Early unpredictability predicts increased adolescent externalizing behaviors and substance use: A life history perspective.

According to evolutionary life history models, environmental harshness and unpredictability can both promote a fast life history strategy characterized by increased risk taking and enacting short-term, opportunistic behaviors. The current longitudinal study tests whether environmental unpredictability during childhood has stronger effects on risky behavior during adolescence than harshness, and whether there may be an early "sensitive period" during which unpredictability has particularly strong and unique effects on these outcomes. Using data from the Minnesota Longitudinal Study of Risk and Adaptation, prospective assessments of environmental unpredictability (changes in residence, cohabitation, and parental occupation) and harshness (mean socioeconomic status) from birth into adolescence were used to predict self-reported externalizing behaviors and substance use at age 16 (N = 220). Exposure to greater early unpredictability (between ages 0 and 5) predicted more externalizing behaviors as well as more alcohol and marijuana use at age 16, controlling for harshness and later unpredictability (between ages 6 and 16). Harshness predicted adolescent substance use, and later unpredictability predicted adolescent externalizing behaviors at the trend level. Early unpredictability and harshness also interacted, such that the highest levels of risk taking occurred in individuals who experienced more early unpredictability and lived in harsher environments. Age 16 externalizing behaviors, but not substance use, mediated the association between early unpredictability and externalizing/criminal behaviors at age 23. We discuss how exposure to early environmental unpredictability may alter biological and social-cognitive functioning from a life history perspective.

The roles of puberty and age in explaining the diminished effectiveness of parental buffering of HPA reactivity and recovery in adolescence.

Parental support is a powerful regulator of stress and fear responses for infants and children, but recent evidence suggests it may be an ineffective stress buffer for adolescents. The mechanisms underlying this developmental shift are not well-understood. The goal of the present study was to examine the independent and joint contributions of pubertal status and chronological age in explaining this shift. A sample of 75 typically developing youth (M age=12.95 years, SD=0.70, range=11.7-14.6 years; 37 females) was recruited to complete a modified Trier Social Stress Test (TSST-M) in the laboratory. Participants were recruited in such a way as to disentangle pubertal stage and chronological age by phone screening for markers of pubertal stage and then recruiting roughly equal numbers of younger and older, pre/early and mid/late pubertal youth who were then randomly assigned within groups to condition. The TSST-M was used as the stressor and youth prepared either with their parent or stranger (parent condition: N=39). Pubertal stage was confirmed by the Petersen Pubertal Development Scale at the time of testing and treated, along with chronological age, as a continuous variable in the analyses. The results revealed an interaction of pubertal stage and support condition for cortisol reactivity to the TSST-M such that preparing for the speech with the parent became a less potent buffer of the HPA axis as pubertal stage increased. Age did not interact with condition in predicting cortisol reactivity. In contrast, the parent's presence during speech preparation decreased in its effectiveness to hasten recovery of the HPA axis as children got older, but pubertal stage was not predictive of recovery rate. These patterns were specific to cortisol and were not observed with salivary alpha-amylase levels or subjective stress ratings for the task. These analyses suggest that the switch away from using parents as social buffers may be the result of neurobiological mechanisms associated with puberty.

FKBP5 moderation of depressive symptoms in peer victimized, post-institutionalized children.

The purpose of this study was to examine whether FKBP5 rs1360780 moderates relations between different forms of life stress/adversity (early institutional rearing and peer victimization) and depressive symptoms in adolescents. As reported previously, PI youth were at risk for being victimized by peers. Here, victimization was associated with elevated depressive symptoms. While FKBP5 did not moderate the association between early life adversity and depressive symptoms for either sex, it moderated the association between current adversity and depressive symptoms for victimized girls carrying the minor allele. Consistent with a differential susceptibility model, girls with the minor allele exhibited more depressive symptoms at higher levels of victimization, but fewer depressive symptoms at lower levels of victimization. Interestingly, boys with the CC genotype had higher rates of depressive symptoms compared to girls with the CC genotype in the context of heightened victimization.