antisocial Personality Disorder/genetics , Genotype , Phenotype , Twins/geneticsABSTRACT
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.
Subject(s)
Sadism , Sexual Behavior , Humans , Adolescent , Young Adult , Adult , Middle Aged , Finland/epidemiology , Prevalence , Masochism , PersonalityABSTRACT
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.
Subject(s)
Psychological Distress , Sexual Behavior , Humans , Sexual Behavior/psychology , Twins , Heterosexuality , Anxiety/psychologyABSTRACT
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.
Subject(s)
Antisocial Personality Disorder , Conduct Disorder , Animals , Mice , Antisocial Personality Disorder/genetics , Genome-Wide Association Study , Conduct Disorder/genetics , Conduct Disorder/psychology , Aggression/psychology , Multifactorial Inheritance/genetics , Membrane Proteins/genetics , Nerve Tissue Proteins/geneticsABSTRACT
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.
Subject(s)
Bullying , Crime Victims , Adolescent , Bullying/psychology , Child , Crime Victims/psychology , Humans , Peer Group , Schools , Students/psychologyABSTRACT
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.
Subject(s)
Child Abuse , Siblings , Aggression , Bias , Child , Female , Finland , Humans , Twins, MonozygoticABSTRACT
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.
Subject(s)
Erectile Dysfunction , Premature Ejaculation , Adult , Androgens , Comorbidity , Ejaculation , Erectile Dysfunction/epidemiology , Erectile Dysfunction/genetics , Finland/epidemiology , Humans , Male , Polymorphism, Genetic/genetics , Premature Ejaculation/epidemiology , Premature Ejaculation/genetics , TestosteroneABSTRACT
Experiencing emotional, physical, and/or sexual abuse in childhood increases the risk (compared with baseline) of developing psychopathological symptoms in adulthood. In the present study, we explored the effects of experiencing only a single abusive event on adulthood psychopathology, and compared this with the risk in individuals with no abusive experiences and with the risk in individuals with several abusive experiences. We used a Finnish population-based sample of 10,980 adult participants (3,766 male and 7,214 female twins and their siblings). The participants reported abuse experiences using the Childhood Trauma Questionnaire (CTQ) and current psychopathology symptoms using the depression and anxiety scales of the Brief Symptom Inventory-18 (BSI-18). We found that in both men and women even single experiences of emotional and sexual abuse were associated with increased psychopathology symptoms compared with no abuse experiences. Single experiences of physical abuse did not, however, increase the risk in either women or men. As expected, experiences of repeated abuse (of all abuse types) increased the risk of psychopathology symptoms compared with experiences of single abuse. When we isolated individuals who only had a single experience of any type of abuse (i.e., emotional, physical, or sexual) to control for possible co-morbidity, no increased risk was found. This study shows that individuals who report experiencing single events of abuse of a specific abuse type have an increased risk of displaying psychopathology symptoms in adulthood. This increase is, however, mainly due to co-morbidity of abuse types.
ABSTRACT
Psychopathy is characterized by callous affect, interpersonal manipulation, a deviant lifestyle, and antisocial behavior. Previous research has linked psychopathic traits to childhood trauma, but also to the upstream variable number tandem repeat (uVNTR) polymorphism of the monoamine oxidase A (MAOA) gene. An interaction between childhood trauma and MAOA genotype has been associated with antisocial behavior, but so far little is known about interaction effects of childhood trauma and the MAOA uVNTR on psychopathy. In order to bridge this gap, we used data of 1531 male and 1265 female twins and their siblings from a Finnish community sample to estimate structural equation models. The psychopathy and childhood trauma constructs were conceptualized as bifactor models with one general and two orthogonal group factors. Data comprised self-reports on childhood trauma and psychopathic traits as well as MAOA uVNTR genotype. In both genders, childhood trauma was associated with the general factor that represents the overarching psychopathy construct, and with the group factor that captures social deviance, but not with the group factor capturing psychopathic core personality traits. Women with a low activity variant of the MAOA uVNTR reported slightly higher levels of psychopathy than those with a high activity allele, but only with respect to the general psychopathy factor. There was no evidence for an interaction effect between MAOA uVNTR genotype and childhood trauma on psychopathy in either gender. Our results suggest that psychopathy in general and social deviance in particular are associated with childhood trauma in men and women, and that psychopathic traits are subject to variation in the MAOA uVNTR genotype in women.
Subject(s)
Antisocial Personality Disorder/genetics , Adolescent , Adult , Adverse Childhood Experiences , Alleles , Antisocial Personality Disorder/psychology , Female , Finland , Gene Frequency/genetics , Genotype , Humans , Life Change Events , Male , Middle Aged , Minisatellite Repeats/genetics , Monoamine Oxidase/genetics , Monoamine Oxidase/physiology , Polymorphism, Genetic/genetics , Promoter Regions, Genetic/genetics , Self Report , Social Behavior , Social Behavior Disorders/genetics , TwinsABSTRACT
In the present study, we investigated the possible gene-environment correlation between the dopamine transporter gene (DAT1) polymorphism and childhood experiences of abuse and neglect. Genetic information was obtained from 1,442 male and 2,178 female twins and their siblings drawn from a Finnish population-based sample. The Childhood Trauma Questionnaire was used to measure the childhood experiences of abuse and neglect. In men, the DAT1 polymorphism was associated with having experienced sexual abuse in childhood, such that men with the 9R9R genotype reported less sexual abuse experiences than men with the 9R10R or the 10R10R genotypes. In women, there was an association between the DAT1 polymorphism and childhood experiences of emotional abuse, such that women with the 9R9R genotype reported less emotional abuse experiences than women with the 9R10R or 10R10R genotypes. No other associations between the DAT1 polymorphism and childhood experiences of abuse and neglect were found. In sum, the results suggested that some genetic components might predispose children to experience childhood abuse and neglect. Possible reasons for this association were discussed.
Subject(s)
Child Abuse/psychology , Dopamine Plasma Membrane Transport Proteins/genetics , Gene-Environment Interaction , Genotype , Polymorphism, Genetic/genetics , Adult , Child , Female , Gene Frequency/genetics , Humans , Male , Surveys and QuestionnairesABSTRACT
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.
Subject(s)
Catechol O-Methyltransferase/genetics , Premature Ejaculation/enzymology , Adult , Alleles , Catechol O-Methyltransferase/metabolism , Ejaculation , Female , Genetic Association Studies , Genotype , Humans , Male , Middle Aged , Mutation, Missense , Polymorphism, Single Nucleotide , Premature Ejaculation/genetics , Premature Ejaculation/physiopathologyABSTRACT
Importance: Antisocial behavior (ASB) places a large burden on perpetrators, survivors, and society. Twin studies indicate that half of the variation in this trait is genetic. Specific causal genetic variants have, however, not been identified. Objectives: To estimate the single-nucleotide polymorphism-based heritability of ASB; to identify novel genetic risk variants, genes, or biological pathways; to test for pleiotropic associations with other psychiatric traits; and to reevaluate the candidate gene era data through the Broad Antisocial Behavior Consortium. Design, Setting, and Participants: Genome-wide association data from 5 large population-based cohorts and 3 target samples with genome-wide genotype and ASB data were used for meta-analysis from March 1, 2014, to May 1, 2016. All data sets used quantitative phenotypes, except for the Finnish Crime Study, which applied a case-control design (370 patients and 5850 control individuals). Main Outcome and Measures: This study adopted relatively broad inclusion criteria to achieve a quantitative measure of ASB derived from multiple measures, maximizing the sample size over different age ranges. Results: The discovery samples comprised 16â¯400 individuals, whereas the target samples consisted of 9381 individuals (all individuals were of European descent), including child and adult samples (mean age range, 6.7-56.1 years). Three promising loci with sex-discordant associations were found (8535 female individuals, chromosome 1: rs2764450, chromosome 11: rs11215217; 7772 male individuals, chromosome X, rs41456347). Polygenic risk score analyses showed prognostication of antisocial phenotypes in an independent Finnish Crime Study (2536 male individuals and 3684 female individuals) and shared genetic origin with conduct problems in a population-based sample (394 male individuals and 431 female individuals) but not with conduct disorder in a substance-dependent sample (950 male individuals and 1386 female individuals) (R2 = 0.0017 in the most optimal model, P = 0.03). Significant inverse genetic correlation of ASB with educational attainment (r = -0.52, P = .005) was detected. Conclusions and Relevance: The Broad Antisocial Behavior Consortium entails the largest collaboration to date on the genetic architecture of ASB, and the first results suggest that ASB may be highly polygenic and has potential heterogeneous genetic effects across sex.
Subject(s)
Antisocial Personality Disorder , Conduct Disorder , Adolescent , Adult , Antisocial Personality Disorder/epidemiology , Antisocial Personality Disorder/genetics , Antisocial Personality Disorder/psychology , Child , Conduct Disorder/epidemiology , Conduct Disorder/genetics , Conduct Disorder/psychology , Environment , Female , Finland/epidemiology , Genetic Variation , Genome-Wide Association Study , Humans , Male , Middle Aged , Multifactorial Inheritance , Sex FactorsABSTRACT
Purpose: We investigated whether participants who reported more often occurring vocal symptoms showed higher salivary cortisol levels and if such possible associations were different for men and women. Method: The participants (N = 170; men n = 49, women n = 121) consisted of a population-based sample of Finnish twins born between 1961 and 1989. The participants submitted saliva samples for hormone analysis and completed a web questionnaire including questions regarding the occurrence of 6 vocal symptoms during the past 12 months. The data were analyzed using the generalized estimated equations method. Results: A composite variable of the vocal symptoms showed a significant positive association with salivary cortisol levels (p < .001). Three of the 6 vocal symptoms were significantly associated with the level of cortisol when analyzed separately (p values less than .05). The results showed no gender difference regarding the effect of salivary cortisol on vocal symptoms. Conclusions: There was a positive association between the occurrence of vocal symptoms and salivary cortisol levels. Participants with higher cortisol levels reported more often occurring vocal symptoms. This could have a connection to the influence of stress on vocal symptoms because stress is a known risk factor of vocal symptoms and salivary cortisol can be seen as a biomarker for stress.
Subject(s)
Hydrocortisone/metabolism , Saliva/metabolism , Voice Disorders/metabolism , Adult , Cohort Studies , Female , Humans , Linear Models , Male , Middle Aged , Risk Factors , Sex Characteristics , Stress, Psychological/metabolism , Surveys and Questionnaires , Voice/physiologyABSTRACT
Purpose: Oxytocin and arginine vasopressin are associated with different aspects of the stress response. As stress is regarded as a risk factor for vocal symptoms, we wanted to explore the association between the oxytocin receptor gene (OXTR) and arginine vasopressin 1A receptor gene (AVPR1A) single-nucleotide polymorphisms (SNPs) and vocal symptoms. We also wanted to explore whether such effects might be mediated by cortisol because oxytocin and vasopressin are associated with cortisol levels. Method: A population-based sample (N = 657) of Finnish twins (born 1961-1989) completed a web questionnaire on the occurrence of vocal symptoms. A total of 170 participants submitted saliva samples for hormone analysis. A total of 20 OXTR and AVPR1A SNPs were analyzed. Results: Three OXTR polymorphisms (rs2270465, rs2268493, rs7632287) and 2 AVPR1A polymorphisms (rs1587097, rs1042615) showed nominal effects (p < .05) on vocal symptoms, of which 1 (rs1587097) remained significant after correcting for multiple testing (p = .003). We found potential mediation of the effect of the OXTR rs2268493 polymorphism on vocal symptoms through levels of cortisol. Conclusions: The associations between variants of OXTR and AVPR1A and vocal symptoms indicate that oxytocin and vasopressin might influence vocal symptoms. The effect of oxytocin seems to be partly mediated through cortisol actions.
Subject(s)
Genetic Predisposition to Disease , Hydrocortisone/metabolism , Polymorphism, Single Nucleotide , Receptors, Oxytocin/genetics , Receptors, Vasopressin/genetics , Voice Disorders/genetics , Female , Finland , Genotyping Techniques , Humans , Male , Saliva/metabolism , Surveys and Questionnaires , Voice Disorders/metabolismABSTRACT
Childhood maltreatment increases the risk of subsequent depression, anxiety and alcohol abuse, but the rate of resilient victims is unknown. Here, we investigated the rate of victims that do not suffer from clinical levels of these problems after severe maltreatment in a population-based sample of 10980 adult participants. Compared to men, women reported more severe emotional and sexual abuse, as well as more severe emotional neglect. For both genders, severe emotional abuse (OR = 3.80 [2.22, 6.52]); severe physical abuse (OR = 3.97 [1.72, 9.16]); severe emotional neglect (OR = 3.36 [1.73, 6.54]); and severe physical neglect (OR = 11.90 [2.66, 53.22]) were associated with depression and anxiety while only severe physical abuse (OR = 3.40 [1.28, 9.03]) was associated with alcohol abuse. Looking at men and women separately, severe emotional abuse (OR = 6.05 [1.62, 22.60] in men; OR = 3.74 [2.06, 6.81] in women) and severe physical abuse (OR = 6.05 [1.62, 22.60] in men; OR = 3.03 [0.99, 9.33] in women) were associated with clinical levels of depression and anxiety. In addition, in women, severe sexual abuse (OR = 2.40 [1.10, 5.21]), emotional neglect (OR = 4.78 [2.40, 9.56]), and severe physical neglect (OR = 9.86 [1.99, 48.93]) were associated with clinical levels of depression and anxiety. Severe emotional abuse in men (OR = 3.86 [0.96, 15.48]) and severe physical abuse in women (OR = 5.18 [1.48, 18.12]) were associated with alcohol abuse. Concerning resilience, the majority of severely maltreated participants did not report clinically significant levels of depression or anxiety (72%), or alcohol abuse (93%) in adulthood. Although the majority of severely abused or neglected individuals did not show clinical levels of depression, anxiety or alcohol use, severe childhood maltreatment increased the risk for showing clinical levels of psychopathology in adulthood.
Subject(s)
Alcoholism/epidemiology , Anxiety/epidemiology , Child Abuse , Depression/epidemiology , Adult , Alcoholism/etiology , Anxiety/etiology , Child , Depression/etiology , Female , Finland/epidemiology , Humans , MaleSubject(s)
Inheritance Patterns , Nausea/genetics , Pregnancy Complications/genetics , Vomiting/genetics , Adolescent , Adult , Aged , Australia , Cohort Studies , Europe/epidemiology , Female , Genome-Wide Association Study , Humans , Middle Aged , Phenotype , Pregnancy , Pregnancy Complications/epidemiology , Twin Studies as Topic , Twins, Dizygotic/genetics , Twins, Monozygotic/genetics , Young AdultABSTRACT
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.
Subject(s)
Inheritance Patterns/genetics , Nausea/genetics , Vomiting/genetics , Adult , Aged , Cohort Studies , Confidence Intervals , Demography , Female , Finland , Humans , Middle Aged , Phenotype , Pregnancy , Spain , Twins, Dizygotic/genetics , Twins, Monozygotic/geneticsABSTRACT
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.
Subject(s)
Coercion , Paraphilic Disorders , Sexual Behavior , Twins , Adolescent , Adult , Female , Humans , Male , Paraphilic Disorders/epidemiology , Paraphilic Disorders/psychology , Risk Factors , Self Report , Sex Offenses , Sexual Behavior/psychology , Sexual Behavior/statistics & numerical data , Twins/psychology , Twins/statistics & numerical data , Young AdultABSTRACT
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.