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This article proposes an evolutionary model of risky behavior in adolescence and contrasts it with the prevailing developmental psychopathology model. The evolutionary model contends that understanding the evolutionary functions of adolescence is critical to explaining why adolescents engage in risky behavior and that successful intervention depends on working with, instead of against, adolescent goals and motivations. The current article articulates 5 key evolutionary insights into risky adolescent behavior: (a) The adolescent transition is an inflection point in development of social status and reproductive trajectories; (b) interventions need to address the adaptive functions of risky and aggressive behaviors like bullying; (c) risky adolescent behavior adaptively calibrates over development to match both harsh and unpredictable environmental conditions; (d) understanding evolved sex differences is critical for understanding the psychology of risky behavior; and (e) mismatches between current and past environments can dysregulate adolescent behavior, as demonstrated by age-segregated social groupings. The evolutionary model has broad implications for designing interventions for high-risk youth and suggests new directions for research that have not been forthcoming from other perspectives.

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Humans learn how to behave directly through environmental experience and indirectly through rules and instructions. Behavior analytic research has shown that instructions can control behavior, even when such behavior leads to sub-optimal outcomes (Hayes, S. (Ed.). 1989. Rule-governed behavior: cognition, contingencies, and instructional control. Plenum Press.). Here we examine the control of behavior through instructions in a reinforcement learning task known to depend on striatal dopaminergic function. Participants selected between probabilistically reinforced stimuli, and were (incorrectly) told that a specific stimulus had the highest (or lowest) reinforcement probability. Despite experience to the contrary, instructions drove choice behavior. We present neural network simulations that capture the interactions between instruction-driven and reinforcement-driven behavior via two potential neural circuits: one in which the striatum is inaccurately trained by instruction representations coming from prefrontal cortex/hippocampus (PFC/HC), and another in which the striatum learns the environmentally based reinforcement contingencies, but is “overridden” at decision output. Both models capture the core behavioral phenomena but, because they differ fundamentally on what is learned, make distinct predictions for subsequent behavioral and neuroimaging experiments. Finally, we attempt to distinguish between the proposed computational mechanisms governing instructed behavior by fitting a series of abstract “Q-learning” and Bayesian models to subject data. The best-fitting model supports one of the neural models, suggesting the existence of a “confirmation bias” in which the PFC/HC system trains the reinforcement system by amplifying outcomes that are consistent with instructions while diminishing inconsistent outcomes.

Accounts of human fears and phobias based on current conditioning models using data from adults are examined and found wanting. Instead, the characteristics of human phobias resemble the kind of learning found during the amnesic period of infancy. As certain neural systems mature, conditioning begins to exhibit adult characteristics: context dependency, sharp generalization, and rapid extinction. Although direct behavioral control by the early learning systems wanes, the adult learning system seems to be structured at least/partially through the lasting influence of infantile experience. Under (hormonal) stress, residues of early experience are reinstated and incorporated into adult memory where they directly control behavior. This control exhibits infantile characteristics. The evidence suggests that once acquired, such conditional fears might never be eliminated using traditional extinction or counterconditioning procedures. The view leads to a renewed emphasis upon the role of experience in human development, accepting the disproportionate importance of infant experience as the foundation upon which subsequent learning and cognitive function rest.It is plain from clinical experience that certain patients experience critical incidents in which the fear has an onset. What is particularly interesting is the fact that quite frequently these same people have been exposed to the same stimulus repeatedly in the past without acquiring the fear. It seems that for acute onset fears, there are certain psychological states in which the person is vulnerable to the acquisition of fears. To take a clinical example, in those agoraphobic patients who report an acute onset of fear, one needs to know why the fear arose on the day that it did, at the time that it did. And why do they acquire a fear of public transport, crowded or open spaces, or whatever the content of their phobia, when on hundreds or thousands The first author acknowledges the fundamental contributions of David Furrow, Scon Mendelson, Michael Buttrick.