Abstract
The binge drinking (BD) pattern of alcohol consumption is prevalent during adolescence, a period characterized by critical changes to the structural and functional development of brain areas related with memory and cognition. There is considerable evidence of the cognitive dysfunctions caused by the neurotoxic effects of BD in the not-yet-adult brain. Thus, the aim of the present study was to evaluate the effects of different blood alcohol concentrations (BAC) on memory during late adolescence (18–19 years old) in males and females with a history of BD. The sample consisted of 154 adolescents (67 males and 87 females) that were classified as refrainers if they had never previously drunk alcoholic drinks and as binge drinkers if they had drunk six or more standard drink units in a row for men or five or more for women at a minimum frequency of three occasions in a month, throughout the previous 12 months. After intake of a high acute dose of alcohol by binge drinkers or a control refreshment by refrainers and binge drinkers, subjects were distributed into four groups for each gender according to their BAC: BAC0-R (0 g/L, in refrainers), BAC0-BD (0 g/L, in binge drinkers), BAC1 (0.3 – 0.5 g/L, in binge drinkers) or BAC2 (0.54 – 1.1 g/L, in binge drinkers). The subjects’ immediate visual memory and working memory were then measured according to the Wechsler Memory Scale (WMS-III). The BAC1 group showed lower scores of immediate visual memory but not of working memory, while lower performance in both memories were found in the BAC2 group. Therefore, the brain of binge drinkers with moderate BAC could be employing compensatory mechanisms from additional brain areas to perform a working memory task adequately, but these resources would be undermined when BAC is higher (>0.5 g/L). No gender differences were found in BAC-related lower performance in immediate visual memory and working memory. In conclusion, immediate visual memory is more sensitive than working memory to the neurotoxic effects of alcohol in adolescent binge drinkers of both genders, being a BAC-related lower performance, and without obvious differences between males and females.
Highlights
The binge drinking (BD) pattern of alcohol consumption is highly prevalent during adolescence
Considering (a) the different criteria that accompany the BD pattern initiated during the critical period of adolescence, (b) the unclear effects of alcohol, either acute consumption or BD history, on memory (IVM and working memory (WM)), and (c) the potential greater vulnerability of women to the neurotoxic effects of alcohol; the aim of the present study was to evaluate the effects of different blood alcohol concentration (BAC) on IVM and WM during late adolescence (18– 19 years old) in healthy male and female individuals with a BD history
The BAC factor was statistically significant [F(3,146) = 9.354, p < 0.001], with a poorer performance of the IVM task registered in adolescents with BAC1 and BAC2 versus BAC0-R (p < 0.05 and p < 0.001, respectively), and in adolescents with BAC2 versus BAC0-BD (p < 0.005)
Summary
The binge drinking (BD) pattern of alcohol consumption is highly prevalent during adolescence. A blood alcohol concentration (BAC) of 0.8 g/L is required by BD criteria (National Institute of Alcohol Abuse and Alcoholism [NIAAA], 2004; Wechsler and Nelson, 2008), with men and women reaching this value after consuming 5 or more drinks and 4 or more drinks, respectively, in a short time period (2 h) This amount of alcohol is equivalent to the intake of approximately 60 g of alcohol in men and 50 g in women (6/5 or more drinks, respectively) (Parada et al, 2011a) when adapted to the Spanish population, the Observatorio Español sobre Drogas [OED] (2016) accepts the criterion of 5/4 drinks (men/women respectively) in a 2-h period. The intermittence between BD episodes (according to the previously mentioned frequency) seems to be the most important factor involved, as the repeated alternation between intoxication and withdrawal is deleterious for the brain, due to the excitotoxic cell death it provokes (Maurage et al, 2012; Petit et al, 2014)
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