The findings suggest that the neural circuits engaged during decision making differ in subjects with ADHD and healthy comparison subjects. This difference may explain observed deficits in motivated behaviors in ADHD. A better understanding of the nature of these deficits could ultimately be applied to refine treatment strategies for ADHD.

OBJECTIVE. Our goal was to examine substance-use initiation in healthy adolescents and in adolescents who have been diagnosed with attention-deficit/hyperactivity disorder. METHODS. Seventy-eight adolescents (28 healthy and 50 with attention-deficit/hyperactivity disorder) participated in an ongoing longitudinal study of predictors of substance use. The substances most commonly reported were tobacco, alcohol, and marijuana. Aggression, conduct problems, hyperactivity, impulsivity, inattention, anxiety/depression, social difficulties, and somatic complaints were assessed at study entry and tested as predictors for later substance use. RESULTS. With an average of 4 years into the study, 37 adolescents had not used any substances, 41 had experimented with at least 1 substance, and 29 experimented with >1 substance. Psychiatric diagnoses (attention-deficit/hyperactivity disorder, attention-deficit/hyperactivity disorder and conduct disorder, and attention-deficit/hyperactivity disorder and depression/anxiety) did not influence reports of substance use. Distinct behavioral measures collected at study entry predicted use of different substances. In a multivariate analysis, aggression had the greatest association with tobacco smoking and marijuana use. Impulsivity was associated with alcohol use. Severity of drug exposure, indexed by the number of substances used, was predicted by aggression. CONCLUSIONS. This 4-year longitudinal study captured the onset of substance use, not abuse. Behavioral predictors differed with the type of substance used. These behavioral characteristics may raise suspicion among pediatricians for enhanced risk for substance-use initiation.

A relationship between parental substance abuse and subsequent alcohol problems in their children has been documented extensively. Children of alcoholics (COAs) are considered to be at high risk because there is a greater likelihood that they will develop alcoholism compared with a randomly selected child from the same community. COAs and children of other drug-abusing parents are especially vulnerable to the risk for maladaptive behavior because they have combinations of many risk factors present in their lives. The single most potent risk factor is their parent's substance-abusing behavior. This single risk factor can place children of substance abusers at biologic, psychologic, and environmental risk. Since the turn of the century, many reports have described the deleterious influence of parental alcoholism on their children. A series of studies measured mortality, physiology, and general health in the offspring of alcoholic parents and concluded that when mothers stopped drinking during gestation, their children were healthier. Today, research on COAs can be classified into studies of fetal alcohol syndrome, the transmission of alcoholism, psychobiologic markers of vulnerability, and psychosocial characteristics. Each of these studies hypothesizes that differences between COAs and children of nonalcoholics influence maladaptive behaviors later in life, such as academic failure or alcoholism. This research supports the belief that COAs are at risk for a variety of problems that may include behavioral, psychologic, cognitive, or neuropsychologic deficits. The vast literature on COAs far outweighs the literature on children of other drug abusers. Relatively little is known about children of heroin addicts, cocaine abusers, or polydrug abusers. Nonetheless, many researchers suggest that the children of addicted parents are at greater risk for later dysfunctional behaviors and that they, too, deserve significant attention to prevent intergenerational transmission of drug abuse. Most research on children of other drug abusers examines fetal exposure to maternal drug abuse. The overview of the research on children of substance abusers points toward the need for better, longitudinal research in this area. Most studies on COAs or other drug abusers are not longitudinal; they examine behavior at one point in time. Given the studies reviewed in this article, it is unclear whether we see true deficits or developmental delay. Longitudinal studies will allow us to predict when early disorders and behavioral deviations will be transient or when they will be precursors to more severe types of maladaptive behavior. Longitudinal research also will enable us to explain specific childhood outcomes. Differences in outcome could be studied simultaneously to understand whether antecedents discovered for one are specific to it or are general antecedents leading to a broad variety of outcomes.

Adult slow nicotine metabolizers have lower smoke exposure, carbon monoxide levels, and plasma nicotine levels than normal and fast metabolizers. Emerging evidence suggests nicotine metabolism influences smoking topography. This study investigated the association of nicotine metabolism (the ratio of plasma 3-hydroxycotinine to cotinine; 3OHCOT/COT) with smoking topography in adolescent smokers (n = 85; 65% female, 68% European American; mean age, 15.3 F 1.2 years; mean cigarettes per day, 18.5 F 8.5; mean Fagerströ m Test for Nicotine Dependence, 7.0 F 1.2) presenting for a nicotine replacement therapy trial. Measures obtained included puff volume, interpuff interval, number of puffs, puff duration, and puff velocity. Linear regression analysis controlling for hormonal contraception use showed that 3OHCOT/ COT ratios predicted mean puff volume in the overall sample (t = 2.126; P = 0.037; adjusted R 2 = 0.067). After gender stratification, faster metabolism predicted higher mean puff volume (t = 2.81; P = 0.009; adjusted R 2 = 0.192) but fewer puffs (t = À3.160; P = 0.004; adjusted R 2 = 0.237) and lower mean puff duration (t = À2.06; P = 0.048; adjusted R 2 = 0.101) among boys only, suggesting that as nicotine metabolism increases, puff volume increases but puffing frequency decreases. No significant relationships were found between nicotine metabolism and total puff volume, mean puff duration, interpuff interval, or puff velocity. If confirmed in a broader sample of adolescent smokers, these findings suggest that as among dependent adult smokers, rate of metabolism among adolescent boys is linked to select parameters of puffing behavior that may affect cessation ability. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1578 -83)

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