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Book Title: Treating and Preventing Adolescent Mental Health Disorders  > pp. [410]-[414]
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pressive symptoms, intrusive memories, and hyperarousal symptoms often associated with PTSD (Davies, Gabbert, & Riggs, 2001; Lohman et al., 2002). Benzodiazepines are contraindicated for anxiety disorders in patients with substance dependence because of their well-known abuse potential.
Pharmacotherapy in Adolescents: Special Considerations in Treating Comorbidity
If the adolescent has a comorbid disorder for which medication is being considered (e.g., ADHD, major depression), abstinence is ideal before initiating medication for comorbidity. However, abstinence is not a realistic goal for many adolescent patients. Clinicians must therefore weigh the risk of potential drug–medication interactions against the risk that the untreated psychiatric illness will thwart treatment engagement or precipitate early dropout. Once the adolescent is engaged in substance abuse treatment, both urine drug screening and self-report should indicate either abstinence or significant reduction in substance use, although it is often necessary to tolerate some ongoing alcohol or cannabis use. The mental health professional or psychiatrist should then develop a plan for regular drug abuse monitoring (e.g., urine toxicology, breath alcohol) and for information exchange regarding compliance with substance treatment, urine toxicology results, target symptom response, and emergence of adverse side effects. When initiating medications, the patient should be compliant with at least weekly therapy sessions. Our clinical experience suggests benefit from motivational enhancement therapy coupled with CBT and an empathic, encouraging therapeutic style. Such an approach typically leads to successful medication stabilization for comorbidity during the first month of treatment. Early treatment of a psychiatric disorder can be critically important in facilitating treatment engagement and retention during the initial months of substance abuse treatment.
The following principles also may be helpful when using medications to treat comorbid disorders concurrently with substance dependence. First, when medication is indicated, consider medications with good safety profiles, low-abuse liability, and once-per-day dosing, if possible. Second, use a single medication if at all possible. Third, provide the patient and family with education about the potential for adverse interactions of medications with substances of abuse and the need for abstinence or reduced substance use to ensure safety and efficacy. Fourth, establish mechanisms to closely monitor medication compliance (initially weekly), adverse effects, target symptom response, and ongoing substance use (using both self-report and urine drug screening). Fifth, monitor compliance with regular substance treatment (generally, individual or family counseling at least weekly) and regular urine drug screening (if not the primary substance abuse treatment provider). Sixth, monitor patient treatment motivation and target symptom response as well as behavior changes and psychosocial functioning throughout treatment. If substance abuse or target symptoms of the comorbid disorder do not significantly improve within the first 2 months after initiating treatment, or if there is evidence of escalation in drug abuse or clinical deterioration, consider several options. First, evaluate the medication efficacy and change the medication. Second, reassess the diagnostic formulation (e.g., bipolar vs. unipolar depression). Third, increase the treatment intensity (frequency or level of care). Adherence to these principles should facilitate pharmacotherapy in adolescents who frequently have comorbid Axis I psychiatric disorders with their substance dependence. Medications primarily targeted at the substance dependence, such as bupropion or NRT for nicotine dependence, might also be considered, but behavior treatments should be tried first for most adolescents with primary substance dependence and no other Axis I psychopathology.
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CHAPTER 19 Prevention of Substance Use Disorders
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On the basis of findings from extensive epidemiological research, the Centers for Disease Control and Prevention (CDC) has identified a set of interrelated problem behaviors, typically originating during childhood and adolescence, that are critically important from a public health standpoint. For youths, central among these risk-related health behaviors are alcohol, tobacco, and other drug use (CDC, 2002b). Prevalence rates of alcohol, tobacco, and marijuana use among adolescents remain high. For example, recent prevalence of lifetime alcohol use among 12th graders was 80%; for cigarette use the lifetime rate was 64.7%, and for marijuana it was 49.7% (Johnston, O'Malley, & Bachman, 2000). Early initiation and use of these substances are associated with a wide range of problems, including risky sexual practices, impaired mental health functioning, and behaviors that result in unintentional and intentional injuries (CDC, 2002a; Duncan, Duncan, Strycker, Li, & Alpert, 1999; Windle & Windle, 2001). Thus, legal and moral implications aside, adolescent substance abuse must be regarded as a public health issue. The effective prevention and treatment of adolescent substance abuse, like that for any public health problem, require a clear understanding of causes and the context in which these causes operate. One cannot effectively stem a pneumonia epidemic without knowing the following:
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Which microbe or microbes produce the disease?
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Under which environmental conditions do the microbes flourish?
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Are there individual sensitivities to the infection?
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What are the most common patterns of contagion?
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To which antibiotic treatments are the microbes most sensitive?
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What are the patterns and factors associated with relapse?
Research on the origins of adolescent substance abuse is asking similar questions: How do different drugs affect the brains of different adolescents at different stages of maturation? How do environmental conditions increase or decrease the probability of substance abuse? Are there individual sensitivities to drugs of abuse that increase the risk of a substance use disorder? How do social factors produce contagion of drug abuse among adolescents? Are there specific treatments or prevention interventions for specific types of adolescent substance abuse? How do biological, psychological, and social factors account for failed prevention efforts or drug treatment relapse, and how common is it? This promising body of research carries with it the potential to create more effective approaches to the prevention of adolescent substance abuse as well as guiding treatment efforts.
THEORETICAL AND CONCEPTUAL MODELS OF PREVENTION AND CHANGE
There is no generally agreed-upon theoretical or conceptual model for prevention of substance abuse. Most prevention interventionists and researchers use both theory and empirical research to plan prevention programs. For example, Hawkins and colleagues Hawkins, Catalano, & Miller, (1992) derive a psychosocial model of drug abuse prevention based on an etiological model that incorporates laws, social norms, substance availability, the quality of the neighborhood, peer values, peer behavior, parental values, parental behavior, individual values, and individual behavior. However, there is no widespread agreement that these domains are the most salient in the cause or prevention of a drug abuse disorder. The development and implementation of a prevention intervention that efficaciously addresses all of these broad domains are daunting tasks.
RISK AND PROTECTIVE FACTORS: THE COMPLEX CAUSES OF ADOLESCENT SUBSTANCE ABUSE
It has been recognized for over 30 years that the risk for becoming a substance abuser is not equally distributed in the population. Originally this observation came from research that followed children into adulthood and used childhood demographic and psychological data to uncover pathways to an adolescent or adult sub
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stance abuse disorder. Subsequently, this view was bolstered by epidemiological surveys in the United States that revealed that only 27% of individuals who have experimentally used drugs six or more times actually progress to become daily drug users, and only about a half of young adult daily drug users go on to develop a drug abuse or dependence disorder (Robins & Regier, 1991). While it is possible that chance plays a role in the acquisition of a substance abuse problem, it is more likely that the complex interplay of risk and protective factors determine who progresses from experimentation to regular use and from regular use to problematic involvement. Furthermore, the interplay of risk and protective factors exists in a maturational context such that at some stages of human development certain biological, psychological, or social factors may be totally benign, while at other stages of development these same factors may confer considerable risk for problematic involvement with drugs of abuse. These risk factors are subject to effects of gender and ethnicity, so risk factors may operate differently in boys and girls, and in Caucasians and African Americans. To further complicate the issue, individual risk and protective factors must be viewed against a backdrop of laws, cultural and social norms, drug availability, economic circumstances, and regional and community factors. For example, a white Chicago adolescent male who has a variety of individual risk factors for alcoholism might develop alcohol problems, but if that same child were raised in Saudi Arabia (where drinking alcohol is forbidden), it is less likely that he would develop an alcohol problem. However, it is possible that these risk factors might manifest themselves in other forms of problematic behavior (e.g., aggressive behavior). Thus, substance abuse is a multifaceted problem.
Geneticists refer to multidetermined problems like substance abuse as “complex disorders” because a multiplicity of individual biological and behavioral factors interact with environmental factors (e.g., social and societal phenomena) in complicated ways across human development to produce a good or bad outcome. To the best of our knowledge, there is no single cause of adolescent substance abuse, and so it is unlikely that there will be a single preventive measure to forestall its development. For this reason, the reader is cautioned to be skeptical of overly simplistic causal explanations for substance abuse problems and of facile and obvious solutions. The likelihood that approaches guided by conventional wisdom will achieve their promised results is diminished by the realities of our current understanding of the complex pathways to a substance abuse disorder.
INFLUENTIAL THEORIES OF THE DEVELOPMENT OF ADOLESCENT SUBSTANCE ABUSE
Theories develop as an effort to summarize and explain research data generated by observation and experimentation. Theories are used to organize future research studies that ultimately test the validity of the original theory and provide an opportunity for the initial theory to evolve and undergo revision. Thus, theories are scientific “works in progress,” not facts. Several influential theories have guided our understanding of the origins of adolescent substance abuse, and provide a framework for ongoing research in this area. These theories also provide a useful structure to guide approaches to the prevention and treatment of adolescent substance abuse problems. The following are among the most influential of these theories. There are many areas of commonality and overlap; yet each has contributed and advanced our understanding of the origins of substance abuse. Other theories abound and it is noteworthy that the “general field theorem” for the vulnerability to adolescent substance abuse has yet to be fully articulated.
The “Gateway” or Stage Theory
This theory comes from epidemiological research that has examined the patterning of alcohol and other drug use progression among adolescents. However, recently this theory has become a battleground for those both for and against the decriminalization of marijuana. The theory is based on the delineation of four stages in the sequence of involvement with drugs. The original findings suggested that surveyed adoles
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cents engage in use of either alcohol or cigarettes (as legal and culturally accepted drugs) then progress to marijuana, and then on to other illicit drugs, such as heroin and cocaine. The legal drugs are necessary intermediates between nonuse and marijuana. Thus, the use of tobacco, alcohol, and marijuana by adolescents was viewed as a crucial step, or “gateway,” to the use of other illicit drugs (Kandel, 1975). However, opponents of this theory suggest that, if there were a risk factor that was common to both marijuana and other drugs, it could easily account for the relationship between both marijuana and other drug use. Examples of a theorized “third factor” include the genetic predisposition to drug use, a predisposition toward adolescent risk behavior in general, or shared opportunities to obtain both marijuana and other drugs (Morral, McCaffrey, & Paddock, 2002). Nonetheless, surveys of American high school students suggest that by 12th grade, 37% of students have tried marijuana, whereas 0.9% have tried heroin and 4.8% have tried cocaine (Johnston, O'Malley, & Bachman, 2002b). The discrepancies in these prevalence rates indicate that although hard drug users may have started with marijuana, it is clear that marijuana use does not invariably progress to adolescent use of hard drugs.
A less controversial aspect of this theory deals with age of initiation of experimentation with drugs of abuse (whether it is alcohol, tobacco, marijuana, or hard drugs), and the timing of stages of regular use and problematic involvement. The literature converges around the observation that the earlier the onset of substance use, the greater the likelihood of problematic involvement (Choi, Gilpin, Farkas, & Pierce, 2001; Choi, Pierce, Gilpin, Farkas, & Berry, 1997; Kandel & Logan, 1984; Schuckit & Russell, 1983; Yamaguchi & Kandel, 1984b). For this reason, substantial effort has been placed on prevention interventions that delay the initiation of initial substance exposure.
Problem Behavior Theory
Problem behavior theory is an influential conceptual framework for understanding not only substance abuse but a wide variety of other types of risky adolescent behaviors (Jessor & Jessor, 1977). The theory proposes that there exists a syndrome of adolescent problem behaviors that may co-occur within the same individual (Jessor, 1991). For example, those who experiment with substance use also tend to engage in risky sexual practices and illegal behavior. These adolescent problem behaviors include
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Problematic involvement with alcohol
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Illicit drug use
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Delinquent behaviors (e.g., truancy, petty theft, vandalism, lying, running away)
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Risky and precocious sexual activity
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Other high-risk behaviors (e.g., drag racing, driving drunk)
These deviant behaviors are thought to emanate from a single underlying factor (perhaps of genetic origin) that may exist prior to adolescence, resulting in a general syndrome of deviance. The risky behaviors may also be adaptive to the extent that they serve a social or maturational goal, such as separating from parents, achieving adult status, or gaining peer acceptance, and these behaviors may help an adolescent cope with failure, boredom, social anxiety or isolation, unhappiness, rejection, and low self-esteem. One example of a risk behavior syndrome is an adolescent's reported use of substances as a means of gaining social status and acceptance from peers and, at the same time, enhancing mood and feelings of low self-worth (DuRant, 1995; DuRant, Getts, Cadenhead, Emans, & Woods, 1995). Thus, this theory posits that substance abuse for some adolescents may be a maladaptive means to cope with the stresses and social pressures that are characteristic of the adolescent stage of development. This theoretical perspective suggests that prevention interventions that offer alternative means of coping and social adaptation might reduce adolescent substance use behavior.
Patterson's Developmental Theory
Patterson's theory was originally proposed to explain the development of juvenile delinquency, and however consistent with the observation
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doi:10.1093/9780195173642.003.0020
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