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Adults with substance use disorders (SUD; alcohol or drug abuse or dependence) were evaluated to determine if childhood-onset psychopathology preceded the onset of SUD. Using structured psychiatric interviews, we assessed 47 clinically referred adults with SUD (27 with opioid dependence and 20 with alcohol dependence), with attention to childhood-onset psychopathology. A sequence of psychopathology and SUD was reconstructed using mean diagnosis onset data. Sixty-two percent of the 47 SUD adults (mean age 39.3±6.6 years) had early-onset SUD (defined as ≤18 years) and 38% had late-onset SUD (≥19 years at onset). Psychopathology preceded the onset of SUD in 56% of adults. Attention deficit/hyperactivity disorder, multiple anxiety, and disruptive disorders typically preceded the onset of SUD; in contrast, mood disorders (specifically depressive and bipolar disorders) followed the onset of SUD. The majority of clinically referred adults with SUD had psychopathology that began in childhood, frequently preceding the onset of their SUD. These findings further highlight the importance of targeting antecedent disorders for preventive and early intervention programs aimed at reducing the risk for SUD.

Objective Previous work in adults has suggested that early-onset bipolar disorder (BPD) is associated with an elevated risk for substance use disorders (SUD). To this end, the authors assessed the risk for SUD in child- versus adolescent-onset BPD with attention to comorbid psychopathology. Method All youths (aged 13–18 years) with available structured psychiatric interviews were studied systematically. From clinic subjects ( N = 333), 86 subjects with DSM-III-R BPD were identified. To evaluate the risk for SUD and BPD while attending to developmental issues, the authors stratified the BPD sample into those with child-onset BPD (≤12 years of age, n = 50) and those with adolescent-onset BPD (13–18 years of age, n = 36). Results In mid-adolescence, youths with adolescent-onset BPD were at significantly increased risk for SUD relative to those with child-onset BPD (39% versus 8%; p =.001). Compared with those with child-onset BPD, those with adolescent-onset BPD had 8.8 times the risk for SUD (95% confidence interval=2.2–34.7; x 2 7 = 9.7, p=.002). The presence of conduct disorder or other comorbid psychopathology within BPD did not account for the risk for SUD. Conclusions Adolescent-onset BPD is associated with a much higher risk for SUD than child-onset BPD, which was not accounted for by conduct disorder or other comorbid psychopathology. Youths with adolescent-onset BPD should be monitored and educated about SUD risk. The identification and treatment of manic symptomatology may offer therapeutic opportunities to decrease the risk for SUD in these high-risk youths.

Despite the increasing awareness of attention deficit hyperactivity disorder (ADHD) in adults, psychotherapeutic interventions for this group remain unstudied. In this study we evaluated the potential benefit of an adapted form of Beck's Cognitive Therapy (CT) for adults with ADHD. Consecutive outpatients with DSM-III-R ADHD treated naturalistically with CT were evaluated for response to treatment using multiple variables assessed both prospectively, and by retrospective review of the medical charts. As a result 26 adults with ADHD were identified of whom all had received prior psychotherapy, 96% had lifetime psychiatric comorbidity with ADHD, and 85% were receiving medications in combination with CT. Patients were treated for a mean (±SD) of 11.7 ± 8 months and 36 ± 24 sessions. Treatment was associated with significant improvements in ADHD, anxiety, and depressive symptoms as well as overall global functioning (p's Attention Deficit Hyperactivity Disorder (ADHD) is an increasingly recognized disorder in adults (Bemporad & Zambenedetti, 1996; Hallowell, 1995; Murphy & Barkley, 1996; Ratey, Greenberg, Bemporad, & Lindem, 1992). In addition to survey studies which indicate that up to 5% of adults may have ADHD (Murphy & Barkley, 1996), ADHD has been demonstrated to be overrepresented in clinical samples of adults with depression and substance abuse (Alpert et al., 1996; Wilens, Spencer, & Biederman, 1995). Conversely, ADHD adults have higher rates of cooccurring depressive anxiety, substance use, and antisocial disorders than corresponding controls (Biederman et al., 1993; Shekim, Asarnow, Hess, Zaucha, & Wheeler, 1990). Although pharmacotherapy remains a mainstay of treatment for adults with ADHD (Wilens, Biederman, & Spencer, 1998), a substantial minority of medicated patients continues to manifest residual ADHD symptomatology and impairment related to ADHD, its comorbidity, and associated sequel (McDermott, 1998). Although not tested under controlled conditions, traditional psychotherapies have been reported to be generally ineffective in treating ADHD adults (Ratey et al., 1992). Hence, a great need exists for the development of effective interventions for adults with ADHD. A recent adaptation of CT for ADHD adults has been proposed by McDermott and is presented in detail elsewhere (McDermott, 1998). These modifications are based on an analysis of the cognitive and emotional components of ADHD, their sequel, and their impediments to standard CT treatment in ADHD adults. This adaptation of CT is based on targeting specific ADHD symptoms (Millstein, Wilens, Biederman, & Spencer, 1998), associated psychopathological conditions (Biederman et al., 1993; Shekim et al., 1990), and cognitive schemes/beliefs in ADHD adults (McDermott, 1998). Moreover, an important component in McDermott's CT model is the concomitant use of pharmacotherapy directed at the ADHD and other psychiatric comorbidities. We now report on results from a systematic assessment of the usefulness of McDermott's adaptation of CT for ADHD (McDermott, 1998) naturalistically administered to 26 largely medicated adults with ADHD. Based on the literature, we hypothesized that the adapted form of CT for ADHD adults (McDermott, 1998) would be effective in reducing ADHD symptomatology, comorbidity, and impairment associated with ADHD. To our knowledge, there are no other reports of focused CT for ADHD adults. METHODS This was an exploratory, retrospective chart review of consecutively referred adults treated naturalistically with a novel, ADHD-based CT for at least 1 month by an experienced cognitive therapist (S. …

As part of a pilot-controlled family-based study of the children of parents with and without substance use disorders (SUD), the influence of parental SUD and ADHD on the risk for ADHD in offspring was evaluated. Using structured psychiatric interviews, 96 families (183 youth; mean age 11.6 years) were assessed. To evaluate the effect of parental ADHD and SUD, the offspring were stratified into four groups based on parental status: children of parents with neither ADHD nor SUD, children of parents with SUD only, children of parents with ADHD only, and children of parents with both ADHD and SUD. Using generalized estimating equation models, parental SUD and ADHD were used to predict ADHD in the offspring. The rate of children with ADHD increased among children of parents with neither disorder (3%), children of parents with SUD (13%), children of parents with ADHD (25%), and children of parents with both ADHD and SUD (50%) (p = .001). Children of parents with ADHD or ADHD plus SUD were more likely to have ADHD in comparison to children of parents with neither diagnosis (p < 0.05). Children of parents with ADHD plus SUD were at greater risk of ADHD in comparison to children of parents with SUD only (p = 0.01). Despite the small sample size, the results of this study seem to suggest that the offspring of SUD or ADHD parents are at elevated risk for ADHD compared to controls. The offspring of parents with both ADHD and SUD appear to be at the highest risk for ADHD, highlighting the need for careful screening of this group of youth for ADHD. Replication studies clarifying the nature and strength of the association are necessary.

In this article, the author sought to use a high-risk study design focused on the children of parents with opioid or alcohol use disorders and children of parents with no substance use disorder (SUD) to evaluate the specificity of the risk conferred by the type of parental SUD. Using structured psychiatric interviews, cognitive assessments, and measures of social, academic, and family functioning, the authors studied 96 families (187 parents and 183 children, mean age of 11.6 years). Sixteen families had parental opioid dependence (22 children; 64% male), 14 families had parental alcohol dependence (22 children; 59% male), and 66 families had no SUD (controls; 139 children; 58% male). Fifty-nine percent of children of opioid-dependent parents had at least one major psychopathological condition, compared to 41% of the alcohol group and 28% of the control group (p < 0.01). The children of opioid- and alcohol-dependent parents were of lower socioeconomic status and had significantly more difficulties in academic, social, and family functioning than did controls. Children of opioid- and alcohol-dependent parents have significantly higher rates of psychopathology as well as more difficulties in academic, social, and family functioning compared to the children of non-SUD parents. In addition, notable trends emerged for the opioid group to have more psychopathology and functional impairment than the alcohol group. With a growing consensus that certain risk factors for later SUD start in childhood with potentially treatable childhood-onset disorders, new preventive approaches for individuals at risk may be developed targeting childhood precursors of SUD.

Despite emerging literature linking juvenile bipolar disorder (BPD) and substance abuse, little is known about a link between BPD and cigarette smoking. To this end, we evaluated the association between BPD and cigarette smoking in youth. Subjects were 31 bipolar adolescents derived from a cohort of boys with DSM-III-R ADHD (N = 128) and non-ADHD comparisons (N = 109) followed prospectively for 4 years into mid-adolescence. Information on cigarette smoking was obtained in a standardized manner blind to the proband's clinical status. Logistic regression models were used to determine risk for smoking at follow-up. BPD was associated with a higher risk for cigarette smoking in mid-adolescence, which was largely accounted for by conduct disorder. The developmental onset of BPD in adolescence (age 13-18 years) conferred a greater risk for cigarette smoking compared to those youths with the onset of their BPD prepubertally (< or = 12 years; odds ratio = 10.8, p < 0.01), even after controlling for conduct disorder and other confounds. The naturalistic treatment of BPD with combined counseling and pharmacotherapy appeared to reduce the risk for cigarette smoking. BPD, particularly when it onsets in adolescence, is a significant risk factor for the early initiation of cigarette smoking in these ADHD youths. These data coupled with the literature strongly suggest that juveniles with BPD need to be carefully monitored for the early initiation of cigarette smoking and substance abuse.