Abstract

Results from studies into the cognitive effects of alcohol hangover have been mixed. They also present methodological challenges, often relying on self-reports of alcohol consumption leading to hangover. The current study measured Breath Alcohol Concentration (BAC, which was obtained via breathalyzer) and self-reported drinking behavior during a night out. These were then related to hangover severity and cognitive function, measured over the internet in the same subjects, the following morning. Volunteers were breathalyzed and interviewed as they left the central entertainment district of an Australian state capital. They were provided with a unique identifier and, the following morning, logged on to a website. They completed a number of measures including an online version of the Alcohol Hangover Severity Scale (AHSS), questions regarding number and type of drinks consumed the previous night, and the eTMT-B-a validated, online analogue of the Trail Making Test B (TMT-B) of executive function and working memory. Hangover severity was significantly correlated with one measure only, namely the previous night’s Breath Alcohol Concentration (r = 0.228, p = 0.019). Completion time on the eTMT-B was significantly correlated with hangover severity (r = 0.245, p = 0.012), previous night’s BAC (r = 0.197, p = 0.041), and time spent dinking (r = 0.376, p < 0.001). These findings confirm that alcohol hangover negatively affects cognitive functioning and that poorer working memory and executive performance correlate with hangover severity. The results also support the utility and certain advantages of using online measures in hangover research.

Highlights

  • The alcohol hangover (AH) is defined as “the combination of mental and physical symptoms, experienced the day after a single episode of heavy drinking, starting when blood alcohol concentration approaches zero” [1]

  • There can be considerable inter-individual variability in the pattern, severity, and temporal characteristics of hangover symptoms [8], with no clear relationship between AH severity and any single physiological process

  • Other mechanisms that may contribute to AH include, but are not limited to, gut dysbiosis, decreased blood glucose concentrations, poor sleep architecture, dehydration, oxidative stress, and inflammatory responses [2,11,12]

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Summary

Introduction

The alcohol hangover (AH) is defined as “the combination of mental and physical symptoms, experienced the day after a single episode of heavy drinking, starting when blood alcohol concentration approaches zero” [1]. Other mechanisms that may contribute to AH include, but are not limited to, gut dysbiosis (including ghrelin-mediated), decreased blood glucose concentrations, poor sleep architecture, dehydration (and concomitant electrolyte imbalances), oxidative stress, and inflammatory responses [2,11,12]. These last two may in part be elevated in response to circulating ethanol metabolites

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