Abstract
Binge drinking is an increasing problem in Western societies, but we are still only beginning to unravel the effects of binge drinking on a cognitive level. While common sense suggests that all cognitive functions are compromised during high-dose ethanol intoxication, several studies suggest that the effects might instead be rather specific. Moreover, some results suggest that the degrees of automaticity and complexity of cognitive operations during response control modulate effects of binge drinking. However, this has not been tested in detail. In the current study, we therefore parametrically modulate cognitive/“mental” workload during response inhibition and examine the effects of high-dose ethanol intoxication (~1.1 ‰) in n = 18 male participants. The results suggest that detrimental effects of high-dose ethanol intoxication strongly depend on the complexity of processes involved in response inhibition. The results revealed strong effects (η 2 = .495) and are in line with findings showing that even high doses of ethanol have very specific effects on a cognitive level. Opposed to common sense, more complex cognitive operations seem to be less affected by a high-dose ethanol intoxication. Complementing this, high-dose ethanol intoxication is increasingly detrimental for action control, as stronger automated response tendencies are in charge and need to be controlled. Binge-like ethanol intoxication may take a heavier toll on cognitive control processes than on automated responses/response tendencies. Therefore, ethanol effects are more pronounced in supposedly “easier” control conditions because those facilitate the formation of automated response tendencies.
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07 January 2022
A Correction to this paper has been published: https://doi.org/10.1007/s00204-021-03208-8
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This research was supported by a grant from the Deutsche Forschungsgemeinschaft (DFG) BE4045/10-2.
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Stock, AK., Riegler, L., Chmielewski, W.X. et al. Paradox effects of binge drinking on response inhibition processes depending on mental workload. Arch Toxicol 90, 1429–1436 (2016). https://doi.org/10.1007/s00204-015-1565-y
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DOI: https://doi.org/10.1007/s00204-015-1565-y