Anyone who’s ever noticed that they feel more relaxed or outgoing after having a drink or two has seen firsthand alcohol’s impact on the brain. But as you may have guessed, beyond the feel-good vibes, the side effects from your go-to rosé or spicy marg are not overwhelmingly positive. In fact, buzzkill alert: No level of alcohol consumption is considered safe. Casual drinking has been linked to various cancers and cardiovascular problems, and chronic drinking (defined as eight or more weekly drinks for women or 15 or more for men) carries additional risks, especially for the brain.
It’s not just a euphemism; booze kills brain cells—kind of, at least. Because it’s a neurotoxin, alcohol can actually damage the frontal lobes and inhibit the formation of new brain cells. It’s one of the few substances (along with things like caffeine, nicotine, THC, and certain medications) that can break through the blood–brain barrier, a layer of cells that filters out harmful substances so they can’t harm our most vital organ. Once alcohol reaches the brain, it can damage the neurons that reside there. Over many years, this ongoing assault on these cells can cause alcohol-related dementia, a form of brain damage that can lead to cognitive challenges with memory and problem-solving.
Unlike other types of dementia, this type of alcohol-induced neurocognitive disorder usually progresses slowly. By contrast, folks with traditional dementia can deteriorate quite quickly.
Stages of alcohol-related dementia
Alcohol-related dementia ranges drastically in terms of its severity, says Lisa Savage, PhD, a professor of psychology at Binghamton University and the scientific director of the Developmental Exposure Alcohol Research Center. At one end of the spectrum, you have mild to moderate cognitive impairment. In these cases, most of the damage occurs in the frontal cortex and hippocampus, the parts of the brain important for things like planning, problem-solving, self-control, and memory, she explains. “In milder cases, if someone quits drinking, imaging studies have shown there can be recovery of gray matter, but white matter can be permanently damaged,” says Savage. This means folks may regain skills like emotional regulation and motor skills, but not memory and attention capacity.
At the more severe end of the spectrum is Wernicke-Korsakoff syndrome, which is actually two different brain disorders, Wernicke encephalopathy and Korsakoff syndrome, that often occur progressively. Both are caused by brain damage associated with a combination of alcohol use disorder and vitamin B1 (thiamine) deficiency. Chronic heavy drinkers generally have a poorer diet and struggle to absorb thiamine from food, which increases their risk for the condition, explains Kasia Rothenberg, MD, PhD, staff neuropsychiatrist at Cleveland Clinic’s Lou Ruvo Center for Brain Health. “Alcohol deprives us of thiamine. It prevents the vitamin from being absorbed and uses it for its own metabolism, so there isn’t enough of it for other cells to use for other processes in the body,” she says of the mechanism behind the disorders. “If you catch [Wernicke encephalopathy] within a few days [of symptom onset] and give the person a large dose of thiamine, they can recover,” Savage says. “But if you get past that, they go into the Korsakoff phase, and there’s no treatment. Loss of brain tissue has already occurred.”
Symptoms of alcohol-related dementia
The symptoms of alcohol-induced neurocognitive disorders differ from person to person, and also depend on how much brain damage has been done and what areas have been impacted. “In general, if someone keeps drinking, the situation becomes more and more severe,” Dr. Rothenberg says.
