Early-life adversity is a major risk factor for psychopathology, but not all who experience adversity develop psychopathology. The current study evaluated whether the links between child and adolescent adversity and depression and anxiety were described by general benefits and/or buffering effects of interpersonal support. Data from 456 adolescents oversampled on neuroticism over a 5-year period were examined in a series of discrete-time survival analyses to predict subsequent disorder onsets. Models examined linear, quadratic, and interactive effects of interpersonal support over time, as measured by chronic interpersonal stress interview ratings. Results did not support buffering effects of interpersonal support against either child or adolescent adversity in predicting depression or anxiety. However, there was support for the general benefits model of interpersonal support as evidenced by follow-up analyses of significant quadratic effects of interpersonal support, demonstrating that higher interpersonal support led to decreased likelihood of depression and anxiety onsets. Secondary analyses demonstrated that effects of interpersonal support remained after accounting for baseline depression and anxiety diagnoses. Further, quadratic effects were driven by social domains as opposed to familial domains when considering child adversity. Implications for interventions and randomized controlled prevention trials regarding interpersonal relationships are discussed.

Maternal stress during pregnancy can cause alterations to the fetal hypothalamus–pituitary–adrenal (HPA) axis, a phenomenon known as fetal programming that may have lasting effects on offspring outcomes, including depression. Evidence suggests that these effects may vary with respect to the offspring's genetic risk. Nonetheless, few studies have examined these effects into adulthood, when risk for depression onset is highest. The present study builds upon the extant literature by examining the interaction of maternal prenatal perceived stress (MPPS) and offspring HPA-axis polygenic risk to predict offspring depression in early adulthood. A total of 381 mother–child dyads participated in a prospective, longitudinal study that spanned from pregnancy until offspring were 20 years of age. Polygenic risk was defined by a multilocus genetic profile score (MGPS) that reflected the additive risk of three HPA-axis candidate genes. The results indicated that the interaction of MPPS and HPA-axis MGPS confers risk for offspring depression at age 20, in line with the differential susceptibility model. This interaction may be specific to prenatal stress, as maternal stress during early childhood did not interact with genetic risk to predict depression. These findings provide the first evidence that genetic variants that are associated with the HPA axis may act in a polygenic, additive fashion to moderate the association between fetal programming and adult depression.

Studies support a link between adolescent romantic involvement and depression. Adolescent romantic relationships may increase depression risk by introducing chronic stress, and genetic vulnerability to stress reactivity/emotion dysregulation may moderate these associations. We tested genetic moderation of longitudinal associations between adolescent romantic involvement and later depressive symptoms by a polymorphism in the serotonin transporter linked polymorphic region gene (5-HTTLPR) and examined contributory roles of chronic stress and family discord. Three hundred eighty-one youth participated at ages 15 and 20. The results indicated that 5-HTTLPR moderated the association between age 15 romantic involvement and age 20 depressive symptoms, with strongest effects for short homozygotes. Conditional process analysis revealed that chronic stress functioned as a moderated mediator of this association, fully accounting for the romantic involvement–depression link among short/short genotypes. Also, romantic involvement predicted later depressive symptoms most strongly among short-allele carriers with high family discord. The results have important implications for understanding the romantic involvement–depression link and the behavioral and emotional correlates of the 5-HTTLPR genotype.

Previous research supports gene–environment interactions for polymorphisms in the corticotropin hormone receptor 1 gene (CRHR1) and the serotonin transporter gene linked polymorphic region (5-HTTLPR) in predicting depression, but it has rarely considered genetic influences on stress sensitization processes, whereby early adversities (EA) increase depressive reactivity to proximal stressors later in life. The current study tested a gene–environment–environment interaction (G × E × E; specifically, gene–EA–proximal stress interaction) model of depression in a 20-year longitudinal study. Participants were assessed prospectively for EA up to age 5 and recent chronic stress and depressive symptoms at age 20 and genotyped for CRHR1 single nucleotide polymorphism rs110402 and 5-HTTLPR. EA predicted stronger associations between recent chronic stress and depression, and the effect was moderated by genes. CRHR1 A alleles and 5-HTTLPR short alleles were associated with greater stress sensitization (i.e., greater depressive reactivity to chronic stress for those also exposed to high levels of EA). The results are consistent with the notion that EA exposure results in neurobiological and cognitive–emotional consequences (e.g., altered hypothalamic–pituitary–adrenal axis functioning), leading to emotional distress in the face of recent stressors among those with certain genetic characteristics, although further research is needed to explore explanatory mechanisms.

This study distinguished between factors that were protective for children at high risk and those that were resources for children regardless of risk level and determined the generality of these factors across three different risk definitions: school-age children of mothers with (a) unipolar depression (n = 22), (b) bipolar disorder (n = 18), and (c) medical illness (n = 18), each compared to a low-risk control group (n = 38). Results were verified at a 1-year follow-up. Positive self-concept, academic success, social competence, and positive perceptions of the mothers were resource factors associated with lower diagnostic ratings for children in all risk groups. Maternal social competence and having a healthy father in the home were resource factors for maternal unipolar risk but, unexpectedly, were vulnerability factors for maternal bipolar risk. Children's friendships were protective for children of medically ill mothers; however, frequent contact with an adult friend was a risk factor for unipolar offspring. The latter finding suggests that such contact might be a consequence of poor parent-child relationships. Findings are discussed in terms of possible interventions for children at risk, and suggestions for additional research are offered.

One pathway to depression in children and adults is hypothesized to result from complex transactions among cognitive, stress, and interpersonal variables. Cognitive vulnerability includes not only appraisals of events and circumstances that emphasize personal unworthiness and incompetence, but also underlying beliefs and “working models” of the self and others. Such cognitions arise in part in the context of maladaptive attachment relations with the parents and may be reinforced by interpersonal incompetencies and difficulties in peer, family, and social relationships. Stressful conditions in early life and throughout development may undermine or erode the development of effective coping competencies. Moreover, maladaptive cognitions about the self and others, and ineffective coping competencies, may contribute to the occurrence of stressful events and circumstances —and these in turn may trigger depressive reactions. For many depressed people with chronic or recurrent depression, therefore, developmental processes play critical roles in the origin and continuation of the disorder.

The validity of a developmentally based life-stress model of depression was evaluated in 88clinic-referred youngsters. The model focused on (a) the role of child–environmenttransactions, (b) the specificity of stress–psychopathology relations, and (c) theconsideration of both episodic and chronic stress. Semistructured diagnostic and life-stressinterviews were administered to youngsters and their parents. As predicted, in the total samplechild depression was associated with interpersonal episodic and chronic stress,whereas externalizing disorder was associated with noninterpersonal episodic andchronic stress. However, the pattern of results differed somewhat in boys and girls. Youngsterswith comorbid depression and externalizing disorder tended to experience the highest stresslevels. Support was obtained for a stress-generation model of depression, wherein childrenprecipitate stressful events and circumstances. In fact, stress that was in part dependent onchildren's contribution distinguished best among diagnostic groups, whereas independentstress had little discriminative power. Results suggest that life-stress research may benefit fromthe application of transactional models of developmental psychopathology, which consider howchildren participate in the construction of stressful environments.

This longitudinal study of 137 female high school seniors investigated therelationship of attachment cognitions, current psychological functioning, and psychologicalfunctioning 12 months later. Attachment cognitions, assessed with the Revised Adult AttachmentScale and the Inventory of Parent and Peer Attachment, were significantly associated with currentsymptomatology. The Revised Adult Attachment Scale, in interaction with initialsymptomatology, predicted depression, substance abuse, eating disorders, and personalitydisorders 12 months later. The Inventory of Parent and Peer Attachment parent subscalespredicted eating disorder and personality disorder symptomatology, whereas the peer subscalespredicted substance abuse, eating disorder, and personality disorder symptomatology.