Alcohol converts to acetaldehyde in the liver, which damages neurons and contributes to neurodegenerative diseases like dementia and Alzheimer's.
"If you look at the uh chemistry of alcohol and as when it converts to, well, your liver, acetaldehyde, it kills the neurons every nanosecond and your liver is trying to detox the acetaldehyde from your blood because it knows your brain is dying slowly. So dementia, Alzheimer's, and all the neurodegenerative diseases, you can prevent that by just not drinking." (said at 0:16:00)
Alcohol is metabolized in the liver to acetaldehyde, a reactive metabolite with well-documented neurotoxic potential through protein and DNA adduct formation, and chronic excessive alcohol intake is an established risk factor for brain damage and dementia. However, claiming that alcohol 'kills neurons every nanosecond' and that 'dementia, Alzheimer's, and all the neurodegenerative diseases, you can prevent that by just not drinking' is vastly overstated. Neurodegenerative diseases like Alzheimer's disease and Parkinson's disease are complex and multifactorial, driven substantially by non-modifiable genetic (e.g., APOE ε4) and age-related factors alongside diverse environmental contributors. Furthermore, epidemiological meta-analyses show that heavy alcohol consumption significantly increases dementia risk, but abstaining from alcohol alone cannot eliminate or prevent all neurodegenerative diseases.
- partial: The Role of Mitochondrial Aldehyde Dehydrogenase 2 (ALDH2) in Neuropathology and Neurodege… (Acta neurologica Taiwanica 2016)
"In particular, the α, β-unsaturated aldehydes derived from lipid peroxidation, 4-hydroxynonenal (4-HNE), DOPAL (MAO product of dopamine), malondialdehyde, acrolein and acetaldehyde, all readily form chemical adductions with proteins, DNA and lipids, thus causing neurotoxicity. Mitochondrial aldehyde dehydrogenase 2 (ALDH 2) is a major aldehyde metabolizing enzyme that protects against deleterious aldehyde buildup in brain... In this review, we highlight the deleterious effects of increased aldehydic load in the neuropathology of ischemic stroke, Alzheimer's disease and Parkinson's disease." (abstract, passage verified)
pubmed - context: Alcohol use and dementia: new research directions. (Current opinion in psychiatry 2021)
"The effects of chronic, heavy alcohol use are clearer, with excessive consumption causing alcohol-related brain damage. Several pathways to this damage have been suggested, including the neurotoxic effects of thiamine deficiency, ethanol and acetaldehyde." (abstract, results, passage verified)
pubmedfull study (doi) - context: Alcohol consumption in relation to cognitive dysfunction and dementia: A systematic review… (Ageing research reviews 2024)
"When compared to the reference group of 0 g/day of alcohol intake, the dose-response meta-analysis revealed a significant non-linear (J-shaped) association between alcohol intake and the risk of each of cognitive dysfunction, (lower dose range: 1-30.5 g/day, RR: 0.97; 95 % CI 0.95-0.99; higher dose range: >30.5 g/day, RR: 1.07; 95 % CI 1.01-1.15) and dementia (lower dose range: 1-17.5 g/day, RR: 0.92; 95 % CI 0.88-0.96, higher dose range: >17.5 g/day, RR: 1.23; 95 % CI 1.09-1.35)." (abstract, results, passage verified)
pubmedfull study (doi)