Alcohol and cognitive function: how drinking affects the brain

Alcohol consumption is deeply embedded in UK culture; in a survey by the Office of National Statistics, 81% of adults reported that they drank alcohol in the past year – with 55% of men and 42% of women¹ reporting alcohol use within the last week.

While moderate drinking is often perceived as benign – or even beneficial² – growing clinical evidence suggests a more complex relationship between alcohol and cognitive function. For practitioners, understanding this interplay is essential, not only in the context of addiction medicine but across general practice, psychiatry, geriatrics, and neurology.

Alcohol is a central nervous system depressant that affects nearly every region of the brain³. Even at low levels, it can impair short-term memory, decision-making, and reaction time. With repeated use, structural and functional brain changes may occur⁴, potentially leading to long-term cognitive decline – particularly in older adults or those with comorbid conditions.

As ‘Through a Glass Brightly’ author Nick Charles once said: “What alcoholics do to themselves becomes a mechanical process of destruction. We become machines that, although malfunctioning, refuse to come to a halt.”

While intended in the context of dependency, this observation also rings true when we consider the gradual and often unnoticed effects of habitual drinking on brain health.

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Acute effects of alcohol on cognitive function

Alcohol’s immediate effects on cognitive performance are well-documented and clinically significant⁵. As a GABA-A receptor agonist and NMDA receptor antagonist, alcohol slows neuronal excitability and disrupts normal synaptic transmission⁶ – leading to a range of cognitive deficits, even at moderate blood alcohol concentrations (BAC).

Short-term cognitive impairments:

• Attention and concentration: reduced ability to sustain focus and filter irrelevant stimuli.
• Working memory: diminished capacity to temporarily store and manipulate information.
• Executive function: impaired judgement, planning, and inhibitory control, increasing risk-taking behaviours.
• Psychomotor performance: slowed reaction times, impaired coordination, and reduced balance.
• Verbal fluency: difficulties in language retrieval and speech coherence, particularly at higher doses.

These impairments can present at BAC levels as low as 0.03–0.05%⁷, well below the UK legal driving limit (0.08%). In clinical settings, even these subtle effects can exacerbate risks in patients with co-existing mental health or neurological conditions.

Transient or dangerous?

For most healthy adults, these cognitive disruptions are temporary.

However, in particularly susceptible populations – older adults, those with pre-existing cognitive vulnerabilities, or individuals in high-pressure roles⁸, for instance – acute alcohol effects can compound existing deficits or provoke episodic confusion, falls, or unsafe behaviours requiring intervention.

Chronic alcohol use and long-term cognitive decline

While acute impairments are often reversible, chronic alcohol use can lead to persistent structural and functional brain changes, resulting in lasting cognitive impairment⁹. These changes are often insidious, with symptoms progressing subtly until function is significantly compromised.

Neuroanatomical changes:

• Cortical atrophy: particularly in the frontal lobes, leading to deficits in executive function and decision-making.¹⁰
• Hippocampal volume loss: impairments in memory consolidation and spatial orientation.¹¹
• White matter degeneration: disrupted connectivity between brain regions, slowing processing speed and cognitive flexibility.¹²

MRI and DTI studies consistently show greater age-related brain shrinkage in chronic drinkers, with heavy drinkers exhibiting structural damage equivalent to a potential additional 10–20 years of ageing.¹³

Alcohol-related brain damage (ARBD):

ARBD is an umbrella term encompassing several clinical syndromes¹⁴ resulting from prolonged alcohol misuse¹⁵. These include:

• Wernicke’s Encephalopathy: acute thiamine deficiency causing confusion, poor muscle control, and ophthalmoplegia.
• Korsakoff’s Syndrome: a chronic amnestic condition characterised by severe memory loss, confabulation, and executive dysfunction.
• Alcohol-Related Dementia: a global decline in multiple cognitive domains due to sustained neurotoxicity.

Dose-response evidence

Even moderate drinking (7–14 units/week) has been associated with measurable cognitive decline¹⁶, especially in older adults.

A 30-year cohort study from the University of Oxford found no protective effect of moderate alcohol consumption on brain health¹⁷; instead, they reported dose-dependent hippocampal atrophy, even in those drinking within current UK guidelines.

Key risk modifiers include:

• Age → older adults are more vulnerable to alcohol-related neurodegeneration.
• Sex → women appear more susceptible¹⁸ to alcohol-induced brain damage at lower doses.
• Genetics → polymorphisms in alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) enzymes may modulate susceptibility.
• Comorbid conditions → nutritional deficiencies, liver disease, and psychiatric disorders compound the risk of cognitive damage.

The debate around ‘moderate’ alcohol consumption

The impact of ‘moderate’ alcohol consumption on cognitive function remains a subject of intense scientific scrutiny and public interest.

For decades, moderate drinking – commonly defined as up to 14 units per week in the UK¹⁹ – was thought to confer certain health benefits, particularly for cardiovascular outcomes. However, emerging evidence challenges this narrative, particularly when it comes to brain health²⁰.

Historical perspective: cardiovascular vs cognitive outcomes

Early epidemiological studies (e.g., the “French Paradox”²¹) suggested that moderate red wine consumption might reduce cardiovascular mortality. These findings were extrapolated to imply cognitive protection via improved vascular health.

However, these associations were non-causal and often confounded by socioeconomic status, diet, and overall health behaviours.

Recent meta-analyses and prospective cohort studies have found no clear cognitive benefit from moderate alcohol intake²². Instead, research increasingly shows that:

• Even low-to-moderate alcohol use is associated with subtle structural brain changes, particularly in the hippocampus and prefrontal cortex.
• Cognitive performance across several domains – especially executive function and memory – tends to decline with increasing alcohol exposure, in a dose-dependent

A study published in the BMJ²³ concluded:

“Alcohol consumption, even at moderate levels, is associated with adverse brain outcomes including hippocampal atrophy. These results support the recent reduction in alcohol guidance in the UK and question the current limits recommended in the US.”

Biological plausibility

At a biological level, one noteworthy point is that (unlike cardiovascular tissue), neuronal tissue lacks regenerative capacity – making the brain particularly vulnerable to sustained toxic insults. Even moderate drinking can disrupt:

• Neurogenesis in the hippocampus
• Neurotransmitter balance, especially involving glutamate, GABA, and dopamine
• Sleep architecture, which plays a crucial role in memory consolidation

Moreover, alcohol interferes with thiamine metabolism, exacerbating risks of neurocognitive compromise, even in individuals without frank dependency.

Rethinking alcohol and cognitive function

The relationship between alcohol and cognitive function is more complex – and potentially more concerning – than once thought. While light-to-moderate drinking has long been culturally and socially accepted, perspectives do appear to be shifting²⁴, and a growing body of high-quality research suggests that no amount of alcohol can be considered entirely ‘safe’ for the brain; much less  ‘protective’.

From acute impairments in memory, attention, and executive function to long-term structural brain changes and an elevated risk of dementia²⁵, the neurological impact of alcohol is both significant and under-recognised in clinical practice. This is especially true in populations with co-occurring vulnerabilities.

As clinicians, we must remain vigilant: not only in identifying alcohol-related neurocognitive risks, but in guiding patients through nuanced conversations about drinking habits. This includes:

• Encouraging realistic self-assessment and harm reduction
• Addressing the myth of ‘healthy’ moderate drinking with clarity and evidence
• Considering the cumulative impact of alcohol on cognitive ageing, particularly when combined with other risk factors

Ultimately, protecting brain health means viewing alcohol use not just through a cardiometabolic or social lens, but from a neurological and cognitive – a whole-person – point of view. As the evidence evolves, so too should our approach to public health messaging, patient education, and clinical screening practices.

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References

1. https://digital.nhs.uk/data-and-information/publications/statistical/health-survey-for-england/2022-part-1/adult-drinking#:~:text=be%20accessed%20here.-,Key%20findings%20for%202022,at%20least%20once%20a%20week.
2. https://www.uchealth.org/today/truth-about-alcohol-is-it-healthy/
3. https://pubmed.ncbi.nlm.nih.gov/26466222/
4. https://alcoholthinkagain.com.au/alcohol-and-your-health/long-term-health-effects
5. https://www.rcpsych.ac.uk/mental-health/mental-illnesses-and-mental-health-problems/alcohol-mental-health-and-the-brain#:~:text=There%20are%20a%20number%20of,panic%20disorder%20and%20impulsive%20behaviour.
6. https://pmc.ncbi.nlm.nih.gov/articles/PMC165791/
7. https://my.clevelandclinic.org/health/diagnostics/22689-blood-alcohol-content-bac
8. https://www.bbc.com/worklife/article/20170425-the-jobs-where-career-success-means-drinking-at-work
9. https://alcoholthinkagain.com.au/alcohol-and-your-health/long-term-health-effects
10. https://pmc.ncbi.nlm.nih.gov/articles/PMC2077939/
11. https://pmc.ncbi.nlm.nih.gov/articles/PMC5595646/
12. https://www.nature.com/articles/s41467-022-28735-5
13. https://pmc.ncbi.nlm.nih.gov/articles/PMC11424507/#:~:text=Volume%20deficits%20in%20the%20AUD,%2C%20&%20Sullivan%2C%202020).
14. https://www.alzheimers.org.uk/about-dementia/types-dementia/alcohol-related-brain-damage-arbd
15. https://www.bbc.co.uk/news/articles/c3e551eqpgdo
16. https://www.theguardian.com/society/2017/jun/06/even-moderate-drinking-can-damage-the-brain-claim-researchers#:~:text=People%20who%20drank%20between%20seven,to%20stick%20to%20recommended%20guidelines.
17. https://pubmed.ncbi.nlm.nih.gov/28588063/
18. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6668882/#:~:text=To%20adequately%20compare%20brain%20damage,men%2C%20the%20evidence%20remains%20inconclusive.&text=Men%20and%20women%20are%20affected,based%20comparisons%20of%20brain%20structure.
19. https://www.nhs.uk/live-well/alcohol-advice/the-risks-of-drinking-too-much/
20. https://www.cdc.gov/alcohol/about-alcohol-use/moderate-alcohol-use.html
21. https://pmc.ncbi.nlm.nih.gov/articles/PMC1768013/
22. https://www.ox.ac.uk/news/2017-06-07-even-moderate-drinking-linked-decline-brain-health
23. https://www.bmj.com/content/357/bmj.j2353
24. https://www.thehrdirector.com/business-news/culture/employees-ditching-office-christmas-party-avoid-colleagues-boozy-behaviour/
25. https://www.alzheimers.org.uk/about-dementia/managing-the-risk-of-dementia/reduce-your-risk-of-dementia/alcohol