Introduction

Adolescents engage disproportionately in problem behaviors, such as delinquency and substance use, that violate social norms and endanger their own and others’ well-being (1–3).¹ In this article, we describe research from behavioral genetics and developmental neuroscience that advances understanding of biological risk for problem behavior. We scaffold our review around three findings from behavioral genetic research: Genetic influences on problem behavior increase with age and puberty, are mediated partially by genetic influences on sensation seeking, and are moderated by peer contexts. We integrate these findings with research on how neurobiological changes during adolescence contribute to teenagers’ propensity for problem behaviors. We focus on developmental changes in the incentive-processing system, including the ventral striatum (VS), the amygdala, and other subcortical areas that respond to rewards and threats. Like genetic risk for problem behavior, the incentive-processing system changes with age and puberty, is linked with sensation seeking, and is activated by peer contexts. These parallels suggest that findings from behavioral genetics and developmental neuroscience can be integrated to formulate hypotheses that can be addressed with interdisciplinary research (see Figure 1).

Figure 1: Overview of pathways from genes to problem behavior Solid arrows represent empirically supported pathways. Dashed arrows represent hypothesized pathways. Note: Numbers in parentheses refer to studies cited in the References.

Three Findings from Behavior Genetic Research on Problem Behavior

Genetic Influences on Problem Behavior Increase with Age and Puberty

Average levels of problem behavior increase from childhood to adolescence (1, 3) and genetic influences on problem behavior also increase during this time. Genetic influences on rule-breaking behavior (e.g., property crime) increase from approximately 20% at age 10 to 80% at age 15 (8), a finding that has been replicated in four independent studies (9–10). In late adolescence, many forms of problem behavior are highly heritable, with genes accounting for more than 80% of the variance in a common latent factor linking antisocial behaviors, drug and alcohol use, and personality disinhibition (11).

The age span during which genetic influences on problem behavior increase most rapidly (10 to 15 years) coincides with puberty, suggesting that genetic influences on problem behavior may be activated by pubertal development rather than (or in addition to) chronological age. Supporting this hypothesis, we recently found that genetic influences on rule-breaking forms of delinquency were moderated by pubertal status, even after controlling for age (12). In contrast, age did not moderate genetic influence on delinquency after controlling for pubertal status.

How might genetic risk for problem behavior be influenced by puberty? One possibility is that the relevant genes influence the timing or tempo of pubertal development itself. In a nationally representative study of adolescent twin girls (13), genetic predispositions toward earlier pubertal development contributed to higher risk for delinquency. Moreover, hormonal changes associated with puberty may activate genes that were not expressed in childhood. During puberty, average levels of gonadal (testosterone, progesterone, estradiol) and adrenal (DHEA and DHEA-S) hormones increase in males and females. These hormones bind to DNA-transcription factors that are distributed throughout the central nervous system and can thus affect gene expression directly (14). Finally, genetic influences on problem behavior may be amplified via transactions with environmental contexts (15). For example, regardless of age, adolescents who are more physically developed affiliate with older and more deviant peers (16). These peer influences, in turn, might influence problem behavior reciprocally, setting up a positive feedback loop that amplifies initial genetically influenced differences.

Genetic Influences on Problem Behavior Are Mediated by Sensation Seeking

Genetic influences on problem behavior increase during adolescence, but it is unclear which genes are involved or how these genetic differences translate into differences in problem behavior. One way to parse the causal chain between genotype and a complex phenotype, such as problem behavior, is to conduct a behavior genetic study that tests whether genetic influences on the complex phenotype are accounted for by genetic influences on a more basic, biologically proximate phenotype that is hypothesized to be intermediary. This study design can delineate complex pathways between genes and behavior by testing intermediary phenotypes at varying levels of analysis, from brain structure (e.g., white matter density) to brain function (e.g., ventral striatum activity) to component psychological process (e.g., selective attention) to personality trait (e.g., novelty seeking) and, finally, to behavior.

In studies using this type of behavioral genetic design, the personality trait of sensation seeking is a key psychological mediator of genetic influences on problem behavior. Sensation seeking—the tendency to prefer and seek novel and thrilling sensations and experiences—correlates phenotypically with many forms of problem behavior (17). At the population level, average levels of sensation seeking increase from childhood to middle adolescence (i.e., around 16 years old), a developmental trend that mirrors increases in problem behavior at this time (18). Given recent evidence that puberty might activate genes for problem behavior, in some studies, average levels of sensation seeking are associated more closely with pubertal development than with chronological age (19). Moreover, twin and family studies suggest that the same genes that influence sensation seeking also influence problem behavior. In a nationally representative study of adolescent twins and siblings ages 10 to 16, individual differences in the rate of increase in sensation seeking were due overwhelmingly to genetic differences (h² ~ 80%). These genetic influences on sensation seeking accounted for nearly half (43%) of the genetic variance in change in adolescents’ delinquent behavior (20). Finally, research using measured DNA (21) provides convergent evidence that genes influencing problem behavior are also relevant for sensation seeking. In this study (21), which constructed a polygenic risk score from a genomewide association study of externalizing disorders in adults, this risk score predicted a small but significant percentage of variance in self-reported impulse control and sensation seeking in adolescents.

Genetic Influences on Problem Behavior Are Moderated by Peer Relationships

Genes account for approximately 80% of the variation in problem behavior by late adolescence. However, this heritability estimate is a population average that masks potential variability in the strength of genetic influences on problem behavior in different environmental contexts—a gene × environment interaction. One of the most consistently replicated gene × environment interaction effects is the moderating effect of peer contexts: Genetic influences on problem behavior are amplified among teenagers who have more deviant peers. This pattern is evident whether examining best friends or peer groups; whether using adolescents’ perceptions of their peers or peers’ own self-report behavior; and whether the key outcome is nonsubstance-related delinquent behavior, alcohol use, or other forms of substance use (22–24). Convergent evidence for the importance of gene × peer interactions has been found using diverse methods, including twin/family studies (e.g., 23), candidate genes (e.g., 24, 25), and polygene methods that aggregate measured genetic risk across the entire genome (e.g., 21). Consistent with the hypothesis that part of the genetic risk for problem behavior is mediated through sensation seeking, the correlation between peer deviance and one’s own delinquent behavior is amplified among adolescents who report high levels of sensation seeking (26).

Adolescent Neurodevelopment and the Emergence of Problem Behavior

As we have described, genetic influences on problem behavior increase with age and puberty, are partially mediated by sensation seeking, and are moderated by peer relationships. At the same time, neuroscience research has begun to elucidate how adolescent-typical patterns of neurodevelopment may heighten teenagers’ propensity for problem behavior. Behavioral genetic research and neuroscience research intersect at several points, particularly on the roles of puberty and peers.

The Dual Systems Model

According to the dual systems model of adolescent neurodevelopment (27), the escalation of risk-taking behavior in adolescence results from asynchronous development in two brain systems. First, the incentive-processing system, including the ventral striatum (VS), amygdala, and orbitofrontal cortex, undergirds processing of motivational and affective information, including information about potential rewards. Second, the cognitive control system, including the prefrontal cortex and anterior cingulate cortex, is involved in self-regulation, planning, and impulse control. The cognitive control system undergoes protracted development through adolescence and young adulthood, whereas the incentive-processing system becomes more responsive in early and middle adolescence. For example, white matter volume—which reflects increasing myelination, a process that allows signals to be conducted through the brain more rapidly and reliably—continues to increase throughout adolescence and young adulthood, particularly in tracts relevant for high-level cognitive control (28). At the same time, adolescents show stronger VS activation in a variety of reward paradigms than children or adults, and VS activation correlates positively with risk-taking and preference for immediate rewards in laboratory tasks, as well as with self-reported problem behavior (reviewed in 28, 29). This neurobiological maturity gap may underlie age-group differences in risky and socially deviant behavior, with adolescents more prone to problem behavior than either children (for whom the incentive-processing system is less active, so they are less sensitive to the potential rewards of problem behavior) or adults (for whom the cognitive control system is more mature, so they can more effectively anticipate the potential adverse consequences of problem behavior).

Puberty and the Incentive-Processing System

The hormonal changes of puberty may be particularly important for the development of the incentive-processing system. Among young adults, both naturally occurring individual differences in testosterone and experimental administrations of testosterone correlate with reward seeking on the Iowa Gambling Task (IGT; 30, 31); performance on the IGT, in turn, is associated with sensation seeking (32, 33). Higher testosterone levels are also associated with greater reward-related VS activation in both adolescent boys and girls (34), and testosterone administration causes higher VS activation in response to rewards among adults (35). Longitudinal increases in testosterone in early adolescence are also associated with increased activation in response to threat cues in both the amygdala and the striatum, which may contribute to adolescents finding ostensibly dangerous situations thrilling and rewarding (36).

Peers and the Incentive-Processing System

The incentive-processing system in adolescents is sensitive to peer environments. Adolescents prefer smaller, more immediate monetary rewards to larger, delayed rewards when they are with peers of the same age (37). The same brain regions (including the VS) that respond to monetary rewards also respond to social stimuli, such as attaining higher social status, receiving positive social feedback, or viewing attractive faces (38, 39). Among adolescents, the presence of peers increases responsiveness of the VS to reward (40, 41). This effect of peer presence is not observed among adults, consistent with the idea that adolescence is a distinct developmental period of elevated sensitivity to social stimuli (40). Moreover, this neural peer effect correlates with risk-taking on a simulated driving task and with self-reported resistance to peer influence (40). Neural responses to peers vary by age and sex, with older female adolescents showing pronounced activity in the VS when they think about being evaluated by socially desirable peers (42). Thus, peer contexts both exacerbate genetic risk for problem behavior and activate neurobiological systems implicated in the rise of problem behavior typical for this age group.

Intersections Between Behavioral Genetic and Neuroscience Research

In summary, based on the behavior genetic and neuroscience findings we have reviewed thus far, average levels of problem behavior, sensation seeking, and reactivity of the incentive-processing system increase during adolescence and are linked with pubertal development. In addition, genetic influences on problem behavior increase with adolescents’ age and pubertal development, and are mediated by sensation seeking. Finally, peer relationships moderate the influence of genes and of sensation seeking on problem behavior, and activate the incentive-processing system. Considering these findings together, we propose a model (see Figure 1) in which genetically influenced individual differences in the structure and function of the incentive-processing system emerge at puberty and widen over adolescence. According to our model, these individual differences in neurodevelopment are also predicted to mediate genetic influences on sensation seeking and ultimately on problem behavior.

Although the studies we have described are consistent with our model, testing these hypotheses directly requires studies that simultaneously examine the links among genes, individual differences in brain structure and function, psychological functioning, and actual behavior. At least one candidate gene study has attempted to link measured genetic polymorphisms, imaging measures of brain activity, and problem behavior (43). In that study, adolescents who used illicit substances had significantly greater activity in the right insula and right anterior cingulate when successfully inhibiting responses on a stop-signal task; this right frontal network, in turn, was significantly associated with a polymorphism in SLC6A2, which codes for the norepinephrine transporter. However, the effect size for this single polymorphism was small (R² ~ 1%) and has not yet been replicated. Additional interdisciplinary research that integrates measures of neurobiology into genetic studies (including both quantitative and molecular genetic designs) is needed.

Looking Ahead at Interdisciplinary Research

Researchers are increasingly interested in interdisciplinary studies that combine genetic and neuroimaging data (e.g., 44). Although quite demanding in terms of sample size, twin and family designs that incorporate measures of brain structure and function (e.g., 45) may be particularly valuable. In initial results from twin studies, some individual differences in brain structure and function are highly heritable. For example, grey matter density in the amygdala (which is involved in the incentive-processing system) is substantially heritable (h² = .80) at the onset of puberty (46), and by adulthood, the heritability of frontal lobe volumes (which are involved in cognitive control) exceeds 90% (47). However, these studies have examined the heritability of phenotypes at a single level of analysis (e.g., brain structure); multivariate twin designs that measure phenotypes that traverse many levels of analysis (e.g., VS activity, sensation seeking, and problem behavior) are needed to test whether these phenotypes are influenced by the same underlying genetic polymorphisms.

Additionally, longitudinal genetically informative designs can answer critical questions about the direction of causation between neurobiological correlates and problem behaviors. Such questions are salient given that problem behavior often involves substance use, and cross-sectional designs provide little information about whether a structural or functional correlate represents an endogenous risk or is a consequence of exposure to substances. More generally, although ostensibly focused on understanding the development of problem behaviors in adolescence, much of the research we have described has been cross-sectional rather than longitudinal. As Loth and colleagues (48) commented, “adolescence-specific maturational growth curves, rather than adult norms, need to be considered when assessing individual differences” (p. 437).

Researchers should take a multivariate approach that considers both unity and diversity in the neurobiological and genetic underpinnings of problem behaviors. Illustrating the utility of a multivariate approach, a recent imaging study of 14- to 16-year-olds examined correlates of a general factor representing common variance across attention deficit hyperactivity disorder, conduct disorder, and symptoms of substance use, as well as unique correlates of behavioral subtypes. Sensation seeking and neural activity while anticipating a reward were associated uniquely with substance use, whereas the general factor was associated with impulsivity and neural activity during response inhibition (49). However, no study has yet investigated this topic using a longitudinal design that can test whether individual differences in neurobiological change are associated uniquely with some forms of problem behavior but not others.

Finally, even rats show heritable individual differences in risk-taking behavior (50). This cross-species consistency suggests that the biological changes characteristic of adolescence have evolved to serve an adaptive purpose—to motivate exploration and separation from caregivers. Adolescents with genetic or neurobiological characteristics associated with problem behavior could engage in forms of risk-taking that are socially sanctioned or even prosocial. Yet the positive trajectories of biologically “at risk” teenagers, as well as the environmental opportunities and individual characteristics that foster prosocial risk-taking, are poorly understood. Addressing this question will stimulate a broader consideration of how the unique characteristics of teenagers can be leveraged to maximize healthy outcomes for themselves and for society as a whole.

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Integrating Behavioral Genetics and Developmental Neuroscience to Understand Adolescent Risk Taking

Adolescents are statistically over-represented in their engagement in behaviors that violate societal norms and pose a danger to themselves and others, such as delinquency and substance use ([1–3]). This article presents research from the fields of behavioral genetics and developmental neuroscience to illuminate the biological underpinnings of this propensity for problem behavior in adolescence. The review is structured around three key findings from behavioral genetic research: the increase of genetic influences on problem behavior with age and puberty, the mediation of these genetic influences by sensation seeking, and the moderating role of peer contexts. These findings are then integrated with developmental neuroscience research highlighting the role of the incentive-processing system in adolescent risk taking. We propose that the parallels between these areas of research offer promising avenues for formulating testable hypotheses through interdisciplinary investigations (see Figure 1).

Three Findings from Behavior Genetic Research on Problem Behavior

Genetic Influences on Problem Behavior Increase with Age and Puberty

Both the prevalence of problem behavior ([1, 3]) and its heritability increase from childhood to adolescence. For instance, genetic influences on rule-breaking behavior (e.g., property crime) escalate from approximately 20% at age 10 to 80% by age 15 ([8]), a finding consistently replicated across multiple independent studies ([9, 10]). By late adolescence, a significant portion of the variance in a latent factor encompassing antisocial behaviors, substance use, and personality disinhibition can be attributed to genetic influences, often exceeding 80% ([11]).

The rapid increase in heritability of problem behavior between the ages of 10 and 15, a period coinciding with puberty, suggests a potential role for pubertal development in activating these genetic influences. This hypothesis is supported by recent findings demonstrating that pubertal status, independent of chronological age, moderates genetic influences on rule-breaking delinquency ([12]).

Several mechanisms could explain the influence of puberty on genetic risk for problem behavior. Genes might influence the timing and pace of pubertal development itself. For example, a study on adolescent twin girls revealed that a genetic predisposition toward earlier puberty correlated with a higher risk for delinquency ([13]). Additionally, hormonal surges during puberty, particularly gonadal (testosterone, progesterone, estradiol) and adrenal (DHEA and DHEA-S) hormones, could directly impact gene expression via DNA-transcription factors distributed throughout the central nervous system ([14]). Finally, genetic influences on problem behavior could be amplified through interactions with environmental contexts, such as the tendency for physically mature adolescents to affiliate with older, more deviant peers, potentially creating a positive feedback loop that escalates problem behavior ([15, 16]).

Genetic Influences on Problem Behavior Are Mediated by Sensation Seeking

While the increase in genetic influences on problem behavior during adolescence is well-established, the specific genes involved and their mechanisms of action remain unclear. To untangle this complex relationship between genotype and phenotype, behavioral genetic studies often examine intermediate phenotypes hypothesized to lie on the causal pathway. One such phenotype, sensation seeking—the proclivity to seek novel and intense sensations—demonstrates a strong phenotypic correlation with various forms of problem behavior ([17]).

Mirroring the developmental trajectory of problem behavior, sensation seeking also increases from childhood to mid-adolescence (around 16 years old) at a population level ([18]). This increase appears more closely linked to pubertal development than chronological age in some studies ([19]). Twin and family studies further suggest a shared genetic basis between sensation seeking and problem behavior. For instance, in a large-scale study of adolescent twins and siblings, genetic factors accounted for a substantial portion (80%) of individual differences in the rate of increase in sensation seeking. Moreover, these genetic influences on sensation seeking explained nearly half (43%) of the genetic variance observed in changes in delinquent behavior ([20]).

Converging evidence from studies utilizing measured DNA ([21]) supports the involvement of genes influencing both sensation seeking and problem behavior. A polygenic risk score for externalizing disorders derived from a genome-wide association study of adults significantly predicted impulse control and sensation seeking in adolescents, albeit with a small effect size.

Genetic Influences on Problem Behavior Are Moderated by Peer Relationships

Although genes account for a significant portion (around 80%) of the variance in problem behavior by late adolescence, this heritability estimate represents a population average that may mask context-dependent variability. One of the most robust gene × environment interaction effects highlights the moderating role of peer relationships: genetic influences on problem behavior are amplified in adolescents with deviant peers ([22–24]).

This pattern persists across various operationalizations of peer influence, including best friend or peer group deviance, adolescent perception of peer behavior, and peer self-reported behavior. It also extends across different outcomes, such as non-substance-related delinquency, alcohol use, and other substance use. The significance of gene × peer interactions is further substantiated by research utilizing diverse methodologies, including twin/family studies ([23]), candidate gene studies ([24, 25]), and polygenic methods ([21]). Consistent with the potential mediating role of sensation seeking in genetic risk for problem behavior, the association between peer deviance and delinquency is amplified in individuals reporting high sensation seeking ([26]).

Adolescent Neurodevelopment and the Emergence of Problem Behavior

The aforementioned findings from behavioral genetics are mirrored by research in neuroscience, which has begun to unravel the neurodevelopmental processes underlying the heightened risk-taking behavior observed during adolescence. These two fields intersect significantly in their focus on the roles of puberty and peers.

The Dual Systems Model

The dual systems model of adolescent neurodevelopment ([27]) proposes that the escalation of risk-taking behavior during this period stems from an imbalance in the maturation of two key brain systems. The first, the incentive-processing system, encompassing the ventral striatum (VS), amygdala, and orbitofrontal cortex, plays a crucial role in processing motivational and affective information, particularly regarding potential rewards. The second, the cognitive control system, which includes the prefrontal cortex and anterior cingulate cortex, is involved in self-regulation, planning, and impulse control.

While the cognitive control system undergoes protracted development throughout adolescence and young adulthood, the incentive-processing system becomes increasingly responsive during early and middle adolescence. For example, white matter volume, reflecting increased myelination for faster and more efficient signal transduction, continues to increase throughout adolescence and young adulthood, particularly in tracts crucial for high-level cognitive control ([28]). Concurrently, adolescents exhibit greater VS activation compared to children or adults across various reward paradigms. This VS activation correlates positively with risk-taking, preference for immediate rewards in laboratory tasks, and self-reported problem behavior (reviewed in [28, 29]). This developmental asynchrony, with a more developed incentive-processing system and a still-maturing cognitive control system, may explain the increased propensity for problem behavior in adolescents compared to children, whose incentive-processing system is less developed and thus less sensitive to potential rewards, or adults, whose more mature cognitive control system allows for better anticipation of potential consequences.

Puberty and the Incentive-Processing System

Hormonal changes during puberty may be particularly influential in shaping the development of the incentive-processing system. Studies in young adults have shown a positive correlation between both naturally occurring and experimentally administered testosterone levels and reward seeking on the Iowa Gambling Task (IGT; [30, 31]). Performance on the IGT, in turn, is associated with sensation seeking ([32, 33]). Higher testosterone levels also correlate with increased reward-related VS activation in both adolescent boys and girls ([34]), and testosterone administration has been shown to increase VS activation in response to rewards in adults ([35]).

Furthermore, longitudinal research has linked increases in testosterone during early adolescence with heightened activation in both the amygdala and the striatum in response to threat cues, which may contribute to adolescents perceiving dangerous situations as thrilling and rewarding ([36]).

Peers and the Incentive-Processing System

Adolescent incentive-processing systems are highly sensitive to peer contexts. When in the presence of peers, adolescents are more likely to choose smaller, immediate monetary rewards over larger, delayed rewards ([37]). Interestingly, the same brain regions involved in processing monetary rewards, including the VS, also respond to social stimuli, such as achieving higher social status, receiving positive social feedback, or viewing attractive faces ([38, 39]).

Research has demonstrated that the mere presence of peers amplifies VS responsiveness to reward in adolescents ([40, 41]), an effect not observed in adults. This suggests a heightened sensitivity to social stimuli during adolescence ([40]). Moreover, this neural peer effect correlates with risk-taking behavior on simulated driving tasks and self-reported resistance to peer influence ([40]). The neural response to peers also varies by age and sex, with older female adolescents exhibiting particularly pronounced VS activity when anticipating evaluation by socially desirable peers ([42]). These findings highlight the role of peer contexts in both exacerbating genetic risk for problem behavior and activating the neurobiological systems implicated in its increase during adolescence.

Intersections Between Behavioral Genetic and Neuroscience Research

In summary, both behavioral genetic and neuroscience research converge on the observation that problem behavior, sensation seeking, and incentive-processing system reactivity increase during adolescence and are linked with pubertal development. Furthermore, genetic influences on problem behavior are amplified by age and pubertal development and are partially mediated by sensation seeking. Lastly, peer relationships moderate the impact of both genes and sensation seeking on problem behavior, while simultaneously activating the incentive-processing system.

Synthesizing these findings, we propose a model (Figure 1) in which genetically influenced individual differences in the structure and function of the incentive-processing system emerge at puberty and become more pronounced throughout adolescence. We hypothesize that these individual differences in neurodevelopment mediate the genetic influences on sensation seeking and, ultimately, on problem behavior.

While the reviewed studies lend support to this model, direct testing of these hypotheses necessitates research that simultaneously examines the intricate relationships between genes, brain structure and function, psychological functioning, and actual behavior. A handful of candidate gene studies have attempted to link measured genetic polymorphisms, brain activity, and problem behavior ([43]). For example, one study found that adolescents who used illicit substances exhibited significantly greater activity in the right insula and right anterior cingulate during successful response inhibition on a stop-signal task. This right frontal network activity was associated with a polymorphism in the SLC6A2 gene, which codes for the norepinephrine transporter. However, the effect size for this single polymorphism was small (R2 ~ 1%) and requires further replication. Additional interdisciplinary research integrating neurobiological measures into genetic studies, employing both quantitative and molecular genetic designs, is crucial for advancing this field.

Looking Ahead at Interdisciplinary Research

Interdisciplinary research combining genetic and neuroimaging data is gaining increasing interest (e.g., [44]). Twin and family designs incorporating measures of brain structure and function ([45]) hold particular promise, despite their inherent complexity and demanding sample size requirements. Initial findings from twin studies indicate that certain individual differences in brain structure and function are highly heritable. For instance, grey matter density in the amygdala, a key component of the incentive-processing system, shows substantial heritability (h2 = .80) at the onset of puberty ([46]). Similarly, the heritability of frontal lobe volumes, which play a crucial role in cognitive control, surpasses 90% by adulthood ([47]). However, these studies have primarily focused on the heritability of individual phenotypes. Multivariate twin designs that incorporate measures across multiple levels of analysis (e.g., VS activity, sensation seeking, and problem behavior) are needed to determine whether these phenotypes are influenced by shared genetic polymorphisms.

Longitudinal genetically informative designs are particularly valuable for elucidating the directionality of causation between neurobiological correlates and problem behaviors. This is especially relevant given the frequent involvement of substance use in problem behavior, which makes it difficult for cross-sectional designs to determine whether an observed structural or functional brain correlate represents a pre-existing risk factor or a consequence of substance exposure. Despite their focus on understanding the development of problem behavior in adolescence, a significant portion of the research reviewed has employed cross-sectional rather than longitudinal designs. As highlighted by Loth and colleagues ([48]), “adolescence-specific maturational growth curves, rather than adult norms, need to be considered when assessing individual differences” (p. 437).

A multivariate approach that considers both the commonalities and distinctions in the neurobiological and genetic underpinnings of various problem behaviors is crucial. Illustrating the value of this approach, a recent imaging study on 14- to 16-year-olds examined the neural correlates of a general factor representing shared variance across attention-deficit/hyperactivity disorder, conduct disorder, and substance use symptoms, as well as correlates unique to specific behavioral subtypes. While sensation seeking and neural activity during reward anticipation were uniquely associated with substance use, the general factor was associated with impulsivity and neural activity during response inhibition ([49]). However, longitudinal research investigating whether individual differences in neurobiological change are uniquely associated with specific forms of problem behavior remains absent.

Finally, it is important to acknowledge that heritable individual differences in risk-taking behavior extend beyond humans and are also observed in rats ([50]). This cross-species consistency suggests an adaptive function for the biological changes during adolescence, potentially serving to motivate exploration and separation from caregivers. Adolescents with genetic or neurobiological characteristics associated with problem behavior may engage in socially sanctioned or even prosocial forms of risk-taking. However, the positive developmental trajectories of biologically "at risk" teenagers, as well as the environmental opportunities and individual characteristics that foster prosocial risk-taking, remain poorly understood. Addressing these questions will broaden our understanding of how to best leverage the unique characteristics of adolescence to promote healthy outcomes for individuals and society as a whole.

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Understanding the Biological Roots of Risky Behavior in Teenagers

Teenagers are known for engaging in risky behaviors more often than children or adults, like breaking rules or using drugs and alcohol. These behaviors go against social norms and can harm themselves and others. This article explores research from behavioral genetics and developmental neuroscience to understand the biological factors that contribute to these risky behaviors. We'll focus on three key findings from behavioral genetics:

• Genetic influences on problem behavior get stronger as kids get older, especially during puberty.

• These genetic influences partly work through a personality trait called "sensation seeking."

• The influence of genes on problem behavior is stronger when teenagers have friends who also engage in risky behavior.

These findings are connected with research on how the brain develops during adolescence, especially the "incentive-processing system," which handles rewards and threats.

Three Findings from Behavior Genetics Research on Problem Behavior

1. Genetic Influences on Problem Behavior Increase with Age and Puberty

As kids transition from childhood to adolescence, risky behaviors become more common. Interestingly, the influence of genes on these behaviors also becomes stronger. For example, genes play a bigger role in rule-breaking behavior (like stealing) as kids get older – increasing from about 20% influence at age 10 to 80% at age 15. This pattern has been seen in multiple studies. By late adolescence, many problem behaviors are strongly influenced by genes. In fact, genes explain over 80% of the differences we see in antisocial behaviors, substance use, and impulsive personality traits.

This increase in genetic influence lines up with puberty, suggesting that puberty itself might be activating these genetic influences. Research supports this idea – a study found that even when controlling for age, the genetic influence on rule-breaking was stronger in kids who were going through puberty. This means puberty, not just getting older, might be a key factor.

There are a few ways puberty could be influencing genetic risk:

• Genes might influence the timing of puberty itself. Early puberty is linked to a higher risk of delinquency, and genes might be playing a role.

• Hormonal changes during puberty could "turn on" certain genes. These hormones can directly affect which genes are expressed throughout the brain.

• Genetic predispositions might lead to experiences that amplify problem behavior. For example, teens who develop physically earlier tend to hang out with older, more rebellious peers. These peer influences can then further encourage problem behavior, creating a cycle.

2. Genetic Influences on Problem Behavior Are Mediated by Sensation Seeking

While we know genes become more influential during adolescence, we don't know exactly which genes are involved or how they lead to problem behavior. One way to figure this out is to look for intermediate factors that connect genes to behavior.

Sensation seeking, or the desire for new and exciting experiences, is one such factor. This personality trait is linked to various risky behaviors. Like problem behavior, sensation seeking increases from childhood to mid-adolescence (around age 16), and this increase might be more closely tied to puberty than age.

Twin and family studies suggest that sensation seeking and problem behavior are influenced by some of the same genes. In one large study of twins and siblings (ages 10-16), genetic differences largely explained why some teens' sensation seeking increased faster than others (80% heritability). These genetic influences on sensation seeking then explained almost half (43%) of the genetic influence on changes in delinquent behavior. This suggests that genes related to sensation seeking are a key part of the genetic risk for problem behavior.

3. Genetic Influences on Problem Behavior Are Moderated by Peer Relationships

Although genes explain about 80% of the differences in problem behavior by late adolescence, this doesn't mean everyone with a genetic predisposition will engage in these behaviors. The environment, especially peer relationships, plays a crucial role.

Numerous studies have found that teens with friends who engage in risky behavior are more likely to do so themselves, and this effect is even stronger for those with a genetic predisposition for such behaviors. This pattern holds true whether we look at best friends or larger peer groups, use teens' own perceptions of their friends or their friends' actual behavior, and examine different types of problem behavior like delinquency, alcohol use, or drug use. The link between having deviant peers and engaging in delinquent behavior is even stronger among teens high in sensation seeking, supporting the idea that sensation seeking is a key link between genes, environment, and behavior.

Adolescent Neurodevelopment and the Emergence of Problem Behavior

The findings from behavioral genetics highlight the increasing influence of genes during adolescence, particularly in the context of puberty and peer relationships. At the same time, neuroscience research sheds light on how the developing adolescent brain contributes to this increased risk-taking.

The Dual Systems Model

The "dual systems model" suggests that the increase in risky behavior during adolescence is a result of uneven development in two brain systems:

1. The Incentive-Processing System: This system, including the ventral striatum (VS), amygdala, and orbitofrontal cortex, processes information about rewards and motivation.

2. The Cognitive Control System: This system, including the prefrontal cortex and anterior cingulate cortex, is responsible for self-control, planning, and thinking ahead.

The cognitive control system develops gradually throughout adolescence and young adulthood. In contrast, the incentive-processing system becomes more sensitive and responsive during early and middle adolescence. This means that teenagers experience a heightened sensitivity to rewards alongside a still-developing ability to control their impulses. This "gap" in brain development might explain why teenagers are more prone to risky behavior compared to children, whose reward systems are less developed, or adults, whose cognitive control systems are more mature.

Puberty and the Incentive-Processing System

The hormonal changes during puberty may be particularly important for the development of the incentive-processing system. Studies show that higher levels of testosterone, a hormone that surges during puberty, are linked to:

• Increased reward-seeking: This has been observed in tasks like the Iowa Gambling Task, which measures decision-making under uncertainty and is related to sensation seeking.

• Greater activation of the VS in response to rewards: This suggests a heightened sensitivity to rewards in individuals with higher testosterone levels.

• Increased activation in the amygdala and striatum in response to threats: This suggests that adolescents, driven by hormonal changes, might find risky and potentially dangerous situations exciting and rewarding.

Peers and the Incentive-Processing System

The adolescent brain's reward system is also highly sensitive to social environments, particularly peers. Research has shown that:

• Adolescents are more likely to choose immediate, smaller rewards over larger, delayed rewards when they are with their peers. This highlights the powerful influence of peers on decision-making.

• The VS, a key area in the reward system, responds not only to monetary rewards but also to social rewards like gaining social status, receiving positive feedback, and seeing attractive faces. This emphasizes the importance of social rewards during adolescence.

• The presence of peers increases VS activity in response to rewards in adolescents but not in adults. This suggests a unique sensitivity to social influences during this developmental period.

• This neural response to peers is linked to real-world behaviors, such as risk-taking while driving and susceptibility to peer pressure. This strengthens the connection between brain activity and real-life behavior.

Intersections Between Behavioral Genetic and Neuroscience Research

The research we've explored suggests that problem behavior, sensation seeking, and the responsiveness of the incentive-processing system all increase during adolescence and are linked to puberty. Genetic influences on problem behavior also increase during this time and are mediated by sensation seeking. Moreover, peer relationships can both strengthen these genetic influences and activate the brain's reward system, making risky behavior more appealing.

These findings point to a model where individual differences in the brain's reward system, influenced by genes, emerge during puberty and become more pronounced throughout adolescence. These differences, in turn, are thought to contribute to variations in sensation seeking and, ultimately, problem behavior.

To directly test this model, we need studies that combine genetic analysis with brain imaging and behavioral assessments. While there have been some attempts to link specific genes, brain activity, and problem behavior, more research is needed, especially studies that consider multiple genes and environmental factors.

Looking Ahead at Interdisciplinary Research

Moving forward, research that combines genetics and brain imaging will be crucial for understanding the complex interplay of nature and nurture in adolescent risk-taking. Studies involving twins and families, which can help disentangle genetic and environmental influences, are particularly promising.

Additionally, longitudinal studies that track individuals over time are essential to determine whether changes in the brain are a cause or consequence of problem behavior, especially substance use. This is particularly important because cross-sectional studies, which provide only a snapshot in time, cannot answer this question.

Future research should also take a broader approach by:

• Examining different types of problem behavior: While some brain regions and genes might be involved in a variety of problem behaviors, others might be specific to certain behaviors, like substance use versus delinquency.

• Investigating both the positive and negative consequences of adolescent risk-taking: While some risk-taking can be harmful, it can also be adaptive, leading to exploration, learning, and social development. Understanding the factors that promote positive risk-taking is crucial for supporting healthy adolescent development.

By combining insights from genetics, neuroscience, and developmental psychology, we can gain a more comprehensive understanding of the biological and environmental factors that contribute to both risky and adaptive behavior during adolescence. This knowledge can then inform interventions and support systems aimed at promoting positive youth development and reducing the negative consequences of risk-taking.

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Why Do Teens Take More Risks? It's in Our Genes (and Our Brains!)

You've probably noticed that teenagers are more likely to engage in risky behaviors like breaking rules or using drugs and alcohol. These actions can be dangerous for everyone involved, but new research suggests there's a biological reason behind this pattern. This article will discuss some fascinating findings from two fields of study – behavioral genetics (how genes affect our behavior) and developmental neuroscience (how our brains change as we grow) – to help us understand why teenagers seem more prone to risky behaviors.

Three Reasons Genes Play a Role in Teen Risk-Taking

1. Genes Get More Influential During Puberty

It's no secret that teenagers get into more trouble than little kids. What's interesting is that the influence of our genes on this behavior also increases as we age, especially during puberty. For example, the impact of genes on rule-breaking behaviors (like stealing) skyrockets from about 20% at age 10 to a whopping 80% by age 15. This suggests that puberty itself might be a trigger for these genetic influences.

So, how does puberty affect our genes? One possibility is that these genes dictate the timing of puberty itself. Another idea is that the hormonal surge during puberty "turns on" specific genes that weren't active during childhood. Finally, puberty might indirectly impact our genes by influencing our environment. For instance, teens who mature physically earlier tend to hang out with older peers, which can lead to increased risk-taking.

2. "Thrill-Seeking" Genes Might Be the Culprit

We know that genes play a role in risky behavior, but which genes? And how do they work? One clue lies in a personality trait called sensation seeking – basically, how much a person enjoys exciting and new experiences. It turns out that sensation seeking is also influenced by genes, and these genes seem to overlap with those linked to risky behaviors. Think of it this way: some people are genetically wired to crave thrills, which might lead them to engage in more risky behaviors.

3. Friends Make a Big Difference (Especially for Those Prone to Risk)

Even though genes are powerful, the environment still matters. And when it comes to risky behavior, friends are a huge influence. Studies show that teens are more likely to act out if their friends are also engaging in risky behaviors. This is especially true for teens who are already genetically predisposed to sensation seeking. In other words, if you're naturally a thrill-seeker and you hang out with people who like to live on the edge, you're more likely to take risks.

Teenage Brains Are Wired for Excitement, But Still Learning Control

While genes lay the groundwork, our brains are also changing dramatically during adolescence. One popular theory, called the dual systems model, suggests that our brains have two systems: one focused on rewards and excitement (the "let's do it!" system), and another focused on planning and self-control (the "hold on a second" system). The problem is that these systems don't develop at the same pace.

During adolescence, the reward system (specifically, a part of the brain called the ventral striatum or VS) becomes super sensitive. We become hardwired to seek out pleasurable experiences, even if they're risky. Meanwhile, the self-control system (located in the prefrontal cortex) is still under construction. It's like having a powerful engine without good brakes – exciting but potentially dangerous.

Puberty Fuels the Reward System

Hormonal surges during puberty aren't just turning on genes, they're also supercharging the brain's reward system. For example, testosterone, a hormone that increases during puberty, has been linked to greater activity in the VS when we anticipate rewards. This might explain why teenagers are so drawn to thrills and why some teens might even find dangerous situations exciting.

Friends Amplify the Excitement

As if the teen brain wasn't already wired for excitement, being around friends makes the reward system even more active. This means that the things teens find rewarding – like hanging out with friends, trying new things, or even breaking the rules – become even more rewarding when they're with their peers. It's no wonder teenagers are so influenced by their social circles.

Putting It All Together: Genes, Brains, and Behavior

Scientists are still unraveling the complex interplay between genes, brain development, and behavior. However, it's clear that the teenage years are a time of incredible change, both biologically and socially. Our genes and our brains are working together, shaping our responses to the world around us.

Understanding these biological underpinnings can help us develop more effective ways to support teenagers as they navigate this exciting but challenging stage of life. By recognizing the power of genes, brain development, and peer influence, we can create environments that encourage healthy risk-taking while minimizing the potential for harm.

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Why Do Teenagers Sometimes Make Bad Choices?

Teenagers sometimes do things that are wrong or dangerous, like stealing or trying drugs. Scientists who study how genes and brains work are trying to figure out why this happens. Here are some interesting things they've discovered.

What Scientists Have Learned About Genes and Bad Behavior

Genes Can Make Teens More Likely to Do Risky Things

Scientists have learned that genes play a bigger role in behavior as people get older, especially during the teenage years. Genes are like instructions inside the body that make us who we are. Some genes might make us more likely to take risks or break rules. These genes might become more powerful as people go through puberty.

Some People are More Excited by New and Exciting Things

Have you ever met someone who loves roller coasters and trying new foods? They might be high in something called "sensation seeking." That means they really like exciting and new experiences. Scientists think genes might make people more or less likely to be sensation seekers. Interestingly, sensation seeking is also linked to those genes that make people more likely to do risky things.

Friends Can Influence Choices

People's friends can have a big influence on their behavior. Scientists have found that teenagers are more likely to do risky things if their friends are also doing them. This is especially true for teenagers whose genes make them more likely to take risks in the first place.

How the Brain Changes During the Teenage Years

Scientists who study the brain, called neuroscientists, have discovered that the brain changes a lot during the teenage years. These changes might also be why some teenagers are more likely to make bad choices.

Two Important Parts of Our Brain

Brains have two important parts that help people make decisions. The first part is called the "incentive-processing system." This part of the brain helps us understand and respond to rewards, like getting a good grade or eating a piece of candy. The second part is called the "cognitive control system." This part helps people control their impulses and make good decisions, even when they are tempted to do something else.

Brains Mature at Different Rates

As we people through puberty, the incentive-processing system becomes more active. This means peolpe become more sensitive to rewards, which can make risky things seem even more appealing. However, the cognitive control system in our brain doesn't finish developing until they are much older. This mismatch, where the brain is very sensitive to rewards but not as good at controlling impulses, might be another reason why teenagers do risky things.

Puberty, Friends, and the Brain

Friends are also connected to these changes in the brain. The hormonal changes of puberty, like increases in testosterone, can make the incentive-processing system even more active. And, being around friends can make the brain even more responsive to rewards, which can make teens more likely to take risks when they are with their friends.

What Does It All Mean?

Scientists are still trying to figure out exactly how genes, brain development, and the environment all work together to influence teenagers' behavior. But we already know that teenagers are going through a lot of changes, both physically and mentally. This is a time when they are learning to be more independent and make their own decisions. By understanding these changes, we can help teenagers make better choices and stay safe.

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