Although distress tolerance is an emerging construct of empirical interest, we know little about its temporal change, developmental trajectory, and prospective relationships with maladaptive behaviors. The current study examined the developmental trajectory (mean- and individual-level change, and rank-order stability) of distress tolerance in an adolescent sample of boys and girls (N=277) followed over a four-year period. Next we examined if distress tolerance influenced change in Externalizing (EXT) and Internalizing (INT) symptoms, and if EXT and INT symptoms in turn influenced change in distress tolerance. Finally, we examined if any of these trends differed by gender. Results indicated that distress tolerance is temporally stable, with little mean- or individual-level change. Latent growth models reported that level of distress tolerance is cross-sectionally associated with both EXT and INT symptoms, yet longitudinally, only associated with EXT symptoms. These results suggest that distress tolerance should be a focus of research on etiology and intervention.

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Background: Previous work reports an association between familial risk factors stemming from parental characteristics and offspring disruptive behavior disorders (DBDs). This association may reflect a) the direct effects of familial environment, and b) a passive gene-environment correlation, wherein the parents provide both the genes and the environment. The current study examined the contributions of direct environmental influences and passive gene-environment correlations by comparing the effects of familial risk factors on child DBDs in genetically related (biological) and non-related (adoptive) families. Method: Participants were 402 adoptive and 204 biological families. Familial environment was defined as maternal and paternal maladaptive parenting and antisociality, marital conflict, and divorce; offspring DBDs included attention deficit/hyperactivity disorder, conduct disorder, and oppositional defiant disorder. Mixed-level regressions estimated the main effects of familial environment, adoption status, and the familial environment by adoption status interaction term, which tested for a presence of passive gene-environment correlations. Results: There was a main effect of maternal and paternal maladaptive parenting and marital discord on child DBDs, indicating a direct environmental effect. There was no direct environmental effect of maternal or paternal antisociality, but maternal and paternal antisociality had stronger associations with child DBDs in biological families than adoptive families, indicating the presence of a passive gene-environment correlation. Conclusions: Many familial risk factors affected children equally across genetically-related and non-related families, providing evidence for direct environmental effects. The relationship of parental antisociality and offspring DBDs was best explained by a passive gene-environment correlation, where a general vulnerability toward externalizing psychopathology is passed down by the parents to the children.

Binge drinking is associated with clinically significant individual-level and public health consequences. The topography of binge drinking may influence the emergence of consequences but studies of topography require a higher level of temporal resolution than is typically available in epidemiological research. To address topography across the five “peak” years of binge drinking (18 to 23 years), we assessed daily binge drinking via successive 90-day Timeline Follow back interviews of 645 young adults (resulting in almost 700,000 data points). Results showed a weekend “pulse” of binge drinking that remained consistent across the entire five year span, with occasional holiday-based perturbations. Two-part latent growth curve (LGC) modeling applied to this dataset showed that the often-observed decrease in drinking associated with “maturing out” was due more to decreased participation in binge drinking occasions, rather than to amounts consumed when drinking (intensity). Similarly, the number of binge drinkers varied by day of the week, but the intensity of binge drinking, for those drinking, varied little by day of the week. This approach also showed distinctive predictors for participation and intensity; baseline expectancies and sociability accounted for individual differences in participation, whereas impulsivity-sensation seeking predicted intensity. Individual patterns of binge drinking participation and intensity also predicted drinking consequences over the 5 years of the study. Given these results, binge drinking patterns may serve as a useful phenotype for future research on pathological drinking.

Comfort eating is a widespread behavior, but does it actually work? The purpose of this review is to provide a summary of the existing research on the potentially comforting effects of comfort food. We begin by summarizing the existing nonhuman animal research in this area, and then summarize the human research. On the basis of this foundational research, we provide a conceptual model of comfort eating that can be used as a hypothesis‐generating tool to guide future research. Finally, we highlight what we consider to be the most exciting future directions in comfort eating. These include (i) determining whether comfort eating is trait‐like or state‐like, (ii) understanding the antecedents and sequelae of comfort eating, (iii) elucidating the types of food implicated in comfort eating, (iv) creating linkages between comfort eating and comfort drinking, (v) incorporating measures of the autonomic nervous and immune systems in addition to the current focus on the hypothalamic‐pituitary‐adrenocortical axis, (vi) studying both short‐term and long‐term effects, and (vii) testing the biological and psychological mechanisms of comfort eating. Given that comfort eating has been practiced for centuries, we conclude that the time is ripe to advance the science of comfort eating.