- Top of page
- Materials and Methods
Background: This study assessed the effects of heavy drinking with high or low congener beverages on next-day neurocognitive performance, and the extent to which these effects were mediated by alcohol-related sleep disturbance or alcoholic beverage congeners, and correlated with the intensity of hangover.
Methods: Healthy heavy drinkers age 21 to 33 (n = 95) participated in 2 drinking nights after an acclimatization night. They drank to a mean of 0.11 g% breath alcohol concentration on vodka or bourbon one night with matched placebo the other night, randomized for type and order. Polysomnography recordings were made overnight; self-report and neurocognitive measures were assessed the next morning.
Results: After alcohol, people had more hangover and more decrements in tests requiring both sustained attention and speed. Hangover correlated with poorer performance on these measures. Alcohol decreased sleep efficiency and rapid eye movement sleep, and increased wake time and next-day sleepiness. Alcohol effects on sleep correlated with hangover but did not mediate the effects on performance. No effect of beverage congeners was found except on hangover severity, with people feeling worse after bourbon. Virtually no sex differences appeared.
Conclusions: As drinking to this level affects complex cognitive abilities, safety could be affected, with implications for driving and for safety-sensitive occupations. Congener content affects only how people feel the next day so does not increase risk. The sleep disrupting effects of alcohol did not account for the impaired performance so other mechanisms of effect need to be sought. As hangover symptoms correlate with impaired performance, these might be contributing to the impairment.
Evidence is mixed on whether the residual effects of heavy drinking cause performance deficits the day after intoxication. “Residual effects” refers to any subjective, physiological, and/or behavioral effects of heavy drinking when blood alcohol concentration (BAC) has fallen to near zero after an episode of heavy drinking. Hangover is the subset of residual effects defined by symptoms, typically headache, nausea, thirst, and fatigue, that peak when BAC reaches 0 g% (Rohsenow et al., 2007). Residual alcohol effects are of importance to the extent that they may affect safety-sensitive occupational performance, driving, or student learning or performance (Howland et al., 2006).
Surveys and qualitative studies find positive relationships between frequency of intoxication or hangovers and the frequency of workplace performance problems (Ames et al., 1997; Mangione et al., 1999), and of poorer college grades (Singleton and Wolfson, 2009). Experimental studies show residual effects of heavy drinking on occupational performance the next morning using workplace simulators (Chait and Perry, 1994; Finnigan et al., 1998; Lemon et al., 1993; Morrow et al., 1990, 1991, 1993; Streufert et al., 1995; Taylor et al., 1994, 1996; Törnros and Laurell, 1991; Wolkenberg et al., 1975; Yesavage et al., 1994; Yesavage and Leirer, 1986). Using neuocognitive tasks specifically, while negative results were found for some measures (Finnigan et al., 1998; Lemon et al., 1993; McCaul et al., 1991; Verster et al., 2003), documented detrimental effects were found for visual perception (Dowd et al., 1973); codification and identification tasks (Myrsten et al., 1980); alertness (Roehrs et al., 1991); divided attention and tracking (Roehrs and Roth, 2001a,b); eye-hand and multi-limb coordination, and attention (Seppälä et al., 1976); immediate and delayed (1 hour) free recall (Verster et al., 2003); visual, memory, and intellectual processing (Kim et al., 2003; McKinney and Coyle, 2004); time-reaction error in a go-no-go task (Alford and Wadling, 2004); sustained attention/reaction time (Finnigan et al., 2005); and choice reaction time (Kruisselbrink et al., 2006; McKinney and Coyle, 2004; Seppälä et al., 1976). Inconsistencies among study findings may be the result of factors such as the type of performance measured, the amount of alcohol administered, age and experience of participants, length of time from drinking to testing, and confounds. When some studies tested residual effects before BAC returned to near zero, alcohol effects confounded the residual effects.
Mechanisms accounting for the residual effects of alcohol on performance have received less investigation, despite a number of hypotheses (Swift and Davidson, 1998; Wiese et al., 2000). Some of the possible mediators considered below include sleep disturbance effects of intoxication (Rohsenow et al., 2006), effects of beverage congeners (Nathan et al., 1970), and distracting effects of unpleasant hangover symptoms.
Consuming alcohol (0.16 to 1.0 g/kg) before bed produces reliable changes in sleep continuity and sleep architecture in young, healthy adults. Alcohol initially reduces sleep onset latency, and may increase total sleep time at low doses (0.16 g/kg) but not at moderate or high doses (Stone, 1980). Most studies with low to moderate doses report no significant changes in sleep efficiency (percent of time devoted to sleep actually asleep) (Roehrs et al., 1991). Light Stage 1 sleep has been found to both increase (Kobayashi et al., 1998; Williams et al., 1983) and decrease (Roehrs et al., 1991) following alcohol ingestion. Sleep effects can differ in the first half of the night, when alcohol is being metabolized, from the second half, when it is being eliminated. The first half of the night typically has enhanced slow wave sleep and reduced rapid eye movement (REM) sleep (less time in REM, longer latency to REM) (Gillin et al., 2005; Kobayashi et al., 1998; MacLean and Cairns, 1982; Roehrs et al., 1991; Williams et al., 1983; Yules et al., 1966, 1967). The second half of the night is characterized by increased wakefulness and light Stage 1 sleep (Gillin et al., 2005; Knowles et al., 1968; MacLean and Cairns, 1982; Roehrs and Roth, 2001a,b; Rundell et al., 1972; Williams et al., 1983) and a rebound in REM (Roehrs and Roth, 2001a,b). Thus, sleep is lighter and more disturbed, particularly during the second half of the night. Subjectively, young adults reported improved sleep quality after drinking beer to 0.11 g% BAC versus placebo; with their perception possibly influenced by the more rapid sleep onset they reported (Rohsenow et al., 2006). However, the objectively poorer sleep particularly in the second half of the night could result in impaired performance after awakening.
Most alcoholic beverages contain small amounts of chemicals other than ethanol as a by-product of the materials used in the fermenting process (e.g., grains and wood casks). Congeners are complex organic molecules with toxic effects including acetone, acetaldehyde, fusel oil, tannins, and furfural, with bourbon having 37 times the amount of congeners as vodka (Nathan et al., 1970). While methanol has also been implicated (Calder, 1997), the elimination of methanol from the body coincides with the onset of hangover, although it does leave formaldehyde and formic acid as byproducts (Jones, 1987). In some studies (Katkin et al., 1970), but not others (McMurphree et al., 1966; Nathan et al., 1970), intoxication with bourbon was more impairing than with vodka. However, high-congener beverages such as bourbon did produce more hangover than low congener beverages (Chapman, 1970) and more electroencephalogram (EEG) signs of drowsiness (McMurphree et al., 1966). While the main cause of hangover symptoms is ethanol (e.g., Chapman, 1970; Ylikahri et al., 1974), congeners may increase symptom severity. However, this aspect has been virtually unstudied as these early studies and never examined for effects on performance measures.
Finally, the experience of headache, nausea, and other physical discomfort might interfere with attention, concentration, or rapid responses, abilities central to many safety-sensitive operations. While symptoms cannot be experimentally manipulated separately from other residual effects, correlational data can be supportive or disconfirming. The only study exploring this hypothesis found no association between next-day psychomotor skill impairment and intensity of hangover (Seppälä et al., 1976).
This study investigated the effects of drinking to above legal intoxication on next-day neurocognitive performance and the extent to which these effects were mediated by alcohol-related sleep disturbance or alcoholic beverage congeners, and correlated with the incidence and intensity of hangover. Sleep was assessed using polysomnography and neurocognitive performance was measured using selected neurobehavioral tasks. While Prat and colleagues (2008) recommended using neuropsychological tests that have shown results across various drug effects (executive or frontal function, impulsive decision making), hangover involves the absence rather than presence of drug. As the primary symptoms expected to affect neurocognitive performance are fatigue, dysphoria, and difficulty concentrating, more specific hypotheses were made based on these effects so as to reduce the number of tests to the most relevant ones. The hypotheses were that heavy drinking would result in decrements in abilities requiring speed or sustained concentration (e.g., sustained attention/vigilance and reaction time), and more disrupted lighter sleep (decreased sleep efficiency because of more time awake and more wake-ups, less time in REM sleep, and increased light Stage 1 sleep), and that the sleep deficits would mediate the effects of alcohol on the performance measures. Hypotheses about congener content were that the high-congener beverage, compared to the low congener beverage, would result in more hangover, decrements in neurocognitive performance requiring speed or sustained concentration, and more disrupted sleep. Finally, degree of hangover was hypothesized to correlate with the sleep decrements and with the degree of performance decrements after heavy drinking.
- Top of page
- Materials and Methods
Drinking to above 0.10 g% BrAC results in residual effects on ability to perform complex cognitive tasks the next morning after alcohol has left the body. While drinking did not have residual effects on tasks that involved either speed or sustained attention but not both, tasks that required speed in using sustained attention were significantly impaired the next morning with medium to large sized effects. As drinking to this level affects complex cognitive abilities the next morning, safety could be affected (Howland et al., 2006). Attentional processing (both sustained and selective) and reaction time along with decision making are tasks considered to be involved in safe automobile driving (Allen et al., 2009) and are likely involved in other safety-sensitive occupational tasks. For example, residual effects of alcohol have been found to impair aspects of ability to fly aircraft that require vigilance across tasks (Yesavage and Leirer, 1986; Yesavage et al., 1994) while not affecting ship engineers’ ability to restart malfunctioning engines (Rohsenow et al., 2006). It is interesting that participants did not think their driving ability was impaired in the morning. Although they did say they would be less willing to drive the morning after alcohol than after placebo, this could be because of the hangover they reported feeling as they did not perceive themselves as impaired.
Beverage congeners in bourbon versus vodka did significantly increase the intensity of hangover that was felt, consistent with results from studies in the 1970s. However, these had no effect on next-day performance, sleep, or perceived impairment either acutely or the next morning, consistent with the only other study that investigated this question (Seppälä et al., 1976). Thus, as congener content affects only how people feel the next day, the congeners in bourbon versus vodka do not appear to increase risk.
Effects of this amount of alcohol on subjective and objective measures of sleep are largely consistent with other studies. After alcohol, sleep was disrupted, characterized by lower sleep efficiency because of spending more time awake during the night, and less time was spent in REM sleep. Participants also reported having slept less well the next morning and feeling sleepier (tiredness is a symptom of hangover, Rohsenow et al., 2007). While effects on sleep efficiency were not found by Roehrs and colleagues (1991), possibly because of a lower dose of alcohol, increased wakefulness is often found, and reduced time in REM sleep is consistent with many other studies. When participants did sleep, their sleep was deeper as indicated by more slow wave sleep, also found in other studies. While we did not find predicted effects on time in Stage 1 sleep, effects on this stage have been inconsistent across studies, as reviewed in the introduction. Thus, drinking impaired sleep in a number of ways. However, the effects of alcohol on sleep were not found to mediate the effects of alcohol on performance the next day. As the sleep disrupting effects of alcohol did not account for the impaired cognitive performance, other mechanisms of these residual effects need to be explored.
Impaired sleep did correlate significantly with hangover symptoms. Correlations with hangover were significant for sleep efficiency, amount of time awake during the night, and time in REM sleep, but the largest effect size was seen with sleep efficiency. People who spent less of their time actually sleeping while in bed felt worse the next morning. While subjective sleepiness also correlated with hangover, tiredness is a component of hangover so this represents overlap in constructs rather than a meaningful relationship.
Hangover symptoms might be a mechanism by which drinking to intoxication impairs performance the next morning. While a true mediation model could not be tested, drinking to this level did increase hangover, and higher hangover scores after alcohol did correlate significantly with poorer performance scores on the neurocognitive measures that had been affected by alcohol. Thus, hangover symptoms might be contributing to impaired performance.
The study had several limitations. First, only young adults were used, to maximize safety, and it is possible that effects would differ in older adults with longer drinking histories and possibly more behavioral tolerance. Second, we excluded people with probable alcohol dependence yet such people are more likely to drink to intoxication on a regular basis. Third, for safety reasons, the target BrAC was set to the minimum at which hangover is reliably induced. Higher doses would produce more hangover, probably more next-day impairment, and more sleep disruption. Fourth, because of the high dose, most people knew what beverage they received so the influence of expectancy effects cannot be ruled out. Placebos are typically not effective at BrACs ≥0.07 g% but these beliefs are usually not checked (Rohsenow and Marlatt, 1981).
Despite these limitations, this study adds to the relatively sparse experimental literature on the nature of hangover and other residual effects of alcohol. In particular, information was added on the types of performance decrements affected residually by heavy drinking, information that could be useful for safety-sensitive occupations. Furthermore, the study contributes to our understanding about possible mechanisms by which drinking to intoxication may produce effects on hangovers or on performance decrements the next day.