Puberty Initiates Cascading Relationships Between Neurodevelopmental, Social, and Internalizing Processes Across Adolescence

Abstract

Adolescence is a period of dramatic developmental transitions-from puberty-related changes in hormones, bodies, and brains to an increasingly complex social world. The concurrent increase in the onset of many mental disorders has prompted the search for key developmental processes that drive changes in risk for psychopathology during this period of life. Hormonal surges and consequent physical maturation linked to pubertal development in adolescence are thought to affect multiple aspects of brain development, social cognition, and peer relations, each of which have also demonstrated associations with risk for mood and anxiety disorders. These puberty-related effects may combine with other nonpubertal influences on brain maturation to transform adolescents' social perception and experiences, which in turn continue to shape both mental health and brain development through transactional processes. In this review, we focus on pubertal, neural, and social changes across the duration of adolescence that are known or thought to be related to adolescent-emergent disorders, specifically depression, anxiety, and deliberate self-harm (nonsuicidal self-injury). We propose a theoretical model in which social processes (both social cognition and peer relations) are critical to understanding the way in which pubertal development drives neural and psychological changes that produce potential mental health vulnerabilities, particularly (but not exclusively) in adolescent girls.

Keywords: Internalizing; Neurodevelopment; Puberty; Social cognition; Social connection; Social rejection.

Figure 1.

Heuristic conceptual model of neural and social mechanisms for the impact of pubertal development on adolescent mental health. The dashed arrow represents mediation of the puberty-internalizing link via neural and social mechanisms. Double-headed arrows represent transactional processes unfolding over time across adolescence. Gender is depicted as a known moderator of the puberty-internalizing link; it is expected to moderate the other paths in this model (e.g., puberty-brain development, puberty-social processes, social processes-internalizing) but these are not depicted for clarity’s sake. Note that neither the brain’s initial trigger of puberty, nor social experiences that affect pubertal timing such as early life adversity, are depicted here as double-headed arrows due to the specific focus on processes happening throughout adolescence.

Figure 2.

This chart depicts the degree of dynamic developmental relevance for each process or system, aligned by chronological age. The values were determined by qualitatively aggregating from the literature referenced in our manuscript, including empirical studies reported on in reviews we cited. Each bar represents a two-year age window across adolescence, from 10–11 years to 24–25 years. Color is saturated in 10% intervals ranging from 0% to 100% saturation (low to high plasticity, respectively). For example, the rapid development of secondary sex characteristics (bodily changes) in early to mid adolescence are conveyed by the highly saturated values during those age windows. Saturation values do NOT represent levels or prevalence rates of the process or system. For example, the slope of increase in testosterone is steepest in early adolescence, as represented by high saturation values, even though absolute levels of testosterone do not peak at the youngest ages. We note that the emphasis is on the relevance of each process or system in developmental tasks across an age cohort, rather than on an individual level. In other words, testosterone remains influential on social behavior in late adolescence and beyond, but this is due to individual differences rather than development. We also note that there are well-documented shifts in pubertal timing such that some racial/ethnic identity minority adolescents (Black and Latinx) enter puberty earlier than others (non-Latinx White and Asian). Finally, in contrast to pubertal processes and internalizing, saturation values for resting-state functional connectivity networks (default mode, salience) and social processes were heavily based on cross-sectional studies and therefore caution is warranted during interpretation until these patterns are confirmed in longitudinal samples. T = testosterone, EST = estrogen, mPFC = medial prefrontal cortex, pgACC = perigenual anterior cingulate cortex, lPFC = lateral prefrontal cortex, fron-stri = frontostriatal connectivity, default = default mode network, salience = salience (cingulo-opercular) network, ment = mentalizing, friend = close friendships, partner = romantic and sexual relationships, anx = worry-based anxiety disorders, depr = depression, NSSI = non-suicidal self-injury.