Childhood abuse can alter biological systems and increase risk for adult psychopathology. Epigenetic mechanisms, alterations in DNA structure that regulate the gene expression, are a potential mechanism underlying this risk. While abuse associates with methylation of certain genes, particularly those in the stress response system, no study to date has evaluated abuse and methylation of the oxytocin receptor (OXTR). However, studies support a role for OXTR in the link between abuse and adverse adult outcomes, showing that abuse can confer greater risk for psychiatric symptoms in those with specific OXTR genotypes. Our study therefore sought to (1) assess the role of epigenetics in the link between abuse and psychopathology and (2) to begin to integrate the genetic and epigenetic literature by exploring associations between OXTR genotypes and DNA CpG methylation. Data on 18 OXTR CpG sites, 44 SNPs, childhood abuse, and adult depression and anxiety symptoms were assessed in 393 African American adults (age = 41±12.8). Overall, 68% of genotypes associated with methylation of nearby CpG sites, with a subset surviving multiple test correction. Child abuse associated with higher methylation of two CpG sites yet did not survive correction or serve as a mediator of psychopathology. However, abuse interacted with CpG methylation to predict psychopathology. These findings suggest a role for OXTR in understanding the influence of early environments on adult psychiatric symptoms.

Polymorphisms in the oxytocin receptor gene (OXTR) are commonly associated with prosocial behaviors in the extant literature, yet their role in antisocial behaviors has rarely been explored, particularly during the transition from adolescence to early adulthood. We examined a prospective cohort (N=404), collecting youth, mother and clinician reports of conduct disordered and antisocial behavior at age 15 and 20. The oxytocin receptor rs53576 polymorphism was hypothesized to interact with social stress to predict antisocial outcomes. Structural equation modeling (SEM) results revealed a significant main effect at age 15 (p=.025); those with the G allele exhibited higher levels of conduct problems. SEM revealed a significant gene-by-environment interaction at age 20 (p=.029); those with the G allele who experienced high social stress exhibited higher levels of antisocial behavior. Heterozygous (AG) grouping models were compared and parameter estimations supported G dominant groupings. These novel findings suggest that rs53576 polymorphisms may influence social salience and contribute to risk for antisocial outcomes, particularly under conditions of high social stress.

Sexuality-related constructs such as sexual arousal, sexual sensation seeking (SSS) and sexual satisfaction have been related to sexual behaviors that place one at risk for adverse consequences such as sexually transmitted infections (STIs), HIV, and unintended pregnancy. The biopsychosocial model posits an array of factors, ranging from social environmental factors, biological, and psychological predispositions that may be associated with these sexuality constructs in adolescent samples. African-American females aged 14-20 were recruited from reproductive health clinics for an HIV intervention. Baseline survey and follow-up DNA data (N=304) was used to assess biological, psychological and social environmental associations with the sexuality constructs of arousal, SSS, and sexual satisfaction. In multivariable linear regressions, a higher depressive symptom rating was associated with higher arousability while short serotonin allele(s) status was associated with lower arousability. Impulsivity and perceived peer norms supportive of unsafe sexual behaviors were associated with increased SSS, and short serotonin allele(s) status was associated with lower SSS. Higher social support was also associated with higher levels of sexual satisfaction while short serotonin allele(s) status was associated with lower satisfaction. The sexuality constructs were also significantly related to number of sex partners, frequency of vaginal sex, and number of unprotected vaginal sex acts in the past six months. These findings emphasize the importance of understanding biopsychosocial factors, including the role of serotonin as an indicator of natural variations in sexual inclination and behaviors, that influence sexuality constructs, which in turn are associated with sexual behaviors, to allow further refinement of sexual health clinical services and programs and promote the development of healthy sexuality.

22q11.2 deletion syndrome (22q11.2DS) is a genomic disorder reported to associate with autism spectrum disorders (ASDs) in 15–50% of cases; however, others suggest that individuals with 22q11.2DS present psychiatric or behavioral features associated with ASDs, but do not meet full criteria for ASD diagnoses. Such wide variability in findings may arise in part due to methodological differences across studies. Our study sought to determine whether individuals with 22q11.2DS meet strict ASD diagnostic criteria using research-based guidelines from the Collaborative Programs of Excellence in Autism (CPEA), which required a gathering of information from three sources: the Autism Diagnostic Interview-Revised (ADI-R), the Autism Diagnostic Observational Schedule (ADOS), and a clinician’s best-estimate diagnosis. Our study examined a cohort of children, adolescents, and young adults (n = 56) with 22q11.2DS, who were ascertained irrespective of parents’ behavioral or developmental concerns, and found that 17.9% (n = 10) of the participants met CPEA criteria for an ASD diagnosis, and that a majority showed some level of social-communication impairment or the presence of repetitive behaviors. We conclude that strictly defined ASDs occur in a substantial proportion of individuals with 22q11.2DS, and recommend that all individuals with 22q11.2DS be screened for ASDs during early childhood.

Introduction Virtually no studies have examined the potential role that chronic stress, particularly the stress associated with socioeconomic (SES) strain, may play on STI risk. This study examined the association between SES-related risk at baseline to STI acquisition and reinfection over 36 months of follow-up. Methods 627 African-American female adolescents, ages 14–20 years, recruited from sexual health clinics in Atlanta, GA participated in a randomized controlled HIV prevention trial, and returned for at least 1 follow-up assessment. Following baseline assessment, 6 waves of data collection occurred prospectively over 36 months. Chronic SES-related risk was assessed as a sum of yes-no exposure to seven risk indicators. Laboratory confirmed tests for C. trachomatis and N. gonorrheoea were performed at each follow-up. Results In multivariable regression analysis, SES-related risk significantly predicted STI acquisition over 36 months (AOR = 1.22) and STI reinfection (AOR = 1.16) above and beyond other known correlates of STI. Discussion Findings demonstrate that SES-related risk was predictive of both STI acquisition and reinfection among young African-American females. They are consistent with propositions that some health disparities observed in adulthood may be linked to earlier chronically stress-inducing life experiences, particularly experiences associated with low SES conditions. Although various explanations exist for the observed connection between SES-related risk and subsequent STI acquisition and/or reinfection across 36 months of follow-up, these findings highlight the need for further research to elucidate the exact pathway(s) by which SES-related risk influences later STI acquisition in order to refine STI prevention interventions for this population.