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Epigenetic processes, including DNA methylation, change reliably with age across the lifespan, such that DNA methylation can be used as an “epigenetic clock”. This epigenetic clock can be used to predict age and age acceleration, which occurs when methylation-based prediction of age exceeds chronological age and has been associated with increased mortality. In the current study we examined epigenetic age acceleration using saliva samples collected from children between ages 6–13 (N = 101). Children’s exposure to neighborhood violence and heart rate during a stressful task were assessed. Age acceleration was associated with children’s direct experience of violence (p = 0.004) and with decreased heart rate (p = 0.002). Children who were predicted to be older than their chronological age had twice as much violence exposure as other children and their heart rate was similar to that of adults. The results remained significant after controlling for demographic variables, such as sex, income and education. This is the first study to show the effects of direct violence exposure on epigenetic aging in children using salivary DNA. Although longitudinal studies are needed to determine whether accelerated epigenetic aging leads to adverse health outcomes later in life, these data point to DNA methylation during childhood as a putative biological mechanism.

Risk for committing child abuse is frequently attributed to an intergenerational “cycle of violence” through which abuse as a child increases risk for committing abuse as a parent. While this hypothesis has support, more research is needed to understand the factors that account for this pattern of risk. Given literature suggesting that adults with a history of child maltreatment have increased risk for a wide range of psychopathology, this study examined the role of two behavioral endophenotypes, emotional dysregulation and negative affect, in the association between maternal experiences of childhood maltreatment and maternal child abuse potential among 83 low-income, primarily African-American mothers of elementary school age children. Results indicate that a mother’s experience of abuse as a child predicts later risk for abusive parenting as measured by child abuse potential scores. However, our data also indicate that the relationship between maternal experience of child abuse and later child abuse potential is mediated by maternal emotional dysregulation and negative affect.

Background: Complex posttraumatic stress disorder (CPTSD) is proposed for inclusion in the ICD-11 as a diagnosis distinct from posttraumatic stress disorder (PTSD), reflecting deficits in affective, self-concept, and relational domains. There remains significant controversy over whether CPTSD provides useful diagnostic information beyond PTSD and other comorbid conditions, such as depression or substance use disorders. Objective: The present study examined differences in psychiatric presentation for three groups: traumatized controls, DSM-5 PTSD subjects, and ICD-11 CPTSD subjects. Method: The sample included 190 African American women recruited from an urban public hospital where rates of trauma exposure are high. PTSD was measured using Clinician Administered PTSD Scale for DSM-5 and CPTSD was measured using clinician administered ICD-Trauma Interview. Psychiatric diagnoses and emotion dysregulation were also assessed. In a subset of women (n = 60), emotion recognition was measured using the Penn Emotion Recognition Task. Results: There were significant differences across groups on current and lifetime major depression (p < .001) and current and lifetime alcohol and substance dependence (p < .05), with CPTSD showing the highest rates of comorbidities. CPTSD women also showed significantly higher levels of childhood abuse and lower rates of adult secure attachment. Multivariate analysis of variance showed significantly more severe PTSD and depression symptoms and, as expected, more severe emotion dysregulation and dissociation, compared to DSM-5 PTSD and traumatized control groups. Individuals with CPTSD also had higher levels of emotion recognition to faces on a computer-based behavioural assessment, which may be related to heightened vigilance toward emotional cues from others. CPTSD women had better facial emotion recognition on a computer-based assessment, which may suggest heightened vigilance toward emotional cues. Conclusions: Our results suggest clear, clinically-relevant differences between PTSD and CPTSD, and highlight the need for further research on this topic with other traumatized populations, particularly studies that combine clinical and neurobiological data.

Cigarette smoking is an environmental risk factor for many chronic diseases, and disease risk can often be managed by smoking control. Smoking can induce cellular and molecular changes, including epigenetic modification, but the short- and long-term epigenetic modifications caused by cigarette smoking at the gene level have not been well understood. Recent studies have identified smoking-related DNA methylation (DNAm) sites in Caucasians. To determine whether the same DNAm sites associate with smoking in African Americans, and to identify novel smoking-related DNAm sites, we conducted a methylome-wide association study of cigarette smoking using a discovery sample of 972 African Americans, and a replication sample of 239 African Americans with two array-based methods. Among 15 DNAm sites significantly associated with smoking after correction for multiple testing in our discovery sample, 5 DNAm sites are replicated in an independent cohort, and 14 sites in the replication sample have effects in the same direction as in the discovery sample. The top two smoking-related DNAm sites in F2RL3 (factor II receptor-like 3) and GPR15 (G-protein-coupled receptor 15) observed in African Americans are consistent with previous findings in Caucasians. The associations between the replicated DNAm sites and smoking remain significant after adjusting for genetic background. Despite the distinct genetic background between African Americans and Caucasians, the DNAm from the two ethnic groups shares common associations with cigarette smoking, which suggests a common molecular mechanism of epigenetic modification influenced by environmental exposure.

The goal of collegial ethics is to actively support our colleagues and to develop the skills needed to do so. While collegial interactions are key for our careers, there is little or no training in this. Many of our actions and reactions with our colleagues are instinctive. Human nature has evolved to be self-protective, but many evolved and automatic responses to others are not always in the best interests of our society or of us. Developing courage and a style of supportive language, avoiding destructive acts, and adhering to the golden rule will improve our relationships and provide a more positive environment for all.

Individuals with posttraumatic stress disorder (PTSD) perform poorer on tests of intelligence than do individuals without PTSD, but the meaning of this finding is controversial. What continues to spark debate is whether either or both variables have a causal impact on the other and whether other factors better explain group differences. One such set of factors may be intergenerational effects of trauma on both cognitive development and risk for PTSD. This dissertation is comprised of three chapters. The first chapter presents three candidate theories to explain the relationship between intelligence and PTSD, namely a social resource theory, a plasticity theory, and a heritability theory. The second chapter presents a quantitative and qualitative review of 29 cross-sectional and 9 prospective studies, demonstrating significant deficits of intelligence, with perhaps more pronounced difference in analytical and analogical reasoning in individuals with PTSD. Results suggested that intelligence may be both an influencing factor prior to traumatic exposure and be impacted following it, supporting both the heritability and the plasticity theories. The third and final chapter presents findings from a cross-sectional study of mother-child pairs, examining intergenerational influences of maternal trauma, PTSD, and parenting (i.e., child abuse potential, overreactivity, and laxness) on the relationship of intelligence to PTSD in children. Participants were 48 mothers and 55 children (29 girls, 26 boys), ages 8 to 12 years, recruited from clinic waiting rooms of a public hospital. Mothers with PTSD performed poorer on a measure of analogical reasoning but, unexpectedly, demonstrated an advantage for nonverbal recognition, even accounting for trauma and other psychopathology. For children, lower verbal intelligence was associated with more frequent symptoms of PTSD, even accounting for child trauma and psychopathology; however maternal factors (i.e., maternal intelligence, trauma, PTSD, and parenting) did not predict child outcomes. Although evidence of an intergenerational impact of intelligence on risk for PTSD was not directly observed in this study, likely due to small sample size, other studies should consider the role of parenting on the relationship between children’s intelligence and symptoms of PTSD.