In this article, we examine the construct of peer contagion in childhood and adolescence and review studies of child and adolescent development that have identified peer contagion influences. Evidence suggests that children's interactions with peers are tied to increases in aggression in early and middle childhood and amplification of problem behaviors such as drug use, delinquency, and violence in early to late adolescence. Deviancy training is one mechanism that accounts for peer contagion effects on problem behaviors from age 5 through adolescence. In addition, we discuss peer contagion relevant to depression in adolescence, and corumination as an interactive process that may account for these effects. Social network analyses suggest that peer contagion underlies the influence of friendship on obesity, unhealthy body images, and expectations. Literature is reviewed that suggests how peer contagion effects can undermine the goals of public education from elementary school through college and impair the goals of juvenile corrections systems. In particular, programs that “select” adolescents at risk for aggregated preventive interventions are particularly vulnerable to peer contagion effects. It appears that a history of peer rejection is a vulnerability factor for influence by peers, and adult monitoring, supervision, positive parenting, structure, and self-regulation serve as protective factors.

A great deal of research has supported James's (1890) observation that the content of people's identities can be meaningfully partitioned into various "constituents." Although researchers have sliced the self-concept pie in different ways, a consensus is emerging that people's self-construals can be classified into three primary sets, reflecting individual, relational, and collective aspects of identity (Brewer & Gardner, 1996;Cheek, 1989; Sedikides & Brewer, 2001; see also chap. 12, this volume). Individual (or personal) identity is composed of physical and psychological characteristics that distinguish the individual from others in his or her social context, specifically, traits that may be described without reference to the person's social relationships. Relational (or social) identity involves aspects of the self-concept that define the person with reference to his or her roles and relationships, particularly those that are based on bonds of attachment (Sedikides & Brewer, 2001; see also chap. 12, this volume). Finally, collective identity is based on one's inclusion and membership in social groups, including large collectives based on race, ethnicity, nationality, and religion, as well as smaller groups, such as clubs, work groups, teams, and other organizations (see chap. 14, this volume).However, philosophical and scientific discussions suggest the presence of a fourth category of self-construal that has received little attention from researchers. In addition to defining themselves in terms of their unique traits, social relationships, and group memberships, some people's self-concepts include broader categories of people, animals, and inanimate objects. For example, a person's identity might include the idea that he or she is a member of the human species; involve his or her kinship with other animals; or incorporate the belief that he or she can be identified as a part of the universe, God, or some other transcendent quality. We call this aspect of identity that goes beyond one's individual, relational, and collective identities allo-inclusive identity (olio = other). Earlier in this program of research, we referred to this construct as the transindividual identity, but we have since realized that its central feature is the inclusion of other entities in one's self-concept instead of merely an iden-137

The role of cognitive mechanisms in the clinical course of neurodevelopmental disorders is poorly understood. Attention Deficit Hyperactivity Disorder (ADHD) is emblematic in that numerous alterations in cognitive development are apparent, yet how they relate to changes in symptom expression with age is unclear. To resolve the role of cognitive mechanisms in ADHD, a developmental perspective that takes into account expected within-group heterogeneity is needed. Method The current study uses an accelerated longitudinal design and latent trajectory growth mixture models in a sample of children ages 7–13 years carefully characterized as with (n=437) and without (n=297) ADHD to: 1) identify heterogeneous developmental trajectories for response inhibition, visual spatial working memory maintenance, and delayed reward discounting and 2) to assess the relationships between these cognitive trajectories and ADHD symptom change. Results Best-fitting models indicated multiple trajectory classes in both the ADHD and typically-developing samples, as well as distinct relationships between each cognitive process and ADHD symptom change. Developmental change in response inhibition and delayed reward discounting were unrelated to ADHD symptom change, while individual differences in the rate of visual spatial working memory maintenance improvement predicted symptom remission in ADHD. Conclusion Characterizing heterogeneity in cognitive development will be crucial for clarifying mechanisms of symptom persistence and recovery. Results here suggest working memory maintenance may be uniquely related to ADHD symptom improvement.

Mindfulness-based interventions for youths have potential utility to improve attentional self-regulation, and future research should consider incorporating measures of attention into interventions that use mindfulness training.

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It has been unclear whether an associations of child ADHD with socio-economic disadvantage (SES) could be accounted for by (a) parental ADHD explaining both low SES and child ADHD, and/or (b) the joint overlap of ODD or CD with low SES and ADHD. Study 1 used a community-recruited case-control sample with detailed evaluation of SES indicators, child ADHD, child externalizing, and parent ADHD symptoms (n = 931 children, 521 ADHD, 577 boys, 354 girls) in a path modeling analysis with latent variables. Study 2 evaluated ADHD and externalizing behavior in a regression model using a poverty index for SES, in 70,927 children (48.2% female) aged 5-17 years from the US 2011-2012 National Survey of Children's Health (NSCH). In Study 1, lower SES was related to the ADHD latent variable, β = -.18, p < .001; 95%CI [-.25,-.12]. This effect held when parent ADHD and child ODD and CD were in the model, β = -.11, p < .01, 95% CI [-.09,-.03], equivalent to OR = 1.50, 95% CI[1.12-2.04]). In Study 2, these results replicated. Adjusting only for age and sex, children from families who were below 200% of the federal poverty line were more likely to have moderate or severe ADHD than no ADHD, versus children above that line, OR = 2.13, 95% CI[1.79,2.54], p < .001. The effect held after adjusting for disruptive/externalizing problems, OR = 1.61, p < .01, 95%CI [1.32,1.96]. The effect size for comparable models was similar across both studies, lending higher confidence to the results. It is concluded that the SES association with child ADHD is not explained by artifact and requires a mechanistic explanation.

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