Alexithymia is a personality construct characterized by difficulties in identifying and verbalizing feelings, a restricted imagination, and an externally oriented thinking style. As alexithymia shows marked overlap with depression, its independent nature as a personality construct is still being debated. The etiology of alexithymia is unknown, although childhood emotional neglect and attachment formation are thought to play important roles. In the FinnBrain Birth Cohort Study, experiences of early-life adversities (EA) and childhood maltreatment (CM) were studied in a sample of 2,604 men and women. The overlap and differences between depression and alexithymia were investigated by comparing their associations with EA types and adult attachment style. Alexithymia was specifically associated with childhood emotional neglect (odds ratio (OR) 3.8, p < .001), whereas depression was related to several types of EA. In depression co-occurring with alexithymia, there was a higher prevalence of emotional neglect (81.3% vs. 54.4%, p < .001), attachment anxiety (t = 2.38, p = .018), and attachment avoidance (t = 4.03, p < .001). Early-life adversities were markedly different in the alexithymia group compared to those suffering from depression, or healthy controls. Depression with concurrent alexithymia may represent a distinct subtype, specifically associated with childhood experiences of emotional neglect, and increased attachment insecurity compared to non-alexithymic depression.

Externalizing behaviors (EBs) pertain to a diverse set of aggressive, antisocial, and potentially destructive behaviors directed toward the external environment. They range from nonclinical to clinical in severity, associated with opposition, aggression, hyperactivity, or impulsivity, and are considered a risk factor for the emergence of psychopathology later in adulthood. Focusing on community adolescents (N = 102; 49 female and 53 male adolescents; age range 12–19 years), this study aimed to explore the relations between EBs and the cortical thickness of regions of interest as well as to identify possible risk markers that could improve understanding of the EB construct. Using a mixed cross-sectional and prospective design (1-year follow-up), we report specific associations with cortical thickness of the left insular, right orbitofrontal, and left anterior cingulate cortex. Specifically, thinner left insular and right orbitofrontal cortex was associated with higher EBs, and thinner left anterior cingulate cortex predicted less reduction in EBs 1 year later. In addition, further examination of the aggression and rule-breaking subscales of the Youth/Adult Self-Report, used to assess EBs, revealed specific associations with insular subregions. Findings suggest that cortical structure morphology may significantly relate to the expression and maintenance of EBs within the general population of adolescents.

While neurodevelopmental disorders (NDDs) are highly heritable, several environmental risk factors have also been suggested. However, the role of familial confounding is unclear. To shed more light on this, we reviewed the evidence from twin and sibling studies. A systematic review was performed on case control and cohort studies including a twin or sibling within-pair comparison of neurodevelopmental outcomes, with environmental exposures until the sixth birthday. From 7,315 screened abstracts, 140 eligible articles were identified. After adjustment for familial confounding advanced paternal age, low birth weight, birth defects, and perinatal hypoxia and respiratory stress were associated with autism spectrum disorder (ASD), and low birth weight, gestational age and family income were associated with attention-deficit/hyperactivity disorder (ADHD), categorically and dimensionally. Several previously suspected factors, including pregnancy-related factors, were deemed due to familial confounding. Most studies were conducted in North America and Scandinavia, pointing to a global research bias. Moreover, most studies focused on ASD and ADHD. This genetically informed review showed evidence for a range of environmental factors of potential casual significance in NDDs, but also points to a critical need of more genetically informed studies of good quality in the quest of the environmental causes of NDDs.

For African American emerging adult men, developmental challenges are evident in their escalating substance abuse and depressive symptoms; this is particularly true for men from low-resource communities. The present study tests a developmental model linking childhood adversity and contemporaneous contextual stressors to increases in emerging adults’ substance use and depressive symptoms, indirectly, via increases in defensive/hostile relational schemas and social developmental risk factors (e.g., risky peers and romantic partners, lack of involvement in school or work). We also advance exploratory hypotheses regarding DNA methylation in the oxytocin receptor gene (OXTR) as a moderator of the effects of stress on relational schemas. Hypotheses were tested with three waves of data from 505 rural African American men aged 19–25 years. Adverse childhood experiences predicted exposure to emerging adult contextual stressors. Contextual stressors forecast increases in defensive/hostile relational schemas, which increased social developmental risk factors. Social developmental risk factors proximally predicted increases in substance abuse and depressive symptoms. OXTR DNA methylation moderated the effects of contextual stressors on defensive/hostile relational schemas. Findings suggest that early exposures to stress carry forward to affect the development of social developmental risk factors in emerging adulthood, which place rural African American men at risk for increased substance abuse and depressive symptoms during the emerging adult years.

Early adolescence is thought to represent a window of vulnerability when exposure to substances is particularly harmful, partly because the neurotoxic effects of adolescent substance use may derail self-regulation development. However, previous studies fail to account for externalizing symptoms, such as aggression and delinquency, that accompany adolescent substance use and may also derail the development of self-regulation. The current study aims to clarify whether the neurotoxic effects of adolescent substance use are associated with deficits in effortful control (EC) after accounting for externalizing symptoms and to examine reciprocal relationships between EC, externalizing symptoms, and substance use. A longitudinal sample of adolescents (N = 387) was used to estimate bifactor models of externalizing symptoms across five assessments (Mage = 11.6 to 19.9). The broad general externalizing factors were prospectively associated with declines in EC across adolescence and emerging adulthood. However, the narrow substance use specific factors were not prospectively associated with EC. Findings suggest that the broader externalizing context, but not the specific neurotoxic effects of substance use, may hamper self-regulation development. It is critical to account for the hierarchical structure of psychopathology, namely externalizing symptoms, when considering development of EC.