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Children with conduct disorders (persistent disruptive, deceptive and aggressive behaviors) are highly likely to require clinical intervention. Furthermore, such children constitute an important opportunity to prevent a future burden of poor adult health and social maladjustment. During childhood, conduct problems cause considerable distress for children, their families and their schools, and conduct problems are associated with consequential social and educational impairments for the child (Lahey, Loeber, Quay et al., 1997). Later, during adolescence and adulthood, children with conduct problems are at substantially increased risk of poor prognosis. This increased risk involves adulthood antisocial outcomes such as antisocial personality disorder, criminal and violent offending, and potential incarceration. Moreover, childhood conduct problems further predict adulthood risk for serious difficulties in education, work and finances, homelessness, abuse and dependence on tobacco, alcohol and drugs, and even compromised physical health including injuries, sexually transmitted infections, compromised immune function, dental health and respiratory health, as well as a variety of mental disorders and suicide attempts (Moffitt, Caspi, Harrington et al., 2002; Odgers, Caspi, Poulton et al., 2007a; Robins 1991). An excess of conduct disorders characterizes the juvenile psychiatric histories of adult patients with substance, affective, anxiety and eating disorders, and even patients with schizophrenia spectrum disorders and mania (Kim-Cohen, Caspi, Moffitt et al., 2003). As adolescents and young adults, children with conduct problems are more likely to enter and contribute to cohabitations and marriages with domestic violence, and to engage in early childbearing and poor parenting practices, hence putting the next generation at risk (Jaffee, Belsky, Sligo et al., 2006; Moffitt & Caspi, 1998). This breadth of compromised long-term outcomes highlights the prevention opportunity afforded when children with conduct problems are successfully treated. The conduct disorders are distinctive among mental disorders in that they are embedded in the patient’s social context and have consequences for victims, apart from conferring harm on the individual patient. Many of the features are seen in social interactions, notably verbal and physical aggression, bullying, oppositional behavior and lying. This means that the symptoms of the disorders are also social behaviors that arise in the context of family, peer, educational and wider social relationships, and which in turn have a detrimental impact on these relationships. The origins, maintenance and cessation of the symptoms cannot be understood independently of these contexts. Equally, the symptoms are not simply the product of social processes, in that individual vulnerabilities are known to play a prominent part. Biological, psychological and social processes are all implicated in the etiology and treatment of the conduct disorders, through additive and interactive effects (Hill, 2002; Rutter, Giller, & Hagell, 1998). This chapter aims to introduce clinicians and researchers to major issues involved in conduct disorders of childhood and adolescence. It covers classification, prevalence, subtypes, associated co-occurring disorders and complicating conditions. Risk factors are examined at the levels of the individual child, the family and the extra-familial social context. Issues in clinical assessment and diagnosis are covered, as are intervention approaches. An exhaustive citation bibliography of all studies of conduct problems is far beyond the scope of this chapter. Thus, only key individual studies with strong methods are cited as examples, and the reader is directed to reviews of the literature when those are available. Classification of Juvenile Antisocial Disorders Conduct Disorder and Oppositional Defiant Disorder in DSM-IV and ICD-10 Two principal classification systems, DSM-IV (American Psychiatric Association, 2000) and ICD-10 (World Health Organization, 1996) are quite similar in that both specify behaviors required for diagnosis. Both emphasize the persistent duration of the symptom behaviors for some months. The principal difference is that, in DSM-IV, Oppositional Defiant Disorder (ODD) and Conduct Disorder (CD) are separated, whereas in ICD-10 the criterion set of items required for CD is very close to what would be obtained by combining the DSM-IV ODD and CD items (Angold & Costello, 2001). ODD is defined as a recurrent pattern of negativistic, defiant, disobedient and hostile behaviors leading to impairment of day to day activities, 543 Conduct Disorders of Childhood and Adolescence Terrie E. Moffitt and Stephen Scott 35 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 543 Rutter’s Child and Adolescent Psychiatry, 5th Edition, Edited by M. Rutter, D. V. M. Bishop D. S. Pine, S. Scott, J. Stevenson, E. Taylor and A. Thapar © 2008 Blackwell Publishing Limited. ISBN: 978-1-405-14549-7

and CD as the repetitive and persistent violation of the basic rights of others and societal norms. Are ODD and CD distinct conditions? It is not clear how valid the distinction is between ODD and CD, because the items in each are clearly age-related (Angold & Costello, 2001). Although some studies have found evidence that CD and ODD symptoms have independent associations with certain clinical correlates, it is commonly accepted that ODD and CD may be different age-related manifestations of the same condition, in which early ODD often develops into eventual CD (Lahey et al., 1997; Loeber, Burke, Lahey et al., 2000; Maughan, Rowe, Messer et al., 2004). Category, or Continuum? Although the principal classification systems, DSM-IV and ICD-10, take a categorical approach, this has disadvantages. Unless there is good evidence that the problems operate in a categorical fashion, the cut-off point will inevitably be arbitrary; studies searching for such evidence have not found it (e.g., Moffitt, Caspi, Rutter et al., 2001). One study has systematically examined the predictive validity of categorical diagnoses versus dimensional measures of ODD and CD (Fergusson & Horwood, 1995). The dimensional variables were better predictors of outcome, and there appeared to be a dose–response relationship of increasing risk for juvenile offending and school dropout associated with increasing severity of disruptive behaviors. Genetic influences appear to operate in a similar manner in relation to conduct problems whether they are assessed as dimensions or categories (Eaves, Silver, Meyer et al., 1997). Although diagnoses are expected in clinical settings, using a categorical approach entails the risk that important differences of severity or type of dysfunction below and above the cut-off will be lost (Hinshaw, Lahey, & Hart, 1993). Other Conceptualizations There has been immense variation in the ways that conduct problems have been conceptualized and measured in the research consulted for this chapter. Many studies have used the DSM diagnoses, but a range of measures such as aggressive personality traits, antisocial behaviors, psychopathic traits and juvenile delinquent offending have also been employed. The terms “conduct problems” and “antisocial behaviors” will be used here to refer broadly to children’s aggressive and disruptive behaviors, measured in a range of ways. Descriptive Epidemiology Overall Prevalence Estimates of the prevalence of conduct problems vary according to the criteria used (Angold & Costello, 2001; Green, McGinnity, Meltzer et al., 2005). However, on the basis of the majority of epidemiological studies from the industrialized west, 5–10% of children and adolescents have significant persistent oppositional, disruptive or aggressive behavior problems. Prevalence by Historical Period, Social Class and Ethnicity With respect to historical period, both short-term changes and longer-term changes in youth antisocial behavior have been examined. One example of short-term change was observed in the USA during the 1990s when rates of youth violence, particularly homicide, increased dramatically and then decreased again, a change attributable to short-term alterations in local drug and firearm markets, and to altered policies in policing and sentencing (Blumstein & Wallman, 2005). A longer-term modest rise in diagnosable conduct disorder over the second half of the 20th century has also been observed in a study comparing assessments of three successive birth cohorts in Britain (Collishaw, Maughan, Goodman et al., 2004). Presumably, this increase arises from some societal level factor that has also been characterized by gradual change during the same time period, such as changing family structure. With respect to socioeconomic class, measured class differences in juvenile antisocial behavior are not as wide as might be expected. Research has consistently failed to find the expected relationship between low family social class and individual youth’s conduct problems or offending, particularly when this behavior is assessed through youth self-reports (Tittle & Meier, 1990). One study found that among low social class adolescents, offending was associated with attitudes of alienation, whereas among high social class, offending was associated with attitudes of unconventionality, suggesting that social class may condition motivation for antisocial conduct (Wright, Caspi, Moffitt et al., 1999). With respect to ethnicity, the over-representation of offenders of Black African ancestry in US and UK jails and prisons has focused much debate, and some research, on the thorny question of ethnic group differences in antisocial behavior (Morenoff, 2005; Smith, 2005). Research into ethnic differences has not really studied childhood conduct problems, but rather is limited to studies of adolescent and adult offending. Recognizing that the over-representation of Black African-ancestry offenders in official statistics could arise from race bias among police and courts, researchers also consult sources of data such as youth self-reports of antisocial behaviors and crime victim survey reports of perpetrators’ ethnicity. These data, although influenced by their own serious sources of ethnicity-related bias, also tend to show an excess of offenders of Black African ancestry, although the Black– White difference is generally somewhat narrower than in official data. Importantly, Hispanic Americans in the USA and British Asians in the UK do not tend to show an excess of offending when compared to their white counterparts. Hypothesized explanations for a Black–White difference in offending include poverty, prejudice, family structure, subculture, neighborhood context and individual characteristics such as intelligence, but research is insufficient to support conclusions (Morenoff, 2005; Smith, 2005). Sex Differences in Prevalence Where studies have included males and females with conduct CHAPTER 35 544 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 544

problems, the sex ratio is approximately 2.5 males for each female overall, with males further exceeding females in the frequency and severity of behaviors (Costello, Angold, Burns et al., 1996; Moffitt et al., 2001). In the light of the gender difference the question arises as to whether the sexes have different risk mechanisms. One study found that the individual and family factors associated with self-reported delinquency were the same for males and females, but were more common in males (Rowe, Vazsonyi, & Flannery, 1995). This same conclusion was reached in a systematic analysis of a wide variety of risk factors comparing the males and females of the Dunedin longitudinal study (Moffitt et al., 2001). Reviews of twin studies have revealed no systematic differences between the sexes in the contributions of genetic and environmental factors (Rhee & Waldman, 2002). On balance, research suggests that the causes of conduct problems are the same for the sexes, but males have more conduct disorder because they experience more of its individual-level risk factors (e.g., hyperactivity, neurodevelopmental delays). However, recent years have seen increasing concern among clinicians about treating antisocial behavior among girls, and this is currently the topic of intense research (Pullatz & Bierman, 2004). Developmental Subtypes Life-Course-Persistent Versus Adolescence-Limited There has been considerable attention paid to the distinction between aggressive and disruptive behaviors that are first seen in early childhood versus those that start in adolescence (Moffitt, 1993a; Patterson & Yoerger, 1993), and these two subtypes are encoded in the DSM-IV diagnostic system for CD. Early onset is a strong predictor of persistence through childhood, and early-onset delinquency is more likely to persist into adult life. Findings from the Dunedin longitudinal study following a 1972–73 birth cohort have shown that those with early onset differ from those with later onset in that they have lower IQ, more attentional and impulsivity problems, poorer scores on neuropsychological tests, greater peer difficulties and they are more likely to come from adverse family circumstances (Moffitt et al., 2001). Those with later onset, by contrast, are thought to become delinquent predominantly as a result of social influences such as association with other delinquent youths, or seeking social status through delinquent behaviors. Moffitt (1993a) termed the early-onset group “lifecourse-persistent” and the later-onset group “adolescencelimited,” thus linking developmental course to the differences in underlying deficits. The distinction between the two groups has been broadly supported in longitudinal studies of several cohorts from a dozen countries (Moffitt, 2006). Findings from the follow-up of the Dunedin cohort support relatively poorer adult outcomes for the early-onset group in domains of violence, mental health, substance abuse, work and family life (Moffitt, Caspi, Harrington et al., 2002). Follow-up to age 32 revealed that the early-onset life-course-persistent group had compromised physical health relative to other cohort men, as shown by increased injuries, primary care physician and hospital visits, and clinical tests of sexually transmitted infections, systemic inflammation, periodontal disease, decayed teeth and chronic bronchitis (Odgers et al., 2007a). However, the “adolescence-limited” group was not without adult difficulties (Moffitt et al., 2002; Odgers et al., 2007a). As adults they still engaged in self-reported offending, and they also had problems with alcohol and drugs. The Cambridge Study in Delinquent Development, a longitudinal study of 411 London males from age 8 to 46 years, also found that those with antisocial behaviors starting in adolescence were likely to continue to commit undetected crimes in adult life, although their work performance and close relationships were not impaired (Nagin, Farrington, & Moffitt, 1995). Thus, the age-of-onset subtype distinction has strong predictive validity, but adolescent-onset antisocial behaviors may have more long-lasting consequences than previously supposed, and thus both childhood onset and adolescent onset conduct problems warrant clinical attention. Childhood-Limited Conduct Problems Robins (1966) first pointed out that half of children with conduct problems do not grow up to have antisocial personalities. Longitudinal studies aiming to document the continuity of antisocial behavior from childhood through adolescence to adulthood have repeatedly revealed the existence of an exceptional group of children who lack such continuity. These are often termed “childhood-limited” conduct problems (Moffitt, 2006). Some studies define this childhood-limited group broadly (as a large group of children having any elevated disruptive behavior), and these draw our attention to the ubiquity of temporary conduct problems in the healthy population of children, and show that so long as mild conduct problems do not persist they need not portend poor prognosis (Odgers, Milne, Caspi et al., 2007b; Tremblay, 2003). In contrast, other studies define this childhood-limited group more narrowly (as a small group of children exhibiting extreme, pervasive and persistent antisocial behavior problems only during childhood). These studies report that such childhood-limited antisocial boys develop into adult men who are depressed, anxious, socially isolated and have low-paid jobs (Farrington, Gallagher, Morley et al., 1988; Moffitt et al., 2002). Thus, boys whose conduct problems are severe and persistent enough to warrant a clinical diagnosis may not later develop antisocial personality, but they will suffer other forms of maladjustment as adults. Thus, all children with conduct disorders warrant clinical attention. When a young child presents for assessment, the clinician’s task is to make a differential diagnosis between childhood-onset CD that will be only childhood-limited, versus childhood-onset CD that will in future have a life-course-persistent course and pathological prognosis. DSM-IV’s age-of-onset distinction cannot help with this task because all child patients, by definition, have childhood onset. Researchers have tried to distinguish life-course-persistent versus childhood-limited CONDUCT DISORDERS 545 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 545

trajectory groups by using childhood risk factors, without much success (Moffitt, 2006). However, initial evidence indicates that comorbid attention deficit/hyperactivity disorder (ADHD), as well as family psychiatric history, characterize the persistent subtype but not the childhood-limited subtype. Alcohol problems in the child’s parents and grandparents seem particularly prognostic (Odgers et al., 2007b). Associated Disorders and Conditions Co-occurring Mental Disorders Epidemiological studies concur that more than 90% of individuals having conduct or antisocial personality disorder also meet diagnostic criteria for other disorders (Moffitt et al., 2001; Robins & Regier, 1991), and conduct disorder has been shown to feature prominently in the developmental history of virtually every adult psychiatric disorder, including schizophrenia and eating disorders (Kim-Cohen et al., 2003). Particularly striking is the frequent overlap between antisocial behaviors and hyperactive-impulsive-inattentive behaviors in the young population (Waschbusch, 2002). A meta-analysis of associations among child psychiatric disorders estimated the odds ratio for ADHD in the presence of conduct disorder is 10.7 (7.7–14.8) (Angold, Costello, & Erkanli, 1999). Children who have both ODD/CD and ADHD have more varied and severe ODD/CD symptoms, greater levels of parental psychopathology, more conflictual interactions with parents, greater peer problems, school difficulties and psychosocial adversity, worse neuropsychological deficits and poorer prognosis into adulthood than those with either condition alone (Angold, Costello, & Erkanli, 1999; Lynam, 1996). Twin studies suggest a common genetic component underlying ADHD and conduct disorder (Moffitt, 2005a). Lynam (1996) reviewed literature suggesting that children with the combination of conduct problems and hyperactivity-attentional difficulties are likely to be “fledgling psychopaths,” who warrant especial clinical attention and may be particularly difficult to treat. Apart from ADHD, young people with conduct problems have also been shown to have other associated disorders at markedly elevated rates (Vermeiren, Jespers, & Moffitt, 2006). The disorders most consistently implicated are adolescent depression and substance abuse. In each case, comorbidity between conduct problems and the co-occurring disorder grows stronger with age, becoming more marked in adolescence. Diagnoses of learning disabilities and reading impairment are also highly prevalent among children with conduct problems (Carroll, Maughan, Goodman et al., 2005). When conduct disorder is diagnosed, any co-occuring behavioral or learning disorders should also be ascertained, as these may afford an opportunity for prevention. Complicating Conditions In addition to the aforementioned diagnosable disorders that often co-occur with conduct problems, certain conditions that are not diagnosable disorders also tend to complicate the clinical picture of children with conduct disorder. This section reviews four such conditions: psychopathy, autistic traits, victimization by others and violence between adolescent romantic partners. Psychopathy The characteristics of the psychopath include grandiosity, callousness, deceitfulness, shallow affect and lack of remorse (see chapter 51). These traits, as assessed by the Hare Psychopathy Checklist, have been shown to predict which individuals will engage in the most serious and violent crime careers, even among prison inmates (Hare, Hart, & Harpur, 1991). Can the “fledgling psychopath” be identified in childhood, as a high priority target for prevention? Contrasting approaches to this question have been taken. One approach has suggested that children showing hyperactivity/attentional problems and conduct problems are at risk for subsequent psychopathy (Lynam, 1996; Lynam & Gudonis, 2005). Another approach emphasizes callous unemotional traits such as lack of guilt, absence of empathy and shallow constricted emotions in children (Barry, Frick, DeShazo et al., 2000). A third approach proposes that psychopathy is associated with a failure to inhibit aggression in response to signs of distress in others, arising from a deficit in processing victims’ distress cues, and reduced ability to recognize fear and sadness (Blair, Mitchell, & Blair, 2005). A number of reliable instruments are now available for the clinical assessment and diagnosis of psychopathic traits in juvenile patients (Farrington, 2005). If childhood psychopathy proves a useful clinical concept, it will be crucial that this provides a more refined background to improved treatments, and not a means of writing off some children. Autistic Traits A very recent development connects conduct disorders with symptoms formerly thought to be key features of autism and limited to patients with autism (Gilmour, Hill, Place et al., 2004). Children with autism, children referred for clinical evaluation of conduct problems and children excluded from school for disruptive behaviors were compared, and all three groups were found to have similar high prevalence of pragmatic language skill deficits and social communication difficulties. Some of the difficulties measured might be secondary to externalizing disorder, such as disrupted social relationships with peers. However, other difficulties such as speech articulation and fluency deficits, misunderstanding of context cues, misuse of gesture and eye contact, and unusual rigid interests have not been previously identified as part of conduct disorder. The importance of this finding is as yet not established, but it may point to new modes of therapy for conduct problems. Bullying The past decade has witnessed growing concerns from parents and schools about young children involved in bullying at or after school (Spivak, 2003; Tolan, 2004). Surveys indicate that nearly half of children are involved in bullying at some CHAPTER 35 546 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 546

time in childhood, although chronic involvement as a victim is somewhat less common (Nansel, Craig, Overpeck et al., 2004). Bullying and cruelty toward other children are key symptom criteria for diagnosing conduct disorder. Risk factors for becoming a bully are thus the same as risk factors for conduct disorder in general (Olweus, 1993). Risk factors that invite victimization by a bully are somewhat different, including emotional problems, low self-regard and poor social skills, as well as physical characteristics such as obesity. Because such risk factors pre-exist involvement in bullying, researchers must control for them in order to determine whether involvement in bullying has any consequences. One longitudinal study was able to control for pre-existing risk factors at age 5 school entry. This study reported that children who were victims in the intervening 2 years before follow-up at age 7 developed more emotional problems, more disruptive behavior problems, fewer prosocial behaviors and were less happy at school (Arseneault, Walsh, Trzesniewski et al., 2006). Thus, being targeted by bullies appears to lead to wide-ranging maladjustment in children, and should be a clinical concern. Crime Victimization Whereas most attention is focused on the potential of youth with conduct problems to harm others, such youth are often victims of violence committed by other people in their communities. Much research has documented that adult psychiatric patients are frequent targets of violence. Although children and adolescents are less often studied as victims, conduct disorder and its co-occurring disorders also place young people in harm’s way (Smith & Ecob, 2007; Snyder & Sickmund, 2006). In the US national Addhealth cohort study, the advent of puberty brought increased victimization risk to adolescents (Haynie & Piquero, 2006). In another cohort study, young people who were regular alcohol and cannabis abusers were twice as likely than healthy young people to become the victim of threatened, attempted or completed physical and sexual assaults in their community, even after controlling for their own prior perpetration of antisocial behaviors (Silver, Arseneault, Langley et al., 2005). Clinicians and researchers should be alert to the potential that their patients will become crime victims, with ensuing symptoms of post-traumatic stress disorder (PTSD). Adolescent Partner Violence The terms “marital violence” and “domestic abuse” generate the impression that partner abuse takes place primarily among adults, but recent research exposes high rates of aggression in the romantic or sexual relationships of teenagers (Halpern, Oslak, Young et al., 2001). Indeed, the peak age for partner aggression is between ages 15 and 25, and early-onset participation in relationship aggression is ominous because it predicts continued high risk for more injurious violence in later adult relationships (Capaldi & Gorman-Smith, 2003). One of the strongest predictors that a teenager will become involved in partner aggression is his or her prior childhood history of conduct problems, suggesting that partner aggression is part of a pre-established long-standing tendency to use violence to solve interpersonal disagreements (Ehrensaft, Moffitt, & Caspi, 2004). Both boys and girls engage in aggression toward partners, but qualitative research with high-school pupils suggests the aggression has shared meaning for the sexes (Tolman, Spencer, Rosen-Reynoso et al., 2003). Boys attributed their partner aggression to the need to appear sexually dominant to peers, aiming to establish their heterosexual credentials beyond doubt. Girls believed boys were sexual predators who exploit girls, but girls were willing to stay in an aggressive relationship rather than to be seen by peers to have no boyfriend. Thus, the almost compulsory pressure among adolescents to prove one can have and keep a heterosexual relationship seems an important context for relationship violence, which warrants attention from clinicians who see adolescents. Etiology Risk Factors Risk factors for conduct problems have been extensively reviewed in many reference sources (Hawkins, Herrenkohl, Farrington et al., 1998; Hill, 2002; Hill & Maughan, 2001; Lahey, Moffitt, & Caspi, 2003; Rutter, Giller, & Hagell, 1998). Here we briefly consider primary risk factors that are present in early childhood before the onset of conduct problems. Individual Level Characteristics Identified Genotypes The search for specific genetic polymorphisms associated with conduct problems is a very new scientific initiative, and little has yet been accomplished. One genome-wide linkage study identified chromosomal regions that are good bets for harboring conduct problem-related polymorphisms, but the polymorphisms have not been specified and the regions have not been replicated (Stallings, Corley, Dennehey et al., 2005). The most-studied candidate gene in relation to conduct problems is the MAOA promoter polymorphism. The gene encodes the MAOA enzyme, which metabolizes neurotransmitters linked to aggressive behavior by previous research in mice, and among men in a Dutch family pedigree. Thus, MAOA was selected as the candidate gene to test a hypothesis that genetic vulnerability might moderate the effect of child maltreatment on later conduct problems in the cycle of violence (Caspi, McClay, Moffitt et al., 2002). Maltreatment history and genotype interacted to predict four different measures of antisocial outcome: diagnosed adolescent conduct disorder; a personality assessment of aggression; symptoms of adult antisocial personality disorder reported by informants who knew the study member well; and adult court conviction for violent crime. Replication of this study was of utmost importance because reports of associations between measured genes and disorders are notorious for their poor replication record. Positive and negative replication studies have appeared, and a meta-analysis of these studies showed the association between MAOA genotype and conduct CONDUCT DISORDERS 547 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 547

problems is modest but statistically significant (Kim-Cohen, Caspi, Taylor et al., 2006). Findings of specific genetic polymorphisms associated with antisocial behavior will probably not be applied for genetic diagnosis purposes, because of the inherent complexity of gene–behavior connections. Rather, gene–environment research will benefit efforts to understand how brain mechanisms connect external risk factors and genomic variation to the conduct disorders (MeyerLindenberg, Buckholtz, Kolachana et al., 2006). Perinatal Complications Birth complications might be a contributory factor to neuropsychological deficits that are associated with conduct problems (Moffitt, 1993b). The evidence regarding this was mixed but recent reports from large-scale general population studies have found associations between life-course-persistent type conduct problems and perinatal complications, minor physical anomalies and low birth weight (Brennan, Grekin, & Mednick, 2003). Most studies support a biosocial model in which obstetric complications might confer vulnerability to other co-ocurring risks such as hostile or inconsistent parenting (Arseneault, Tremblay, Boulerice et al., 2002; Kratzer & Hodgins, 1999; Raine, Brennan & Mednick, 1997; Tibbetts & Piquero, 1999). Studies have further indicated that smoking in pregnancy is a statistical risk predictor of offspring conduct problems (Brennan, Grekin, & Mednick, 2003), but a causal link between smoking and conduct problems has not been established (Fergusson, 1999). Temperament Individual differences in infancy that might contribute to subsequent risk of psychopathology were conceptualized by Thomas, Chess, and Birch (1968) in terms of temperament, which they viewed as inherited and not significantly influenced by experience. Several prospective studies have shown associations between temperament and conduct problems (Keenan & Shaw, 2003), and also predicted antisocial personality disorder and criminal offending into adulthood (Caspi, Moffitt, Newman et al., 1996). Temperament, as originally conceived, should be strongly heritable and experience-free. However, measures of temperament are only moderately heritable, and a child’s engagement with the social world from birth means that temperament measures inevitably assess the outcome of social processes. It may be that the contributions of temperament will be seen most consistently in combination with environmental risk factors (Nigg, 2006). Neurotransmitters Neurotransmitters have been linked to antisocial behavior in adult samples, and in non-human animal models (Nelson, 2006). It would be a major advance if it were possible to link neurotransmitter levels and activity to conduct problems in children. However, in general, the findings with children have not been consistent (Hill, 2002). For example, in the Pittsburgh youth cohort, boys with long-standing conduct problems showed downward changes in urinary epinephrine level following a stressful challenge task, whereas prosocial boys showed upward epinephrine responses to the challenge (McBurnett, Raine, Stouthamer-Loeber et al., 2005). However, other studies have failed to find an association between conduct disorder and measures of norepinephrine in children (Hill, 2002). Some limited evidence supports the view that, as in adults, serotonin is linked with aggression in children, but findings for indices of serotonin function in children are also markedly inconsistent (Pine, Coplan, Wasserman et al., 1997). It should be borne in mind that neurotransmitters in the brain are only indirectly measured, most measures of neurotransmitter levels are crude indicators of activity and little is known about neurotransmitters in the juvenile brain. Verbal Deficits Children with conduct problems have been shown consistently to have increased rates of deficits in language-based verbal skills (Lynam & Henry, 2001; Nigg & Huang-Pollock, 2003). Conduct-disordered children, delinquent adolescents and adult antisocial individuals show poor performance on standardized tests of verbal ability, and in tests of IQ, poor verbal and performance scores. These associations hold after controlling for potential confounds such as race, socioeconomic status, academic attainment and test motivation (Lynam, Moffitt, & Stouthamer-Loeber, 1993). Longitudinal studies show that persistence in antisocial behavior over periods of years is predicted by low verbal IQ in childhood (Farrington & Hawkins, 1991; Lahey, Loeber, Hart et al., 1995; Lynam & Henry, 2001). Deficits in verbal capacities are found also with oppositional defiant disorder among preschool-aged clinic-referred boys (Speltz, McClellan, DeKlyen et al., 1999). Several possible ways in which poor verbal ability might influence behavior can be drawn from Luria’s theory of the role of verbal memory and verbal abstract reasoning in the development of self-control (Luria, 1961). The abilities to recall oral instructions and to use language to think through the consequences of actions contribute to the effective control of actions. Children who cannot reason or assert themselves verbally may attempt to gain control of social exchanges using aggression (Dodge, 1993). It is likely that there are also indirect effects in which low verbal IQ contributes to academic difficulties which in turn mean that the child’s experience of school becomes unrewarding, rather than a source of self-esteem and support. Executive Dysfunction Children and adolescents with conduct problems have been shown consistently to have poor tested executive functions (Ishikawa & Raine, 2003; Lynam & Henry, 2001; Moffitt, 1993b; Nigg & Huang-Pollock, 2003). Executive functions comprise those abilities implicated in successfully achieving goals through appropriate effective actions. Specific skills include learning and applying contingency rules, abstract reasoning, problem-solving, self-monitoring, sustained attention and concentration, relating previous actions to future goals and inhibiting inappropriate responses. These mental functions are largely, although not exclusively, associated with frontal CHAPTER 35 548 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 548

lobes (Pennington & Ozonoff, 1996). Important data come from a Montreal cohort studied from the age of 6 years (Séguin, Boulerice, Harden et al., 1999). The study used executive function tests that have been shown to be associated with different anatomical structures in the brain, on the basis of lesion and functional imaging studies. Chronic aggression was associated with lower scores on tests tapping executive functions of the frontal brain region, and the findings held after controlling for general memory, IQ and ADHD. Although most studies of executive deficit involve adolescents, such deficits have also been linked with disruptive behaviors in very young preschool children (Hughes, Dunn, & White, 1998; Speltz, DeKlyen, Calderon et al., 1999). Autonomic Reactivity A low resting pulse rate or slow heart rate has been found consistently to be associated with antisocial behavior, and a meta-analysis of 40 studies suggested it is the best replicated biological correlate of antisocial behavior (Ortiz & Raine, 2004). For example, in the longitudinal Cambridge Study in Delinquent Development, slow heart rate was associated with convictions for violence after controlling for all other risk variables (Farrington, 1997). Other psychophysiological indicators of slow autonomic system reactivity have also been examined. For example, in a longitudinal study of Pittsburgh boys, those most antisocial and psychopathic were also slowest to show a skin-conductance response to aversive blasts of noise (Fung, Raine, Loeber et al., 2005). The explanation for the link between slow autonomic activity and antisocial behavior remains unclear. Information Processing and Social Cognition Dodge (1993) proposed the leading information-processing model for the genesis of aggressive behaviors within social interactions. The model hypothesizes that children who are prone to aggression focus on threatening aspects of others’ actions, interpret hostile intent in the neutral actions of others and are more likely to select and to favor aggressive solutions to social challenges. Several studies have demonstrated that aggressive children make such errors of social cognition. An extensive review of the many studies of social cognition among children with conduct problems has been presented elsewhere (Dodge, Coie, & Lynam, 2006). Dodge (1993) hypothesized that the tendencies to encode hostile aspects of situations and to attribute hostile intent to ambiguous social cues, and to access and favor aggressive responses to social challenges, are the result of repeated exposure to physical maltreatment. This prediction was tested prospectively (Dodge, Petit, Bates et al., 1995). Physical abuse documented in kindergarten was strongly associated with conduct problems in primary school; 28% of the abused group developed conduct problems compared to 6% of the non-abused. Encoding errors, hostile attributions and biases toward accessing and favoring aggressive responses were each associated with conduct problem outcome, and with having experienced physical abuse. Encoding errors and accessing aggressive responses mediated the link between physical abuse and conduct problems, but hostile attributions and positive evaluation of aggressive responses did not. This prospective study thus provided some support for the social cognition model. Risks Outside the Family Risks in the Neighborhood It has long been assumed that bad neighborhoods have the effect of encouraging children to develop conduct problems. Parents strive to secure the best neighborhood and school for their child that they can afford. Although it is obvious that some local areas have higher crime rates than others, it has been difficult to document any direct link between neighborhood characteristics and child behavior, for a number of reasons. For example, neighborhood characteristics were conceptualized in overly simple structural demographic terms such as percentage of non-White residents or percentage of single-parent households. Moreover, research designs could not rule out the alternative possibility that families whose members are antisocial tend to selectively move into bad neighborhoods. A new generation of neighborhood research is addressing these challenges (Beyers, Bates, Petit et al., 2003; Caspi, Taylor, Moffitt et al., 2000; Sampson, Raudenbusch, & Earls, 1997). New research suggests that the neighborhood factors that are important go beyond structural demographic characteristics. Neighborhood-level social processes such as “collective efficacy” and “social control” do influence young children’s conduct problems, probably by supporting or failing to support parents in their efforts to rear children. Peer Influences Children with conduct problems have poorer peer relationships than non-disordered children in that they tend to associate with children with similar antisocial behaviors, they have discordant interactions with other children and experience rejection by non-deviant peers (Vitaro, Tremblay, & Bukowski, 2001). Three principal explanations have been tested, and evidence found for all three. Either children’s antisocial behaviors lead them to have peer problems, or deviant peer relationships lead to antisocial behaviors, or some common factor leads to both. Peer Rejection in Childhood Regarding the possibility that conduct problems lead to peer difficulties, there is ample evidence that children with established conduct problems are more likely to have more conflict with peers, and to be rejected by non-deviant peers (Coie, 2004). This peer rejection has been shown to contribute to declines in academic achievement and increases in aggression across the first year of primary schooling (Coie, 2004). One consequence of rejection by healthy peers is that from as young as 5 years aggressive-antisocial children are obliged to associate with other deviant children (Farver, 1996; Fergusson, Woodward, & Horwood, 1999). Peer Groups Promote Conduct Problems in Adolescence In the light of the limited evidence that peer difficulties prompt the onset of childhood conduct problems, and the rather more CONDUCT DISORDERS 549 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 549

substantial evidence that children’s peer difficulties are a consequence of their conduct problems, is there any reason to think that peer processes influence the long-term course of conduct problems? Regarding the possibility that peers lead to conduct problems, this has been shown to come about in several ways. Youth who are aggressive are attracted to each other, and deviant youth reinforce each others’ antisocial behaviors and attitudes (Boivin & Vitaro, 1995). Evidence that peer influences do increase antisocial behaviors applies primarily to the adolescent developmental stage (Warr, 2002). Strong evidence comes from treatment experiments: in two controlled clinical trials, boys treated in groups did worse than untreated controls; treatment was followed by increased adolescent problem behaviors and poorer outcomes (Dishion, McCord, & Poulin, 1999). After group-level treatment brought the boys together they mutually reinforced each others’ antisocial activities, a finding that argues for individual treatment approaches. A natural experiment study tracked change in antisocial behavior among boys who joined a gang, to reveal that joining a gang increased each adolescent’s individual offending over his pre-gang baseline, whereas leaving the gang decreased each individual’s personal offending rate (Thornberry, Krohn, Lizotte et al., 1993). Overall, we must consider the dynamic and reciprocal manner in which children’s conduct problems influence who their friends are, and in which those friends later promote the young person’s conduct problems (Vitaro, Tremblay, & Bukowski, 2001). Family Level Influences Concentration of Crime in Families Fewer than 10% of the families in any community account for more than 50% of that community’s criminal offenses (Farrington, Jolliffe, Loeber et al., 2001; Rowe & Farrington, 1997). This familial concentration of crime most certainly reflects the co-incidence of genetic and environmental risks, directing researchers who wish to understand the origins of conduct problems to look for interactions between both types of risk. Familial Genetic Liability There is now solid evidence from twin and adoption studies that conduct problems assessed both dimensionally and categorically are substantially heritable (Moffitt, 2005a; Rhee & Waldman, 2002). However, knowing that conduct problems are under some genetic influence is less useful clinically than knowing that this genetic influence appears to be reduced, or enhanced, depending on interaction with circumstances in the child’s environment. Several genetically sensitive studies have allowed interactions between family genetic liability and rearing environment to be examined. Adoption studies have reported an interaction between antisocial behavior in the biological parent and adverse conditions in the adoptive home that predicted the adopted child’s antisocial outcome (Bohman, 1996; Cadoret, Yates, Troughton et al., 1995). The genetic risk was modified by the rearing environment. A twin study also yielded evidence that family genetic liability and environmental risks interact (Jaffee, Caspi, Moffitt et al., 2005). In this study, the experience of maltreatment was associated with an increase of 24% in the probability of diagnosable conduct disorder among children at high genetic risk, but an increase of only 2% among children at low genetic risk. Thus, awareness of a familial liability toward psychopathology increases the urgency to intervene to improve a child’s social environment (Odgers et al., 2007b). Family Poverty There is an association between severe poverty and early childhood conduct problems (Farrington & Loeber, 1998). Early theories proposed direct effects of poverty related to strains arising from the gap between aspirations and realities, and from lacking opportunity to acquire social status and prestige. Subsequent research has indicated that the association between low income and childhood conduct problems is indirect, mediated via family processes such as marital discord and parenting deficits (Maughan, 2001). As one example of this research, the Iowa longitudinal study of 378 rural families found that family economic stress was associated with adolescent conduct problems, but this was mediated via parental depression, marital conflict and parental hostility (Conger, Ge, Elder et al., 1994). Another study took advantage of a naturally occurring experiment (Costello, Compton, Keeler et al., 2003). Native American families in North Carolina, formerly living below the poverty line, benefitted from increased income from newly opened casinos. In many families, the children’s behavior problems decreased markedly as a result. However, the effect of increased income was mediated through better parent–child relationships. This mediation is not limited to poverty in recent times. Glueck’s study of delinquency from the historical period of economic depression also found that harsh discipline, low supervision and weak parent–child attachments accounted for the effects of poverty on children’s antisocial behaviors in the 1930s (Sampson & Laub, 1984). Parent–Child Attachment Parent–child relationships provide the setting for the development of later social functioning, and disruption of these attachment relationships (e.g., through institutional care) is associated with subsequent difficulties in relating (Robins, 1966; Rutter, Quinton, & Hill, 1990). Thus, conduct problems might be expected to arise from infant attachment difficulties. Indeed, attachment theory had its origins in Bowlby’s (1944) study of adolescent thieves. However, the evidence is rather mixed (Vondra, Shaw, Swearingen et al., 2001). One study found an increased rate of each of the categories of insecure attachment (avoidant, ambivalent, controlling) in preschool boys referred with ODD (Speltz, DeKlyen, & Greenberg, 1999). However, in a follow-up of the clinic boys, attachment did not predict the severity of conduct problems. By contrast, another study found that ambivalent and controlling attachment predicted CHAPTER 35 550 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 550

disruptive behaviors after controlling for baseline differences (Moss, Smolla, Cyr et al., 2006). Early studies of low-risk samples, using the secure–insecure classification, failed to find robust associations with disruptive behavior problems, but subsequent studies of higher risk samples using the disorganized classification report that disorganized attachment can predict conduct problems (Van IJzendoorn, Schuengel, & Bakermans-Kranenburg, 1999). Disorganization is identified in Ainsworth’s Strange Situation Test if the child shows bizarre or contradictory behaviors with the caregiver when reunited after separation (Main & Solomon, 1986). However, low rates of infants with disorganized attachment in study samples mean that findings should be viewed with caution. Although it seems obvious that poor parent–child relations in general predict conduct problems, it has yet to be established whether attachment difficulties as measured by observational paradigms have an independent causal role in the development of behavior problems. Attachment classifications could be markers for other relevant family risks. Discipline and Parenting Patterns of parenting associated with conduct problems were delineated by Patterson (1982) in his seminal work Coercive Family Process and subsequent publications. In brief, parents of antisocial children were found to be more inconsistent in their use of rules; to issue more, and unclear, commands; to be more likely to respond to their children on the basis of mood rather than the characteristics of the child’s behavior; to be less likely to monitor their children’s whereabouts; and to be unresponsive to their children’s prosocial behavior. Patterson proposed a specific mechanism for the promotion of oppositional and aggressive behaviors in children. A parent responds to mild oppositional behavior by a child with a prohibition to which the child responds by escalating his or her behavior, and mutual escalation continues until the parent backs off, thus negatively reinforcing the child’s behavior. The parent’s inconsistent behavior increases the likelihood of the child showing further oppositional or aggressive behavior. In addition to specific tests of Patterson’s reinforcement model (Gardner, 1989; Snyder & Patterson, 1995) there is ample evidence that conduct problems are associated with hostile, critical, punitive and coercive parenting (Rutter, Giller, & Hagell, 1998). In considering the role of coercive processes in the origins or maintenance of conduct problems, we need to consider possible alternative explanations: (i) that the associations reflect familial genetic liability toward children’s psychopathology and parents’ coercive discipline; (ii) that they represent effects of children’s behaviors on parents; and (iii) that coercive parenting may be a correlate of other features of the parent–child relationship or family functioning that influence child behaviors. There is considerable evidence that children’s difficult behaviors do evoke parental negativity. One experiment observed the interactions of normal and conduct disordered children when with their own parents, the parents of normal children and the parents of other conduct disordered children (Anderson, Lytton & Romney, 1986). Conduct disordered children elicited more negative reactions from all groups of parents than did non-conduct disordered children. Adoption studies (Ge, Conger, Cadoret et al., 1996; O’Connor, Deater-Deckard, Fulker et al., 1998) have shown that adoptees at genetic risk of antisocial disorders are more likely than low-risk children to evoke negative parenting in the adoptive home. The role of the child in influencing parental monitoring has also received attention. Stattin and Kerr (2000) pointed out that studies of parental monitoring have generally assessed how much knowledge parents have of their children’s whereabouts, but not how parents acquired it. They showed, in a study of 14-year-olds, that the majority of this knowledge came from what the child chose to tell the parent, and conduct-problem adolescents told their parents less about what they were doing. The fact that children’s behaviors can evoke negative parenting does not, however, mean that negative parenting has no impact on children’s behavior. One study reported that negative maternal control at age 4 was significantly associated with conduct problems at age 9, after controlling for children’s initial behavior problems at age 4 (Campbell, Pierce, Moore et al., 1996). The Environmental-Risk longitudinal twin study of British families examined the effects of fathers’ parenting on young children’s aggression (Jaffee, Moffitt, Caspi et al., 2003). As expected, a prosocial father’s absence predicted more aggression by his children. But, in contrast, an antisocial father’s presence predicted more aggression by his children, and his harmful effect was exacerbated the more time each week he spent taking care of the children. In another report, the E-Risk study evaluated the hypothesis that because depressed mothers provide inept parenting, maternal depression promotes children’s aggression (KimCohen, Moffitt, Taylor et al., 2005). Children of depressed mothers often develop conduct problems, but it has not been clear that this correlation represents environmental transmission. Although the connection between mothers’ depression and children’s conduct problems decreased somewhat after stringent control for familial liability to psychopathology, it remained statistically significant. Further, depressed women might exaggerate their ratings of their children’s problem behaviors, but the pattern of findings remained the same when teachers rated the children’s behavior. A temporal analysis showed that if E-Risk mothers experienced depression only before their children’s birth, the children were not unusually aggressive. In contrast, only if mothers suffered depression while rearing their children were the children likely to develop aggression. Finally, the possibility that the association was spurious because children’s aggression provoked their mothers’ depression was ruled out by documenting that children exposed to an episode of maternal depression between ages 5 and 7 became even more aggressive by age 7 than they had been at age 5. Taken together, these and other findings provide good evidence for the role of discipline in conduct problems (Moffitt, 2005b). CONDUCT DISORDERS 551 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 551

Exposure to Adult Marital Conflict and Domestic Violence It is likely that family processes other than parenting skills and quality of parent–child attachment relationships have a role. Many studies have shown that children exposed to domestic violence between adults are subsequently more likely to become aggressive themselves (Moffitt & Caspi, 1998). Davies and Cummings (1994) proposed that marital conflict influences children’s behavior because of its effect on their regulation of emotion. For example, a child may respond to frightening emotion arising from marital conflict by down-regulating his or her own emotion through denial of the situation. This in turn may lead to inaccurate appraisal of other social situations and ineffective problem-solving. Repeated exposure to family conflict is thought to lower children’s thresholds for psychological dysregulation, resulting in greater behavioral reactivity to stress (Cummings & Davies, 2002). Children’s aggression may also be increased by marital discord because children are likely to imitate aggressive behavior modeled by their parents (Bandura, 1977). Through parental aggression, children may learn that aggression is a normative part of family relationships, that it is an effective way of controlling others and that aggression is sanctioned, not punished (Osofsky, 1995). Maltreatment Physical punishment is widely used, and parents of children with conduct problems frequently resort to it out of desperation. However, links with conduct problems are not straightforward. One study found that physical punishment was clearly associated with behavior problems in White American children, but not in African-American children (DeaterDeckard, Dodge, Bates et al., 1996). Furthermore, the risk for conduct problems does not apply equally to all forms of physical punishment. The E-Risk longitudinal twin study was able to compare the effects of corporal punishment (smacking, spanking) versus injurious physical maltreatment using twin-specific reports of both experiences (Jaffee, Caspi, Moffitt et al., 2004). Results showed that children’s genetic endowment accounted for virtually all of the association between their corporal punishment and their conduct problems. This indicated a “child effect,” in which children’s bad conduct provokes their parents to use more corporal punishment, rather than the reverse. Findings about injurious physical maltreatment were the opposite. There was no child effect provoking maltreatment and, moreover, significant effects of maltreatment on child aggression remained after controlling for any genetic transmission of liability to aggression from antisocial parents. Overall, associations between physical abuse and conduct problems are well established (Hill, 2002). In the Christchurch cohort, child sexual abuse predicted conduct problems, after controlling for other childhood adversities (Ferguson, Horwood, & Lynskey, 1996). In a large prospective study of court substantiated cases of abuse and neglect, 26% of abused and neglected adolescents were antisocial, contrasted with 17% in a well-matched comparison group, implying a modest but long-lasting effect of abuse and neglect (Widom, 1997). Investigating the relationship of child maltreatment to psychopathology is particularly difficult for ethical reasons. Little is known about the possible mechanisms linking maltreatment to conduct problems, although threats to security of attachment, difficulties in affect regulation, distortions of information processing and self-concept reviewed elsewhere in this chapter are likely to be relevant. From Risk Predictor to Evidence for Causation Associations have been documented between conduct problems and a wide range of risk factors. A variable is called a “risk factor” if it has a documented predictive relation with antisocial outcomes, whether or not the association is causal. The causal status of most of these risk factors is unknown; we know what statistically predicts conduct problem outcomes, but not how or why (Kraemer, 2003). Establishing a causal role for a risk factor is by no means straightforward, particularly as it is unethical to experimentally expose healthy children to risk factors to observe whether those factors can generate new conduct problems. There is no one solution to the problem, although the use of genetically sensitive designs and the study of within-individual change in natural experiments and treatment studies have considerable methodological advantages for suggesting causal influences on conduct problems (Moffitt, 2005b; Rutter, 2000; Rutter, Moffitt, & Caspi, 2006). This chapter has emphasized risk factors that have research evidence to support a causal role in conduct problems. For example, above we have cited research that supports causation by depressed mothers’ poor discipline (Kim-Cohen, Arseneault, Caspi et al., 2005), child maltreatment (Dodge et al., 1995; Jaffee et al., 2004), family poverty (Costello et al., 2003), familial genetic liability (Moffitt, 2005a) and affiliating with delinquent peers (Dishion, McCord, & Poulin, 1999; Thornberry et al., 1993). These studies’ designs either took advantage of natural experiments or otherwise were able to rule out alternative explanations to causation (Moffitt, 2005b). Other risk factors described here have not been decisively tested for causation yet, but they do have evidence that they are robust predictors of conduct problems across many studies carried out in different contexts (e.g., perinatal complications, temperament, verbal and executive deficits, slow heart rate, social cognitions, exposure to parental conflict). Still other risk factors benefit from strong causal theory, warranting inclusion in this chapter, but the evidence base to show reliable association with conduct problems is not yet strong (e.g., attachment, neurotransmitters, MAOA genotype, pregnancy smoking, neighborhood context). Contemporary Issues in Clinical Assessment and Diagnosis How Young Can a Diagnosis of Conduct Disorder be Made? One controversy about the diagnosis of conduct disorders is particularly current: How young can and should a child be CHAPTER 35 552 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 552

diagnosed? Evidence suggests that conduct problems emerge in preschoolers, that the youngest age of onset is associated with the poorest long-term prognosis and that long-established conduct problems are difficult to treat. This evidence base has resulted in calls for intervention at preschool ages to prevent conduct problems from becoming chronic. However, to intervene early in individual cases, valid methods must be available to diagnose conduct disorders in young children. Whether valid diagnoses of conduct disorders can, or should, be made in very young children has been a focus of controversy (Campbell, 2002; Keenan & Wakschlag, 2002). Some argue that disruptive behaviors in young children should not be pathologized, because aggressive, disruptive and defiant behaviors are thought to be common and developmentally normative in the preschool period, and most children will outgrow them. Others believe that children falsely identified as having conduct disorder will be stigmatized, and unnecessary referral for treatment will waste health care resources. Some argue that the predictive accuracy of conduct problems for prognosis improves only when children are older, and applying diagnostic criteria meant for older children may promote overdiagnosis. One study tested the validity of the DSM-IV conduct disorder diagnosis for preschoolers, by applying it to screen a birth cohort of 2200 4- to 5-year-olds (Kim-Cohen et al., 2005). The diagnosis successfully identified the children in the cohort who most needed treatment: they were aggressive and antisocial, had co-occurring cognitive deficits and ADHD symptoms, came from adverse family backgrounds, and were likely to have experienced harsh parenting and physical maltreatment. Followed up 2 years later, at age 7, over half of the diagnosed children still met diagnostic criteria for conduct disorder, but even the apparently remitted children continued to evidence clinically significant behavioral and academic difficulties at school, suggesting preschool intervention with them would not have been wasted. The study indicated that clinicians wishing to minimize false positives can adopt a conservative approach by requiring the more stringent number of criteria specified by DSM-IV for moderate conduct disorder (five symptoms) as opposed to mild conduct disorder (three symptoms). Even better, standardized interview, checklist, and observational methods and guidelines for diagnosing preschool children have been developed (Egger & Angold, 2006). Thus, when necessary to support intervention, the conduct disorder diagnosis can be made for a very young child, albeit with very careful attention to developmental considerations. Resource Instruments and Multiple Informants to Enhance Diagnostic Validity There are many different measurement instruments for assessing conduct problems for research and clinical practice; systematic evaluation of their strengths and weaknesses is beyond the scope of this chapter. Earlier we mentioned that juvenile antisocial behavior can be defined in terms of diagnostic categories or continuous distributions of symptom behaviors. Assessment tools reflect these two options. Structured interviews aim to operationalize the specific DSM and ICD criteria to achieve a categorical diagnosis (Costello et al., 1996; Goodman, Ford, Richards et al., 2000; Shaffer, Fisher, Lucas et al., 2000). Symptom checklists aim to broadly cover a variety of conduct and oppositional behavior problems, operating on the evidence-based principle that variety of antisocial behaviors is the best predictor of poor prognosis (Achenbach & Rescorla, 2000; Elander & Rutter, 1996; Goodman, 1997). Whatever instruments are applied, the field has reached consensus that information must be obtained from multiple informants, including if possible parents, teachers, police, clinicians and the child (Arseneault, Kim-Cohen, Taylor et al., 2005; Koot, Crijnen, & Ferdinand, 1999). Multiple informants are an essential part of assessment because no single reporter can have the opportunity to observe all manifestations of antisocial conduct and thus they provide complementary information. In addition, poor prognosis characterizes children who show conduct problems pervasively across multiple different settings such as home, school and neighborhood (Loeber, Green, Lahey et al., 1991). Risk Assessment and Treatment Planning Approaches A recent approach to diagnosis and assessment of children with conduct problems may prove especially useful for clinicians. In this approach, assessment is guided by a manual. Examples of such manuals are the SAVRY (Structured Assessment of Violence Risk in Youth; Borum, Bartel, & Forth, 2002), the EARL-20B (Early Assessment Risk List for Boys; Augimeri, Koegl, Webster et al., 2001) and the EARL-21G (Early Assessment Risk List for Girls; Levene, Augimeri, Pepler et al., 2001). These easy-to-use manuals are grounded in the scientific literature, providing operational definitions to assist clinicians in assessing risk factors that are the most valid predictors of a child’s poor antisocial prognosis. Scales are included for rating the severity of each risk factor, resulting in a risk profile that points to key intervention targets in a particular child’s life. Each child’s specific areas of strength are highlighted to exploit in treatment planning, as are specific factors known to predict engagement in treatment versus resistance to treatment. Risk and protective factors can then be linked to approaches for case management, tailored for each juvenile patient and their family members. Formal evaluation of these manual-guided assessments has not been reported, and their long-term predictive validity is unknown, but they are evidence-based and they have strong inherent appeal to many clinicians. Interventions The following sections cover treatment of children aged 2– 12 years. (For prevention see chapter 61. For treatment of teenagers with conduct disorder, and of delinquents, including CONDUCT DISORDERS 553 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 553

functional family therapy and multisystemic therapy, see chapter 68. For further reviews of treatments see Farmer, Compton, Burns et al., 2002; Bloomquist & Schnell, 2002.) Principles of Intervention Basing Treatment on the Assessment The intervention needs to fit the particular needs of the child and family. Many risk factors have been delineated in this chapter, but usually not all occur in the same child. Intervention needs to be tailored according to the needs and strengths of the family revealed by the assessment, which should include all aspects of the child’s environment and functioning – the multiaxial framework of ICD-10 provides a helpful framework for doing this (World Health Organization, 1996). Choosing Which Treatment Modality to Use The behavior may predominantly occur in the home, at school, with peers, in the community, or it may be pervasive. If possible, interventions need to address each context specifically, rather than assuming that successful treatment in one area will generalize to another. Thus, improvements in the home arising from a successful parent training program will not necessarily lead to less antisocial behavior at school (Scott, 2002). Therefore, for cases with difficulties that are mainly at home, where the child is doing reasonably at school and has a friend or two, parent training would be the first line of treatment. If classroom behavior is a problem and a school visit shows that the teacher is not using effective methods, then advice to the teacher and other school staff can be very effective. Where there are pervasive problems including fights with peers, then individual work on anger management and social skills should be added; on it own, anger management is unlikely to be nearly as successful as when it is combined with other approaches. Medication is controversial and generally best avoided; possible indications are discussed below. Developing Strengths Identifying strengths of the young person and the family is crucial. This helps engagement, and increases the chances of effective treatment. Encouragement of abilities helps the child spend more time behaving constructively rather than destructively (e.g., more time spent playing football is less time spent hanging round the streets looking for trouble). Encouragement of prosocial activities (e.g., to complete a good drawing, or to play a musical instrument well) also increases achievements and self-esteem and hope for the future. Stattin and Magnusson (1995) found that for children with antisocial behavior living in high-risk areas (which the majority do), those with strengths or skills ended up with far lower rates of criminality than those without. Engaging the Family Any family coming to a mental health service is likely to have some fears about being judged as bad and possibly mad. Families of children with conduct problems are more likely to be disadvantaged and disorganized, to have had arguments with official agencies such as schools and welfare officers and to be suspicious of officialdom. Dropout rates in treatment for conduct problem families are high – often up to 60% (Kazdin, 1996a). Practical measures, such as assisting with transportation, providing child care and holding sessions in the evening or at other times to suit the family are all likely to facilitate retention. Forming a good alliance with the family is especially important, and Prinz and Miller (1994) showed that adding engagement strategies during the assessment such as showing parents that the therapist clearly understood their viewpoint led to increased attendance at treatment sessions. Once engaged, the quality of the therapist’s alliance with the family affects treatment success, accounting for 15% of the variance in outcome in the meta-analysis by Shirk and Carver (2003). Treating Comorbid Conditions Child antisocial behavior often affects others so strongly that comorbid conditions can easily be missed. Yet, in clinical referrals, comorbidity is the rule rather than the exception. Common accompaniments are depression and ADHD; a number will have PTSD (e.g., in the context of violence inflicted on them by a father, or witnessing beatings received by their mother from a partner). In recent years there has been increasing recognition of the overlap with autistic spectrum disorders (Gilmour et al., 2004), and that a minority will have psychopathic traits (see chapter 51). Each of these conditions requires appropriate management in its own right. Promoting Social and Scholastic Learning Treatment involves more than the reduction of antisocial behavior – for example, stopping tantrums and aggressive outbursts, while helpful, will not lead to good functioning if the child lacks the skills to make friends or to negotiate: positive behaviors need to be taught too. Specific learning disabilities such as reading retardation, which is particularly common in these children, need treatment, as do more general difficulties such as planning homework. Making Use of Guidelines The American Academy of Child and Adolescent Psychiatry (AACAP) has published sensible practice parameters for the assessment and treatment of conduct disorder (AACAP, 1997), and the UK National Institute for Health and Clinical Excellence (NICE, 2006) has published a “technology appraisal” of the clinical and cost effectiveness of parent-training programs. This sets out criteria for choosing parent-training programs, such as being backed by evidence from randomized controlled trials. NICE guidelines are strongly influential on service commissioners and should help improve practice considerably. Treating the Child in their Natural Environment Most of the interventions described below are intended for out-patient or community settings. Psychiatric hospitalization is very rarely necessary; there is no evidence that in-patient CHAPTER 35 554 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 554

admissions lead to gains that are maintained after the child is returned to their family. The objective of treatment is to enable the child to cope with the environment he or she lives in, and alter the environment where necessary. Where there is parenting breakdown or total inability to manage the child, then foster care may be necessary. Family Interventions Several studies have repeatedly found that family factors are strongly associated with antisocial behavior and, as reviewed above, these appear to have a causal role in many cases. Even where the antisocial behavior appears to have arisen “in a clear blue sky” without adverse family risk factors, living with a child with marked antisocial behavior can itself lead to coercive parenting styles, which in turn may exacerbate the problems (O’Connor et al., 1998). Therefore, improving family risk factors such as coercive parenting is likely to be beneficial, whether or not they were originally implicated as a cause. Family interventions can be divided into two main types, those derived from family systems theory, which tend to be more broadly based, and those derived from social learning theory, which tend to be more specifically focused on training parents to improve moment-to-moment interactions with their children. Family Systemic Therapies Typically, family systemic therapies involve all family members attending. Their goals differ according to the style and underlying theory of the particular variant of therapy. For example, structural family therapy as pioneered by leaders such as Minuchin (1974) would try to restore clear boundaries of authority of the parents over the child, because often antisocial children have become domineering in their own homes. Other forms of family therapy try to improve patterns of communication that have gone wrong, and “systemic” variants try to reveal and address relevant factors that impinge on the family system from both within and outside the family. There have been rather few good quality evaluations of family or systemic therapies for childhood antisocial behavior; for a fuller discussion see chapter 65. One exception is functional family therapy pioneered by Jim Alexander (Barton & Alexander, 1985), which is particularly focused on antisocial children and has several trials to support it (see chapter 68). Parent Management Training Parent management training programs are designed to improve parents’ behavior management skills and the quality of the parent–child relationship. Most target skills such as promoting play and developing a positive parent–child relationship, using praise and rewards to increase desirable social behavior, giving of clear directions and rules, using consistent and calm consequences for unwanted behavior, and reorganizing the child’s day to prevent problems. Parenting interventions may also address distal factors likely to inhibit change (e.g., parental drug or alcohol abuse, maternal depression and relational violence between parents). Treatment can be delivered in individual parent–child appointments, or in a parenting group. Individual approaches offer the advantages of in vivo observation of the parent–child dyad and therapist coaching and feedback regarding progress. Examples of Good Practice Helping the non-compliant child (McMahon & Forehand, 2003) and Parent Child Interaction Therapy (PCIT; Eyberg, 1988) are two examples of well-validated individual programs. Group treatment has been shown to be equally effective, and offers opportunities for parents to share their experience with others who are struggling with a disruptive child. Group treatments emphasize discussion among group leaders and parents, and may use videotaped vignettes of parent–child interactions that illustrate the “right” and “wrong” ways to handle situations. Two well-known group treatments are the Incredible Years Program (IY; Webster-Stratton, 1981) and the Positive Parenting Program (Triple P; Sanders & MarkieDadds, 1996; Sanders, Markie-Dadds, & Turner, 2000). Effectiveness Behavioral parent training is the most extensively studied treatment for conduct problems, and there is considerable empirical support for its effectiveness (Weisz, Hawley, & Doss, 2004). Several of the programs are considered “wellestablished,” according to American Psychological Association criteria, with multiple randomized trials (e.g., Patterson, Chamberlain, & Reid, 1982; Webster-Stratton, Reid, & Hammond, 2001a) and replications by independent research groups (e.g., Scott, Spencer, Doolan et al., 2001). There have also been randomized trials showing the effectiveness of PCIT and Triple P (e.g., Bor, Sanders, & Markie-Dadds, 2002; Sanders, Markie-Dadds, Tully et al., 2000), and there is at least one independent replication of the PCIT model (Nixon, Sweeney, Erickson et al., 2003). Studies suggest that behavioral parent training leads to short-term reductions in antisocial behavior, with moderate to large effect sizes of d = 0.5− 0.8. Follow-up studies suggest enduring effects at up to 6 years post-treatment (Hood & Eyberg, 2003; Reid, Webster-Stratton, & Hammond, 2003). Recently, some programs have included an element training parents to read with their children in addition to behavior management, with the idea of targeting multiple risk factors for antisocial behavior. Although teaching parents to read with their children has not always proved successful, Scott, Sylva, Doolan et al. (in press) combined a 12-week behavior management program with a relatively intense, detailed reading program (10 2-hour sessions) for 5- and 6-year-olds. In a randomized controlled trial, this combination reduced the rate of ODD by half and increased reading age by 6 months; ADHD symptoms were also reduced. This kind of approach is promising because it is relatively inexpensive, using parents as the only vehicle for treatment, yet hits multiple risk factors for poor outcomes in antisocial behavior (parenting, ODD, ADHD symptoms, reading ability; for more details of parenting programs see chapter 64). CONDUCT DISORDERS 555 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 555

Child Therapies Cognitive–behavioral therapy (CBT) and social skills therapies can have several targets: 1 To reduce children’s aggressive behavior such as shouting, pushing and arguing. 2 To increase prosocial interactions such as entering a group, starting a conversation, participating in group activities, sharing, cooperating, asking questions politely, listening and negotiating. 3 To correct the cognitive deficiencies, distortions and inaccurate self-evaluation exhibited by many of these children. 4 To ameliorate emotional regulation and self-control problems so as to reduce emotional lability, impulsivity and explosiveness, enabling the child to be more reflective and able to consider how best to respond in provoking situations. In practice, most programs cover all four target areas to a greater or lesser extent. While child CBT was originally mainly used with school-age children and older, more recently it has been successfully adapted for preschoolers. These interventions may be delivered in individual or group therapy formats. Although groups offer several advantages (e.g., opportunities to practice peer interactions), there is some research documenting iatrogenic effects (Dishion, McCord, & Poulin, 1999). This appears to be particularly problematic in larger groups and those with inadequate therapist supervision, where children may learn deviant behavior from their peers and encourage each other to act in antisocial ways. A lower patient : therapist ratio is therefore recommended for group work. Examples of Good Practice Two of the more popular treatment models for conduct disorder are Kazdin’s Problem Solving Skills Training with in vivo Practice (PSST-P; for a review see Kazdin, 1996b) and Lochman and Wells’ (1996) Coping Power Program. In PSST-P, which is used from the age of 7 upwards, the child receives individual training in interpersonal cognitive problem-solving techniques for 12–20 1-hour sessions. The focus is on identifying problem situations, learning a series of problem-solving steps and applying the steps first to hypothetical situations, then in role plays and finally in real-life situations. Therapeutic strategies include games, therapist modeling and role play with therapist feedback. A token system is used in session to reinforce children’s efforts to practice target skills. Parents are involved periodically for conjoint sessions, and may receive behavioral parent training as an adjunctive treatment. The Coping Power program is for children aged 8 years upwards, and is fairly lengthy, comprising 33 one-to-one and half-hour group sessions, with periodic (at least monthly) individual meetings. Training focuses on interpretation of social cues, generating prosocial solutions to problems and anger management with arousal reduction strategies. Treatment is delivered in groups of 5–7 children by a therapist and co-therapist. Sessions include imagined scenarios, therapist modeling, role plays with corrective feedback and assignments to practice outside of sessions. Parent and teacher training components have also been developed as adjunctive treatments. Specifically targeting younger children with conduct problems aged 4–8, Webster-Stratton, Reid, and Hammond (2001b, 2004) have added a group child social skills training component to their IY program, called Dinosaur School. The program lasts for 20–22 2-hour sessions, during which parents usually attend a parallel parenting group. It covers interpersonal problem-solving for young children in a group format with about six children at a time. Sessions include discussion of hypothetical situations and possible solutions, therapist modeling of prosocial responses and practice role playing with therapist feedback. Videotaped vignettes are used to present situations for discussion. Puppets are used for interactive role plays, as well as child-friendly cue cards, coloring books and cartoons. The Dinosaur School program dovetails with other interventions in the IY program, including parent training and a curriculum to train teachers in classroom management skills. Effectiveness In two randomized controlled trials, Kazdin, Esveldt-Dawson, French et al. (1987) and Kazdin, Bass, Siegel et al. (1989) found that PSST results in significant decreases in deviant behavior and increases in prosocial behavior. Outcomes were superior to a client-centered relationship-based treatment and were maintained at 1-year follow-up. The addition of in vivo practice and a parent training component were both found to enhance outcomes. Evaluations of the Coping Power program demonstrate reductions in aggression and substance use, and improved social competence (e.g., Lochman & Wells, 2002). Treatment effects were maintained at 1-year follow-up, particularly for those who also received parent training components (Lochman & Wells, 2004). Now replications by independent research groups are needed. In studies by Webster-Stratton, Reid, & Hammond (2001b, 2004), Dinosaur School has been found to result in significant decreases in behavior problems and increased prosocial behavior; treatment gains appeared to be maintained after 1 year. These findings have been independently replicated (Hutchings, Lane, Owen et al., 2004). The literature is generally not supportive of the effectiveness of individual psychodynamic psychotherapies, art and drama therapies in this population, especially when used as a sole treatment modality, although decisive studies are yet to be undertaken. One or two studies, although methodologically limited, suggest that an attachment-based approach (Moretti, Holland, & Peterson, 1994) or a classic exploratory approach (Fonagy & Target, 1993) might possibly be helpful, at least for a subset of antisocial children; again, properly conducted randomized controlled trials are needed. Interventions in School Interventions to Promote Positive Behavior Typically, teachers are taught techniques that they can apply to all children in their class as well as to those exhibiting the most antisocial behavior. Successful approaches use proactive strategies and include a focus on positive behavior and group interventions, and combine effective instructional strategies with CHAPTER 35 556 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 556

effective behavioral management. Typically, they target four areas of functioning: 1 Promote positive behaviors such as compliance and following established classroom rules and procedures. 2 Prevent problem behaviors such as talking at inappropriate times and fighting. 3 Teach social and emotional skills such as conflict resolution and problem-solving. 4 Prevent the escalation of angry, acting out behavior. A number of these targets can be met by training teachers in similar methods as parents, as described above. However, other techniques are classroom specific. For example, establishing and teaching rules and procedures involves setting rules such as “use a quiet voice,” “listen when others are speaking,” “keep your hands and feet to yourself” and “use respectful words.” Note that these rules are all expressed positively, describing what the child should do, rather than as prohibitions stating what they should not do. Streipling (1997) offers six “rules for making rules”: 1 Make few rules (3–6). 2 Negotiate them with the children. 3 State them behaviorally and positively. 4 Make a contract with the children to adhere to them. 5 Post them in the classroom. 6 Send a copy home to parents. Crucial to all this is a systematic and consistent response to children following or not following the rules. Rewards can be social (teacher praise, peer recognition, notes home to parents), material (stickers, certificates, tokens to exchange for food, etc.), or privileges (e.g., extra breaktime, games, parties, computer time). Mild punishments include reprimands, response-costs procedures (losing privileges or points) and time out (being sent to the corner of the room or to another boring place). Interventions to Promote Academic Engagement and Learning These include self-management and self-reinforcement training programs, for example, to help children spend more time on task and to complete written work more quickly and accurately. An older review of 16 studies found moderate to large effects of such programs (Nelson, Smith, Young et al., 1991), and subsequent trials uphold this (e.g., Levendoski & Cartledge, 2000). A number of programs build on the evidence that antisocial failing children often have parents who do not get involved in their academic schoolwork, and indeed may not value it highly. They do not read with their children, encourage homework or attend school meetings. Approaches include removing barriers to home–school cooperation through training parents to approach teachers positively (often their own memories of school and teachers will be negative and discouraging) and, equally, training teachers to be constructive in solving children’s difficulties and helping parents engage in academic activities with their children. Although there are good descriptions of programs (e.g., Christenson & Buerkle, 1999), to date rigorous evaluations are lacking. For more details of special education programs see chapter 74. Medication At present, there are no pharmacological interventions approved specifically for conduct disorder. Nonetheless, in the USA, medications are used relatively frequently and increasingly in this population (Steiner, Saxena, & Chang, 2003; Turgay, 2004). Primary care physicians are often placed in the position of managing such medications. Concerns have been raised because primary care clinicians often lack adequate training in developmental psychopathology, and adequate time for thorough assessment and monitoring (Vitiello, 2001). In the UK, medication would not generally be supported as good practice because, as discussed below, well-replicated trials of effectiveness are limited, particularly for children without ADHD. The best-studied pharmacological interventions for youth with conduct problems are psychostimulants (methylphenidate and dexamfetamine), as used with children with comorbid ADHD and conduct disorder. In these circumstances, there is evidence that reduction in hyperactivity-impulsivity will also result in reduced conduct problems (Connor, Glatt, Lopez et al., 2002; Gerardin, Cohen, Mazet et al., 2002). There is insufficient reliable evidence to decide whether stimulants reduce aggression in the absence of ADHD; one study by Klein, Abikoff, Klass et al. (1997) found that improvements in conduct disorder symptoms were independent of ADHD symptom reduction, but this needs replication. Other pharmacological approaches for antisocial behavior have tended to target reactive aggression and overarousal, primarily in highly aggressive and psychiatrically hospitalized youth. Medications used in these conditions include those purported to target affect dysregulation (e.g., buspirone, clonidine), mood stabilizers (e.g., lithium, carbamazepine). Whereas Campbell et al. found that lithium reduced aggression and hostility in psychiatrically hospitalized youth (Campbell, Adams, Small et al., 1995; Malone, Delaney, Luebbert et al., 2000), others have failed to show effectiveness in out-patient samples (e.g., Klein, 1991) and in studies of shorter treatment intervals (i.e., 2 weeks or less; Rifkin, Karajgi, Dicker et al., 1997). Carbamazepine failed to out-perform placebo in a double-blind placebo controlled study (Cueva, Overall, Small et al., 1996). In children with aggression and hyperactivity, Hazell and Stuart (2003) in a placebo controlled randomized trial of stimulants plus placebo versus stimulants plus clonidine found the latter was more effective. However, it should be noted that the use of polypharmacy treatment also carries the risk of increased side-effects (Impicciatore, Choonara, Clarkson et al., 2001). In the last few years, the use of antipsychotics such as risperidone, clonidine and others in out-patient settings has been increasing. However, there is only modest evidence for their effectiveness in conduct disorder in normal IQ children without ADHD. The review by Pappadopoulos, Woolston, Chait et al. (2006) found that effect sizes were larger where ADHD CONDUCT DISORDERS 557 9781405145497_4_035.qxd 29/03/2008 02:51 PM Page 557

or intellectual disability were present. Findling, McNamara, Branicky et al. (2000), in a small (n = 10 per group), doubleblind placebo controlled study, found significant short-term reductions in aggression. The Risperidone Disruptive Behavior Study Group used a placebo controlled double-blind design to study the effects of risperidone in 110 children with subaverage IQ and conduct problems. Results suggested that risperidone leads to significant improvements in behavior versus placebo (Aman, De Smedt, Derivan et al., 2002; Snyder, Turgay, Aman et al., 2002), but it remains unclear whether the same findings would apply to normal IQ children. Even newer antipsychotics, while not especially sedating, have substantial side-effects (e.g., risperidone typically leads to considerable weight gain) and the prevalence of movement disorders in the long term is unknown. When might they be contemplated? Clinical experience suggests they can lead to dramatic reductions in aggression in some cases, especially where there is poor emotional regulation characterized by prolonged rages. Prescribing antipsychotics for relatively short periods (say, up to 4 months) in lower doses (say, no more than 1–1.5 mg/day risperidone) can help families cope; during this time it is crucial to introduce more effective psychological management. Conclusions and the Way Forward Conduct disorder is a common disorder among children, and intervention is essential because most children with conduct disorder show poor health and social outcomes for many years, ultimately accounting for a substantial proportion of the adulthood health burden. In coming years we expect to see new research into the following unanswered questions. First, given the plethora of statistical risk factors for conduct problems at the levels of individual, family and community, which among them are causal and which are the best candidates for intervention? Second, what factors can help clinicians predict long-term prognosis and select which youth with conduct problems most warrant scarce treatment resources? Third, given that preschool-onset conduct problems and psychopathic traits are good predictors of prognosis in research settings, how can these features be safely used in clinical settings without the iatrogenic effects of assigning derogatory labels to young children? Fourth, do girls with conduct problems need a different causal theory from boys, and perhaps different interventions? Fifth, what biomarkers are reliably associated with conduct problems, and do any of these suggest new treatment possibilities? As our review of treatments demonstrated, psychological therapies are the mainstay of treatment for conduct problems. However, despite this strong evidence base, in both the USA and the UK only a minority of children receive any treatment, and even fewer receive empirically supported interventions. Further, the “effectiveness” of these interventions as practiced in community settings tends to lag behind documented “efficacy” in controlled trials (e.g., Curtis, Ronan, & Borduin, 2004). As can already be seen in recent efforts with many of the interventions described here, the next generation of evidence-based treatments for conduct problems will likely include much greater attention to dissemination, including strategies for ongoing training and supervision of practitioners to ensure treatment fidelity. The ultimate goal, of course, is to ensure that children with these disorders have access to highquality empirically based care. Acknowledgments We are indebted to Jonathan Hill, who assisted us with this chapter. 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Adolescent and pre-adolescent substance use and substance use disorder bring immediate risks of harm. The acute effects of intoxication can be devastating: alcohol-related motor vehicle accidents remain one of the leading causes of mortality among youth; sharing needles and related injecting paraphernalia has emerged as a leading vector for the transmission of blood borne viruses; and acute intoxication has also been associated with sexual risk taking, sexual victimization and unintentional injury (Hingson & Kenkel, 2004). In treatment samples, excessive alcohol use has been reported to be associated with neurocognitive deficits (Brown & Tappert, 2004) which, if confirmed to be a consequence of alcohol misuse rather than predisposing deficits, would raise the possibility of longer-term disadvantages as a consequence of misuse. Adverse health effects of smoking have been shown in adolescent smokers, including adverse effects on lung function (Gold, Wang, Wipij et al., 1996). Despite these risks, and despite the high rates of co-occurrence of substance use or substance use disorders with other childhood disorders seen in clinical practice (Abrantes, Strong, Ramsey et al., 2005; Wilens, Biederman, Abrantes et al., 1997), adolescent substance use has been relatively neglected in clinical practice and in research studies. The societal costs of this neglect of adolescent substance use are high. The Global Burden of Disease project identified tobacco, alcohol and illicit drugs as, respectively the 2nd, 9th and 20th leading causes of mortality globally (Ezzati, Lopez, Rodgers et al., 2003). If current trends continue, tobacco smoking alone is projected to lead to 1 billion premature deaths globally during the 21st century (Mackey, Eriksen, & Shafey, 2006). Continued and heavy use of these substances has a spectrum of adverse outcomes including physical, social and legal consequences. While many of these conditions, and particularly those relating to physical ill health, develop only after chronic use spanning several decades, and are therefore rare in children and adolescents, an understanding of substance use and substance use problems during adolescence is critical to any approach aimed at lessening these consequences, as it is during childhood and adolescence that the use of these substances typically first occurs. Some studies suggest that, if substance use has not been initiated by age 21, it is unlikely to ever be initiated (Chen & Kandel, 1995). Further, age at initiation to substance use has consistently been shown to be associated with higher lifetime consumption, more risky patterns of use, and with the onset, duration and severity of dependence (see p. 570). While the interpretation of these associations remains controversial, it is clearly the case that early-onset use is a robust indicator of risk for future substance-related problems. In this chapter we first outline research characterizing patterns of adolescent substance use, the assessment of substance use and substance use problems in adolescents, and diagnostic criteria for substance use disorders, including issues relating to the extent to which such criteria may be applicable to adolescents. We also examine outcomes associated with adolescent substance use. We next consider research findings on the etiology of substance use disorders, and their comorbidity with other disorders. Finally, we review treatment approaches and prevention strategies. Epidemiology Much of the literature on the prevalence of substance use in children and adolescents is hampered by methodological challenges including small and unrepresentative samples and varying definitions of substance involvement. We limit our consideration to a relatively small number of studies using large and representative samples that have examined prevalence of substance use. We attempt where possible to provide accurate estimates of the ages at which substance use has been assessed, because childhood and adolescence is a time of very rapid escalation in the prevalence of lifetime use and escalation in involvement and thus even relatively small age differences may be associated with quite large changes in the extent of substance use. Tobacco Use Tobacco, principally but not exclusively in the form of smoked cigarettes, is widely used among children and adolescents. Perhaps the most comprehensive information on patterns of licit and illicit drug use among children and adolescents comes from the USA Monitoring the Future project, which has conducted large surveys of the school-aged population at annual intervals since 1975 ( Johnston, O’Malley, Bachman et al., 2006). The most recent data available from this study are for the year 2005, which indicate that about 50% of 12th grade 565 Substance Use and Substance Use Disorder Andrew C. Heath, Michael T. 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students (ages 17–18) and 25.9% of 8th grade students (ages 13–14) have smoked cigarettes while 17.5% and 10.1%, respectively, have used smokeless tobacco products. Further, 13.7% of 12th graders and 4.1% of 8th graders reported smoking cigarettes daily during the 30 days preceding the survey while about 2.5% and 0.7% reported using smokeless tobacco products about once a day or more often. While international comparisons show considerable variability in the prevalence of tobacco smoking and the use of smokeless tobacco products, the use of these products among youth is widespread. For example, the Global Youth Tobacco Survey, which surveyed 13- to 15-year-old school students from 131 countries, reported that rates of past 30- day tobacco use ranged from 11.4% to 22.2% of students (Warren, Jones, Eriksen et al., 2006). Alcohol Consumption In the 2005 Monitoring the Future study, by 12th grade, 75.1% of all students had used alcohol at least once and 57.5% reported having been drunk at least once, with corresponding percentages of 41% and 19.5% in 8th grade. By 12th grade, rates of lifetime alcohol use were approximately equal across genders (75.7% in males and 74.5% in females), although more males (60.5%) than females (54.4%) reported lifetime drunkenness. There was also evidence of a relatively small subgroup of students who were drinking heavily regularly: 18.1% of students in their final year at high school, and 18.1% of 8th graders, reported having five or more drinks in a row on at least two occasions in the preceding 2 weeks. There is also information available on patterns of alcohol use internationally. Schmid, Ter Bogt, Godeau et al. (2003) reported on patterns of consumption among 15-year-olds in 22 countries: the prevalence of lifetime alcohol use across these countries ranged from 66% (in the USA and Norway) to 92.2% (in Greece and Denmark) among males and from 66% (in the USA) to 91% (in Denmark) among females. Among students who had drunk alcohol, the prevalence of ever having been drunk was 47–85% of males and 42–93% of females. Illicit Drug Use Prevalence estimates derived from the Monitoring the Future Survey lead to several important conclusions. First, at least some lifetime use of illicit drugs is widespread – 21.4% of 8th graders reported using illicit drugs on at least one occasion, and by the final year of high school in excess of 50% of school attendees report some illicit drug use. Second, cannabis is by far the most widely used illicit drug, with 44.8% of 12th graders and 16.5% of 8th graders reporting having used this drug. Relatively few individuals reporting lifetime use of illicit drugs have not used cannabis (22.9% of 8th graders and 11.1% of 12th graders who report any illicit drug use). The lifetime use of other illicit drugs is less prevalent but substantial minorities report some experience with amphetamines (13.1% of 12th graders, 7.4% of 8th graders), inhalants (11.4%, 17.1%, suggesting younger respondents are considering a wider range of experiences as inhalant use, or older respondents are forgetting), sedatives (10.5%, no data for 8th graders), tranquilizers (9.9%, 4.1%), hallucinogens (8.8%, 3.8%), cocaine (8.0%, 3.7%), MDMA (ecstasy; 5.4%, 2.8%) and heroin (1.5%, 1.5%). In addition, there are marked gender differences with the prevalence of use of all drugs being higher among males than among females (e.g., 49.1% versus 40.2% for cannabis use among 12th graders). However, gender differences in the prevalence of illicit drug use appear to have declined in more recent years, with rates of use among females converging on rates among males, a trend that mirrors similar findings in the tobacco and alcohol literatures (Johnson & Gerstein, 1998). Finally, rapid escalation in use occurs over the high school years: rates of ever use of cannabis rose from 16.5% among 8th graders to 44.8% among 12th graders. While these estimates of the prevalence of illicit drug use may appear high, it is worth noting that, because of the sampling frame of this study (school attendees) it is likely, in fact, to underestimate the true prevalence of illicit drug use among youth. School surveys such as this exclude individuals who no longer attend school as well as those who, for whatever reason (e.g., habitual truancy), are unavailable on the day of testing, a group likely to have higher rates of illicit drug use (Johnston et al., 2006). Finally, the figures cited above are for any lifetime use and it is also important to consider the frequency and progression of illicit drug use among youth. While the Monitoring the Future Survey does not provide good information on the frequency or extent of illicit drug use, it appears that the majority of those reporting any lifetime illicit drug use have used the drug on relatively few occasions. For example, while 44.8% of 12th grade high school students in the Monitoring the Future Survey reported lifetime cannabis use, 22.3% of these (10.0% of the entire sample) reported using cannabis on only one or two occasions in their life. Nonetheless, there is a smaller minority of youth who report relatively frequent illicit drug use: 4.9% of these students reported using cannabis on 10 or more occasions in the previous 30 days. Substance Use Disorders There is generally less information on the prevalence of substance use disorders (e.g., abuse, dependence as operationalized in DSM-IV [American Psychiatric Association, 2000]) in youth. This likely reflects a convergence of factors: potential difficulties in the application of standard abuse/dependence criteria to samples of youth (see p. 569); the need for exceptionally large and representative samples given the relatively low base rate of these disorders within the general population; and the fact that they are likely to be concentrated in subgroups of the population (e.g., homeless, those who have left school) who are difficult to capture using traditional survey methodologies. 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disorders. Published studies have either not reported any information on the prevalence of substance abuse/dependence or have adopted the convention of combining all (typically nontobacco) diagnoses to form a single category of substance use disorder. For example, in a representative sample of approximately 1000 New Zealand children studied at age 15 years, Fergusson, Horwood, and Lynskey (1993) reported that 7.7% of this sample met criteria for a substance use disorder, defined as nicotine dependence, or alcohol or other substance abuse or dependence. Such studies were reviewed by Costello, Egger, and Angold (2005), who reported that the median estimate from studies of substance use disorders was in the region of 5%, although there was wide variation among studies in these estimates. An alternative strategy for estimating the prevalence of substance use disorders among youth is to consider retrospective reports of the age of onset of substance use disorders from large and representative samples of the general population. For example, in the NCS Replication survey of adults aged 18 years and older, Kessler, Berglund, Demler et al. (2005) reported, for 50% of all those meeting lifetime criteria for a substance use disorder (not including nicotine dependence), the onset of these disorders occurred before age 21 for alcohol abuse, before age 23 for alcohol dependence, before age 19 for drug abuse, before age 21 for drug dependence and before age 20 for any substance use disorder. Implications for the Assessment of Adolescent Substance Use and Problems Research suggests that face-to-face interview assessment leads to underreporting of substance use by adolescents. In the USA, the discrepancy between rates of self-reported substance use in early national household surveys of drug use that used traditional interview methods, and self-reports based on responses to questionnaires administered in schools, led to several changes in strategy: first to using a self-administered questionnaire, during an interview, to obtain drug use history information; and then to using a computer self-administered interview to obtain this same information (Gfroerer, Eyerman, & Chromy, 2006). Self-report data obtained by questionnaire (e.g., Rutgers Alcohol Problem Index: White & Labouvie, 1989; Drug Use Screening Inventory: Kirisci, Mezzich, & Tartar, 1995) or computer self-administered interview (Turner, Ku, Rogers et al., 1998), particularly where this can be supplemented by toxicology screens, are likely to become the norm for adolescent research assessment. We know of no research comparing the accuracy of information gathered by a standard clinician interview with supplementation by self-report checklist or computer-based assessment, but would anticipate that substantial underreporting at interview would also occur in this clinical context, suggesting that supplementation by checklist or computer-based assessment be used. Brief screens for use and problem use should be utilized across a spectrum of clinical settings as such use and/or problems are common – and elevated – in youth accessing treatment. Diagnosis At the time of writing, the development of the next generation of diagnostic criteria for drug use disorders by the American Psychiatric Association (DSM-V) remains a work in progress. However, while important innovations have been proposed (e.g., use of semicontinuous ratings for each dependence criterion, to permit a more nearly continuous assessment of level of problems), the need to preserve continuity of clinical and research practice, and lack of the necessary empirical base to support more radical change, are expected to limit changes from DSMIV to DSM-V. The application of diagnostic criteria developed for drug use problems in adults to adolescents remains controversial, with many areas of difficulty (Crowley, 2006), but some of these difficulties highlight shortcomings in the existing diagnostic criteria. In discussions of the assessment and diagnosis of substance use problems in children and adolescents, four important shortcomings of existing evidence are faced. 1 The lack of large general population psychiatric surveys of children and adolescents of the magnitude (minimally, tens of thousands of participants) that is necessary to give confidence in attempts to use advanced statistical methods (e.g., Muthen, 2006) to refine diagnostic criteria for specific drug use disorders in general community samples. This has the implication that much of what we can guess about the applicability of diagnostic criteria sets to adolescent substance use disorders derives from retrospective recall of adults about their past history of drug use and problems. While such “back-testing” of diagnostic schema to determine their applicability to adolescents has been underutilized by researchers, the pitfalls associated with reliance on retrospective reports are considerable. 2 The lack of large-scale follow-up studies of clinically treated adolescents with drug use disorders with sample sizes of the magnitude (500–1000 or more participants) available for adults. This makes prospective validation of proposed diagnostic criteria sets, by comparing prediction of future course, treatment–response and other outcomes, a special challenge for pediatric substance use disorders. 3 The narrow focus of most contemporary research assessments of substance use disorders on existing (and in some cases earlier) diagnostic criteria sets, which leaves a weak evidence base for modifying existing criteria. 4 The predominant focus of much research on the nosology of substance use disorders on one drug, alcohol, because of its widespread use and the recognition by psychiatrists of the clinical significance of alcohol use disorders. Tobacco dependence, although widespread and associated with severe long-term physical health risks, is widely neglected in psychiatry. Cannabis use disorders, also increasingly prevalent, have likewise tended to be neglected, perhaps because viewed by many psychiatrists as benign. The Dependence Syndrome Current operationalizations of substance dependence, in both DSM-IV and ICD-10, derive ultimately from the formulation SUBSTANCE USE DISORDERS 567 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 567

of the “dependence syndrome” by Edwards (1986), developed initially with respect to alcohol dependence and then generalized to other drug classes, which represented an attempt to define a physiological syndrome of dependence. Primacy was given to: 1 The experiencing of repeated symptoms of withdrawal, with other defining symptoms being; 2 Relief or avoidance of withdrawal symptoms by further drug use; 3 Increased tolerance; 4 Subjective awareness of compulsion to use the drug, including loss of control; 5 Rapid reinstatement after abstinence; 6 Narrowing of the drug use repertoire; and 7 Salience of drug-seeking behavior. Withdrawal, Withdrawal Relief; Tolerance Both DSM-IV (American Psychiatric Association [APA], 2000) and ICD-10 (World Health Organization, 1996) specify withdrawal syndromes separately for each drug, but using the same criterion for each drug – namely, that the syndrome is due to the cessation or reduction in substance use that has been heavy or prolonged. In DSM-IV no cannabis withdrawal syndrome was recognized, but subsequent laboratory-based studies (Budney, Hughes, Moore et al., 2004), supported by psychometric data (Budney, 2006), make it likely that a cannabis withdrawal syndrome will be included in DSM-V, leaving hallucinogens as the main drug class with no known withdrawal syndrome. Tolerance is defined in DSM by a need for markedly increased amounts of a drug to achieve intoxication or a desired effect or (as may occur after a history of chronic heavy use) by a markedly diminished effect with continued use of the same amount (APA, 2000). At least two schools of thought exist concerning the assessment of drug withdrawal, and of tolerance. One, in its most extreme form, emphasizes the severe and sometimes lifethreatening withdrawal syndromes seen with very long-term opiate, alcohol or sedative dependence that may include grand mal convulsions and delirium tremens. Caetano and Babor (2006) emphasized the development of withdrawal after 25–30 years of heavy drinking, and contrasted this with the problems reported by young adults, arguing that the latter are not truly describing withdrawal symptoms. Likewise, it is possible to operationalize tolerance in such a way that it describes individuals with prolonged histories of excessive substance use (Caetano & Babor, 2006) whose acquired tolerance enables them to function at levels of consumption that would cause severe impairment in most of the population. From this perspective, the alcohol withdrawal syndrome will almost never be encountered in adolescents, and the tolerance reported by adolescents is the acquired behavioral tolerance (VogelSprott, 1997) that comes from learning to adapt to intoxicating levels of alcohol or other drugs, rather than the chronic adaptations that occur after a prolonged history of substance use. However, a consequence of this approach is that the alcohol dependence syndrome as originally conceptualized (with withdrawal as a cardinal feature) becomes a severe but rare disorder, with the majority of individuals who experience problems with alcohol needing to be covered by a residual alcohol use disorder category, an unfortunate consequence given the desirability of providing clinical help before individuals reach the stage of such severe dependence. Alternatively, if a broader conceptualization of dependence is used, drug withdrawal and tolerance defined this stringently become essentially irrelevant to diagnosis, because most individuals reporting drug withdrawal or tolerance will also report many other less severe symptoms. While retention of stringent criteria for a severe withdrawal syndrome requiring careful medical management is clearly essential, this, together with stringently defined tolerance, will usually be irrelevant in pediatric practice. The second school of thought considers withdrawal and tolerance as symptoms arising relatively early in the course of drug use, that may indeed impact the development of other symptoms of dependence. Tolerance may be defined more broadly, so that it is endorsed by many individuals with few or no other dependence symptoms (Muthen, 2006). For alcohol withdrawal, support for a broader operationalization (Muthen, 2006) derives primarily from research using structured diagnostic assessments with quite non-specific wordings to assess withdrawal, which may indeed be endorsed by youngsters who are confusing effects of alcohol intoxication with effects of alcohol withdrawal (Caetano & Babor, 2006). Other research studies that have used a more stringent operationalization of alcohol withdrawal find it to be a relatively severe symptom (e.g., Bucholz, Heath, Reich et al., 2006) that would be quite rare in adolescents. We do not have good empirical data to support preference for either narrower or broader definitions, and need to be sensitive to the possibility that we are arbitrarily dichotomizing continuums of tolerance or withdrawal severity and thereby sacrificing diagnostic precision. Basic science studies have shown acute alcohol withdrawal effects after a single high dose (e.g., handling-induced seizures in mice; Metten et al., 1998) with evidence for genetic overlap of vulnerability to chronic versus acute withdrawal effects (Metten et al., 1998). It has been speculated that hangover in humans may represent such an acute alcohol withdrawal effect, and rates of reported hangover are certainly elevated in those at high risk of alcohol dependence by virtue of a positive family history of alcoholism (Piasecki, Sher, Slutske et al., 2005). Such acute withdrawal effects may be not uncommon in adolescent heavy drinkers, because many have a typical pattern of intermittent heavy consumption; they simply have not been usually assessed, because not a part of the DSM-IV criteria, and their prognostic significance is therefore unknown. Consideration of tobacco dependence suggests that tolerance and withdrawal can be important in adolescence. Koob (2006) cited evidence that “measures of brain reward function during acute abstinence from all major drugs with dependence potential have revealed increases in brain reward thresholds as measured by brain stimulation reward,” suggesting that withdrawal symptoms involving dysphoria may be a common feature, across drug classes, of drug withdrawal. Nicotine CHAPTER 36 568 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 568

withdrawal symptoms, which in DSM-IV predominantly involve affective symptoms, are reported by adolescents relatively early in their smoking careers, as well as by adults (Prokhovov, Hudmon, de Moor et al., 2001), and it is plausible that this pattern for affective symptoms of withdrawal will be confirmed across drug classes. In contrast with alcohol, nicotine is not a drug used for intoxication (hence the more severe operationalizations of tolerance are irrelevant for this drug), and most smokers would not describe their smoking in terms of achieving a “desired effect” (Hughes, 2006). Nicotine in doses smoked by some heavy smoking adolescents (e.g., 20 cigarettes per day; Hurt, Croghan, Beede et al., 2000), however, would be extremely toxic in someone with no prior smoking history: by this example, tolerance is clearly acquired by many adolescent smokers. In the absence of careful laboratory-based studies of adolescent withdrawal, and of real-time field assessments of adolescent withdrawal and tolerance (such as are now possible using palm-pilot based ecological momentary assessment techniques), the present state of the science must be to assess both broadly and stringently and determine whether either or both measures have predictive value for adolescent substance use disorders. Compulsive Use – Loss of Control; Difficulty Quitting/Cutting Down The notion of “loss of control,” as experienced by an individual with alcohol problems who, across repeated drinking sessions, intends to limit his or her drinking but drinks to intoxication, has little relevance to tobacco dependence, where the smoker typically maintains a very stable pattern of smoking from day to day. If defined broadly (the language of DSM-IV includes “often taken in larger amounts... than intended,” relaxing the requirement for intoxication), it does not discriminate very well in heavy-drinking cohorts (Bucholz et al., 1996). Loss of control is more likely to be experienced by a smoker as difficulty quitting, despite a persistent desire to quit. Concern has been expressed about whether adolescents understand questions about such experiences in the same way as adults, and thus may overreport dependence symptoms because of difficulty distinguishing symptoms from the normal fluctuations of adolescence (Prokhovov, Hudmon, Cinciripini et al., 2005). It may also be the case that an adolescent who has progressed from occasional experimentation to more regular use of a drug is actually a better informant about the experience of compulsion to use than, say, an adult chronic heavy smoker who has adapted to drug use over a period of many years. DSM-IV defines as a separate dependence symptom (also considered an indicator of compulsive use) spending a great deal of time obtaining, using or recovering from the effects of the substance, which applies in quite different ways to illicit drug use (seeking out drugs from a dealer), drinking (recovering from effects of hangover) and also is made to apply to smoking (by giving chain-smoking as an example of spending a great deal of time using), but the connection with compulsive use appears far more remote in these cases. Continued Use Despite Negative Consequences Hasin, Hatzenbuehler, Keyes et al. (2006) correctly drew attention to the rather idiosyncratic ways in which continued use despite substance-related problems is handled in current diagnostic criteria. In DSM-IV, continued use despite knowledge that this is causing physical or emotional problems is considered a symptom of dependence. Giving up important social, occupational or recreational activities because of substance use is considered a separate symptom of dependence. Both are inferred to be manifestations of loss of control, although the evidence to support the implicit assertion that it is the compulsion to use that leads ultimately to the pattern of continued use despite negative consequences is not supplied. In contrast, continued use despite interference with major role responsibilities (e.g., schooling, parenting, work); continued use despite social problems (e.g., disruption of relationships) or legal problems; or continued use in situations that are physically hazardous (e.g., drunk driving), are considered manifestations of “abuse,” a residual category whose survival or demise in DSM-V remains controversial (Schuckit & Saunders, 2006). DSM-IV uses the phrase “recurrent” to describe these latter problems (although continued use is clearly implied). It is precisely the latter types of problem that adolescents are more likely to encounter through substance use. Continued use despite being aware of other negative consequences that do not involve immediate physical hazard (e.g., heavy drinking leading to inappropriate sexual behavior by an adolescent) is discounted. Continued smoking that is increasing an individual’s long-term risk of cancer is also discounted. The adolescent who is continuing to use at medically unsafe levels, or the adolescent who is experiencing distress because their substance use is leading to inappropriate sexual behavior or sexual risk-taking, may be experiencing symptoms of comparable importance to the older adult who is already experiencing physical problems associated with their substance use, but these problems are classified quite differently. Clinically Significant Distress/Impairment DSM-IV includes a requirement, for a diagnosis of substance abuse or dependence, that there be evidence of clinically significant distress or impairment, thereby excluding all those cases whose significance lies purely in the realm of physical medicine (e.g., alcohol-related liver damage; smoking-related health risks), or where individuals’ behavior puts themselves or others in danger (e.g., recurrent driving under the influence) without personal remorse or impairment in daily life. Reliance on subjective evaluations of distress or impairment may be particularly problematic for adolescents whose social milieu discourages recognition of impairment. The wisdom of such exclusions must be questioned. Reconceptualizing Adolescent Substance Use Disorder There remains debate about how well criteria for substance use disorders developed for adults apply to adolescents, and whether indeed separate criteria should be developed for SUBSTANCE USE DISORDERS 569 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 569

adolescents or young adults (Crowley, 2006; Martin, Chung, Kirisci et al., 2006). We argue that consideration of: (i) heaviness of use (indexed by tolerance); (ii) loss of control (including difficulty quitting); (iii) continued use despite awareness of negative consequences of use; and in some cases, (iv) problems associated with cessation of use (withdrawal) will identify significant numbers of adolescents experiencing substance-related problems; and that the same profile of problems occurring in a 17-year-old and a 47-year-old would not be an indicator that the 47-year-old does not have problems. There is accumulating evidence in support of a “dimensional” conceptualization of alcohol dependence symptoms (which have been more extensively studied than is the case for other substance use disorders), with individuals with more severe problems more likely to endorse particular symptoms, individuals with less severe problems less likely to endorse the same symptoms, but with no unique symptom profiles identifying particular subclasses of dependent patients (e.g., Bucholz et al., 1996). Under these conditions, defining diagnostic criteria sets that correctly classify severely affected chronic substance dependent individuals is easy; the real challenge is posed by ensuring that individuals with milder problems are correctly classified, a group in which an increased proportion of adolescents will be represented. From this perspective, difficulties identified in the application of diagnostic criteria to adolescents are highlighting broader limitations of these criteria. Risks Associated With Early Use A consistent – albeit controversial – finding is that age of initiation to substance use is strongly associated with later risks of problems. For example, using data from a diagnostic interview survey of a representative sample of US adults (the NESARC study), Hingson, Heeren, and Winter (2006) reported that age of onset of alcohol use was inversely related not only to lifetime risks of alcohol dependence, but also to the severity and duration of dependence. Specifically, individuals who commenced drinking before age 14, compared to those who commenced after age 21, were more likely to meet the criteria for alcohol dependence in the 10 years immediately following drinking initiation, in the 12 months prior to the interview and ever in their lifetimes. They were also more likely to experience multiple distinct episodes of alcohol dependence. Comparisons restricted to those experiencing lifetime alcohol dependence indicated that early-onset alcohol dependence was also associated with higher rates of long duration episodes and with meeting six or more dependence criteria. Hingson, Heeren, Zakocs et al. (2003) reported a 3.5-fold increased risk of being involved in an alcohol-related accident among individuals who began drinking at age 14 relative to those who started drinking after age 21. Importantly, these associations persisted after control for a range of covariates including alcohol dependence and length of drinking career, and when consideration was limited to alcohol-related accidents in the 12 months prior to the interview. These results parallel findings from other studies that an earlier age of alcohol initiation is associated with heavy and more prolonged drinking (Fergusson, Horwood, & Lynskey, 1995; Pitkanen, Lyyra, & Pulkkinen, 2005), alcohol dependence (Hingson, Heeren, & Winter, 2006) and unsafe sexual practices (Hingson et al., 2003). Analogous, although less striking, results have also been reported for tobacco use, with early-onset tobacco use being associated with heightened risks for the development of nicotine dependence (Hu, Davies, & Kandel, 2006) and also for illicit drug use (Lynskey, Heath, Bucholz et al., 2003). Some commentators have implied that these associations are causal and therefore advocated delaying the onset of alcohol use as a potential means of reducing longer-term exposure to alcohol-related harm (Pitkanen, Lyyra, & Pulkkinen, 2005). Alternatively, it has been argued that these associations are likely to be non-causal and arise from the effects of social, family and related (including genetic) factors preceding the onset of alcohol consumption that increase risks both of early initiation of alcohol use and of subsequent alcohol-related harm, for which there may have been inadequate statistical control (Prescott & Kendler, 1999). Prescott and Kendler (1999), using a genetically informative research design, reported that apparent associations between age of onset of alcohol consumption and lifetime alcohol dependence could largely be attributed to shared genetic vulnerabilities. An alternative possibility, not excluded by those analyses, is that genetic differences in dependence risk and early-onset alcohol use are combining interactively (a genotype × early-onset use interaction effect) to determine dependence risk, so the controversy remains unresolved. The Gateway Hypothesis A highly controversial theory concerns whether early-onset cannabis use may act as a risk factor that increases risks for the initiation and escalation in use of other drugs such as heroin and cocaine. This theory, sometimes referred to as the stage or gateway theory, is largely based on findings that, among those reporting the use of drugs such as heroin or cocaine, nearly all people report having also used cannabis and also, among these individuals, use of cannabis is almost always initiated before the use of these other drugs. These findings, and the interpretation placed on them, have been described as one of the most influential research findings in drug policy and have been used as a major rationale for sustaining legal prohibitions against cannabis in the USA and other countries where cannabis use and possession remain illegal. However, temporal sequence alone does not imply causality and it is equally possible that the observed patterns of association between cannabis use and other drug use could be explained by a model assuming no causal associations between cannabis use and subsequent use of illicit drugs (Morral, McCaffrey, & Paddock, 2002). Nonetheless, a number of studies that have attempted to control for observed covariates have reported that, even after such control, significant associations remain between earlyonset cannabis use and subsequent illicit drug use (Fergusson, CHAPTER 36 570 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 570

Boden, & Horwood, 2006). Using a cotwin methodology to control for both genetic and shared environmental risk factors that may be associated both with early-onset cannabis use and with subsequent use of other illicit drugs, Lynskey et al. (2003) reported that early-onset cannabis users had odds of sedative, hallucinogen, cocaine/other stimulants and opioid use that were 2.6–5.2 times higher than those of their non-early using cotwin. Subsequent studies using a variety of genetically informative research strategies have also failed to discount the possibility that the use of cannabis may influence subsequent risks for the development of illicit drug use (Agrawal, Neale, Prescott et al., 2004; Lynskey, Vink, & Boomsma, 2006). There are a number of different possible explanations for the mechanisms underlying the observed associations. First, it remains possible that the associations are wholly noncausal and arise both from the joint influence of shared risk factors (including genetic and shared environmental risk factors that were controlled for in the genetically informed research studies mentioned above), and from non-shared risk factors – such as peer affiliations – that were not controlled. While popular interpretations of the “gateway” properties of cannabis imply pharmacological effects of adolescent exposure to cannabis, such mechanisms seem unlikely; the levels of exposure typically employed in animal models are often many times higher than is typical in early-onset cannabis users. An alternative explanation of the observed associations is that they arise because use of and access to cannabis increase exposure and opportunity to use other drugs (Wagner & Anthony, 2002). Psychosocial and Genetic Risk Factors In evaluating pertinent literature on the etiology of substance use disorders, ideally one would wish to know about at least four dimensions of risk: 1 Predictors of early onset, because early initiation of substance use will itself predict increased risk of later problems (see p. 570); 2 Predictors of heaviness of use (or other aspects of substance use patterning that may be associated with increased risks of problems); 3 Predictors of dependence vulnerability, conditional upon duration and heaviness of use; and 4 Predictors of desistance (i.e., protective factors that may facilitate quitting or overcoming substance use-related problems). It is rare to find that these different dimensions of risk have been considered in a single study. Genetic Research We know relatively little about the genetics of adolescent substance use and substance use disorder, with the limited information deriving from a small number of studies (McGue, Iacono, Legrand et al., 2001; Rose, Dick, Viken et al., 2004; Slutske, Cronk, Sher et al., 2002a) that are mostly ongoing at the time of writing but should eventually provide important information about how genetic influences on adolescent substance use and substance use disorder overlap with genetic influences on adult substance use disorder. For the time being, what we may anticipate in adolescents is largely guided by information about genetic contributions to risk of adult substance dependence, which derives from multiple sources. Family, Including Prospective High-Risk Studies From the 1950s onwards, a growing literature acknowledged the strong familiality of alcoholism, with some families having large numbers of alcohol-dependent cases. In the recent multisite US COGA study, rates of alcohol dependence in the relatives of an index case ascertained through treatment sources were increased three- to eight-fold, varying by gender (Reich, Edenberg, Goate et al., 1998). This work has been extended to examine outcomes associated with index case illicit drug dependence (Merikangas, Stolar, Stevens et al., 1998; Rounsaville, Kosten, Weissman et al., 1991), with research finding support for at least partial drug specificity of familial risks. Intergenerational transmission of smoking has been surprisingly weak in many studies (Avenevoli & Merikangas, 2003), although this may in part reflect generational change in the determinants of smoking associated with pronounced secular changes in rates of smoking and recognition of the health hazards of smoking: sibling and twin correlations typically have been much higher (Avenovoli & Merikangas, 2003; Heath & Madden, 1995). Increasingly, family studies have been implemented for the purposes of discovering genetic linkage (i.e., co-segregation of a genetic marker and a “trait” locus that influences risk of a disorder) in order to identify individual genes that contribute to risk, with some positive findings reported initially for alcohol dependence (Prescott, Sullivan, Kuo et al., 2006; Reich et al., 1998) and more recently for other substance use disorders including cocaine dependence (Gelernter, Panhuysen, Weiss et al., 2005), opiate dependence (Gelernter, Panhuysen, Wilcox et al., 2006) and tobacco dependence (Li, Payne, Ma et al., 2006). Specific features of the design of a study (e.g., an emphasis on ascertainment of large extended pedigrees; Reich et al., 1998) may also define the types of genes that are more or less likely to be discovered in that study (in this case, making it less likely that genetic risk factors associated with antisocial alcoholism will be discovered, because of the decreased likelihood of large full sibships in the case of an antisocial personality disordered father). The evidence for significant parent–offspring and sibling correlations from family studies establishes the importance of familial factors, but of course does not exclude non-genetic causes for family resemblance. Family studies also provide evidence for significant spousal concordance for substance use and substance use disorder which, at least some studies suggest (Agrawal, Heath, Grant et al., 2006) may be explained by assortative mating, the tendency for like to marry like, and which may vary over time. Any increased tendency for an alcoholic to marry another alcoholic (or, more broadly, substance abusing) partner will increase genetic risk to the offspring SUBSTANCE USE DISORDERS 571 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 571

generation, compared to random mating. Thus, while the genes that are segregating in a population will not change over time, and thus cannot account for secular changes in rates of disorder, changes in the intensity of assortative mating (e.g., in periods of disruption such as war) do have the potential to impact on the distribution of risk in the next generation. Recognition of the strong familiality of alcoholism has in turn produced a large literature of high-risk research studies contrasting outcomes in offspring of alcohol-dependent parents (typically fathers) and controls (Sher, Walitzer, Wood et al., 1991), with some important prospective studies beginning either in early childhood (Zucker, Wong, Puttler et al., 2003) or in adolescence (Chassin, Rogosch, & Barrera, 1991). Such studies can provide important information about early precursors of substance use disorders, but at the cost of lengthy delays before early outcomes can be conclusively linked to adolescent or adult substance use. Because of the extensive psychiatric comorbidity of substance use with other psychiatric disorders, and the extensive environmental risk-exposures of offspring of a parent with a substance use disorder history (which typically will be associated with risks that are not specific to offspring substance use disorder), it is only by the time that offspring are mostly through their period of risk for substance use disorder onset that the connection of early behaviors with later substance use disorder can be confirmed. The sampling strategy used to ascertain high-risk families incurs important limitations to the generalizability of findings from a particular study: for example, the work of Chassin (Chassin, Rogosch, Barrera, 1991) is unusual in requiring that a custodial parent be alcoholic at the time a family was entered into the study but, in the general population, a relatively high proportion of families with parental alcoholism will have experienced parental divorce by the time the offspring reach early adolescence (see p. 575). Of particular note have been the prospective high-risk studies of Schuckit (e.g., Schuckit, Smith, Pierson et al., 2006), using an alcohol challenge paradigm, with administration of a standardized dose of alcohol under the controlled conditions of the research laboratory, to compare level of response to alcohol in young adult offspring from high-risk with control families. While the precise interpretation of Schuckit’s findings remains controversial, because the adult offspring that he was testing were not alcohol-naïve, it is clear that level of response to alcohol, indexed by such measures as self-reported intoxication, differentiates high-risk from control offspring, and is prospectively predictive of alcohol dependence risk, with low level of response associated with familial alcoholism history and independently predictive of increased risk of dependence, findings that emphasize that individual differences in drug response may themselves be important (and heritable; Heath, Madden, Dinwiddie et al., 1999) determinants of risk. A similar association is also seen in a (non-genetic) prospective study of marijuana reactions and subsequent dependence risk (Fergusson, Horwood, Lynskey et al., 2003). The high-risk paradigm has been relatively fruitful in alcohol research, but underutilized for illicit drug dependence (but see e.g., Tarter, Kirisci, Mezzich et al., 2003). A new generation of studies is emerging as the children and adolescent offspring of adult linkage samples are followed prospectively, which should allow prospective characterization of the behavioral effects of genes identified as associated with alcohol dependence risk in the parental generation. Adoption, Twin and Children-of-Twins Studies Detailed reviews of individual studies are available elsewhere for alcoholism (Heath, Slutske, & Madden, 1997), smoking (Heath & Madden, 1995) and marijuana dependence (Agrawal & Lynskey, 2006). Here we emphasize overall findings and conceptual issues concerning the interpretation of research from these studies, noting that most have been based on adult samples from older twin cohorts (typically born in the 1970s or earlier), but that a new generation of prospective studies including studies of international adoptees (McGue, Sharma, & Benson, 1996) and of open adoptions (where the biological mother remains in contact with the adoptive family), and prospective twin studies (cited earlier), as well as the emerging children-of-twins studies (Jacob, Waterman, Heath et al., 2003) are characterizing adolescent substance use and its adult outcomes. From the adoption study literature, there is very consistent evidence that alcoholism or more broadly defined substance dependence (which will be chiefly alcohol or marijuana dependence) in adoptees is significantly correlated with alcoholism or antisociality in biological fathers, and uncorrelated, or only weakly correlated, with alcoholism in adoptive parents. A similar pattern is seen for antisocial traits (Langbehn, Cadoret, Yates et al., 1998). This consistency of evidence is seen despite considerable variability in how biological parent alcoholism was assessed: by direct interview in the original Danish adoption study (Goodwin, Schulsinger, Hermansen et al., 1973); by a record review that would have classified as positive individuals with a single drunk-driving conviction (i.e., defining a relatively mild, high-prevalence phenotype) in the case of the Scandinavian adoption studies (Cloninger, Bohman, & Sigvardsson, 1981); and by a record review that disproportionately identified alcoholic fathers through the prison and hospital systems, defining a low-prevalence severe antisocial alcoholic/substance abusing paternal phenotype, in the case of the Iowa adoption studies (Cadoret, Troughton, & Woodworth, 1994). However, the adoption study literature is less consistent with the hypothesis that the comorbidity of depression and alcoholism is largely determined by genetic factors (Cadoret, Winokur, Langbehn et al., 1996). The adoption study literature must be interpreted with recognition of certain important limitations. Because of the much higher prevalence of alcoholism in males than females, particularly for the older birth cohorts from which the older adoption studies were based, the studies have mainly been informative about outcomes associated with paternal alcoholism, although the Swedish studies do provide some data about associations with maternal alcoholism. Selective placement (i.e., the possibility that individuals from high-risk genetic CHAPTER 36 572 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 572

backgrounds will be more likely to be placed with high-risk adoptive parents) is probably an overstated problem, given the typically quite limited sophistication, from a psychiatric perspective, of the evaluations conducted in the adoption process, and random placement a closer approximation to reality. On the other hand, it is clear that by selecting children given up for adoption, there is overrepresentation of biological parent antisociality, and, conversely, adoptive home environments may not represent the full range of environmental adversity encountered in non-adoptive families (because adoptive parents will include fewer young parents with active substance use disorder at the time of their parenting). (However, rates of prenatal substance exposure may be more elevated in adoptees, given higher rates of maternal antisociality, and mothers who were not planning to keep their offspring: certainly prenatal effects appear more pronounced than would be anticipated for general population samples; Yates, Cadoret, Troughton et al., 1998.) Thus, the early adoption studies are most likely to be informative about genetic influences on alcoholism occurring in the context of a history of antisocial traits, and while the adoption study design may provide useful insights into pertinent environmental risk mechanisms, it is information that cannot easily be generalized, in terms of magnitude of effects or their importance relative to other environmental risk mechanisms, to non-adoptive families. A new generation of studies is emerging that takes advantage of international adoptions (McGue, Sharma, & Benson, 1996) and open adoptions (where adoptive and biological parents remain in contact with one another) in the USA that may overcome some of the limitations of the earlier studies. Twin Studies A series of diagnostic interview and record-linkage twin studies provide additional support for the importance of genetic factors in the familial transmission of alcohol dependence risk (Heath, Slutske, & Madden, 1997; Knopik, Heath, Madden et al., 2004). A smaller number of diagnostic interview studies have provided evidence for genetic influences on nicotine dependence (Lessov, Martin, Statham et al., 2004) and illicit drug dependence (Agrawal, Lynskey, Bucholz et al., 2007; Kendler, Jacobson, Prescott et al., 2003), although many questionnaire studies have documented genetic effects on various non-diagnostic aspects of smoking behavior including heaviness of smoking and persistence versus successful desistance (Heath & Madden, 1995). As far as concerns alcoholism, studies have ranged from analyses of medical record or hospital discharge data in the Swedish and US World War II twin panels – which will have defined a relatively severe alcoholism phenotype – to diagnostic interview surveys which typically will have defined a much broader phenotype. In general, these studies have confirmed the inference of important genetic effects on substance use disorder inferred from adoption studies, and provided evidence for important genetic influences in women (where assessed) as well as men, and for severe phenotypes as well as milder phenotypes. If one twin has a history of substance use disorder, it is much more likely that the cotwin will also have a history if the cotwin is monozygotic (genetically identical) than if the cotwin is dizygotic (an ordinary full sibling). Quantity of alcohol consumed also appears to be influenced by genetic factors (Heath & Martin, 1994), emphasizing that genetic effects on dependence risk may be at least partially, or substantially, mediated through effects on consumption patterns (Whitfield, Zhu, Madden et al., 2004). Multivariate genetic analyses have also documented high genetic correlation between substance use disorder (principally alcohol dependence) and traits that might be broadly characterized as indicators of behavioral disinhibition (Iacono, Malone, & McGue, 2003; Slutske, Heath, Madden et al., 2002b), but also moderately strong genetic correlation between history of major depression and alcohol dependence risk (Kendler, Heath, Neale et al., 1993). As with adoption studies, limitations of the traditional twin study design must be considered carefully. Foremost is the question of whether the assumption of equally correlated environmental exposures in monozygotic compared to dizygotic pairs is justified for drug use. While investigations of this question for a broad range of behavioral and psychiatric phenotypes have generally found support for this assumption (Hettema, Neale, & Kendler, 1995; Kendler, Neale, Kessler et al., 1994), the very low proportion of monozygotic pairs who are discordant for use of some drug classes (e.g., tobacco) must make us suspect that frequently once one twin uses, he or she initiates his or her cotwin. Where investigated, it has not been found that this biases inferences about the later outcomes of substance use: for example, conditioning upon whether or not a twin pair start smoking at the same time still leads to consistent estimates for the importance of genetic effects on later smoking outcomes (Pergadia, Heath, Agrawal et al., 2006). Additional limitations to consider in the interpretation of twin data are: (i) the confounding of shared environmental and non-additive genetic effects, which can lead to the underestimation of the importance of shared environmental influences on risk; and (ii) the confounding of genetic and genotype × shared environment interaction effects, which leads to reported genetic variances or heritabilities (or, in the multivariate case, genetic correlations) combining both the main effects of genes on risk, and the effects of genotype × shared environment interaction (Heath, Todorov, Nelson et al., 2002). It is possible to model explicitly the interaction of latent genotype with a measured environmental modifier; however, power to detect such interaction effects will be low, particularly if a low-prevalence binary environmental modifier is used for analysis, and published reports have not always excluded the full range of alternative explanations before claiming such interaction effects (e.g., variance differences between exposure conditions can lead to erroneous inference of G × E effects, unless appropriately modeled). Thus, while convincing demonstration of the importance of G × E interaction effects in the substance use disorder literature have been relatively few, we shall see in our review of environmental risks (see p. 574) that it is probably quite unsafe to assume the absence of such effects. SUBSTANCE USE DISORDERS 573 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 573

An informative extension of the classic twin design examines outcomes of children of twins who are concordant or discordant for history of substance use disorder ( Jacob et al., 2003). Assuming adequate statistical control for psychopathology in the coparent (Jacob et al., 2003), the children-of-twins design allows contrasts of outcomes in children at high genetic and high environmental risk (twin parent has a history of substance use disorder); high genetic but reduced environmental risk (twin parent is unaffected but parent’s monzygotic [MZ] cotwin has a history of substance use disorder); intermediate genetic but reduced environmental risk (twin parent is unaffected but parent’s dizygotic [DZ] cotwin has a history of substance use disorder); and low genetic and low environmental risk (twin parent, and parent’s cotwin, both have no history of substance use disorder). Unexpectedly, the one study for which results have been published to date found increased offspring risk of alcohol use disorder only in the presence of both genetic risk (parent or MZ cotwin alcohol dependent) and environmental exposure (the parent, if not alcohol dependent, had a history of alcohol abuse; Jacob et al., 2003). However, these are results for a single study, whose offspring were relatively early in their period of risk for the onset of alcohol use disorder, so it remains to be determined whether this pattern (for which one interpretation is important genotype × shared environment interaction effects) is confirmed. Genetic Association Studies: Effects of Metabolism Genes We shall not attempt to review the early case–control literature on genetic association studies of substance use disorders: by contemporary standards, most early research was severely underpowered, lacked correction for multiple testing of the very many plausible candidate genes that can be identified for substance use disorders, and thus had high probability of generating false positive findings. More systematic approaches guided by linkage findings are now beginning to identify and replicate genetic associations (Edenberg & Faroud, 2006), and the new era of Genome-Wide Association Studies and highthroughput candidate gene studies (Bierut, Madden, Breslau et al., 2007; Saccone, Hinrichs, Saccone et al., 2007), provided studies are adequately powered, is likely to lead to rapid advances in this literature. Some of the same studies that have been used to identify genetic linkage have also been obtaining prospective data from the pre-adolescent and adolescent offspring in their families, so findings of more direct relevance to adolescent substance use disorder are to be anticipated. We use a concrete example to illustrate some of the issues raised, for clinical practice as well as research, by the identification of a gene with (in this example) important effects on risk. Arguably the best example of how a polymorphism at a single genetic locus may affect a major psychiatric phenotype is provided by the example of alcoholism, and its associations with ALDH2 (aldehyde dehydrogenase) genotype in individuals of Asian ancestry. Ethanol is converted by the enzyme alcohol dehydrogenase to the toxic metabolite acetaldehyde, which in turn is converted by the enzyme acetaldehyde dehydrogenase to acetic acid. A single point mutation in the gene for ALDH2 leads to an inactive enzyme, so that those who are heterozygotes (ALDH2*1/*2) have substantially elevated blood acetaldehyde concentrations after ingestion of alcohol and experience a characteristic flushing response (Wall, Peterson, Peterson et al., 1997). Individuals who are homozygous for the null allele but develop alcohol problems are extraordinarily rare, reflecting their typically very low consumption of alcohol (a 10-fold difference in average consumption in males between the normal and null homozygotes in one community sample; Higuchi, Matsushita, Muramatsu et al., 1996). In the Japanese context where much of this research was conducted, pronounced genotype × gender effects are also seen, with women with the high-risk genotype drinking at the same level as men with the lowest risk genotype (Higuchi et al., 1996). Heterozygotes are also rarer in alcoholic patient series than in control series, although at least among Japanese this difference appears to be declining over time (Higuchi, Matsushita, Imazeki et al., 1994), a trend that the authors attributed to increased social pressures on Japanese males to drink after work. At the same time, those heterozygotes who progress to heavier drinking appear to be at increased risk of adverse medical consequences, including increased frequency of alcohol-related cancers (e.g., Hori, Kawano, Endo et al., 1997), presumably because of impaired metabolism of alcohol. Among Asian American youth, however, genotype effects on consumption levels have not been found (Hendershot, MacPherson, Myers et al., 2005). Thus, in considering this single example we find evidence for: (i) an important single gene effect on alcohol dependence risk, which may at least in part be mediated through heaviness of consumption; (ii) important modifiers of this effect, including gender, age-cohort and/or society, and secular change in drinking practices; and (iii) evidence for increased vulnerability (to adverse medical outcomes) in the heterozygote group that were at low risk of becoming heavy drinkers. This example also raises the interesting issue of whether genetic information should be used in counseling adolescents (or adults) about their substance use. In this case, a subset of youth, of Asian ancestry, are at substantially increased risk of adverse medical consequences from alcohol misuse, but they and their families may be unaware of this (particularly in the case of international adoptions by European ancestry parents). Environmental Risks The existing research literature has identified a range of environmental risk factors that are associated with increased rates of adolescent substance use and substance use problems. These risk factors are not specific to substance use problems, being also associated with increased risk of conduct disorder (see chapter 35) and in many cases other disorders (e.g., major depression and attention deficit/hyperactivity disorder [ADHD]; see chapters 37 and 34), but their associations with substance use are not, in general, limited to those with coCHAPTER 36 574 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 574

occurrence of these other disorders. A brief summary of key domains of putative risk is provided below, with comment on methodological considerations pertinent to each domain. We conclude with a discussion of significant clustering observed among environmental risks and between environmental risks and parental substance use disorder history. Prenatal Alcohol and Other Drug Exposure Maternal heavy alcohol use during pregnancy is now rare in most contemporary western cultures. Its association with fetal alcohol syndrome is well documented and characterized in clinical follow-up studies, with an extensive supporting basic science literature (see chapter 30). Broader literatures have also developed examining possible consequences of milder levels of prenatal alcohol exposure (fetal alcohol effects) as well as effects of other prenatal drug exposures, and in particular tobacco and cocaine. Parental history of substance use disorder is associated with increased risk of offspring prenatal alcohol and other substance exposure (Yates et al., 1998), which in turn predicts cognitive and behavioral self-regulation difficulties (Knopik, Sparrow, Madden et al., 2005; Weissman, Warner, Wickramaratne et al., 1999), which also increase risk of adolescent substance use and abuse (Biederman, Monuteaux, Mick et al., 2006). However, it is by no means clear that these associations are causal. Higher rates of substance use disorders and antisocial traits in both the pregnant woman who smokes or uses other drugs during pregnancy, and her partner (Knopik et al., 2005), will predict increased risk of externalizing problems for her offspring, quite apart from any prenatal exposure effect. In the Iowa adoption study (Yates et al., 1998), maternal alcohol use during pregnancy, as abstracted from adoption records (and therefore most probably limited to cases of heavy alcohol use) was predictive of increased risk of offspring drug involvement. However, because biological mothers’ psychopathology could be inferred only indirectly from records, it is quite possible that reported maternal alcohol use during pregnancy is functioning merely as an index of greater maternal antisociality, so the possibility of genetic confounding cannot be excluded. This possibility will become clearer with a new generation of studies taking advantage of open adoptions, where the biological mothers can be directly evaluated. While basic science literatures have developed that indicate that deficits associated with prenatal exposure might be anticipated (for reviews see Ernst, Moolchan, & Robinson, 2001; Slawecki, Thomas, Riley et al., 2004), imperfect control for parental and situational risk factors is likely to make identification of such effects in clinical research challenging. More convincing characterization of such prenatal exposure effects will arise only when systematic within-mother between-pregnancy comparisons are made of full sibling offspring born to mothers who used during one pregnancy but not during a second pregnancy, so that heritable traits in the biological parents can be controlled for. Even these comparisons will have important limitations, because the most severely dependent mothers are the least likely to have refrained from substance use during at least one pregnancy. Child Maltreatment and Abuse Childhood neglect, physical abuse (PA), sexual abuse (CSA) and other forms of childhood maltreatment are predictive of early onset tobacco, alcohol, marijuana and other illicit drug use (Anda, Croft, Felitti et al., 1999; Dube, Felitti, Dong et al., 2003; Dube, Miller, Brown et al., 2006), and alcohol or other drug problems during adolescence (Fergusson, Horwood, & Lynskey, 1996) and into adulthood (Molnar, Buka, & Kessler, 2001; Nelson, Heath, Lynskey et al., 2006), especially among women (Widom, Ireland, & Glynn, 1995). Whereas the association between childhood trauma (CSA, in particular) and early and escalating substance involvement observed during adolescence is well documented, debate continues regarding the magnitude of reported effects, and importantly, the causal role of maltreatment in the development of problem substance use. Methodological differences, such as use of retrospective versus prospective assessments and recruitment of study participants from individuals in treatment for substance use disorder or other psychiatric disorders versus large-scale community or population-based sampling, contribute to continued debate. In addition, abuse during childhood is variously defined in terms of age of onset and severity, with some researchers limiting analysis to abuse occurring during younger childhood years (e.g., before age 12 or 16) or to more severe forms of abuse, such as CSA involving penetration or intercourse, or court documented cases of abuse. Researchers also differ in whether or not, and to what extent, potential third variable confounds are controlled. Rates of maltreatment are higher for children raised in families characterized by a host of other risks, including parental substance use disorder, which might directly impact on vulnerability to early and problem substance use during adolescence. Thus, parental substance use disorder and correlating risks that pre-date both maltreatment and substance initiation may account for at least some of the reported effects. Many recent studies of childhood maltreatment and later outcome include statistical controls for a variety of potentially confounding risk factors; however, few include prospective assessment of offspring outcomes and/or confounded risks. Work by Fergusson, Horwood, and Lynskey (1996) on CSA is an exception, and one of few population-based longitudinal studies in which adolescent substance use disorder is examined. With growing interest in identifying causal mechanisms underlying the association between childhood maltreatment and early and problem substance involvement, genetically informed methodologies have been increasingly employed to rule out heritable third variables that might independently contribute to substance use disorder risk in adolescence and adulthood. To date, genetically informed research is limited to the examination of substance use disorder in adults. In several studies employing a discordant twin design, higher rates of substance use and substance use disorder among individuals reporting CSA have been observed (Kendler, Bulik, Silberg et al., 2000; SUBSTANCE USE DISORDERS 575 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 575

Nelson et al., 2006). However, even in discordant twin comparisons it is not clear to what extent substance use outcomes are secondary to other deficits and early disadvantages that are not shared by members of the twin pair. Marital Conflict, Parental Divorce and Repartnering Parental divorce, subsequent repartnering and marital conflict often preceding separation, are associated with increased rates of offspring alcohol, tobacco, marijuana and other illicit drug use initiation (Hoffman & Johnson, 1998), heavier use of these substances (Doherty & Needle, 1991; Hoffman, 1995; Needle, Su, & Doherty, 1990) and greater risk of problem use (Fergusson, Horwood, & Lynskey, 1994; Hoffman & Johnson, 1998; Needle, Su, & Doherty, 1990). However, interpretation of these associations is complicated by confounded risks associated with family disruption that might independently contribute to offspring substance involvement, including parental substance use disorder. Results from a handful of studies that assess prospectively offspring outcomes and/or confounded risks that pre-date family disruption suggest small but significant effects of family disruption on adolescent substance use and substance use problems (Fergusson, Horwood, & Lynskey, 1994; Doherty & Needle, 1991). In addition, behavioral genetic studies have noted genetic effects on the risk of divorce (McGue & Lykken, 1992), a not unexpected finding given the importance of genetic effects on parental characteristics such as substance use disorder history that are associated with increased divorce risk. Thus, it may be questioned to what extent risks associated with parental divorce are mediated environmentally, rather than by genetic transmission. This issue has been the focus of a number of recent genetically informed studies of substance use disorder in adults. For example, Kendler, Neale, Prescott et al. (1996) examined environmental mediation of parental loss effects on risk for alcoholism in a large sample of adult female twins. Kendler reported parental loss through separation (but not death) had both causal and non-causal effects. Specifically, associations between alcoholism risk and parental separation were mediated by environmental factors specific to parental separation as well as genetic factors associated with susceptibility to alcoholism. In a recent study of adolescent and young adult offspring of Australian twins discordant for divorce, D’Onofrio, Turkheimer, Emery et al. (2005) report divorce-specific environmental mediation of associations between parental divorce prior to age 16 and marijuana use. However, mediation by environmental factors specific to divorce either before or after age 16 was not observed for ever use of alcohol or cigarettes, age at first use of alcohol, cigarettes or marijuana, having experienced alcohol intoxication, or age at first alcohol intoxication. In both studies, inferences about environmental mediation are model-dependent, so that unmeasured genetic confounders in the parental generation would potentially lead to false positive (or false negative) inference. Additional, more robust support for environmental mediation of divorce effects (and parental psychopathology) on offspring substance involvement is provided by Cadoret, Troughton, O’Gorman et al. (1986), who in an early report on a cohort of Iowa adoptees found an increased risk for drug abuse among adoptees whose adoptive parents divorced or had a history of psychiatric difficulties compared to adoptees whose adoptive parents remained together and had no history of psychiatric difficulties. Similar results were reported in a separate study of male adoptees (Cadoret, Yates, Troughton et al., 1995), with marital and psychiatric problems in adoptive parents contributing to adoptee risk of drug abuse independently of genetic influences. Overall, it is clear that children in disrupted families show increased risk of early substance involvement and abuse and/or dependence, but the underlying mechanisms remain uncertain. It remains unclear whether, and certainly cannot be assumed that, removal of a parent with a history of substance use disorder from the home produces better outcomes for offspring: indeed, one study using a children-of-twins design failed to find any significant effect of duration of paternal presence in the home as a moderator of paternal alcoholism effects (Duncan, Scherrer, Fu et al., 2006). Parenting Influences Results from cross-sectional and an increasing number of prospective longitudinal studies of adolescent substance involvement support the importance of a range of parenting influences. Inconsistent, ineffective discipline and poor supervision and monitoring (Chilcoat & Anthony, 1996), parent–child conflict (Brook, Brook, Gordon et al., 1990; Sokol-Katz, Dunham, & Zimmerman, 1997), low levels of parent support and parent– child attachment (Allen, Hauser, & Borman-Spurell, 1996) and permissive or tolerant attitudes about substance use (Ary, Tildesley, Hops et al., 1993; Brook, Whiteman, Gordon et al., 1986) are among parenting behaviors predictive of both early and problem alcohol, tobacco, marijuana and other illicit drug use during adolescence. Identification of mediating and moderating effects of parenting on adolescent substance involvement is the focus of much recent research on parenting influences. In addition to parsing direct from indirect effects of parental substance use disorder (Urberg, Goldstein, & Toro, 2005), this work has documented significant moderation by parenting of associations between parental substance use disorder and adolescent substance use and misuse (Doherty & Allen, 1994). Consistent with results from cross-sectional studies (Brook et al., 1990; Kung & Farrell, 2000), there is now longitudinal evidence that some parenting behaviors, particularly monitoring, work to moderate peer influences on adolescent substance use and substance use problems (Ary, Duncan, Duncan et al., 1999; Barnes, Hoffman, Welte et al., 2006; Marshal & Chassin, 2000). Peer Influences Whereas deviant peer affiliation continues to be one of the best predictors of early and problem substance use during the CHAPTER 36 576 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 576

adolescent years (Fergusson, Swain-Campbell, & Horwood, 2002), mechanisms underlying this association remain largely unknown. Among competing explanations is the possibility that deviant peers have a direct influence through peer pressure and socialization, both modeling and providing reinforcement of alcohol and other drug use. However, selective processes are also likely; for example, parental substance use disorder increases risk for both substance involvement and affiliation with deviant peers, and might thereby account for their association. In addition, substance-using adolescents may seek out peers who also use substances, a form of social homophily (Bauman & Ennett, 1994). To disentangle direct and indirect effects of deviant peer affiliation on early and problem use of alcohol and other substances, an increasing number of researchers are capitalizing on the strengths of prospective longitudinal designs in attempts to rule out third variable confounds. Results from this work largely support both socialization and selection explanations, together suggesting parental substance use disorder, along with impairments in parenting, increase the likelihood of affiliating with substance-using peers (Fergusson & Horwood, 1999; Larzelere & Patterson, 1990) which, in turn, has direct effects on adolescent substance involvement. Conclusions: Clustering of Risks In interpreting the literature on putative risk factors, it is important to note the high degree of overlap or clustering of these risk factors, and their associations with conduct disorder and other disorders. For example, prenatal drug exposure is more common among children of parents with substance use disorder. These offspring are also at heightened risks for experiencing family disruption, childhood abuse, neglect and otherwise compromised parenting that together increase the likelihood of affiliations with delinquent or substance-using peers. Despite the high degree of overlap and clustering of risk factors, most of the accumulated literature on potential risk factors in fact derives from research that has considered relatively few risk factors, ignoring others, and that may have imperfect or no characterization of parental psychopathology. However, these challenges do not reduce the importance of considering the total effects, both direct and through correlated environmental risks, in so far as they help identify particular groups of individuals (e.g., children of divorced parents; children with a history of abuse) at increased risk of early substance involvement and problems. A further issue concerns the interplay between genetic and environmental risks. Despite the extensive evidence for genetic effects on risks of substance use disorders, it must be remembered that most of this evidence derives from non-adopted families, so that genetic effects are occurring in these same contexts of environmental risks such as prenatal substance exposures, early trauma and parental conflict and separation/ divorce. While there has been only limited characterization of gene–environment interaction effects at the time of writing, the likely importance of such effects should not be ignored. Behavioral and Pharmacotherapies The efficacy of pharmacotherapies for adolescent drug use disorders has not been established, although some promising pharmacotherapies are emerging for use with adults. Clinical trials with adolescents have been few in number and underpowered. Whereas some studies using complex combination cognitive–behavioral interventions have been able to demonstrate improved adolescent desistance rates, there is at this time limited understanding of the mechanisms by which adolescent desistance or reduction in use is achieved, and of the risk or protective factors that influence these outcomes, whether in or out of the context of treatment. Thus, while appealing treatment programs have been developed for therapy with adolescent substance abusers (MacPherson, Frissell, Brown et al., 2006), the evidentiary base for identifying particular components of therapy as critical for successful outcome, or particularly efficacious with particular adolescents, does not yet exist. This is further complicated by substantial comorbidity between substance use disorders and the range of psychiatric disorders, particularly disruptive behavior disorders, and mood disorders. Despite high rates of comorbidity, there is relatively little research evidence addressing the extent to which specific treatment approaches may be best suited for specific patterns of co-occurring substance use and psychiatric disorders. In summary, randomized clinical trials focused on adolescent substance abusers have been rare and typically single-site (therefore of uncertain generalizability to patient populations across diverse clinical settings), underpowered and with little attention to the potential influence of comorbid conditions on clinical outcomes. Some insights can be obtained from randomized clinical trials with adult patient populations; however, such trials have the advantage of adult participants who have usually volunteered to participate precisely because they are at a point in their life where they are motivated to change their pattern of drug use; the challenge with adolescents, who commonly are referred to treatment through parental, school or legal influences, is much greater. Furthermore, the specific ethical challenges of clinical research with minors (requirement to obtain parental consent for participation; potential for confidentiality breach in obtaining parental consent) raise additional (but not insurmountable) difficulties. Tobacco It is common in psychiatric practice for smoking and tobacco dependence to be ignored, a peculiar oversight given that smoking accounts for a substantial proportion of early deaths in most western societies. This relative neglect of tobacco use has been no less the case for children and adolescents. While nicotine replacement therapy (NRT) has been used successfully for adult smoking cessation, an early open-label trial using nicotine patch with adolescent smokers desiring to quit reported no benefit (5% abstinence rate at 6 months; Hurt, Croghan, Beede et al., 2000), and a single underpowered clinical trial SUBSTANCE USE DISORDERS 577 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 577

failed to find a significant improvement in abstinence rates at 6 months using the nicotine patch (Grimshaw & Stanton, 2006; Moolchan, Robinson, Ernst et al., 2005). Use of amfebutamone, in combination with NRT patch, for adolescent smoking cessation has also not been found to be useful (Grimshaw & Stanton, 2006). In adults, there is a substantial clinical trial literature documenting improved smoking cessation rates with NRT (1.5- to two-fold, across a range of different modalities for nicotine administration, compared with placebo or other control group; Silagy, Lancaster, Stead et al., 2006), and some antidepressants (amfebutamone, nortriptyline; a doubling of the odds of cessation) but not selective serotonin reuptake inhibitors (Hughes, Stead, & Lancaster, 2004). There have also been promising developments using a selective α4β2-nicotinic receptor partial agonist, with a phase II trial reporting, at the 1 mg twice daily dose, increased long-term success rates compared to sustainedrelease amfebutamone and to placebo, with 48% reporting 4 or more weeks without smoking during the 6-week treatment phase (versus 33%, 17%) and continuous quit rates at 12-month follow-up also higher (approximately a three-fold increase: 14.4% versus 6.3%, 4.9%; Nides, Oncken, Gonzales et al., 2006). A phase III trial with a 12-week treatment phase has confirmed increased rates of continuous abstinence, compared with both placebo and amfebutamone, during the final month of treatment, and at follow-up at up to 52 weeks ( Jorenby, Hays, Rigotti et al., 2006). Given the weak evidentiary basis for assessing pharmacotherapy effects for adolescent smokers, and the fact that NRT products in many countries are available over-the-counter, it seems premature to conclude that pharmacotherapies for smoking cessation by adolescents will not be successful. Despite shorter smoking histories, a significant number of adolescents are smoking at levels similar to those of adults being entered into clinical trials (e.g., 20 cigarettes per day, scores on the Fagerstrom Test of Nicotine Dependence of 5 or more; Hurt, Croghan, Beede et al., 2000). However, the case for efficacy for pharmacological treatment of adolescent smokers remains to be established. Some evidence from controlled trials for efficacy of behavioral interventions for smoking cessation in adolescents has been obtained (Grimshaw & Stanton, 2006). Some of this has been generated within the theoretical framework of the Transtheoretical Model (TTM; DiClemente, Prochaska, Fairhurst et al., 1991) and, despite the considerable limitations of the TTM framework (Sutton, 2001), these studies have achieved reasonable increases in rates of adolescent smoking cessation (pooled odds ratio of 1.70 at 12 months), a testament to the loose coupling between theoretical perspective and behavioral intervention results. Cognitive–behavioral therapy (CBT) interventions (pooled odds ratio 1.87) and interventions including a motivational interviewing component (pooled odds ratio 2.05) have also shown some success. These effect sizes are generally consistent with those obtained using non-pharmacological individual or group-based treatments in adult smoking cessation (Lancaster & Stead, 2005; Stead & Lancaster, 2005). Alcoholism and Illicit Drug Use Disorders The treatment of adult alcoholism has shifted from inpatient to out-patient-based treatments. While this change occurred largely because of economic factors, it appears that the effectiveness of out-patient-based treatment is comparable to in-patient treatment, except in cases of serious comorbid medical or psychiatric conditions (Finney, Hahn, & Moos, 1996). Large-scale multisite randomized clinical trials of alcoholism have been limited to samples of adults. In the 1990s, the US Project MATCH (Project MATCH Research Group, 1997a,b) investigated matching client characteristics to treatments, but found approximate comparability of outcomes with the three contrasted approaches: motivational enhancement therapy (MET), which uses structured feedback to motivate the client to utilize his or her resources to change behavior; 12-step facilitation, an approach popular in the USA which makes use of the 12-step framework developed by Alcoholics Anonymous (AA) and makes attendance at and participation in AA meetings an important component of recovery; and a CBT-based approach. There is only limited evidence for the value of patient–treatment matching. There have been no multisite randomized clinical trials of pharmacotherapies for alcoholism in adolescents, and in the absence of such data, the most recent findings from large US multisite trials with adults suggest that behavioral interventions should remain the treatment of choice for adolescents with alcohol problems. In a multisite trial involving almost exclusively males, with chronic severe alcohol dependence (n = 627, median age approximately 50), supplementation of 12-step facilitation counseling with short-term (3 month) or long-term (12 month) administration of naltrexone (50 mg/ day), an opioid receptor antagonist, compared with placebo, produced no differences in time to relapse at 13 weeks, nor in percentage drinking days or drinks per drinking day, at 12- month follow-up. Substantial decreases in percent days abstinent were achieved across all conditions (from approximately 35% at baseline to 82% at 12-month follow-up), with more modest reductions in number of drinks per drinking day (from 13–14 at baseline to 9–10 at 12-month follow-up; Krystal, Cramer, Krol et al., 2001). Other studies using naltrexone have reported modest short-term and medium-term improvements in time to first drink and diminished craving, compared with placebo, with some evidence for improved outcome when combined with an intensive psychosocial treatment (Srisurapanont & Jarusuraisin, 2005). More recently, Project COMBINE (Anton, O’Malley, Ciraulo et al., 2006), using a 16-week treatment period (n = 1383, twothirds male, median age 44), found no improvements in outcome associated with use of acamprosate (a medication that had been reported to be efficacious in some European trials; 3 g/day), either alone or in combination with naltrexone or a combined behavioral intervention (CBI); a modest increase in abstinence days (versus 25% at baseline) compared with placebo plus medical monitoring (75%) under conditions of naltrexone administration (100 mg/day) plus medical monitoring (81%), or the combined behavioral intervention plus CHAPTER 36 578 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 578

medical monitoring (79%), but not both (77%), these differences being rather modest and no longer significant (but with trends in the same direction) at 12 months. While Project COMBINE was in very many respects a model for its quality control procedures, one unfortunate aspect of its design complicates interpretation of findings: a CBI-only group was included that showed worse outcomes (67% days abstinent) compared to the CBI plus placebo plus medical monitoring group. However, medical management involved an initial baseline 45-minute session with 20-minute follow-ups at 1, 2, 4, 6, 8, 10, 12 and 16 weeks, conducted by a nurse, physician, pharmacist or physician assistant, and included a focus on the alcohol dependence diagnosis and negative consequences of drinking, and the importance of medications compliance, at baseline, with review of medication compliance, adverse effects, and drinking and overall functioning, at subsequent follow-ups. The medical practitioner contact under the CBI-only condition was more limited, leaving open the possibility that it was the intermittent nurse/physician contact, combined with CBI, rather than taking of pills, that explained the improved success under the CBI plus placebo condition. From these studies of older adults one may conclude that in adults wishing to overcome problems with alcohol, substantial harm reduction may be achieved through behavioral interventions in terms of reduction in drinking days, even without the use of pharmacotherapy, as other have noted (Miller, Walters, & Bennett, 2001). Given the absence of adolescent pharmacotherapy trial data, reliance on behavioral interventions seems the preferred strategy at this time. Unfortunately, rigorous clinical trial data on the components of behavioral interventions that are effective with adolescents, and the mechanisms by which changes in drinking are achieved, are lacking: thus, the clinician is left to select from a menu of strategies that have been found to give improved outcome (e.g., motivational enhancement; cognitive–behavioral skills training), sometimes packaged as an esthetically pleasing package (MacPherson et al., 2006) but nonetheless having relatively weak empirical support to justify the necessity of individual components of the package. Although there is now considerable evidence that methadone maintenance – and other opioid agonist maintenance agents such as buprenorphine – are effective at reducing illicit opioid use (Ward, Hall, & Mattick, 1999), relatively little research has been conducted on the effectiveness of these treatments in children and adolescents. This may be a reflection of a number of factors including the lower rate of heroin dependence (relative to tobacco or alcohol) in the general population, the later mean age of onset of this disorder and a widespread belief among clinicians that maintenance therapies are better suited to older individuals with a long-term history of chronic heavy opioid use. Nonetheless, findings from the limited adolescent-focused research converge on those from larger, more carefully controlled studies with adult samples to suggest that methadone (and, by extension, other maintenance therapies) is likely to be effective in reducing long-term use of heroin and other illicit opioids in those adolescents who have developed severe dependence (Kellogg, Melia, Khuri et al., 2006). There is considerably less research on pharmacotherapies for cannabis or other illicit drugs, although there are a number of possible therapies being considered for use. These include the use of antidepressant medication, particularly among those with comorbid substance use disorders and major depressive disorder (Cornelius, Clark, Bukstein et al., 2005), the use of CBI agonists specifically for tobacco dependence (Cohen, Kodas, & Griebel, 2005), and maintenance stimulant prescription for treatment of cocaine and other illicit stimulant dependence (Grabowski, Shearer, Merrill et al., 2004). There is little research evaluating these treatments empirically, what literature is available is based almost entirely on adult, rather than adolescent samples and evaluations of the efficacy of these alternative pharmacotherapies have produced, at best, equivocal results regarding their efficacy (DeLima, Soares, Reisser et al., 2002). Coerced Treatment Largely in the area of illicit drug use and related problems, there has been ongoing interest in the extent to which mandated or coerced treatment, either as an adjunct to, or in replacement of, criminal justice interventions (e.g., imprisonment), may be efficacious in reducing the use of illicit drugs and related problems (Harrison & Scarpitti, 2002). While such interventions, including so-called drug courts, have been most popular in the USA (Turner, Longshore, Wenzel et al., 2002), there is increasing interest in implementing them in other countries (Bean, 2002). Evaluations of such programs have generally shown them to be both effective and cost effective (relative to alternatives), suggesting that, provided the myriad ethical issues involved in such mandated treatment (Caplan, 2006) can be addressed, they may have a role in the treatment of drug use problems, particularly among those more severely afflicted. Similarly, diversion from the criminal justice system for more minor drug offences (principally possession of small amounts of cannabis) may be an effective strategy to continue discouraging illicit drugs while avoiding imposing the potentially heavy individual consequences of a drug conviction for what may be relatively minor drug use (Barratt, Chanteloup, Lenton et al., 2005). As with many issues surrounding the legal status of illicit drugs and legal approaches to limiting the use of licit drugs (e.g., taxation, licensing hours), consideration of such interventions raises a number of social, political and ethical issues, the resolution of which may be only slightly influenced by empirical evidence of effectiveness. Brief Interventions Spanning the intersection of treatment and public health interventions, there has also been considerable interest in the extent to which brief interventions, targeted at individuals who may be using substances heavily but who are not seeking treatment SUBSTANCE USE DISORDERS 579 9781405145497_4_036.qxd 29/03/2008 02:51 PM Page 579

nor necessarily meet criteria for a substance use disorder, may reduce substance use and/or prevent escalation to heavier, problematic or dependent use. Evaluations of such interventions have been conducted in a number of settings including general medical practices, hospital emergency departments and other health care providers and have generally been positive. For example, in a sample of 152 13- to 17-years-olds presenting at an emergency department after an alcohol-related event, Spirito, Monti, Barnett et al. (2004) reported that a brief intervention involving motivational interviewing reduced the average number of drinking days per month and frequency of heavy drinking at 12-month follow-up, relative to those receiving standard care. Similarly, Colby, Monti, O’Leary Tevyaw et al. (2005) reported 6-month follow-up in a group of 85 14- to 19-year-olds randomized to receive a brief intervention or no intervention for tobacco use, delivered in medical settings (hospital out-patient or emergency departments). Results indicated some reductions in smoking among those treated, but overall reductions were small. Whereas the bulk of brief interventions with adolescents have been targeted at either tobacco or alcohol use, there is emerging evidence of their feasibility for use with cannabis use (Martin, Copeland, & Swift, 2005) and across multiple substances, including illicit drugs (McCambridge & Strang, 2004). Prevention Legislative Approaches Aimed at Limiting Availability of and Access to Substances Among Youth These include policies regulating the sale and availability of alcohol (Chikritzhs & Stockwell, 2006; Stockwell & Grunewald, 2004), restrictions on the sale of alcohol and tobacco to youth (Ahmad & Billimek, 2007; Wagenaar & Toomey, 2002), as well as legal prohibitions against the supply and possession of cannabis and other illicit drugs (MacCoun & Reuter, 2001). In terms of the licit drugs – tobacco and alcohol – there seems to be considerable evidence supporting the efficacy of legal and policy approaches limiting access to these substances among youth. Research indicates that raising the minimum legal age for purchasing alcohol results not only in a reduction in use, but also a reduction in alcohol-related harm among youth (Wagenaar & Toomey, 2002), while demonstrated price elasticity of cigarettes indicates that raising prices through the imposition of taxation is likely to decrease both the prevalence of smoking among youth and the frequency of smoking among youthful smokers (Hopkins, Briss, Ricard et al., 2001; Zhang, Cohen, Ferrence et al., 2006). Evidence in favor of legal sanctions for reducing illicit drug – and especially cannabis – use appears more mixed (MacCoun & Reuter, 2001) with crossnational comparisons indicating that lifetime prevalence of cannabis use is lower in some countries that have relatively liberal legal approaches (e.g., the Netherlands) compared to countries with more restrictive legal approaches (e.g., the USA; Vega, Aguilar-Gaxiola, Andrade et al., 2002) highlighting that differences in legal approach alone cannot explain the often quite large differences between countries in rates of substance use and substance use disorders. Community and Mass Media Campaigns There have also been a variety of media campaigns or interventions including both laws to limit or eliminate tobacco or alcohol advertising and mass media campaigns designed to limit or reduce licit and illicit drug use. Within the tobacco field there is evidence that such campaigns can be successful (Farrelly, Niederdeppe, & Yarsevich, 2003), although it is uncertain what specific components of these campaigns are likely to be most effective. Similarly, some alcohol-related campaigns, focused primarily on reducing alcohol-related harm rather than alcohol use per se, have been shown to be effective in reducing such behaviors (Elder, Shults, Sleet et al., 2004), although, to the extent that these have often be implemented in the context of a comprehensive array of interventions, it is often difficult to isolate the impact of a specific intervention. Within the illicit drug field, it has also been recently suggested that there may be a synergistic effect between media and school-based interventions aimed at reducing the uptake of illicit drugs. Thus, the greatest benefit of these programs may be in helping to provide a milieu that is supportive of and conducive to other more intensive interventions by helping to create a social milieu that is generally supportive of drug abstinence. School and Educational Interventions A variety of school-based interventions – including both knowledge-based educational programs and others focused more broadly on social skills, assertiveness and related training – have been widely adopted. Nonetheless, the enthusiasm with which such programs are adopted appears to be unmatched by empirical evidence of efficacy or effectiveness. Indeed, there is controversy surrounding the extent to which some such interventions – and particularly those focused on imparting knowledge about drugs – may actually increase experimentation and use of these substances. Nonetheless, there is some evidence that well-conducted interventions not focusing on drug knowledge but instead focusing on social skills training may lead to consistent, yet modest, reductions in drug use uptake (Faggiano, Vigna-Taglianti, Versino et al., 2005). Increasingly in the USA there has been interest in implementing drug-testing procedures whereby students are tested on a regular basis. Comprehensive assessments of the efficacy of such programs appear lacking and, whereas a study indicated that rates of self-reported drug use did not differ between schools with drug testing programs and those without (Yamaguchi, Johnston, & O’Malley, 2003), problems with the interpretation of such findings (in particular, the fact that there are likely to be pre-existing differences in rates of drug use between schools that adopt such measures and those that do not), mean that it is difficult to draw any firm conclusions regarding the utility of such programs. 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Parenting Programs Interventions aimed at parents include broad communitybased interventions, such as media campaigns discussed above, more family focused interventions aimed at delaying or preventing substance use in adolescents (Gerrard, Gibbons, Brody et al., 2006; Komro, Perry, Veblen-Mortenson et al., 2006) and highly intensive interventions, typically targeted at families identified as “high risk” (Fergusson, Grant, Horwood et al., 2005; Olds, Robinson, Pettitt et al., 2004). Such interventions often address a range of risk factors and, while not targeted specifically at substance use, likely have the advantage of limiting risk across a range of adverse outcomes including substance use, delinquency and psychiatric disorder. Harm Reduction Initiatives Whereas a major focus of many prevention efforts involves the delay or avoidance of substance use onset and/or cessation of use (particularly for tobacco and the illicit drugs), there are also a number of interventions aimed at limiting or reducing the harm caused by substance use, even if substance use itself continues. These include campaigns that aim to reduce alcoholrelated harm not necessarily by reducing alcohol consumption but by reducing driving under the influence (Elder, Shults, Sleet et al., 2004). Similarly, needle and syringe exchange programs have been successful in reducing transmission of bloodborne viruses without reducing drug use per se (Lurie & Drucker, 1997; Wodak & Cooney, 2006), although it is also important to note that, despite claims by critics of these programs, there is no evidence indicating that such programs increase either the prevalence of drug use or the frequency of drug use among users (Fisher, Fenaughty, Cagle et al., 2003). Conclusions Throughout this chapter we have emphasized the need for greater attention to be paid to adolescent substance use and dependence, both in clinical practice and in research. We have tried to draw attention to areas of uncertainty in the literature on adolescent substance use disorders, including uncertainty concerning classification and diagnosis, etiology, consequences of adolescent substance use and substance use disorder, and treatment, prevention and intervention strategies. We have also attempted to encourage critical awareness of the limitations of many existing research strategies. We have done so because we see this area of research as being extraordinarily rich in opportunities for rapid research advances, but currently underserved by the research community. Given the long-term economic costs of substance use disorders in most western societies and their origins in adolescence, and the immediate personal, family and societal costs of adolescent substance use disorder, the relative neglect of this area of research cannot be justified. The problem of adolescent substance use and substance use disorders, more than most areas of child and adolescent psychiatry, also has a strong societal component. As the substantial reductions in rates of smoking that were achieved in California illustrate (Fichtenberg & Glantz, 2000), much can be achieved through local and national policies to reduce rates of adolescent (and adult) substance use. 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