A Review of the Literature on the Cognitive Effects of Alcohol Hangover

Richard Stephens; Jonathan Ling; Thomas M. Heffernan; Nick Heather; Kate Jones


Alcohol Alcohol. 2008;43(2):163-170. 

In This Article


Several pathophysiological changes that both follow and outlast acute alcohol intoxication (i.e. are present after all the acute alcohol has been metabolized) may give rise to the alcohol hangover. Wiese et al. (2000) note increased levels of acetaldehyde, hormonal alterations due to deregulated cytokine pathways and the inhibition of the availability of glucose via a process mediated by insulin. Calder (1997) lists additional phenomena associated with dehydration, metabolic acidosis, disturbed prostaglandin synthesis, increased cardiac output and vasodilation. Other potential mechanisms include sleep deprivation and insufficient eating (Verster et al., 2003). Calder (1997) suggests that the complex organic molecules found in alcoholic beverages known as congeners may have an important role in producing hangover effects because some, such as methanol, are metabolized to the notably toxic substances formaldehyde and formic acid. Congeners tend to be present in greater concentrations in darker drinks (e.g. whisky) compared with clear drinks (e.g. vodka).

These mechanisms have in common the prediction of the presence of hangover effects when the blood alcohol level (BAL) has returned to zero, after having become elevated during and following the drinking episode. Indeed, a defining characteristic of alcohol hangover effects is their presence at zero BAL. This is necessary for research purposes in order to distinguish between hangover and acute alcohol intoxication. However, there appears to be inconsistency in the way that some of these physiological changes would be predicted to affect cognitive functioning. For example, sleep deprivation is known to impair executive functioning (e.g. Jones and Harrison, 2001). On the other hand, increased cardiac output is associated with improved cognitive performance (e.g. Tomporowski and Ellis, 1986). The wide range of mechanisms and the lack of a unitary direction of effect make predicting the effects of hangover complex. Fisk and Scerbo (1987) found that, during acute alcohol intoxication, controlled processes were affected more than automatic processes, implicating an effect on executive function. Such an effect may persist into the hangover phase. Likewise, Jones and Harrison (2001) found executive function decrements following modest amounts of experimentally induced sleep loss, one of the mechanisms thought to underlie hangover. Therefore, executive function, or certainly higher cognitive functions, should be considered as candidate functions to be affected by hangover.

Humans have been drinking alcohol, and presumably experiencing hangovers, since the first mead was brewed from fermented honey around 8000 BC (Meyer and Quenzer, 2005). Nevertheless, although a number of studies have been carried out addressing hangover effects on cognition and performance, we argue in the following sections that their interpretation is severely limited due to a variety of methodological considerations.


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