Evidence regarding the use of inner speech by individuals with autism spectrum disorder (ASD) is equivocal. To clarify this issue, the current study employed multiple techniques and tasks used across several previous studies. In Experiment 1, participants with and without ASD showed highly similar patterns and levels of serial recall for visually presented stimuli. Both groups were significantly affected by the phonological similarity of items to be recalled, indicating that visual material was spontaneously recoded into a verbal form. Confirming that short-term memory is typically verbally mediated among the majority of people with ASD, recall performance among both groups declined substantially when inner speech use was prevented by the imposition of articulatory suppression during the presentation of stimuli. In Experiment 2, planning performance on a tower of London task was substantially detrimentally affected by articulatory suppression among comparison participants, but not among participants with ASD. This suggests that planning is not verbally mediated in ASD. It is important that the extent to which articulatory suppression affected planning among participants with ASD was uniquely associated with the degree of their observed and self-reported communication impairments. This confirms a link between interpersonal communication with others and intrapersonal communication with self as a means of higher order problem solving.

Cardiovascular response patterns to laboratory-based social and physical exercise challenges were evaluated in 69 children and adolescents, 20 with selective mutism (SM), to identify possible neurophysiological mechanisms that may mediate the behavioral features of SM. Results suggest that SM is associated with a dampened response of the vagal brake to physical exercise that is manifested as reduced reactivity in heart rate and respiration. Polyvagal theory proposes that the regulation of the vagal brake is a neurophysiological component of an integrated social engagement system that includes the neural regulation of the laryngeal and pharyngeal muscles. Within this theoretical framework, sluggish vagal brake reactivity may parallel an inability to recruit efficiently the structures involved in speech. Thus, the findings suggest that dampened autonomic reactivity during mobilization behaviors may be a biomarker of SM that can be assessed independent of the social stimuli that elicit mutism.

It has been reported that borderline personality related characteristics can be observed in children, and that these characteristics are associated with increased risk for the development of borderline personality disorder. It is not clear whether borderline personality related characteristics in children share etiological features with adult borderline personality disorder. We investigated the etiology of borderline personality related characteristics in a longitudinal cohort study of 1,116 pairs of same-sex twins followed from birth through age 12 years. Borderline personality related characteristics measured at age 12 years were highly heritable, were more common in children who had exhibited poor cognitive function, impulsivity, and more behavioral and emotional problems at age 5 years, and co-occurred with symptoms of conduct disorder, depression, anxiety, and psychosis. Exposure to harsh treatment in the family environment through age 10 years predicted borderline personality related characteristics at age 12 years. This association showed evidence of environmental mediation and was stronger among children with a family history of psychiatric illness, consistent with diathesis–stress models of borderline etiology. Results indicate that borderline personality related characteristics in children share etiological features with borderline personality disorder in adults and suggest that inherited and environmental risk factors make independent and interactive contributions to borderline etiology.

The influence of five monoamine candidate genes on depressive symptom trajectories in adolescence and young adulthood were examined in the Add Health genetic sample. Results indicated that, for all respondents, carriers of the dopamine receptor D4 5-repeat allele were characterized by distinct depressive symptom trajectories across adolescence and early adulthood. Similarly, for males, individuals with the monoamine oxidase A 3.5-repeat allele exhibited unique depressive symptom trajectories. Specifically, the trajectories of those with the dopamine receptor D4 5-repeat allele were characterized by rising levels in the transition to adulthood, while their peers were experiencing a normative drop in depressive symptom frequency. Conversely, males with the monoamine oxidase A 3.5-repeat allele were shown to experience increased distress in late adolescence. An empirical method for examining a wide array of allelic combinations was employed, and false discovery rate methods were used to control the risk of false positives due to multiple testing. Special attention was given to thoroughly interrogate the robustness of the putative genetic effects. These results demonstrate the value of combining dynamic developmental perspectives with statistical genetic methods to optimize the search for genetic influences on psychopathology across the life course.

The longitudinal associations of older sibling substance use as well as dyadic sibling conflict and collusion to younger sibling substance use were examined in a community-based sample of 244 same-sex sibling pairs. Indirect effects of older siblings on younger sibling substance use were hypothesized via younger sibling deviant peer affiliation and conflict with friends. Adolescents, parents, friends, and teachers completed measures of substance use, conflict, and deviant peer involvement. Observational data were used for both measures of collusion and conflict. Findings suggest that older sibling substance use has a direct effect on younger sibling use, but relationship dynamics and reinforcement played a significant role as well. Specifically, collusion and conflict in the sibling relationship both had indirect effects through younger siblings’ deviant peer affiliation. Findings validate the powerful socializing role of both siblings and peers, and elucidate the complex mechanisms through which socialization occurs. Furthermore, data underscore the importance of considering how multiple dimensions of socialization operate in the elaboration of antisocial behavior.

This study examined how the development of aggressive/rule-breaking behaviors (9–17 years) is related to the development of overreactive and warm parenting, and explored gender differences in development and interrelations. Externalizing was assessed using combined mother/father reports of the Child Behavior Checklist (N = 516). Overreactivity was assessed using self-reports of the Parenting Scale; warmth was measured using self-reports of the Parenting Practices Questionnaire. All constructs were assessed three times across 6 years. The interrelated development of externalizing and parenting was examined by cohort-sequential multigroup latent growth models. Timing of effects was investigated using multigroup cross-lagged models. The results from latent growth models suggest that boys and girls change similarly in the extent to which they show externalizing behaviors, and indicate that mothers and fathers show somewhat different parenting toward boys than girls. No gender differences were found for interrelations between externalizing and parenting. Initial levels of aggression were related to changes in overreactivity and warmth, and vice versa. Changes in externalizing were related to changes in parenting. Cross-lagged models showed that relations between overreactivity and aggression/rule breaking were reciprocal. Together, results from this study show that adolescent externalizing and parenting affect each other in important ways, regardless of the gender of the child or the parent.

Girls receiving lower quality paternal investment tend to engage in more risky sexual behavior (RSB) than peers. Whereas paternal investment theory posits that this effect is causal, it could arise from environmental or genetic confounds. To distinguish between these competing explanations, the current authors employed a genetically and environmentally controlled sibling design (N = 101 sister pairs; ages 18–36), which retrospectively examined the effects of differential sibling exposure to family disruption/father absence and quality of fathering. Consistent with a causal explanation, differences between older and younger sisters in the effects of quality of fathering on RSB were greatest in biologically disrupted families when there was a large age gap between the sisters (thus maximizing differential exposure to fathers), with greater exposure within families to higher quality fathering serving as a protective factor against RSB. Further, variation around the lower end of fathering quality appeared to have the most influence on RSB. In contrast, differential sibling exposure to family disruption/father absence (irrespective of quality of fathering) was not associated with RSB. The differential sibling-exposure design affords a new quasi-experimental method for evaluating the causal effects of fathers within families.