Squeglia LM, Spadoni AD, Infante MA, Myers MG, Tapert SF. Initiating moderate to heavy alcohol use predicts changes in neuropsychological functioning for adolescent girls and boys. Psychol Addict Behav 23: 715-722

San Diego State University/University of San Diego Joint Doctoral Program in Clinical Psychology and VA San Diego Healthcare System, San Diego, California, USA.
Psychology of Addictive Behaviors (Impact Factor: 2.75). 12/2009; 23(4):715-22. DOI: 10.1037/a0016516
Source: PubMed


This study prospectively examines the influence of alcohol on neuropsychological functioning in boys and girls characterized prior to initiating drinking (N = 76, ages 12-14). Adolescents who transitioned into heavy (n = 25; 11 girls, 14 boys) or moderate (n = 11; 2 girls, 9 boys) drinking were compared with matched controls who remained nonusers throughout the approximately 3-year follow-up period (N = 40; 16 girls, 24 boys). For girls, more past year drinking days predicted a greater reduction in visuospatial task performance from baseline to follow-up, above and beyond performance on equivalent measures at baseline (R2Delta = 10%, p < .05), particularly on tests of visuospatial memory (R2Delta = 8%, p < .05). For boys, a tendency was seen for more past year hangover symptoms to predict worsened sustained attention (R2Delta = 7%, p < .05). These preliminary longitudinal findings suggest that initiating moderately heavy alcohol use and incurring hangover during adolescence may adversely influence neurocognitive functioning. Neurocognitive deficits linked to heavy drinking during this critical developmental period may lead to direct and indirect changes in neuromaturational course, with effects that would extend into adulthood.

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Available from: Lindsay M Squeglia
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    • "An important question that arises from these findings is whether these deficits are present prior to and predict the onset of drinking or whether the (heavy) use of alcohol induces these deficits. Although this relationship has been investigated in several studies (Fernie et al., 2013; Hanson et al., 2011; Khurana et al., 2012; Nigg et al., 2006; Squeglia et al., 2009; Tapert et al., 2002), none of these studies have included alcohol-naïve adolescents at baseline, which clearly limits the interpretation of the associations found. "
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    ABSTRACT: Recently, it has been suggested that impairments in executive functioning might be risk factors for the onset of alcohol use rather than a result of heavy alcohol use. In the present study, we examined whether two aspects of executive functioning, working memory and response inhibition, predicted the first alcoholic drink and first binge drinking episode in young adolescents using discrete survival analyses. Adolescents were selected from several Dutch secondary schools including both mainstream and special education (externalizing behavioral problems). Participants were 534 adolescents between 12 and 14 years at baseline. Executive functioning and alcohol use were assessed four times over a period of two years. Working memory uniquely predicted the onset of first drink (p=.01) and first binge drinking episode (p=.04) while response inhibition only uniquely predicted the initiating of the first drink (p=.01). These results suggest that the association of executive functioning and alcohol consumption found in former studies cannot simply be interpreted as an effect of alcohol consumption, as weaknesses in executive functioning, found in alcohol naïve adolescents, predict the initiating of (binge) drinking. Though, prolonged and heavy alcohol use might further weaken already existing deficiencies. Copyright © 2015. Published by Elsevier Ltd.
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    • "Adolescent alcohol drinking is increasingly becoming a major health concern and appears to be responsible for the development of psychiatric disorders including substance abuse in adulthood (Grant et al., 2001; Miller et al., 2007; Brown et al., 2008; Squeglia et al., 2009). "
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    ABSTRACT: Epigenetic mechanisms appear to play an important role in neurodevelopment. We investigated the effects of acute ethanol exposure on anxiety measures and function of histone deacetylases (HDAC) and DNA methyltransferases (DNMT) in the amygdala and bed nucleus of stria terminalis (BNST) of adolescent rats. One hour after ethanol exposure, rats were subjected to anxiety measures. A subset of adolescent rats was exposed to two doses (24 h apart) of ethanol (2 g/kg) to measure rapid ethanol tolerance to anxiolysis. The HDAC and DNMT activities and mRNA levels of DNMT isoforms were measured in the amygdala and BNST. The lower dose of ethanol (1 g/kg) produced neither anxiolysis, nor inhibited the HDAC and DNMT activities in the amygdala and BNST, except DNMT activity in BNST was attenuated. Anxiolysis by ethanol was observed at 2 and 2.25 g/kg, whereas higher doses (2.5 and 3 g/kg) were found to be sedative. DNMT activity in the amygdala and BNST, and nuclear HDAC activity in the amygdala, but not in the BNST were also inhibited by these doses of ethanol. A lack of tolerance was observed on ethanol-induced inhibition of DNMT activity in the amygdala and BNST, and nuclear HDAC activity in the amygdala, as well to anxiolysis produced by ethanol (2 g/kg). The DNMT1, DNMT3a, and DNMT3b mRNA expression in the amygdala was not affected by either 1or 2 doses of 2 g/kg. However, DNMT1 and DNMT3a expression in the BNST was increased, whereas DNMT3l mRNA was decreased in the amygdala, after 2 doses of 2 g/kg ethanol. These results suggest that reduced sensitivity to anxiolysis and the lack of rapid tolerance to the anxiolytic effects of ethanol and inhibition of HDAC and DNMT functions may play a role in engaging adolescents in binge drinking patterns.
    Full-text · Article · Jun 2014 · The International Journal of Neuropsychopharmacology
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    • "Participants were assessed using rigorous follow-up procedures (Kleschinsky et al., 2009; Twitchell et al., 1992), with an overall follow-up rate of 99% through Year 6. Specifically , every three months after the baseline interview and imaging were complete, participants were interviewed to assess current substance use and psychiatric functioning . Those who met criteria for heavy drinking (see Squeglia et al., 2009 for classification) were invited to return and complete annual full in-person assessments (see Section 2.2), including neuroimaging. Each participant that endorsed heavy drinking was matched to a demographically similar participant who continued to endorse no substance use throughout the follow-up (i.e., continuous non-drinkers) for comparison. "
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    ABSTRACT: Brain abnormalities in adolescent heavy drinkers may result from alcohol exposure, or stem from pre-existing neural features. This longitudinal morphometric study investigated 40 healthy adolescents, ages 12-17 at study entry, half of whom (n=20) initiated heavy drinking over the 3-year follow-up. Both assessments included high-resolution magnetic resonance imaging. FreeSurfer was used to segment brain volumes, which were measured longitudinally using the newly developed quantitative anatomic regional change analysis (QUARC) tool. At baseline, participants who later transitioned into heavy drinking showed smaller left cingulate, pars triangularis, and rostral anterior cingulate volume, and less right cerebellar white matter volumes (p<.05), compared to continuous non-using teens. Over time, participants who initiated heavy drinking showed significantly greater volume reduction in the left ventral diencephalon, left inferior and middle temporal gyrus, and left caudate and brain stem, compared to substance-naïve youth (p<.05). Findings suggest pre-existing volume differences in frontal brain regions in future drinkers and greater brain volume reduction in subcortical and temporal regions after alcohol use was initiated. This is consistent with literature showing pre-existing cognitive deficits on tasks recruited by frontal regions, as well as post-drinking consequences on brain regions involved in language and spatial tasks.
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