Adolescent Risk-Taking, Impulsivity and Brain Development - Essay Example

? Critique Paper on “Adolescent Risk Taking, Impulsivity and Brain Development: Implications for Prevention” Introduction Adolescence is a life stagethat mediates the end of childhood and the beginning of adulthood and is often perceived as the most turbulent of all phases in a person’s life. Susceptibility of the youth to such high-risk activities as drug addiction, smoking, premarital sex, and binge drinking, among others, are often the cause of much anxiety to parents, the community and the government. Their perceived vulnerability from such risky activities stemmed from lack of maturity to make the right decisions and also face their consequences. The underlying causes of adolescent susceptibility to risk-taking behavior are thus often the subject of many important researches and in their wake many theories and school of thoughts were born. One such theory is the subject of the article “Adolescent Risk-Taking, Impulsivity, and Brain Development: Implications for Prevention” by David Romer, where he suggested a two-factor model as the primary underlying sources of adolescent risk-taking propensity. Romer posited that this ehaviro is caused primarily by early childhood stressful experiences and the activation of the nucleus accumbens in the brain during adolescence. While these two factors are credible sources of risk-taking behavior, they cannot convincingly explain risk-taking behavior in adolescents that have no early adverse childhood experiences or the absence of risk-taking behavior in some adolescents. Thus, Romer’s model of adolescent risk-taking model is too simplistic because of its inability to account for all patterns of risk-taking behavior of adolescents. Summary of the Article Daniel Romer’s article entitled “Adolescent Risk-Taking, Impulsivity, and Brain Development: Implications for Prevention” discusses adolescent risk-taking behavior. According to him, the scientific community generally believes that there are two underlying factors that make adolescents prone to risk-taking activities: the early maturation of frontostriatal reward circuits involving the ventral striatum, and; the immaturity of the prefrontal cortex (PFC) during adolescence. The first drives adolescents to engage in adult-like activities while the other one makes them incapable of gauging the safeness of their decisions. The non-synchronic pace of maturity between these two parts of the brain is thought to cause an “inevitable period of risk for adolescents.” For Romer, however, adolescent risk-taking is underpinned primarily by the following: pre-existing impulsivity that starts early in life, and; increased sensation-seeking brought about by the activation of the ventral striatum. To support his position, Romer cited the longitudinal researches of the Seattle Social Development Project on binge drinking and Nagin and Tremblay (1999) on physical aggression. Both studies show, according to Romer that risk-taking is not a general pattern in adolescents and those few who started with such behavior early in childhood continued in their adolescence. He pointed out the three forms of impulsivity as acting without thinking, impatience, and sensation-seeking and stated that a combination of the first and the third usually underpins early problems and risky behavior while a combination of the first and the second results in weaker executive functions. According to him, these forms of impulsive behavior can be brought about by stressful experiences in childhood such as physical and emotional abuse, emotional neglect, exposure to violence and sexual abuse. He cited the National Annenberg Survey of Youth in 2000, which shows that sensation-seeking behavior begins to escalate at the age of 14 peaking at the ages of 18 for boys and 17 for girls. This is attributed by Romer to the dopaminergic activation of the nucleus accumbens, which peaks during adolescence. Romer played down the role of brain structure development to adolescent risk-taking behavior as unproven and inconclusive. As an example, he cited a study of children from 5 to 11 years old with the same IQ where it shows vocabulary development influences cortical thinning and in another research showing that those with higher IQ started their cortical thinning later than those with lesser IQ and still in another study where cortical thickening is thought to be the reason behind language skill development. More importantly, in yet another study, it was shown that myelination of the corpus callusom in youth alcoholism is more advanced that those adolescents who do not drink. Finally, Romer suggested that interventions should be made at an early age, and during adolescence. In the first, mothers-to-be who will potentially subject her children to early stressful experiences should be subjected to intensive programs to avert it. The second type would involve, according to Romer, well-crafted information drives that would inform, but not increase the perception that certain risk-taking behavior are exciting. He cited the graduated licensing strategy, where teens are first allowed to drive only with an adult in the daytime for a certain period before granting them driver’s license. Analysis Romer’s article is well-organized and the statement of his thesis clear and concise. Topics are segregated well and are easily identifiable under clear headings, which make for an easier reading. After commencing with the common theories underpinning adolescent risk-taking behavior, Romer proceeded with supporting the meat of his thesis by discussing his arguments one after the other in separate sub-headings. Romer’s thesis relies on the twin elements of early adverse childhood experiences and activation of ventral striatum at the onset of adolescence. Romer’s narrowing down of the causes of adolescent risk-taking behavior to two factors necessarily relegated factors commonly cited by researchers such as genetic predispositions, hormonal influences and asynchronous pubertal timing that have not been discussed nor rebutted by Romer. More importantly, the article has consigned various valuable researches linking adolescent risk-taking behaviors to brain development into the dustbin. The most crucial objection against Romer’s model, however, is that it fails to account other adolescent risk-taking behavior patterns in cases where early adverse childhood experiences are absent or the absence of risk-taking behavior in some adolescents. In 1995, the Youth Risk Behavior Surveys (YRBS) conducted a survey of nationally representative students from the 7th up to the 12th grades. It involved blacks, whites and Hispanic students. The results reflected that the following engaged in risk-taking behavior: 64% of the black students, 3% of which engaged in multi-risk activities; 55% of the Hispanic students, 4% of which are multi-risk engaging, and; 52% of the whites, 5% of which engaged in multi-risk behavior. Thus, 39% of the blacks, 45% of the blacks and 47% of the whites did not engage in risk-taking behavior at all (Lindberg et al 2000:21). In another study of the YRBS on early sexual debut, African Americans had the highest percentage at 26.8% for males and 7.1% for females, the Latinos at 11.1% and 3.6% for males and females, respectively, and the American European at 5% and 2.9% for males and females, respectively (Tercek et al 2008: 6). The immediately preceding paragraph illustrates that Romer’s model of risk-taking behavior involving the two factor elements of activation of nucleus accumbens during adolescence and early childhood stressful experiences are incapable of fully explaining the underpinning factors why Hispanics have higher rates in overall adolescent risk-taking behavior, but more whites engaged in multi-risk activities than both blacks and Hispanics, both of which had higher overall risk-taking behavior. In addition, Romer’s model also cannot explain why there are students, a majority of them, in fact, from all races, that did not engage at all risk-taking behavior. Neither does the same model sufficient to clarify why adolescent males generally have a higher early sex debut than females, or why African Americans have the highest percentage of adolescents engaging in early sex debuts than other races. In addition, Romer’s two-factor model discounted findings of other researches that point to other factors as underlying sources of adolescent risk-taking behavior. For example, various studies have confirmed that during adolescence, the brain undergoes specific alterations that accompany hormonal and neuroendocrine events. Cellular, molecular and anatomical changes take place in brain during adolescence. In the study of adolescent mice by Cunningham et al, the researchers noted increased fiber connectivity between the amygdala, the seat of learning, and the prefrontal cortex (or PFC), the executive decision-making region, implying the immaturity of the cognitive and assessment skills of adolescents, which may account for the fact that adolescents cannot fully comprehend the risks entailed in some activities. In the rat study, the hyperactivity and novelty-seeking nature as well as distractibility commonly found in human adolescents were also reflected (Kelley et al 2004: 29-31). Romer suggested that there is inconclusive proof that brain structure development underlies the risk-taking behavior of adolescents because of the discordant findings of researchers as to its role in this type of behavior resulting in a “chicken or the egg” dilemma. Thus, he concluded that brain structure development cannot be conclusively used to account for the risk-taking behavior of adolescents. According to Ronald Dahl, Staunton Professor of Psychiatry and Pediatrics, it is precisely the combination of downstream and upstream changes and puberty-independent maturational changes that creates the “potential for dys-synchrony among the components of adolescent brain maturation” that may result in the adolescent’s propensity for risk-taking. Dahl observed that certain brain changes results in pubertal changes, which he called upstream changes and at the same time certain pubertal processes affect brain changes, which he referred to as downstream changes. On top of these, there are aspects of brain maturation during adolescence that are independent of the pubertal stage and continue even after the stage of puberty. The combination of all these three, according to Dahl, can account for the characteristic vulnerable period of an adolescent’s life (2004: 16-18). It is also suggested by Spears (2002) that developing activities in the different regions of the brain do not follow a pattern, but through a dynamic process become interrelated over time. Thus, changes in a brain region are specific to that region alone and may not reflect those being undergone by other areas and Casey added that changes in different regions occur at dissimilar paces. Like Cunningham et al, Casey observed the steep curve of disproportion pace between the limbic system, where the amygdala is, and the PFC during the period of adolescence, which, according to him, may account for the propensity for risk-taking by adolescents (Institute of Medicine and National Research Council 2011: 37-38, 40). Aside from the influence of brain structure development during adolescence, there are other compelling findings in various researches that point to a host of other sources that may combine with brain structure development and early stressful experiences that may influence adolescent risk-taking behavior. Unlike Romer’s two-facto adolescent risk-taking model, DiClemente et al suggests that a more complete and non-unidimensional model should take into account not only one or two aspects, but include biological, psychosocial, and environmental influences. This means a combination of factors such as genetic predisposition, hormonal influences, asynchronous pubertal timing, brain and central nervous system development together with self-esteem, sensation-seeking, and cognitive and affective states as well as school, parental and peer influences (2009: 41-42). A multi-dimensional approach such as that of DiClemente et al accounts for the behavioral variance among adolescents, some of which exhibit a greater propensity for risk-taking behavior than some of their peers. Conclusion Romer’s article is well-organized, concise and his thesis well-laid out. Nonetheless, it is inadequate to answer and fully explain a lot of statistical findings regarding adolescent risk-taking behavior. If, for example, the activation of the nucleus accumbens is a primary factor of the behavior and is a common occurrence during the period of adolescence, then how is the absence of the risk-taking behavior of many adolescents explained? The idea that Romer’s two-factor model primarily underpin early sexual debut is doubtful considering the absence of logical rationale that makes male adolescents more prone to this risky behavior than their female counterparts. Moreover, by primarily attributing to these factors adolescent risk-taking behavior, Romer discounted researches on the influence of brain structure development during adolescence. Substantial evidence, however, have been uncovered that the brain undergoes a lot of changes during this period especially in the executive-making area of the PFC. Works Cited Dahl, Ronald. ‘Adolescent Brain Development: A Period of Vulnerabilities and Opportunities.’ Annals New York Academy of Sciences 1021:1-22 (2004). DiClemente, Ralph and John Santelli, Richard Crosby. Adolescent Health: Understanding and Preventing Risk Behaviors. San Francisco: John Wiley & Sons, 2009. Institute of Medicine and National Research Council. The Science of Adolescent Risk-Taking: Workshop Report. Washington, DC: National Academies Press, 2011. Kelley, Ann and Terri Schochet, Charles Landry. ‘Risk-Taking and Novelty in Adolescence.’ Annals New York Academy of Sciences 1021:27-32 (2004). Lindberg, Laura and Scot Boggess, Laura Porter, Sean Williams. Teen Risk-Taking: A Statistical Portrait. Washington DC: Urban Institute, 2000. aspe.hhs.gov/health/reports/teenrisk/teenrisktaking.html. Romer, Daniel. ‘Adolescent Risk-Taking, Impulsivity, and Brain Development: Implications for Prevention.’ Developmental Psychobiology, 263-273, 2009. Tercek, Rachel and Rosalind Franklin. Impulsivity: Examining Links to Risk-Taking Behavior among Adolescent Detainees. ProQuest, 2008 Read More