Journal of Studies on
Alcohol
Volume 66
Number 1
January 2005
Issues Available Online
September 2006
July 2006
May 2006
March 2006
January 2006
November 2005
September 2005
Supplement 15 July 2005
July 2005
May 2005
March 2005
January 2005
November 2004
September 2004
July 2004
May 2004
March 2004
January 2004
November 2003
September 2003
July 2003
May 2003
March 2003
January 2003
November 2002
September 2002
July 2002
May 2002
Selected Abstracts
SIMONS-MORTON, B. AND CHEN, R. Latent Growth Curve Analyses of Parent Influences on Drinking Progression among Early Adolescents
ABSTRACT. Objective: The nature of parent influences on early adolescent substance use was examined. Method: Latent growth curve analyses were used to examine data on a sample of 2,453 adolescents from seven middle schools who were randomized to a problem behavior prevention program or a control condition and were assessed a total of five times during sixth to ninth grade. Results: Whereas the growth in the number of friends who drink was positively associated with adolescent drinking, parental involvement, monitoring and expectations over time provided direct protective effects against drinking progression and indirect effects by limiting increases in the number of friends who drink. Conclusions: The results provide evidence in a sample of early adolescents that parenting behavior—including involvement, monitoring and expectations—protected against progression in drinking directly as well as indirectly by limiting growth in the number of friends who drink. (J. Stud. Alcohol 66: 5-13, 2005)
ABSTRACT. Objective: This study examines the relationship between parental alcohol use disorders (AUDs) and child violent and nonviolent delinquency. It also explores the mediating effects of executive functioning and chronic family stress on the parental AUD/child delinquency relationship. Method: Participants were 816 families with children (414 boys and 402 girls) born between 1981 and 1984 at Mater Misericordiae Mother’s Hospital in Brisbane, Australia. Parents and children completed semistructured interviews, questionnaires and neuropsychological tests that assessed parental alcohol use, family psychiatric history, chronic family stress, child delinquency and child executive functioning. Results: Paternal (but not maternal) AUDs predicted child violent and nonviolent delinquency. Executive functioning mediated the relationship between paternal AUDs and violent delinquency, whereas family stress mediated the relationship between paternal AUDs and both violent and nonviolent delinquency. Conclusions: Results support a biosocial conceptualization of the paternal AUD/delinquency relationship. They suggest that paternal AUDs may be associated with child executive functioning and family stress, which may in turn lead to child delinquency. (J. Stud. Alcohol 66: 14-22, 2005)
ABSTRACT. Objective: The present study used structural equation modeling to test whether prospective relations between prematriculation social influences and alcohol involvement in college were most consistent with peer selection, peer socialization or reciprocal determinism explanations and to determine if observed relations varied according to measurement interval. We tested the hypotheses that “active” (alcohol offers) and “passive” (social modeling, perceived norms) social influences would be uniquely and reciprocally associated with alcohol use and alcohol-related consequences across two and three waves of assessment. Method: Prospective undergraduates (N = 388) completed self-report assessments in the summer before matriculation (Wave 1), in the spring of their freshman year (Wave 2) and in the spring of their sophomore year (Wave 3). Results: Reciprocal effects were observed between social influences and alcohol use in both two- and three-wave models. Some evidence was observed for reciprocal associations for social modeling with alcohol use and alcohol problems. Overall, however, only modest support was found for a reciprocal influence conceptualization of social influences in alcohol problems. For alcohol problems, the results were more consistent with selection effects. No significant reciprocal associations were observed for perceived norms. Conclusions: Findings generally support the Social Learning Theory concept of reciprocal determinism but suggest the relationship between individual drinking behaviors and the social environment varies when distinguishing between alcohol use and alcohol problems. These findings also point to the importance of distinguishing among different types of social influences when delineating processes that result from and lead to heavy drinking in college. (J. Stud. Alcohol 66: 23-34, 2005)
ABSTRACT. Objective: The Oct 2 POU homeodomain gene has been shown to increase during late juvenile development; the upstream control of Oct 2 is not known, however. The insulin-like growth factor-1 (IGF-1) is known to act centrally to stimulate luteinizing hormone (LH)-releasing hormone (LHRH) release and advance female puberty. We therefore sought to determine if this peptide induces transcription of Oct 2 genes as an early pubertal event. Furthermore, as alcohol (ALC) blocks IGF-1-induced LHRH and LH release acutely, we aimed to determine if it could affect the ability of IGF-1 to stimulate Oct 2 gene expression. Method: Female rats, 25 days old, were administered saline or IGF-1 (rat IGF-1 20 ng/3 µl) in the third ventricle at 0900 hours and killed 2, 4 and 6 hours later for assessment of Oct 2 gene expression in the preoptic area (POA) and the medial basal hypothalamus (MBH). In another experiment, we determined whether ALC (3 g/kg) could block IGF-1-induced Oct 2 gene expression. Results: In the POA, IGF-1 did not affect the expression of Oct 2a, but it increased the Oct 2c mRNA levels at 2 hours. In the MBH, both transcripts were elevated 4 hours after IGF-1 stimulation. ALC did not alter basal expression of either of the Oct 2 gene isoforms. In both regions, however, ALC blocked IGF-1-induced gene expression. Conclusions: IGF-1 induced Oct 2 genes prior to the normal increase during the late juvenile period, indicating this IGF-1 induction may be an early event in the activation of the LHRH secretory pathway. ALC blocks this action, suggesting the Oct 2 POU gene is a likely target by which ALC can interfere with glial-neuronal interactions and interrupt LHRH secretion during prepubertal development. (J. Stud. Alcohol 66: 35-45, 2005)
ABSTRACT. Objective: Alcohol misuse early in life is associated with an increased risk of alcoholism. It is possible that this increased risk in adolescent drinkers is in part related to the susceptibility of the adolescent brain to ethanol. This study assessed the effects of ethanol exposure on several neuropeptides to begin to elucidate potential substrates that could mediate the differential effects of ethanol on adolescent and adult rats. Method: Male Sprague Dawley rats were exposed to ethanol vapor or air during adolescence (30 days old, n = 9, controls = 8) or adulthood (80-90 days old, n = 9, controls = 8) for 10 days. Blood alcohol concentrations averaging 250 mg/dl were maintained during this period. After 7 weeks of cessation from ethanol vapor, brain tissue was collected from the frontal cortex, caudate, hippocampus, amygdala and hypothalamus to assess the immunoreactivity levels of neuropeptide Y (NPY-LI), corticotropin-releasing hormone, substance P (SP-LI) and neurokinins (NK-LI). Results: Ethanol exposure decreased overall hippocampal NPY-LI and increased SP-LI and NK-LI in the caudate, but these effects were more prominent in adult rats. Rats in the adult treatment groups (both ethanol exposed and controls) also had significantly lower levels of frontal cortical NK-LI, frontal cortical SP-LI and hypothalamic SP-LI relative to rats in the adolescent treatment groups. Conclusions: These data indicate that brief exposure to alcohol has long-term effects on levels of NPY-LI, SP-LI and NK-LI. As these effects were primarily the result of changes in rats exposed to ethanol during adulthood, however, they are unlikely to contribute to the increased susceptibility of adolescents to the effects of chronic ethanol exposure. (J. Stud. Alcohol 66: 46-52, 2005)