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12 BIOLOGICAL AND SOCIAL UNIVERSALSbut also because of other potential adaptive consequences of these behaviors.Indeed, engaging in some risk taking becomes normative during adolescence,with >50% of human adolescents engaging in drunk driving, sex without contraception,use of illegal drugs, fighting, or other risk-taking behaviors (Irwin,1989).Although adolescent-associated increases in risk-taking behaviors may havebeen highly conserved in part because they served to facilitate emigration or otherwiseenhance adaptive fitness during evolution, such risk taking bears considerablecost for some adolescents. There are elevated mortality rates duringadolescence in virtually all species, including humans (e.g., Crockett & Pope, 1993;Irwin & Millstein, 1992). This increase, during the otherwise relatively healthyage period of adolescence, is attributable largely to risk-taking behaviors per se(e.g., Muuss & Porton, 1998), with the three highest sources of mortality amongmodern human adolescents being accidents, homicides, and suicides (Irwin et al.,2002). Although it is likely that those adolescents who exhibit the most risk takingare at the greatest risk of adverse outcome, for even those adolescents engagingin moderate amounts of risk taking, there is a chance for harm.Adolescent Brain Sculpting: Pruning of Synapses,Declines in Energy Utilization, and Changesin White/Gray MatterDevelopment of the neocortex during adolescence is characterized more by a lossof connections rather than creation of substantial new connectivity, with an almost50% loss of the synaptic connections between neurons estimated in somecortical regions during adolescence in the brain of nonhuman primates (Bourgeoiset al., 1994; Rakic et al., 1994). A similar decline in synaptic density is seen inhuman neocortex between 7 and 16 years (Huttenlocher, 1979), with limitationsin the amount of human autopsy material restricting more precise delineation ofthe time course of this decline.The functional implications of the synaptic pruning during adolescence haveyet to be determined. More synapses are not necessarily better, with some formsof mental retardation associated with elevated numbers of synapses (Goldman-Rakic et al., 1983). Indeed, “overproduction followed by pruning” is a well-knowncharacteristic of brain ontogeny during the prenatal and early postnatal periods(see Rakic et al., 1994). Yet, an adolescent-associated synaptic decline wouldseemingly reflect more than the elimination of nonfunctional synapses, given thecostliness of maintaining synapses with no functional role throughout infancy andthe juvenile period prior to their belated demise during adolescence. Some supportfor this notion is seen in data from Lewis (2005) showing that properties ofsynapses eliminated during adolescence are similar to those that were maintained,