Due to conflicting results across studies, the impact of alcohol consumption on dementia risk has been difficult to determine. While heavy drinking has been consistently linked to increased dementia risk, the evidence regarding light to moderate alcohol use on brain health has been quite variable, with some studies showing a protective effect [1]. How is it possible that alcohol could potentially be both harmful and helpful to the brain? If it is simply a matter of dose, is it possible to find a level that maximizes benefit and minimizes harm? In an effort to try to make sense of all of this conflicting information, we will unpack some of the reasons why it has been difficult to get a clear answer. Then, we will apply this knowledge to better understand the evidence and what it means for us.
COMPLICATING FACTORS
Comparison group: To understand whether alcohol use impacts dementia risk, we need to compare people who drink with those who abstain. For it to be a fair comparison, those two groups should be matched in areas other than alcohol use, such as age, gender, income, etc., which impact dementia risk. This is especially challenging because across the globe, the populations of drinkers and non-drinkers are fundamentally different along these attributes [2]. The most consistent trend is that alcohol use tracks with income, such that higher income countries tend to have a higher percentage of people who drink [3]. And, within a given country, higher income individuals are more likely to drink. Women are more likely to be non-drinkers. Additionally, health status affects the decision to drink, as some medications can interact with alcohol. Since abstainer groups are more likely to have more dementia risk factors due to socioeconomic status, gender, and overall health, the association between drinking and dementia risk could be skewed if these factors are not taken into account.
Lifetime pattern: A person’s pattern of alcohol consumption tends to change over the course of his lifetime, with a tendency to decrease consumption in late life [4]. Many studies use one-time self-reporting of alcohol use conducted during late life, which may underestimate lifetime use and impact findings. An accurate assessment of lifetime dementia risk requires a related assessment of lifetime alcohol consumption. This could help address whether alcohol use during a particular stage of life has an outsized effect on the brain, in either direction. Since brain pathology tends to start several decades before the onset of cognitive symptoms, middle age has emerged as a critical period of future dementia risk. Recent longitudinal studies tracking alcohol consumption and brain health starting in middle age may help find an answer [4; 5].
Quantity of alcohol: One of the most confusing aspects of alcohol studies is the categorization of ‘light’, ‘moderate’, and ‘heavy’ drinking. This is further complicated by the question of what constitutes a standard drink, as this can vary across countries [1]. To get around this problem, most studies instead measure alcohol in terms of units, such that 1 unit = 8 grams of pure alcohol [6]. Depending on the alcohol content, there are typically around 2 to 3 units per serving of wine or beer. Due to the lack of standardization across studies as to how many units qualify as ‘light’, ‘moderate’, and ‘heavy’, these distinctions are hard to interpret.
Frequency: While most studies measure the units of alcohol consumed over the course of a week, many don’t relate it to the pattern of consumption [1]. For example, a person drinking 7 units of alcohol per week could spread them out to have 1 unit per day, or drink all 7 units in one night. At high quantities, alcohol is toxic to the brain [7]. Binge drinking increases the potential for alcohol levels to get high enough to harm the brain, and is consistently associated with worse outcomes than regular consumption at a low level [5].
Type of alcohol: Alcoholic beverages can differ in their alcohol content and nutritional profile. Different types of beverages are preferentially consumed in different parts of the world, and by particular segments of the population [8]. This makes it difficult to determine if there is an optimal type for the brain. Wine is most consistently associated with protective effects. The antioxidant-rich polyphenols in wine are thought to mediate the protective effects, suggesting that the benefits stem from the non-alcoholic components [9]. Wine consumption is also more common in European countries that consume a brain-healthy Mediterranean diet. In the absence of these other dietary components, wine alone may not offer the same benefits. Wine drinkers also tend to have higher socioeconomic status. Relative to the alcohol content, beer tends to have more calories than wine, which may lead to weight gain [10]. Due to their high alcohol content, spirits lend themselves toward binge drinking, which may explain their tendency to be associated with harm [11].
WHAT DOES THE EVIDENCE SAY?
Two large longitudinal cohorts in the UK tracked participants starting in middle age, taking periodic assessments of alcohol use and brain health over the course of 20 to 30 years [4]. One study found that drinking more than 14 units per week (~5 to 7 drinks) was associated with an increased risk for dementia [4]. Brain imaging indicated that those who drank more than 14 units per week were more likely to show brain volume loss [13]. Brain volume was not significantly impacted for occasional drinkers, who drank less than 7 units per week. In the other study, the negative impact to brain volume was detected at consumption levels greater than 7 units per week [5]. Brain volume loss can be considered a form of brain aging. Relative to the average 50-year-old, the brains of those consuming 2 units per day looked two years older than those consuming 1 unit per day, and the degree of brain aging was accelerated even further at higher consumption levels [13]. The brain effects were most prominent in binge drinkers, and those with other risk factors, such as hypertension. A similar study following twins in Sweden for over 40 years, found that consumption of over 12 grams of alcohol per week was associated with an increased risk for dementia, while consumption of less than 5 grams per week did not impact risk [11].
IMPLICATIONS
Taking all of these considerations into account, the evidence generally suggests that the association between ‘light to moderate’ drinking and dementia risk is likely driven by other lifestyle factors, and that the level of alcohol associated with potential harm is lower than most people realize.
In their most recent update, the Lancet Commission added alcohol consumption greater than 21 units per week as modifiable risk factor for dementia [14]. Meanwhile, brain imaging studies suggest that as little as 7 units per week may promote adverse brain changes. The difference may be explained by the higher degree of protective lifestyle factors typically seen in the ‘light to moderate’ (1 to 14 units/week) drinkers, which may allow their brains to better adapt to these changes. However, a role for low level alcohol consumption as part of the protective effects of a healthy diet cannot be ruled out. Based on these studies, the level of alcohol consumption estimated to minimize negative impacts to the brain is the equivalent of two to three drinks per week, which is lower than the current US guidelines [15], but is in line with the recently updated Canadian guidelines [16]. Ideally, this is spread out over the course of the week, which would equate to about one-third of a standard drink per day. Reassuringly, these studies also suggest that, for most people, occasional low volume drinking, such as a glass of wine during special occasions does not meaningfully impact brain trajectories.
Betsy Mills, PhD, is a member of the ADDF's Aging and Alzheimer's Prevention program. She critically evaluates the scientific evidence regarding prospective therapies to promote brain health and/or prevent Alzheimer's disease, and contributes to CognitiveVitality.org. Dr. Mills came to the ADDF from the University of Michigan, where she served as the grant writing manager for a clinical laboratory specializing in neuroautoimmune diseases. She also completed a Postdoctoral fellowship at the University of Michigan, where she worked to uncover genes that could promote retina regeneration. She earned her doctorate in neuroscience at Johns Hopkins University School of Medicine, where she studied the role of glial cells in the optic nerve, and their contribution to neurodegeneration in glaucoma. She obtained her bachelor's degree in biology from the College of the Holy Cross. Dr. Mills has a strong passion for community outreach, and has served as program presenter with the Michigan Great Lakes Chapter of the Alzheimer's Association to promote dementia awareness.
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