Key result
Individual cognitive performance impairments induced by ethanol and sleep deprivation were highly correlated (r = 0.62), and acute ethanol administration increased cerebral A1 adenosine receptor availability by up to 26%.
Why the study?
Does individual vulnerability to ethanol predict cognitive impairment from sleep deprivation, and does ethanol increase cerebral A1 adenosine receptor availability?
Does individual vulnerability to ethanol predict cognitive impairment from sleep deprivation, and does ethanol increase cerebral A1 adenosine receptor availability?
Individual trait vulnerabilities to cognitive impairment from alcohol and sleep deprivation are highly correlated and may share a common mechanism involving the up-regulation of cerebral A1 adenosine receptors.
May implicate shared adenosine mechanisms in ethanol and sleep deprivation effects; hypothesis-generating and should not yet change practice.
Significance Modern work environments favor working around the clock, at the cost of insufficient sleep and increased risk for fatigue-related human error. Performance impairments caused by sleep loss show great variability among individuals and resemble the effects of ethanol intoxication. We found that there are individual trait characteristics that make individuals either vulnerable or resilient to both alcohol and to sleep deprivation. We also provide evidence by molecular brain imaging that ethanol induces an up-regulation of cerebral A 1 adenosine receptors, reminiscent of the effects of sleep deprivation. Targeting the brain’s adenosine system might help to identify countermeasures for fatigue- and alcohol-related human error.
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Elmenhorst et al. (2018) studied Healthy (n=59). Ethanol and sleep deprivation vs. Baseline / Placebo was evaluated on Correlation between performance impairments (mean speed) induced by ethanol and total sleep deprivation (r = 0.62, p=<0.0001). Individual cognitive performance impairments induced by ethanol and sleep deprivation were highly correlated (r = 0.62), and acute ethanol administration increased cerebral A1 adenosine receptor availability by up to 26%.
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