Literature DB >> 21952669

Binge drinking differentially affects adolescent male and female brain morphometry.

Lindsay M Squeglia1, Scott F Sorg, Alecia Dager Schweinsburg, Reagan R Wetherill, Carmen Pulido, Susan F Tapert.   

Abstract

RATIONALE: Adolescent binge drinking is concerning, as important neurodevelopments occur during this stage. Previous research suggests that binge drinking may disrupt typical brain development, and females may be particularly vulnerable.
OBJECTIVES: We used magnetic resonance imaging (MRI) to examine cortical thickness in adolescent females and males with and without histories of binge drinking.
METHODS: Participants (N = 59) were 16-19-year-old adolescents recruited from local schools. Recent binge drinkers (n = 29, 48% female) were matched to non-drinkers (n = 30, 50% female) on age, gender, pubertal development, and familial alcoholism. Participants completed a neuropsychological battery and MRI session. Cortical surfaces were reconstructed with FreeSurfer.
RESULTS: Binge × gender interactions (p < .05) were seen for cortical thickness in four left frontal regions: frontal pole, pars orbitalis, medial orbital frontal, and rostral anterior cingulate. For all interactions, female bingers had thicker cortices than female controls, while male bingers had thinner cortices than male controls. Thicker left frontal cortices corresponded with poorer visuospatial, inhibition, and attention performances for female bingers (r = -0.69 to 0.50, p < 0.05) and worse attention for male bingers (r = -0.69, p = 0.005).
CONCLUSIONS: Adolescent females with recent binge drinking showed ~8% thicker cortices in left frontal regions than demographically similar female non-drinkers, which was linked to worse visuospatial, inhibition, and attention performances. In contrast, adolescent binge-drinking males showed ~7% thinner cortices in these areas than non-drinking males. These cross-sectional data suggest either different gray matter risk factors for males as for females toward developing heavy drinking, or differential adverse sequelae.

Entities:  

Mesh:

Year:  2011        PMID: 21952669      PMCID: PMC3527131          DOI: 10.1007/s00213-011-2500-4

Source DB:  PubMed          Journal:  Psychopharmacology (Berl)        ISSN: 0033-3158            Impact factor:   4.530


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