A distinct adolescent phase as the transition between childhood and adulthood is characteristic for several mammalian species, defined by sexual maturation and a period of brain remodeling. Depending on species this process happens over a few weeks or several years, as in humans. Next to distinct maturation in the brain, adolescence is accompanied by notable behavioral changes. For instance, adolescents show more grooming behavior, social interactions, and playfulness, as well as increased novelty seeking, risk-taking and altered reward sensitivity (Spear, 2000). Those behavioral modifications are believed to have adaptive value. For example, becoming independent, by exploring the environment and leaving the protected childhood nest, as well as developing social skills that are important to become an adult member of their social environment (Crews, He, & Hodge, 2007). But those rapid changes observed in brain and behavior seem to make adolescents as well more vulnerable to adverse developments, such as depression, eating disorders and substance abuse (Kelly, Schochet, & Landry, 2004). Especially novelty-seeking and risk-taking have been suggested to be involved in increased susceptibility to adolescent drug-using behaviors. Likewise, substance abuse in adolescence seems to be connected to an increased risk for continued or later reemerging drug consumption.
Adolescence is related to widespread changes in hormonal production, such as the activation of the hypothalamus-pituitary-gonadal axis (HPG), gonadotropin-releasing hormone (GnRH), and the consequent production of luteinizing hormone (LH) and follicle stimulating hormone (FSH). While those hormones are involved in maturational aspects of puberty, risk-taking behavior in adolescence can be connected to the steroid hormone testosterone. During adolescence, testosterone increases in both genders, though this increase is more significant in boys (Grumbach, 2002). This gender difference is in line with the finding that risk-taking behavior is more prominent in adolescent boys than girls (Kelly et al., 2004). Further, individual differences in testosterone have been attributed to behavioral problems and other psychopathology in adolescent boys and girls (Granger, Shirtcliff, Zahn-Waxler, Usher, Klimes-Dougan, & Hastings, 2003). One study found, that in adolescent boys the level of testosterone was associated with non-aggressive risk-taking (Vermeersch, T’sjoen, Kaufman, & Vincke, 2008). However, those results were related to social factors, meaning that boys with higher levels of testosterone tended to have friends who engage in increased risk-taking. Similar results have been shown in adult males who showed increased risk-taking behavior after drug-induced elevation of testosterone (Goudriaan, Lapauw, Ruige, Feyen, Kaufman, Brand, , 2010). Moreover, Peper, Koolschijn, and Crone (2013) reported that testosterone levels in male and female adolescents were not just related to risk-taking behavior, but characteristics of the orbitofrontal cortex (OFC). The OFC is involved in decision-making processes, and OFC morphology was identified as a significant mediator between testosterone and risk-taking behavior. Interestingly, there was a gender difference in this association. For males, smaller grey matter volume in the OFC was linked to higher testosterone, whereas for females it was a smaller OFC surface area. But not just risk-taking behavior can be linked to testosterone levels, novelty-seeking and sensation-seeking have been found to be correlated to salivary testosterone levels in females (Kerschbaum, Ruemer, Weisshuhn, & Klimesch, 2006). Further, a study with all male subjects suggests that testosterone and a variant of the dopamine receptor gene (7R+ allele) may both predict novelty-seeking behaviors in adolescence (Campbell et al., 2010). But while testosterone is linked to risk-taking as well as novelty seeking behaviors in several studies, it has been implied that this characteristic adolescent behavior may be even more initiated by significant changes in brain structure and the dopaminergic system (Spear, 2000; Steinberg, 2008).