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Book Title: Treating and Preventing Adolescent Mental Health Disorders
> pp. [xxx]-[xxxiv]
UNDEFINED: AUTHORS
Treating and Preventing Adolescent Mental Health Disorders
Print ISBN 9780195173642, 2005
pp. [xxx]-[xxxiv]
which are presumed to be excitatory, accompanied by a reduction in brain energy utilization, transforms the adolescent brain into one that is more efficient and less energy consuming (Chugani, 1996; Rakic et al., 1994). These changes may permit more selective reactions to stimuli that in younger children activate broader cortical regions (Casey, Giedd, & Thomas, 2000). Myelination is another brain process that occurs during adolescence. The speed of neural transmission is greatly increased during myelination as a result of the glial cell membranes wrapping around axons. Although certain areas of the brain, such as the visual cortex, show maturation of myelin during childhood, myelination continues for the long-distance neural connections in the frontal, parietal, and temporal areas throughout adolescence (Luna & Sweeney, 2004). It is hypothesized that the myelination seen during adolescence further contributes to the development of executive functions of the brain, including faster information processing, by facilitating the integration of distributed brain areas and enhancing local connections (Luna & Sweeney, 2004). Adolescence is also marked by changes in the relative volume and level of activity in different brain regions. For example, there is an increase in cortical white matter density (due to myelination) and a corresponding decrease in gray matter, especially in frontal and prefrontal regions (Giedd et al., 1999; Sowell et al., 1999a, 1999b). The overall result of these varied changes is a net decrease in volume of the prefrontal cortex (Sowell et al., 1999b; van Eden, Kros, & Uylings, 1990). In the hippocampus and the amygdala, however, gray-matter volumes continue to increase during late childhood and adolescence (Giedd, Castellanos, Rajapakse, Vaituzis, & Rapoport, 1997; Yurgelun-Todd, Killgore, & Cintron, 2003). While frontal white-matter volume peaks at about 11 years of age in girls and 12 years of age in boys, temporal gray matter volume peaks at about 16.7 years in girls and 16.2 years in boys (Giedd, 2004). In contrast, the dorsal lateral prefrontal cortex, which controls impulses, doesn't reach adult size until the early 20's (Giedd, 2004). Consistent with these changes in brain structure is the finding that by
the end of adolescence there is improvement in prefrontal executive functions, including response inhibition and organizational and planning skills (Fuster, 1989). There are also developmental shifts in patterns of innervation, including the circuits involved in the recognition and expression of fear, anxiety, and other emotions (Charney & Deutsch, 1996). The responsiveness of the cortical GABA–benzodiazepine receptor complex to challenge increases as animals approach puberty (Kellogg, 1998), and there are maturational changes in the hippocampus in humans and in animals (Benes, 1989; Wolfer & Lipp, 1995), especially increases in GABA transmission (Nurse & Lacaille, 1999). Further, pubescent animals show lower utilization rates of serotonin in the nucleus accumbens than do younger or older animals (Teicher & Andersen, 1999). Developmental increases in amygdala–prefrontal cortex connectivity are seen during adolescence, in work conducted in laboratory animals (Cunningham, Bhattacharyya, & Benes, 2002). There are also alterations in amygdala activation (Terasawa & Timiras, 1968) and in the processing of emotional and stressful stimuli. Lesions of the amygdala have opposite effects on fearfulness to social stimuli according to whether those lesions are in infant or adult monkeys (Prather et al., 2001). Although levels of negative affect and anxiety have been correlated with amygdala activity in adults (Davidson, Abercrombie, Nitschke, & Putnam, 1999), recent studies using functional magnetic resonance imaging (fMRI) to examine amygdala activation in response to emotionally expressive faces in younger individuals have yielded a varying mosaic of evidence (Killgore, Oki, & Yurgelun-Todd, 2001; Pine et al., 2001). Maturational changes in the cerebellum and in the circuitry connecting the cerebellum to the prefrontal cortex continue throughout adolescence. Lesions of the adult cerebellum disrupt the regulation of emotion and interfere with performance of tasks requiring executive functions (Schmahmann & Sherman, 1998), although this is less apparent in those younger than 16 years of age (Levisohn, Cronin-Golomb, & Schmahmann, 2000).
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These brain changes related to the circuitry that involves emotions interact with hormonal changes during this period, leading to parallel emotional and behavioral changes during adolescence. Early adolescence is characterized by a lack of emotional regulation, but by the end of adolescence there is substantially greater emotional stability and control over behavior, particularly impulsive behavior. There are several other changes in the human brain that, while not unique to adolescence, occur from birth through adulthood. One of these is postnatal neurogenesis (development of new neurons). This ongoing development of new neural cells is now known to occur in several brain areas, including the hippocampus, the olfactory bulb, the cingulate gyrus, and regions of the parietal cortex (Nelson, 2004). Neurotransmitter systems in the brain, which are key to current biological perspectives on many mental disorders, also do not reach full maturity until adulthood (White & Nelson, 2004).
Hormonal Changes in Adolescence
Puberty results from increased activation of the hypothalamic–pituitary–gonadal (HPG) axis, which in turn results in a rise in secretion of sex hormones (steroids) by the gonads in response to gonadotropin secretion from the anterior pituitary. Rising sex steroid concentrations are associated with other changes, including increased growth hormone secretion. There is also more activity in the hypothalamic–pituitary–adrenal (HPA) axis during adolescence. This neural system governs the release of several hormones and is activated in response to stress. Cortisol is among the hormones secreted by the HPA axis, and researchers can measure it in body fluids to index the biological response to stress. Beginning around age 12, there is an age-related increase in baseline cortisol levels in normal children (Walker, Walder, & Reynolds, 2001). The significance of postpubertal hormonal changes has been brought into clearer focus as researchers have elucidated the role of steroid hormones in neuronal activity and morphology
(Dorn & Chrousos, 1997; Rupprecht & Holsboer, 1999). Neurons contain receptors for adrenal and gonadal hormones. When activated, these receptors modify cellular function and influence neurotransmitter function. Short-term effects of steroid hormones on cellular function are believed to be mediated by membrane receptors. Longer-term effects (genomic effects) can result from the activation of intraneuronal or nuclear receptors. These receptors can influence gene expression. Brain changes that occur during normal adolescence may be regulated by hormonal effects on the expression of genes that govern brain maturation. Gonadal and adrenal hormone levels are linked with behavior in adolescents. In general, both elevated and very low levels are associated with greater adjustment problems. For example, higher levels of adrenal hormones (androstenedione) are associated with adjustment problems in both boys and girls (Nottelmann et al., 1987). Children with an earlier onset of puberty have significantly higher concentrations of adrenal androgens, estradiol, thyrotropin, and cortisol. They also manifest more psychological disorders (primarily anxiety disorders), self-reported depression, and parent-reported behavior problems (Dorn, Hitt, & Rotenstein, 1999). The more pronounced relationship between testosterone and aggressive behavior in adolescents who have more conflicts with their parents demonstrates the complex interactions between hormonal and environmental factors (Booth, Johnson, Granger, Crouter, & McHale, 2003). It is conceivable that hormones partially exert their effects on behavior by triggering the expression of genes linked with vulnerability for behavioral disorders. Consistent with this assumption, the heritability estimates for antisocial behavior (Jacobson, Prescott, & Kendler, 2002) and depression (Silberg et al., 1999) increase during adolescence. Further, the relationship between cortisol and behavior may be more pronounced in youth with genetic vulnerabilities. For example, increased cortisol is more strongly associated with behavior problems in boys and girls with a mutation on the long arm of the X chromosome (fragile X syndrome) than in their unaffected siblings (Hessl et al., 2002).
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Genetics plays a significant role in our understanding of adolescent mental health. Historically, diathesis–stress models of mental illness suggested that a constitutional vulnerability interacting with environmental stress led to the development of mental disorders. Research in recent years, however, has shown that more complex models are needed to understand many disorders. Genes are turned on and turned off throughout one's lifetime, and multiple genes are likely involved in many mental disorders. Many of the mental disorders prevalent in adolescents are the subject of promising, ongoing genetic research. Schizophrenia is one example. Several candidate genes have been identified that influence the development of the brain, including processes that have been linked to schizophrenia such as the excitability of glutamate neurons, hippocampal function, and regulation of dopamine neurons by the cortex. The authors of Chapter 5 on schizophrenia speculates that disruptions in these processes during adolescence may be particularly problematic because of the dramatic changes in cortical development that occur during this period. Another example of the role of genetics is recent research on the relationship between a genetic variable, polymorphism of the serotonin transporter gene, and the development of depression after exposure to child abuse (Caspi et al., 2003). Individuals with a certain polymorphism of the serotonin transporter gene were found to be immune to the depressogenic affects of child abuse, whereas those with a different form of the polymorphism were highly likely to develop depression after child abuse (Caspi et al., 2003).
The Environmental Context of Adolescence
In the developing adolescent, the environmental context provides an influence that interacts (positively or negatively) with that child's biology to produce behavior. Families, schools, peers, youth sports and after-school activities, and community and religious organizations are the main social contexts in which adolescents
spend time and model interactions with adults and peers, and these contexts provide the general framework for adolescents to develop their own outlook on life. As youth move from childhood to adolescence, there is an increase in time spent with peers and a corresponding decrease in time spent with their family. Typically, there is also a natural tendency for conflicts with authority figures, including parents, to increase. These conflicts allow adolescents to find their own path in life and to begin to acquire the skills needed to succeed as an independent adult. As mentioned previously, the successful acquisition and application of skills to live independently mark the definition of the transition from adolescence to adulthood. There are also cultural differences in the nature and timing of the acquisition of these adult living skills during adolescence. Thus, environmental and cultural factors are inherently interwoven into the fabric of adolescence. Each of the major external environmental contexts to which adolescents are exposed can have positive or negative influences on their mental health. Parents, friends, coaches, and teachers provide social support to adolescents that can bolster them during difficult times and help them develop in positive ways by serving as role models. But if these people are abusive, rejecting, or overly controlling toward a youth who is emotionally attached to them, the youth can suffer detrimental effects. Abuse, which is all too often physical and/or sexual abuse from adults, and trauma are also clearly risk factors for the development of mental disorders, such as posttraumatic stress disorder and major depression. Unfortunately, trauma and abuse are not uncommon in some settings. For example, a study of African-American male youth living in low-income housing in Alabama found that over three-fourths of the youth had been victims of violence. An even larger proportion (87%) reported witnessing at least one violent act (Fitzpatrick, 1997). Finally, a measurable impact of parental mental health, particularly parental depression, on child and adolescent mental health is beginning to be uncovered (see Chapter 1). Although parental behavior or mental health has an impact on that of the child or adolescent, a case can be made that, beyond the extreme sit
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uation of abuse or neglect, parents are not the major influence on adolescents; instead, socialization that occurs in peer groups outside the home may be the more potent influence. Harris ( 1995) describes a number of influential processes that occur in peer groups. Adolescents who are part of a peer group are subject to “in-group” favoritism and “out-group” hostility. Peer groups also elicit within-group jockeying for status. Moreover, peer groups encourage adolescents to form close dyadic relationships, including the development of love relationships. Disruptions in these processes are part of the emotional turmoil of adolescence. Peer groups, along with the media, also expose adolescents to popular culture, which can impact adolescent beliefs, values, and sexual behavior. One important example of this is described in Chapter 17: particularly during the 1960s to 1980s, popular culture affected the degree and nature of adolescent substance abuse. Within each of the parts on mental disorders in adolescents, the role of environmental contexts as contributing factors or triggers in the development of such disorders is discussed. The positive influence of such environmental contexts is highlighted in Chapter 26 on positive youth development. These environmental contexts are important to understand, not only because of their etiologic or protective factors in regard to mental health, but also because they are the settings and vehicles for interventions among youth, as we discuss below.
Intervention in Adolescence
With all of the changes occurring during adolescence and the associated neurobehavioral vulnerabilities and resiliences, it is clear that this phase of life is an ideal time to target with interventions aimed at improving young people's lives. This is true for both the treatment of adolescent disorders and the prevention of both adolescent-onset and adult-onset disorders. For many mental disorders, it is increasingly clear that the earlier the intervention, the better. For example, disorders such as schizophrenia and bipolar disorder have a progressive course, with onset in adolescence or early adulthood,
followed by the potential for further deterioration with the occurrence of each subsequent episode of illness. Therefore, rather than waiting for an individual to meet all diagnostic criteria from the Diagnostic and Statistical Manual for Mental Disorders (DSM) for a psychiatric disorder, it may be far better to identify and treat individuals who have risk factors or display some of the early signs of the illness. In the case of schizophrenia, such early-intervention programs have shown promise in reducing the annual incidence of first-episode psychosis (see Chapter 6; Falloon, Kydd, Coverdale & Laidlaw, 1996). These early-intervention efforts and the targeting of high-risk and other nondisordered populations speak to the importance of interventions that have a preventive perspective. Although treatment of actual disorders in adolescence will remain an essential aspect of adolescent mental health research and practice, prevention may be the key to diminishing the burden of adolescent and adult disorders on society. Accordingly, the current volume has a major focus on prevention. There are many forms of prevention, therefore, a brief history of the concept and definitions of relevant terms are presented here.
Early Public Health Prevention Classification System
Different types of disease prevention efforts were first defined from a public health point of view in 1957 by the Commission on Chronic Illness (Commission on Chronic Illness, 1957). Three types of preventive interventions were identified: primary, secondary, and tertiary.
Primary prevention was defined as the reduction of the incidence of a disease or disorder through the prevention of the occurrence of new cases of a disease or disorder before they occur (Commission on Chronic Illness, 1957). This definition was expanded to include interventions designed to promote general optimum health by the specific protection of persons against disease agents or the establishment of barriers against agents in the environment (Leavell & Clark, 1965). Widespread vaccination is an example of primary prevention.
Secondary prevention was defined as the reduc
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tion in the prevalence in the general population of recurrences or exacerbations of a disease or disorder that already has been diagnosed (Commission on Chronic Illness, 1957). This includes early detection and intervention to reverse, halt, or at least retard the progress of a condition (Rieger, 1990). An example of secondary prevention is the use of antihypertensive medications among those with high blood pressure to reduce the risk of cardiovascular complications such as stroke. In contrast to primary and secondary prevention, tertiary prevention efforts do not seek to reduce the prevalence of a disease or disorder. Tertiary prevention is only concerned with the reduction of the disability associated with an existing disease or disorder (Commission on Chronic Illness, 1957). For those with allergies, removal from exposure to the allergen would be a tertiary prevention approach. Although these prevention terms were widely used in various public health domains, there are clear problems in attempting to apply this classification system for prevention efforts to the mental health field. The system requires an appreciation of the linkage between a disease or a disorder and the cause of that disorder at different stages of development (Haggerty & Mrazek, 1994). For example, the primary prevention of adolescent depression requires knowledge of the causal factors related to depression and their operational relationships. Secondary and tertiary prevention require a similar knowledge base. In practice, however, prevention interventions are often applied without this level of knowledge. As a practical matter, many preventive interventions have been based on indirect associations or statistical relationships with an outcome that is desirable to prevent. The strength or lack of strength of these associations has often diminished the effectiveness of these efforts. As more has been learned about etiology, it has become clear that physical and mental health events and outcomes cannot be explained by simple causal relationships. Rather, they are the result of the complex interplay of biological, social, environmental, and intrapersonal risk and protective factors. Thus, the original definitions of prevention break down when applied to adolescent mental health.
Gordon's Definitions of Prevention
An alternative to the Commission on Chronic Illness ( 1957) definitions of prevention was proposed by Robert Gordon. This new system was based on the “empirical relationships found in practically oriented disease prevention and health promotion programs” (Gordon, 1983). These included programs designed for universal, selective, and indicated prevention. The definition of universal prevention included all interventions targeted to the general public or to an entire population group not selected on the basis of risk (Gordon, 1987). This would include interventions such as use of seat belts and immunization programs that are desirable for everyone in the eligible population. Selective prevention is defined by Gordon as interventions that target individuals, or a specific subgroup of the population, whose risk of developing a disorder is higher than average (Gordon, 1987). For example, condom use programs among sexually active adolescents is a selective prevention effort. Once an individual in a high-risk group exhibits the early signs or symptoms of a disorder, indicated prevention efforts would apply (Gordon, 1987).
Institute of Medicine Definitions
To reduce confusion emanating from the use of both the Commission on Chronic Illness ( 1957) and Gordon ( 1983) systems, and to suggest definitions more appropriate to the mental health field, the 1994 Institute of Medicine report, Reducing Risk for Mental Disorders: Frontiers for Prevention Intervention Research, offered new definitions. The term prevention was used in this report to refer only to interventions that occur before the initial onset of a disorder. Prevention included all three elements of Gordon's system. Efforts to identify cases and provide care for known disorders were called treatment, and efforts to provide rehabilitation and reduce relapse and reoccurrence of a disorder were called maintenance. Further distinctions were made within the prevention category using Gordon's ( 1983) terms. These are the definitions that we have used for the current volume. The specific dis
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doi:10.1093/9780195173642.003.0001
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