Alcohol consumption has been linked to having both beneficial and harmful effects on the human body and brain
Research studies often contradict each other and findings are difficult to reproduce as methodologies differ vastly. Some researchers study the effects of wine, while others examine the effects of beer or other alcoholic beverages, making their findings a challenge to interpret for clinicians, as most are unable to pinpoint the ingredient responsible for the results.
Should I tell my patients to start drinking if they don’t already drink? Should I tell my patients who already drink to drink more? Should I tell them to drink less? Let’s take a look at four recent studies that examine the effect of alcohol consumption on the brain.
A systematic review, published in Current Clinical Pharmacology, found that light-to-moderate drinking may decrease the risk of Alzheimer’s disease and dementia, while excessive drinking may instead increase the risk.1 Definitions of light-to-moderate drinking and excessive drinking were not provided in the study, and specific beverages remain unknown. Bottom line, if patients don’t drink, there is insufficient evidence to suggest that they should start drinking to protect against dementia.
A more recent study investigated the alcohol type and consumption. The analysis indicated the risk of dementia and Alzheimer’s was highest in patients that surpassed 23 drinks per week, or 38 Gm per day. Modest alcohol consumption, defined as ≤ 12.5 Gm per day, was associated with a reduced risk of dementia, with 6 Gm a day conferring an even lower risk. The risk reduction effect was greatest in patients under 60 years of age, and wine was the drink of choice.
Another study, published in Alcoholism, Clinical and Experimental Research, investigated the association between the consumption of beer and amyloid beta aggregation in the brain. Interestingly enough, beer drinking was associated with a lower extent of amyloid beta aggregation, a statistically significant finding (p=0.02).3 But is it enough to hit the pint? Not really, the authors themselves said no.
Most recently, a study investigated the effects of alcohol on the central nervous system, more specifically, the brain metabolite clearance system (glymphatic function) in mice. They found that 0.5 Gm/kg ethanol exposure increased glymphatic function, whereas 1.5 Gm/kg ethanol exposure suppressed glymphatic function.4 Glymphatic function suppression has been considered a contributing factor to the higher risk of dementia observed in heavy drinkers.
What to tell our patients?
So far evidence points to the old adage, “all excesses are bad.” For patients who don’t drink, none of the evidence suggests they start. For patients who do drink, delve deeper into how much they are really drinking and get more precise answers beyond the usual, “I only drink socially,” or many patients’ favorite, “I only drink one glass a day.” Share with them current evidence that points towards drinking in moderation for the potential of benefit, but definitely to reduce the risk of harm and prolong their health.
References
- Ilomaki, J., Jokanovic, N., Tan, E.C., & Lonnroos, E. (2015). Alcohol consumption, dementia and cognitive decline: an overview of systematic reviews. Current Clinical Pharmacology, 10(3), 204-212.
- Xu, W., Wang, H., Wan, Y., Tan, C., Li, J., Tan, L., & Yu, J.T. (2017). Alcohol consumption and dementia risk: a dose-response meta-analysis of prospective studies. European Journal of Epidemiology, 32(1), 31-42.
- Kok, E.H., Karppinen, T.T., Luoto, T., Alafuzoff, I., & Karhunen, P.J. (2016). Beer drinking associates with lower burden of amyloid beta aggregation in the brain: Helsinki sudden death series. Alcoholism, Clinical and Experimental Research, 40(7), 1473-1478. doi: 10.1111/acer.13102.
- Lundgaard, I., Wang, W., Eberhardt, A., Vinitsky, H.S., Reeves, B.C., Peng, S., Lou, N., Hussain, R., & Nedergaard, M. (2018). Beneficial effects of low alcohol exposure, but adverse effects of high alcohol intake on glymphatic function. Scientific Reports, 8(1), 2246. doi: 10.1038/s41598-018-20424-y.
