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Natural Course of Alcohol Use Disorders From Adolescence to Young Adulthood

ROHDE, PAUL PH.D.; LEWINSOHN, PETER M. PH.D.; KAHLER, CHRISTOPHER W. PH.D.; SEELEY, JOHN R. M.S.; BROWN, RICHARD A. PH.D. Volume 40(1), January 2001, pp 83-90 [Articles] Copyright 2001 American Academy of Child and Adolescent Psychiatry Accepted August 22, 2000. Drs. Rohde and Lewinsohn and Mr. Seeley are with the Oregon Research Institute, Eugene. Drs. Kahler and Brown are with Brown University School of Medicine, Butler Hospital, Providence, Instituciones: RI. This research was supported in part by NIMH awards MH40501, MH50522, and MH52858. Reprint requests to Dr. Rohde, Oregon Research Institute, 1715 Franklin Boulevard, Eugene, OR 97403-1983; e-mail: paulr@ori.org. Palabras clave: alcohol use disorders, course, comorbidity
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ABSTRACT
Objectives: To examine the course of alcohol use disorder (AUD) and determine the extent to which AUD in adolescence is a risk factor for AUD and other psychopathology in young adulthood. Method: Nine hundred forty participants from a large community sample in western Oregon were interviewed twice during adolescence (1418 years of age the first assessment; between 1987 and 1991) and once at age 24 (19931999). Between 1995 and 1998, parents were assessed for lifetime AUD. Participants were classified into nonproblematic use (NON), problem drinker (PROB) (symptoms of AUD but no diagnosis), and AUD groups. Results: Adolescent AUD significantly predicted AUD, substance use disorder, depression, and elevated levels of antisocial and borderline personality disorder symptoms by age 24. Compared with the NON group, adolescents in the PROB group were at increased risk for AUD, substance use disorder, depression, and antisocial personality disorder symptoms. However, the PROB group had lower rates of future AUD and antisocial personality disorder symptoms than the adolescent AUD group. Gender interactions were nonsignificant. Daily smoking and conduct/oppositional defiant disorders predicted future AUD, when adolescent AUD and other disorders were controlled. Paternal, but not maternal, AUD was associated with greater risk of future AUD. Conclusions: For the majority of adolescents, AUD are not benign conditions that resolve over time. Assessment, treatment, and prevention recommendations are discussed.

Problematic alcohol consumption tends to begin early in life. Among adults in the Epidemiologic Catchment Area study with a lifetime diagnosis of alcohol use disorder (AUD) (abuse or dependence), more than 80% developed their first symptoms before age 30 and more than 35% had developed at least one symptom between the ages of 15 and 19 (Helzer and Burnam, 1991). Knowledge of the longitudinal course of AUD is essential to determine the prognosis of these disorders and to understand the continuities and discontinuities between adolescent and adult psychopathology. Longitudinal information also provides an opportunity to examine diagnostic validity (e.g., Hasin and Paykin, 1999). Our primary goal in the present study was to examine the extent to which AUD in adolescence is a risk factor for AUD in young adulthood. This study is the third in a series focusing on the patterns and consequences of alcohol consumption in the Oregon Adolescent Depression Project (OADP), a large community sample of older adolescents (1418 years of age) who were initially assessed for depression, AUD, and other psychiatric disorders at two time points (T1 and T2) over a 1-year period. The first article in this series (Lewinsohn et al., 1996) presented information regarding the occurrence, frequency, and structure of alcohol use and AUD during adolescence. Although regular alcohol use was not a frequent occurrence, approximately three quarters of the sample had tried alcohol, and those adolescents who drank often consumed large quantities of alcohol. Six percent met criteria for a lifetime diagnosis of AUD, and an additional 17% had problematic alcohol use, as indicated by the occurrence of behaviors that met criteria for one or two DSM-IV symptoms of alcohol dependence but not AUD. The second paper in this series (Rohde et al., 1996) delineated the degree to which various levels of problematic alcohol use were associated with psychiatric disorders in adolescence. More than 80% of adolescents with AUD had some form of comorbid psychopathology, with increased rates of depressive disorders, disruptive behavior disorders, drug use disorders, and daily tobacco use. There was a trend for increased alcohol use in girls to be associated with anxiety disorders. AUD, in general, followed rather than preceded the onset of other psychiatric disorders. Psychiatric comorbidity was associated with an earlier age of AUD onset and with a greater likelihood of mental health treatment. In this study, we extend our research by following the sample into young adulthood. Problematic alcohol use does not occur in isolation. In previous research, primarily with adult samples, heavy alcohol consumption and AUD have been found to have the highest degree of comorbidity with other substance use disorders (SUD), disruptive behavior disorders, personality disorders (especially antisocial and borderline), and habitual cigarette smoking (e.g., Costello et al., 1999; Deykin et al., 1987; Helzer and Burnam, 1991; Kandel et al., 1997; Kessler et al., 1997; Merikangas et al., 1998). Less robust associations have been noted between AUD and mood and anxiety disorders (e.g., Grant and Harford, 1995; Regier et al., 1990). Given this degree of comorbidity, the second goal of this study was to examine whether adolescent AUD potentiates the development of other disorders during young adulthood. Problematic alcohol use occurs on a continuum. It has been suggested (e.g., Martin et al., 1996) that traditional diagnostic criteria for alcohol abuse and dependence may miss individuals whose drinking is clinically significant, especially in adolescence, when AUD symptoms are first coming into existence. For this reason, adolescents with AUD were contrasted with two comparison groups: adolescents who reported problematic alcohol use (i.e., experiencing symptoms of AUD but no

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diagnosis) and adolescents with no history of alcohol abuse or dependence symptoms. The presence of other psychiatric disorders during adolescence and a family history of AUD are examined as two potential predictors or moderators of the course of AUD. Mental disorders in childhood and adolescence, especially conduct disorder, have been shown to be associated with or to predict AUD (e.g., Cohen et al., 1993; Costello et al., 1999; Kandel et al., 1997), and parental AUD is a well-established risk factor for problematic alcohol use in adults and adolescents (e.g., Chassin et al., 1991; Merikangas et al., 1998; Sher, 1991). We examined whether each variable predicted AUD in young adulthood, after controlling for the effects of adolescent AUD. Finally, because gender differences in the prevalence of AUD are marked (e.g., Helzer and Burnam, 1991; Kessler et al., 1997), we examined the degree to which gender affected the course of AUD.

METHOD
Participants and Procedures
T1 and T2 Assessments. A total of 1,709 adolescents, randomly selected from nine high schools in western Oregon (ages 1418; 61% participation) completed the initial (T1) assessments between 1987 and 1989 (see Lewinsohn et al., 1993, for additional details). Approximately 1 year later (T2), 1,507 participants (88%) returned for a readministration of the interview and questionnaire (mean T1-T2 interval = 13.8 months, SD = 2.3). Although differences between T2 participants and those who discontinued participation were small (Lewinsohn et al., 1993, 1996), T1 participants who failed to participate at T2 were significantly (p < .05) more likely to have used alcohol prior to T1 (82% of T2 nonparticipants versus 75% of T2 participants), reported a higher T1 quantity of alcohol consumed per drinking episode (mean on 8-point scale: 3.3 for nonparticipants versus 2.8 for T2 participants), and reported a greater lifetime number of times being drunk (mean on 5-point scale: 2.8 for nonparticipants versus 2.1 for T2 participants). Differences between the two groups in lifetime and current diagnoses of AUD and frequency of current drinking at T1 were nonsignificant. T4 Assessments. Between 1993 and 1999, as participants reached their 24th birthday, all individuals with a history of psychopathology and a randomly selected set of participants with no history of mental disorder were invited to the T3 telephone interview ( N = 1,101). Sampling of the no-disorder comparison group was proportional to age and gender within age; all participants with nonwhite ethnicity were retained in the sample. Data were obtained from 940 individuals (85% participation), with a mean interval between T2 and T3 of 6.8 years (SD = 1.4). Attrition at T3 was related to gender (57% of T3 participants were female versus 42% of T3 nonparticipants; [chi] 2 [1, N = 1,101] = 13.54, p < .001) and T2 age (T3 participants mean = 17.8 [SD = 1.3] versus T3 nonparticipants mean = 17.5 [SD = 1.2] years old; t 1,095 = 2.64, p < .01), but was unrelated to ethnicity, parental education, residing with both biological parents at T2, or alcohol use or AUD at T2. Given their small numbers and the severity of their psychopathology, 32 participants with a history of bipolar disorder or schizophrenia were deselected from the present study. Parents. Biological parents of T3 participants were recruited and interviewed for lifetime AUD, with the goal of obtaining two sources of data for each parent (either direct and informant interviews or two informant interviews). Data were obtained between 1995 and 1998 on 800 mothers (85%; direct interview = 64%) and 785 fathers (84%; direct interview = 39%).

Diagnostic Interviews: OADP Participants

T1 and T2. Adolescents were interviewed at T1 with a version of the Schedule for Affective Disorders and Schizophrenia for School-Age Children (Orvaschel et al., 1982). Participants at T2 were interviewed with the Longitudinal Interval Follow-up Evaluation (Keller et al., 1987), which provided detailed information about the onset and course of disorders since the T1 interview. Although designed to collect information according to DSM-III-R criteria, information was collected in the T1 and T2 interviews to ascertain AUD symptoms as per DSM-IV criteria. Five additional diagnostic categories were examined for occurrence before T2: (1) SUD ( n = 101, 11.1%); (2) depressive disorders (DEP) (combining major depressive disorder and dysthymia) (n = 314, 35%); (3) anxiety disorders (ANX) ( n = 107, 12%); (4) conduct or oppositional defiant disorders (CD/ODD) ( n = 54, 6%); and (5) daily smoking (n = 193, 21%), which was selected as a proxy measure of nicotine dependence. All interviews were recorded, and 12% were randomly selected and reviewed by a second interviewer. With few exceptions, interrater [kappa] values (Cohen, 1960) for current and lifetime diagnoses at T1 and T2 exceeded 0.80, and reliabilities for lifetime and current AUD were excellent ([kappa] = 0.84 and 0.91, respectively). T3. The T3 interview repeated the T2 procedures, expanding the interview to assess all disorders as per DSM-IV criteria. Interrater reliability ranged from very good to excellent (Rohde et al., 1997); AUD reliability between T2 and T3 was [kappa] = 0.77. The T3 interview also used relevant portions of the Personality Disorder Examination (PDE) (Loranger, 1988) to assess antisocial and borderline personality disorders. Interrater reliability of the PDE dimensional scores (i.e., summation of partial and full symptom criteria) was excellent (intraclass correlation coefficients > 0.80). The PDE dimensional scores were dichotomized at approximately the 90th percentile (antisocial cutoff score > 7; borderline cutoff score > 4). On the basis of adequate prevalence rates, seven T2-T3 diagnostic categories were examined: (1) AUD ( n = 243, 27%); (2) SUD (n = 143, 16%); (3) DEP ( n = 295, 33%); (4) ANX ( n = 97, 11%); (5) antisocial personality disorder symptoms (n = 44, 5%); (6) borderline personality symptoms ( n = 82, 9%); and (7) daily smoking ( n = 100, 11%).

Diagnostic Interviews: Parents

Parents took part in telephone interviews for AUD with the Structured Clinical Interview for DSM-IV , Nonpatient Version (First et al., 1996; Williams et al., 1992). Family history information was obtained with a modified version of the Family Informant Schedule and Criteria (Klein et al., 1994; Mannuzza and Fyer, 1990). Interviewers were blind to proband diagnosis and assessed no more than two relatives per family. Best-estimate diagnoses were independently derived by pairs of senior clinical psychologists who were blind to information about the probands; disagreements were resolved by consensus. Interrater reliability for lifetime AUD in a randomly selected subsample of family members (n = 157) was excellent ([kappa] = 0.97). A total of 129 mothers (16%) had lifetime AUD (67 abuse, 62 dependence); 326 fathers (42%) had lifetime AUD (154 abuse, 172 dependence). Failure to obtain parental AUD data was unrelated to rates of AUD (T2 lifetime or T2-T3) or demographic variables in the probands, with one exception: parents of nonwhite participants were more likely to decline participation (20% versus 9%; [chi]2 [1, N = 908] = 14.3, p < .001).

Sample for the Present Study

On the basis of AUD symptoms occurring before T2, participants were classified into three adolescent alcohol use groups: (1) nonproblematic use (NON) (n = 685, 75%), defined as no DSM-IV symptoms of alcohol abuse or dependence; (2) problem drinkers (PROB) ( n = 141, 16%), defined as one or two symptoms of alcohol dependence but no AUD diagnosis; and (3) AUD ( n = 82, 9%), defined as a lifetime DSM-IV diagnosis of alcohol abuse ( n = 23) or dependence ( n = 59).

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So that adolescent versus young adult AUD and chronic AUD versus recovery and recurrence could be more clearly differentiated, 20 participants (2%) with AUD at T2 were omitted from the analyses of the course of AUD. Of these 20 participants, 2 (10%) remained in an AUD diagnosis for the entire T2-T3 period, 3 (15%) escalated from alcohol abuse to dependence, 5 (25%) recovered from the AUD but experienced a recurrence before T3, and the remaining 10 (50%) recovered from the AUD at some point after T2 and did not experience a recurrence by T3. Demographic characteristics of participants in the three adolescent alcohol groups are shown in Table 1. Because there were significant group differences in T2 age and T1 household composition, these variables, in addition to gender, were controlled for in subsequent analyses.

TABLE 1 Demographic Characteristics of the Three Diagnostic Groups at Times 1 and 2Note: Means or percentages having the same superscript letter are not significantly different at p < .05. AUD = alcohol use disorder diagnosis; PROB = problematic alcohol use; NON = nonproblem (no symptoms of alcohol abuse or dependence).* p < .05; *** p < .001.

RESULTS
Effects of Demographic Variables on AUD in Young Adulthood
When other demographic variables and adolescent alcohol group were controlled for (AUD versus PROB and NON), male gender increased the likelihood of AUD diagnosis between T2-T3 (adjusted odds ratio [OR] = 2.41, 95% confidence interval [CI] = 1.773.30). In addition, participants who were younger at T2 had a higher likelihood of AUD by T3 (adjusted OR = 1.15, 95% CI = 1.011.32), probably because they had a longer time interval between the T2 and T3 interviews.

Psychopathology in Young Adulthood as a Function of Adolescent Alcohol Group

Table 2 shows the frequency of psychiatric disorders occurring between T2 and T3 as a function of T2 alcohol group status. To ensure that the included disorders were new episodes (as opposed to continuations of an adolescent-onset episode), participants in a current episode of the disorder of interest at T2 were deselected from that specific analysis. Occurrence of each disorder in the adolescent AUD group was contrasted with the combined PROB and NON groups, followed by two planned contrasts: AUD versus PROB and PROB versus NON. Group differences were evaluated with hierarchical logistic regression models, with the adolescent alcohol group entered as the first block. If a significant effect was found, the OR (with 95% CI) for the contrast was calculated. Significant unadjusted ORs for the three contrasts are presented in Table 2.

TABLE 2 Frequency of Diagnosis in Young Adulthood as a Function of Adolescent Alcohol GroupNote: OR = odds ratio; CI = confidence interval; AUD = alcohol use disorder diagnosis; PROB = problematic alcohol use; NON = nonproblem (no symptoms of alcohol abuse or dependence); NS = nonsignificant; A vs. (P/N) = AUD versus (PROB and NON); A vs. P = AUD versus PROB; P vs. N = PROB versus NON; SUD = substance use disorder; SMOK = daily smoking; DEP = depressive disorder; ANX = anxiety disorders; BORD = elevated borderline personality disorder symptoms; ANTI = elevated antisocial personality disorder symptoms. a Adjusted for gender, T2 age, T1 family structure, and history of the respective disorder in adolescence. No adjustments for adolescent history were made for BORD or ANTI. Gender, T1 household composition, and T2 age were entered as a second block, along with adolescent history of the disorder being examined (e.g., for SUD, history of SUD at T2 was entered as a covariate; no psychiatric adjustments were made for the analyses of borderline and antisocial personality disorder symptoms). Significant adjusted ORs (with 95% CI) are shown in Table 2. In the third block of the hierarchical analysis, the interaction between adolescent alcohol group and gender was considered for entry. Adolescent AUD predicted future disorders in five of the seven categories. The PROB group was at increased risk for four of the seven categories but was at significantly less risk than the adolescent AUD group in three of seven categories. Adjustment for demographics and previous history of the outcome disorder reduced differences in the rates of future SUD between the AUD and PROB groups to the level of a trend ( p = .09); other adjusted ORs remained significant. Interactions

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between AUD and gender were nonsignificant.

Effects of Comorbid Adolescent Psychopathology on AUD in Young Adulthood

Hierarchical logistic regression models were used to assess the effects of adolescent psychopathology on AUD between T2 and T3; adolescent AUD, demographic variables, and five adolescent diagnoses (SUD, daily smoking, DEP, ANX, CD/ODD) were entered in one block. A history of daily smoking (adjusted OR = 1.67, 95% CI = 1.112.49) and CD/ODD (adjusted OR = 1.98, 95% CI = 1.053.73) predicted future AUD, when adolescent AUD and other disorders were controlled for. The other disorders and all interactions between AUD and adolescent diagnoses were nonsignificant in predicting the occurrence of AUD between T2 and T3 .

Effects of Maternal and Paternal AUD on AUD in Young Adulthood

Rates of maternal and paternal AUD were significantly higher in participants with AUD by T2 (27% and 57%, respectively) compared with the remaining adolescents (16% and 42%, respectively; [chi]2 [1, N = 773] = 5.13, p < .05, and [chi] 2 [1, N = 758] = 6.27, p < .05, respectively). Maternal and paternal AUD in the PROB group (17% and 47%, respectively) did not differ significantly from rates in either the NON (16% and 41%) or AUD (27% and 57%) groups. Maternal and paternal AUD were examined as unadjusted predictors of participant AUD between T2 and T3. Maternal and paternal AUD were then entered simultaneously into hierarchical logistic regression models, along with adolescent alcohol group (AUD versus PROB and NON) and participant demographic variables. In the bivariate model, paternal AUD was significantly associated with greater risk of future AUD (33% of participants with paternal AUD developed AUD between T2 and T3 versus 22% of participants without paternal AUD; OR = 1.70, 95% CI = 1.222.36); this association remained significant when maternal AUD, participant demographics, and adolescent AUD were controlled for (adjusted OR = 1.62, 95% CI = 1.142.29). Maternal AUD was unrelated to future AUD in the OADP participants in both the bivariate and multivariate models (31% of participants with maternal AUD developed future AUD compared with 26% of participants without maternal AUD). Interactions between parental AUD and adolescent AUD status and between parental AUD and gender were nonsignificant.

DISCUSSION
This study adds to the literature describing the longitudinal course of AUD and problematic alcohol use in a community-based sample of adolescents. As expected, there was a high degree of continuity of AUD from adolescence to young adulthood. Odds of future AUD increased in a stepwise progression, doubling in the problematic alcohol use group compared with the NON group, and doubling again in the AUD group compared with the PROB group. Overall, rates of AUD between T2 and T3 in the sample were high, which has implications for the DSM-IV diagnostic system (i.e., the relatively low threshold required for diagnosis). However, given that the average time interval between T2 and T3 was 6.8 years, the rates of AUD translate into an annual recurrence rate of approximately 8% for the adolescent AUD group and annual first incidence rates of 5% and 3% in the adolescent PROB and NON groups, respectively. Our previous research (Orvaschel et al., 1995) found that SUD (which included alcohol abuse and dependence) had among the highest rates of continuity from the first to the second episode of psychopathology during adolescence. This study extends those findings over a much longer time interval and into a new developmental period. The high degree of continuity into young adulthood increases our confidence in the clinical significance and diagnostic validity of these diagnoses during adolescence. Sher and Gotham (1999) have described several trajectories of the course of AUD in early adulthood, distinguishing between chronic (continued AUD from adolescence to young adulthood), developmentally limited (present in adolescence but diminishing by adulthood), and late onset (first becoming problematic in young adulthood). In addition to documenting the differential trajectories of problematic alcohol use from adolescence to adulthood, future research needs to identify the predictors of differential course and whether interventions can prevent or ameliorate the negative course of AUD by adulthood. Adolescents with AUD also experienced elevated rates of SUD and depression as young adults. These associations remained significant after we controlled for occurrence of the outcome disorder during adolescence. Adolescent AUD was unrelated to subsequent onset of daily smoking or anxiety disorders in young adulthood, although the prevalence rates of these two outcomes were low, which reduced our ability to detect differences. Adolescent AUD was associated with both measures of Axis II disorder, with particularly striking results for antisocial personality disorder. Numerous classification systems for alcoholism distinguish groups on the basis of antisocial personality disorder features (e.g., Babor et al., 1992; Cloninger, 1987; Hesselbrock et al., 1985; Zucker, 1987). Almost all of these typologies suggest that adult alcoholics with comorbid antisocial personality disorder have a more pernicious outcome, which emphasizes the importance of studying comorbidity in understanding the course of AUD. Consistent with the present study, Brook et al. (1998) found that daily alcohol drinking in adolescents (mean age = 16 years) was predictive of antisocial personality disorder in young adulthood (mean age = 22 years). This study also confirmed that problematic adolescent drinking at subthreshold levels should not be ignored. Compared to adolescents with no symptoms of AUD, adolescents with subthreshold problematic alcohol use had significantly higher rates of future AUD, SUD, depression, and antisocial personality disorder symptoms as young adults. The present study supports the conclusion of Sobell and Sobell (1993) that individuals experiencing subdiagnostic levels of problematic alcohol use often require treatment. Even when the presence of adolescent AUD was controlled for, a history of daily smoking and conduct or oppositional defiant disorders were significant risk factors for future AUD. Our results are consistent with research indicating that cigarette smoking is predictive of increasing alcohol use (Duncan et al., 1998) and that disruptive behavior problems often predict an early onset and faster progression of problematic levels of alcohol use (e.g., Baer et al., 1995; Costello et al., 1999; Windle and Davies, 1999). Although both paternal and maternal AUD were related to adolescent AUD, only paternal alcoholism was significantly associated with greater risk of future AUD by young adulthood. The influence of paternal AUD remained significant after we controlled for maternal AUD, participant demographics, and adolescent AUD. This finding is consistent with Chassin et al. (1996), who found that adolescents with alcoholic fathers were more likely to use substances (alcohol and other drugs) and had greater increases in their substance use over three annual assessments, whereas maternal alcoholism predicted initial substance use but not escalation at subsequent assessments. Also consistent with the present findings, Cuijpers et al. (1999) found that adult children of fathers with problematic drinking had elevated rates of SUD (including AUD, 15% versus 9% in adult children of fathers with no problematic drinking). Differences for adult children of problem-drinking and nonproblem-drinking mothers were nonsignificant (11% versus 9%, respectively). One hypothesis to explore in future research is that maternal AUD negatively impacts the offspring only when they live at home, whereas paternal AUD continues to impact the child even after he or she has left home. Although men in the sample were twice as likely to develop AUD in the period between T2 and T3, interactions with gender were nonsignificant. The absence of gender interactions suggests that young men and women with AUD do not differ significantly in the course of their alcohol disorder or in the extent to which AUD predicts other disorders. Although gender interactions in the impact of parental AUD were also nonsignificant in the present study, previous research has suggested that female offspring may be more strongly impacted than male offspring by a family history of alcoholism (e.g., Jacob et al., 1999).

Limitations
To the degree that the sample was not completely representative, conclusions from the present study are limited. There was some evidence that the early heavy

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drinkers were more likely to discontinue participation at T2. Fortunately, this potential bias did not extend to adolescents who had a diagnosis of alcohol abuse or dependence. Nonetheless, additional differences may have emerged if participation rates at various points in the study had been higher. Second, although the sample was large, the relatively low base rate of some disorders required us to aggregate diagnoses into larger categories (e.g., anxiety disorders) or not to examine other disorders (e.g., schizophrenia). A larger sample size would have also provided an opportunity to examine differences in the course of alcohol abuse versus dependence. Third, only two personality disorders were assessed. However, the two selected personality disorders have repeatedly been shown to be the most prevalent among substance abusers (e.g., Kessler et al., 1997; Poling et al., 1999). We cannot comment on the associations between AUD and the other personality disorders. Fourth, it needs to be remembered that individuals with AUD and other disorders at T2 were oversampled for the T3 interview. Thus, the prevalence and incidence rates are higher than would have been found if all T2 participants had been assessed. Finally, the sample was primarily white and middle class, and results need to be replicated with more diverse populations. Although the present study was prospective and longitudinal, we did not establish a causal connection between adolescent problematic alcohol use and subsequent alcoholism and related disorders in young adults. A number of causal associations are possible. For example, previous research has documented the physiologically depressive effects of prolonged or excessive alcohol use on adults (e.g., Schuckit and Hesselbrock, 1994).

Clinical Implications
Clearly, for many adolescents, AUD and problematic alcohol consumption are not benign conditions that self-resolve. Instead, they are often indicators of persistent and recurrent psychopathology, resulting in significant and potentially long-term dysfunction. Therefore, strong consideration should be given to the appropriate referral and treatment of these problems in order to prevent or at least reduce the severity of subsequent pathology. Assessment recommendations from the present study include the need for systematic screening of subthreshold alcohol problems. The fact that the presence of a single AUD symptom in adolescence predicted young adult AUD was striking and has important public health implications. Also, clinicians are advised to probe thoroughly for the presence of psychiatric disorders in any adolescent seeking treatment for alcoholism. Given the high degree of continuity of alcohol problems from adolescence to young adulthood, treatment recommendations should include the development of booster or maintenance treatments. Also, given the high degree of comorbidity and the risk for the development of other psychopathology, greater efforts are needed to develop empirically supported treatments for the patient who has a dual diagnosis. The presence of comorbid psychiatric disorders with AUD has been shown to be associated with poorer treatment outcome and greater suicidality, disability, and functional impairment (e.g., Regier et al., 1990). Prevention recommendations can also be offered. The present findings lead to the hypothesis that smoking prevention or cessation efforts and the treatment of childhood externalizing disorders may prevent future onset of AUD in young adulthood. Another clinical recommendation that emerges from this study is that the children of alcoholic fathers are at particularly high risk for future alcoholism, which warrants active follow-up and monitoring of their alcohol use. In addition, future research needs to examine whether modifying the levels of adolescent problematic drinking changes the development of other disorders. We cannot say that alcohol use prevention and cessation in adolescence will prevent drug abuse and dependence or depression during young adulthood. However, consistent with this suggestion, Kessler and Price (1993) have called for interventions in which the treatment of one disorder is conceptualized as a preventive intervention for a secondary, comorbid condition.

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