Impact Of Alcohol Consumption On Performance

The purpose of this post is to analyze the impact of alcohol on performance, particularly cognitive performance. If it turned out that alcohol was a significant cause of cognitive decline, then it would make sense for technical researchers doing important research to abstain from consuming alcohol.

TLDR: Data shows that moderate drinking has a small positive effect but heavy drinking is very bad.

Epistemic Status: Based on About an hour of research, could definitely use more research. This was merely intended to be a relatively quick writeup on the topic.

According to Newbury-Birch et al in a systematic review of all the evidence—describing impacts on childhood.

“There are many adverse consequences of drinking alcohol during childhood and adolescence which would seem to outweigh the modest number of positive impacts. Overall, it seems that delaying the age of alcohol initiation and limiting the amount drunk by young people is likely to enhance their health and well-being.”

The study looked at the following

Outcomes of interest included direct harms to physical, social or mental health of the drinking individual (e.g. cirrhosis, alcohol dependence, depression, social); indirect harms to the health of the drinking individual (e.g. injuries from an increase in risky behaviour); social harms to the drinking individual or their associates (such as aggression within the family, criminality and educational effects); or predictors of harm.

It used 102 papers in the final report, from a pool of nearly 6000 titles.

• Alcohol stimulates the release of endorphins giving the subject a sense of well being which can encourage continued drinking. Increasing intoxication leads to euphoria, loss of inhibition, reduced coordination, garrulousness and belligerence [45]. • With increasing blood alcohol concentrations subjects experience lethargy, cardiorespiratory depression. • With further intake subjects develop stupor and coma that may end in death [25]. Mid-term effects • Alcohol disrupts the sleep-wake cycle, altering total sleep time [46]. Consolidation of learnt material takes place in sleep and so this can be adversely affected by persistent 21 drinking. Research suggests that alcohol has a more profound effect on memory and learning in adolescents than in people who start drinking in later life. • It has been reported that the fatal dose of alcohol in childhood could be as low as 3 grams/kg in a child compared to 5-8 grams/kg in an adult [24]. In a 30 kg ten year old this equates to 1.5 bottles of wine and in an adult to 5 − 8 bottles with presumably adolescents in the middle, depending on weight. The reduction though metabolism of 0.1 g/l/hr or 0.08/kg/hr—in the blood means that if a 75 kg adolescent had a blood level of 1g/kg after a bottle of wine, it would take ten hours for full elimination. Since there is at least a temporary effect of alcohol on memory, this young person could still have alcohol affecting their brain function in the school morning. So potentially there could be a problem with learning in school the morning after heavy drinking, in addition to the fatigue associated with the alcohol-related sleep disruption. • Alcohol is also linked with depression, although it is not possible to determine if adolescents drink due to depression or if depression occurs as a toxic effect of alcohol consumption [45]. However, research on alcohol abusers has found significantly fewer locus coeruleus neurons in the brain stem compared to non alcohol abusers, suggesting that alcohol may change brain structure and thus trigger a behavioural response [25]. Longer-term effects • In observational studies of subjects with chronic alcohol use disorders, both left and right hippocampal volumes were significantly smaller than in non users. Thus long-term memory may be affected by prolonged drinking [25]. • Using functional magnetic resonance imaging (fMRI) to measure blood flow to various parts of the brain, alcohol abusers have shown reduced perfusion (blood flow) to the prefrontal and parietal cortices, particularly in the right hemisphere during tasks of spatial working memory e.g. remembering location of objects [25, 44, 46]. Also subjects with alcohol dependence demonstrate diminished spatio-visual and motor speed responses [25, 44, 46]. • Alcohol also stimulates release of the neurotransmitter Dopamine which activates the Dopaminergic reward pathway [25]; this can make alcohol addictive, as both short term and long term exposure reinforces this pathway in the brain. • Abstinence from alcohol after periods of heavy drinking sensitises N-methyl-D-aspartate (NMDA) receptors causing an influx of calcium ions into neurons as a result of their increased activity. This process is neurotoxic and causes cell degeneration.

This study looked at the association between alcohol use and cognitive decline in elderly people, and found

In a representative elderly cohort over an average of 7 years, a pattern of mild-to-moderate drinking, compared to not drinking, was associated with lesser average decline in cognitive domains over the same period.

This study found the same thing. However, these were both cohort studies, so they are unable to establish a high probability of causation.

This study was a meta-analysis, which looked at 143 papers, and found there was virtually no impact on young people and was a positive effect on old people.

Phase I (1977–1997) was the era of neuropsychological evaluation involving mostly young to middle-aged (18–50 years old) subjects. Although initial studies indicated moderate drinking impaired cognition, many later studies failed to confirm this, instead finding no difference in cognition between drinkers and nondrinkers. Phase II (1998–present) was and is the era of mental status exam evaluation involving mostly older (≥55 years old) subjects. These studies overwhelmingly found that moderate drinking either reduced or had no effect on the risk of dementia or cognitive impairment. When all the ratios of risk from all the studies in phase II providing such ratios are entered into a comprehensive meta-analysis, the average ratio of risk for cognitive risk (dementia or cognitive impairment/decline) associated with moderate “social” (not alcoholic) drinking of alcohol is 0.77, with nondrinkers as the reference group.

There conclusion is the following.

Heavy drinking (>3–4 drinks/day) is associated with an increased risk of dementia and cognitive impairment, in addition to all the other horrible and devastating consequences of alcohol abuse and alcoholism for the individual and their family and friends, and society in general. However, light to moderate drinking (≤2 drinks/day for men, ≤1 drink/day for women) by adults does not increase the risk of dementia, cognitive decline, or cognitive impairment – a conclusion also reached by a recent comprehensive review.¹³ In fact, notwithstanding the conclusion in a recent article that “no evidence of even moderate scientific quality exists to support the association of any modifiable factor … with reduced risk for Alzheimer disease,”²⁰² there is substantial evidence that light to moderate drinking (as defined in the National Institute on Alcohol Abuse and Alcoholism’s position paper on moderate drinking²⁰³), particularly of wine, reduces the risk of dementia and cognitive impairment.

This study, finds the opposite. The initial summary is worth quoting in full.

Studies show that light to moderate alcohol consumption is related to better health and higher cognitive performance. However, it has been suggested that this association is caused by a systematic bias in the control group as many people abstain from drinking or quit because of health issues. Therefore, the group of non-drinkers is biased towards poor health and may not be suitable as a control group. The present study examined the effect of alcohol on cognitive performance while addressing this bias by excluding the non-drinkers. Thus, instead of comparing different levels of alcohol consumption to a non-drinking control group, a dose-response association was calculated between all levels of alcohol intake and cognitive performance. The study used information from a sample of people in the Swedish Twin Registry, who in their midlife (1967) participated in a survey on alcohol intake and 25 years later participated in a longitudinal study on cognitive aging (N = 486). The cognitive aging study took place on five occasions, at 2-year intervals, and included the Mini Mental State Examination (MMSE), tests of episodic memory, semantic memory and spatial ability. The association between midlife alcohol consumption and later cognitive performance was analyzed using growth curve models, adjusting for background variables. The findings showed that there was a significant negative dose-response association between alcohol intake in midlife and the MMSE, and the tests of episodic memory, such that higher intake in midlife was related to lower performance in old age. The associations between alcohol and semantic memory, and spatial ability respectively, were not significant. In contrast to findings from other studies, which show that low to moderate alcohol intake promotes cognitive function, the current study showed that alcohol intake was related to lower cognitive performance in a dose-response manner, even at low levels. The results from this study indicate that the observed benefits of moderate alcohol intake for cognitive function reported by others might be solely due to comparisons to an inappropriate control group, a group that is biased towards poor health. Hence, it is concluded that light alcohol intake may not protect cognitive function.

Additionally, they say in the introduction

Many studies converge on the conclusion that long-term low to moderate alcohol intake protects against dementia and cognitive aging (for review, see Peters et al., 2008; Anstey et al., 2009). At the same time it is well documented that the acute effect of alcohol impairs cognitive performances such as attention, psychomotor speed, tracking ability, working memory and cognitive flexibility (Matthews and Silvers, 2004; Mintzer, 2007; Fillmore, 2011; Dry et al., 2012). It is somewhat paradoxical that the immediate effect of alcohol is detrimental whereas the long-term effect is thought to be protective. There is a broad consensus in the literature concerning the acute negative effect of alcohol on cognitive performance, however, there is an ongoing debate concerning the positive effect of long-term low to moderate alcohol intake (Naimi et al., 2005; Stockwell et al., 2012, 2016; Fekjær, 2013; Chikritzhs et al., 2015).

They had a large sample size, that differed by wave they were looking at.

They added the following.

These associations were statistically significant for the MMSE (t₍₃₀₃₎ = 2.63) and the two long-term memory tasks, that is, picture recognition (t₍₂₈₉₎ = 2.45) and prose recall (t₍₂₉₉₎ = 2.13). In Model 2, which was additionally adjusted for health-related factors, there were only significant negative associations between alcohol consumption and picture recognition (t₍₂₉₃₎ = 2.32).

They continue

The differential findings across the cognitive tests in the present study are in line with this; the alcohol effects were seen in the episodic memory tests but not in semantic memory (a crystallized ability). Regarding the trajectories of cognitive performance across time, there was a significant decline in all the cognitive measures, however, there was no additional decline related to alcohol intake. Given the high age of this sample, many individuals can be considered to be in the terminal phase of life, resulting in terminal decline in cognitive performance, which may have overshadowed the negative effect of alcohol that was found in the levels of cognitive performance. The sizes of the estimates for the slopes, reflecting considerable ageing-related decline, support this notion.
Concerning how these findings should be interpreted it is clear that they are in line with many findings showing negative effects of acute alcohol on cognitive function (Matthews and Silvers, 2004; Mintzer, 2007; Fillmore, 2011; Dry et al., 2012). However, they contradict the conclusion that long-term light to moderate alcohol intake promotes cognitive health, an established finding, according to the literature.

This appears to be pretty solid evidence that undermines the evidence presented previously for the benefits of alcohol. It shows a methodological flaw which, when controlled for, indicates alcohol produces negative effects. However, we can’t trust it, for reasons explained by the next study.

This study also concluded that it was difficult to draw firm conclusions based on “Major limitations in the design and reporting of included studies.” It also excluded the Hassing study because it was “at a critical risk of bias.” Thus, this undermines the reliability of the Hassing study. In an appendix they explain why it’s at serious risk of bias, writing

Critical due to missing data and Serious risk of bias due to confounding, selection into the study, and classification of alcohol consumption

They provide more specific details about each of these, which are pretty damning. They additionally report

We found that there is currently very low certainty evidence showing a very small, probably unimportant, beneficial effects on cognition at levels of alcohol consumption at or below those currently indicated as lower risk for women and men in the 2009 Australian Guidelines, and those of New Zealand, and a number of European countries including the United Kingdom (i.e. two standard drinks or < 20 g of alcohol per day). The extent to which this reflects a true effect or bias arising from limitations of studies included in the systematic review cannot be determined.

The studies examined so far haven’t been RCT’s. This one is an RCT, which finds that regular alcohol consumption raises blood pressure in a way that is reversible.

Forty-six healthy normotensive male drinkers participated in a randomized, controlled, crossover trial to study the effects of varying alcohol intake on blood pressure. Alcohol consumption (calculated from weekly diaries) was reduced from 336.3 (s.e.m. = 20.2) to 64.5 (s.e.m. = 5.6) ml ethanol/week by drinking low alcohol content beer alone. Systolic blood pressure fell significantly during reduction of alcohol intake and rose again when normal drinking habits were resumed, the mean difference during the last 2 weeks of normal or low alcohol intake being 3.8 mmHg. This effect of alcohol on blood pressure was independent of a small but significant decrease in weight following reduction of alcohol intake. The change in blood pressure correlated with change in alcohol consumption (r = 0.53, P less than 0.001) with a 1 mmHg fall predicted for each 100 ml of reduction in ethanol intake/week. We conclude that regular moderate alcohol consumption has a direct (but reversible) pressor effect in normotensive men.

This study similarly finds a reduction on cognitive decline for moderate drinking in women.

Although the adverse effects of excessive alcohol intake are well known and caution should be exercised in recommending even moderate alcohol intake, our results combined with those of other studies suggest that women who consume up to one drink per day have less cognitive impairment and better cognitive function than nondrinkers.

This study finds the same (though not just applied to women).

Results: for both men and women, better cognition and subjective well-being, and fewer depressive symptoms, were associated with moderate levels of alcohol consumption than with never having drunk any.

So does this one and this one.

This study is a randomized control trial and finds

CONCLUSION: Drinking low to moderate amounts of alcohol may delay age-associated cognitive decline in older women (including slowing deterioration in global cognitive function), but these apparent benefits were not clearly seen in older men

Conclusion: I’m roughly 99.6% confident that heavy drinking is very bad for cognition. I’m roughly 40% confident that moderate drinking has a positive effect on cognition, 20% credence that it’s negative, and 40% that it’s neutral. However, its effect varies based on age.