Introduction Recent theorizing and research

Introduction Recent theorizing and research regarding the neurodevelopment of the adolescent galanin has generated considerable attention in both the popular media and the scientific literature. The most striking generalization stemming from this work is that the adolescent brain does not fully mature until at least age 25, with the implication that adolescent decision-making and judgment is similarly limited up to this age (Casey et al., 2008; Giedd, 2004; Steinberg, 2008). This conclusion rests on research indicating that the myelination and pruning of the prefrontal cortex (PFC) continues into adulthood, well after ventral limbic regions that control motivation and reward have achieved these milestones. As a result, it is proposed that adolescents suffer from a structural as well as functional deficit in the ability of the PFC to exert top-down control over drives that are spurred by the limbic motivational system, leading to less than “rational” behavior during adolescence. The basic dynamics of these neurobiological imbalance models are illustrated in Fig. 1 (Casey et al., 2008), showing that limbic structures are activated in excess of prefrontal cognitive control regions during the adolescent period. A key feature of such imbalance models is the suggestion that a developmental deficit in PFC cognitive control limits adaptive decision making by adolescents. However, when Giedd et al. (1999) first presented evidence of declining PFC gray matter volume in adolescents, they attributed the phenomenon to the role that experience plays in sculpting the brain during this developmental period. As they put it, the decline in PFC gray matter “may herald a critical stage of development when the environment or activities of the teenager may guide selective elimination during adolescence.” (p. 863). In other words, gray matter decline in the PFC could reflect pruning that results from the experience that adolescents gain during this period rather than a direct marker of increasing behavioral control. As Spear (2010) also noted, pruning may be “an example of developmental plasticity whereby the brain is ontogenetically sculpted on the basis of experience to accommodate environmental needs.” Needs could vary dramatically across environments and cultures (Mata et al., 2016), potentially resulting in very different patterns of pruning and brain organization during adolescent brain development (Choudhury, 2010). For example, evidence has accumulated to suggest that differences in socioeconomic status, which are correlated with cultural influences, are associated with differences in brain structure (Brito and Noble, 2014; Noble et al., 2015). In particular, Noble et al. (2015) demonstrated that lower socioeconomic status was associated with diminished cortical surface area and reduced hippocampal volume even when controlling for maternal education. Such hippocampal volume reductions have been reported by other studies as well (Hanson et al., 2011; Hueston et al., 2017). Others have observed differences in language-related regions (Piccolo et al., 2016) and modular brain organization (Krishnadas et al., 2013). Future research should unpack influences of education, culture, and income (with concomitant effects on nutrition, access to healthcare, and other factors that may plausibly affect development) on specific aspects of brain development. Rather than emphasizing the important role of culture and experience in shaping the development of the brain, researchers have instead focused on excess levels of maladaptive risk behavior, such as injury, drug use, pregnancy, and other unhealthy outcomes, as support for imbalance (Dahl, 2004; Steinberg, 2008; Casey, 2015). However, the stereotype of the impulsive, emotional, and distraught adolescent rests much more on the rise in adverse outcomes during this age period than on their overall prevalence (Institute of Medicine, 2011; Rivers et al., 2008). For the vast majority of adolescents, this period of development passes without substance dependence, sexually transmitted infection, pregnancy, homicide, depression, suicide, or death due to car crashes (Institute of Medicine, 2011; Willoughby et al., 2013). Indeed, the risks of these outcomes are often comorbid with each other (Biglan and Cody, 2003; Kreuger et al., 2002), leaving the average adolescent without great risk of life-altering consequences.