Binge-drinking has long been associated with an increased risk of early-onset dementia, such as Alzheimer’s disease. Alzheimer’s disease is characterized by beta-amyloid plaques in the brain. These are clumps of amyloid protein that interfere with transmissions between brain cells. Previous scientific research has suggested that alcohol can affect genes that are important for regulating inflammation and beta-amyloid breakdown in the brain.
Microglial cells are immune cells found in the brain and spinal cord and are associated with brain inflammation. In a healthy brain, these microglial cells break down the amyloid-beta which forms the iconic plaques in Alzheimer’s. When exposed to alcohol, microglial cells express high levels of inflammatory markers and start to suppress their ability to break down the amyloid-beta in the brain.
Interestingly, when researchers from the University of Chicago exposed microglia to alcohol levels similar to those found in binge drinkers, the microglia had a 15% suppression of their ability to break down amyloid-beta.[1]Kalinin, S., Gonzalez-Prieto, M., Scheiblich, H., Lisi, L., Kusumo, H., Heneka, M.T., Madrigal, J.L.M., Pandey, S.C. and Feinstein D.L. (2018) Transcriptome analysis of alcohol-treated microglia reveals downregulation of beta amyloid phagocytosis. Journal of Neuroinflammation 15 (141) This led the researchers to conclude that alcohol may impair the microglia, leaving the brain vulnerable to neurodegeneration.
However, the argument over the link between alcohol consumption and dementia has been recently rekindled by a study in PLOS Medicine.[2]Kim, J.W., Byun, M.S., Yi, D., Lee, J.H., Jo, K., Jeon, S.Y., Sohn, B.K., Lee, J-Y., Kim, Y.K., Shin, S.A., Sohn, C-H. and Lee, D.Y. (2020) Researchers in Korea studied a large sample of 414 individuals with an average age of 71. They found that those who drank one to thirteen standard drinks a week (a ‘standard drink’ is usually a bottle or beer, a small glass of wine or roughly one shot of liquor) had a 66% lower rate of beta amyloid deposits in the brain than abstainers. This suggests that drinking in moderation may actually have a beneficial influence on the development of Alzheimer’s disease.
Another 2018 study found similarly surprising results.[3]Sabia, S., Fayosse, A., Dumurgier, J., Dugravot, A., Akbaraly, T., Britton, A., Kivimaki, M. and Singh-Manoux, A. (2018) Alcohol consumption and risk of dementia: 23 year follow-up of Whitehall II cohort study. British Medical Journal 362 In a large group of 9,000 individuals working in London aged between 35 and 55 back in the 1980s when the study began. Twenty-three years after the study ended, medical records were investigated to identify cases of dementia. They found that abstinence during midlife was associated with a 45% higher risk of developing dementia when compared to those who drank in moderation (one to fourteen units of alcohol per week).
Although these results sound exciting for those of us who enjoy an after-work beer or a glass of wine on the weekend, it’s important to remember that moderation is the key. This study also found, unsurprisingly, that those who drank above the recommended 14 units of alcohol a week had a significantly increased risk of dementia.
So, enjoy sharing this article with your friends and family over a guilt-free glass of wine but remember that no study has ever found excessive drinking beneficial for your brain!
References
↑1 | Kalinin, S., Gonzalez-Prieto, M., Scheiblich, H., Lisi, L., Kusumo, H., Heneka, M.T., Madrigal, J.L.M., Pandey, S.C. and Feinstein D.L. (2018) Transcriptome analysis of alcohol-treated microglia reveals downregulation of beta amyloid phagocytosis. Journal of Neuroinflammation 15 (141) |
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↑2 | Kim, J.W., Byun, M.S., Yi, D., Lee, J.H., Jo, K., Jeon, S.Y., Sohn, B.K., Lee, J-Y., Kim, Y.K., Shin, S.A., Sohn, C-H. and Lee, D.Y. (2020) |
↑3 | Sabia, S., Fayosse, A., Dumurgier, J., Dugravot, A., Akbaraly, T., Britton, A., Kivimaki, M. and Singh-Manoux, A. (2018) Alcohol consumption and risk of dementia: 23 year follow-up of Whitehall II cohort study. British Medical Journal 362 |