O God, that men should put an enemy in their mouths to steal away their brains!”
Cassio (Act II, Scene iii) William Shakespeare
The Diagnostic and Statistical Manual of Mental Disorders, the official compendium of acceptable psychiatric diagnoses, lists a syndrome called “alcohol-induced persistent dementia.” This condition was once described as the “common end reaction of all alcoholics who do not recover from their alcoholism or do not die of some accident or intercurrent episode.” But alcoholic dementia has never been a frequent diagnosis and alcohol is still not listed as one of the risk factors for dementia. In guidelines for reduction in harm from alcohol consumption, the governments of the US, Canada, Australia, Great Britain and the EU all acknowledge the role alcohol plays in a host of chronic health and social problems, but dementia is not mentioned. Growing epidemiological evidence suggests that this omission is an error, and even that alcohol-related dementia might be a “21st-century silent epidemic.”
Some evidence comes from a 2018 British study that correlated the appearance of dementia with the alcohol habits of British civil servants over a period of 23 years. The data showed that people consuming more than 14 units of alcohol a week (the equivalent of 60gm of alcohol or about 6 drinks) had an increased risk of developing dementia. The more they consumed, the higher the risk. A 2018 French study concluded, from a vast analysis of hospitalizations related to alcohol disorders, that there was a distinct association of alcohol use disorders with all kinds of dementia, that alcohol was responsible for a much greater proportion of dementia than previously estimated, that alcohol should be considered as one of the main causes of dementia appearing before age 65, and that, of all the risk factors related to dementia, alcohol was the easiest one to change.
A subject that doctors and patients avoid
Abstinence, over time, improves the symptoms of alcohol related dementia. Why, then, do we not make vigorous attempts to educate patients and families in the early stages of dementia evaluations about the possibility that ceasing all alcohol intake might be beneficial, and certainly not harmful, no matter what the cause of the dementia? Doctors who evaluate patients for symptoms of dementia should question patients carefully about their current and past alcohol use patterns. Often, they do not. Patients being evaluated for dementia, and the concerned family members who bring them to the doctor, should provide honest and accurate accounts of alcohol use. Often, they do not. Alcohol use is a subject which people tiptoe around for many different reasons, but one which should be addressed openly and compassionately, with an educational goal.
The path of alcohol through the body
The first goal is understanding how alcohol affects the brain, and how age and sex influence its effects. Alcohol is absorbed into the bloodstream within five minutes of entry to the stomach. On its first pass around the body, it is metabolized by an enzyme called alcohol dehydrogenase. This enzyme declines with age and is less active in women than in men. Alcohol that is not metabolized immediately circulates in the blood and is measurable as a “blood alcohol level.” Some of it goes to the liver where it is broken down to a substance called acetaldehyde and some is broken down to acids – all these chemicals escape in urine, as well as in your breath and through the skin (the source of the “morning after” boozy smell that lingers long after the party is over). In the brain, the un-metabolized alcohol enters brain cell membranes and dissolves some of their fats, changing receptors that transmit information from cell to cell. As more and more alcohol is absorbed, blood alcohol levels rise and a predictable sequence of events occurs: mild euphoria, mild in-coordination, then imbalance, confusion, depressed mental activity, stupor, deep anesthesia, and, ultimately, death.
Tolerance reflects changes in brain cell membranes
Depending on tolerance, alcohol’s effects on brain function occur at varying blood alcohol concentrations, with some alcoholics able to remain awake and alert at blood alcohol levels that might kill novice drinkers. Enzymatic breakdown of alcohol occurs a little faster in people accustomed to heavy drinking, but most of their tolerance to alcohol’s effects comes from persistent changes in their brains.
Altered brain cell membranes change the personality
Brain scans of chronic alcoholics typically show atrophy – shrinkage of the brain tissue, and, at autopsy, the brain of a chronic heavy drinker may show loss of some cells and white matter. But unless there are coexisting problems like old trauma, Alzheimer’s disease or vascular damage, there is no specific pathology that identifies alcoholic dementia. In life though, the result of altering brain cell membranes chronically by dissolving parts of them in alcohol is dementia – the gradual disintegration of a personality structure with persistent impairments in attention and memory, problem solving, language use, planning abilities, visuo-spatial understanding, and in emotional control and responsiveness. Memory problems can be the most prominent feature in alcoholic dementia, and emotional instability and paranoia also occur.
Not all bad
Is all alcohol bad for the brain? Not necessarily. Both studies mentioned earlier confirm a modest increased risk of dementia in strict teetotalers, an observation made many times in the past and never well understood. Research in the last decade suggests that small amounts of alcohol enhance the function of the “glymphatic” system, a term coined to describe the way spinal fluid flows deep into the brain and clears waste from it. Sleep and exercise also heighten this pattern of spinal fluid flow. (Exercise is known to have a protective effect on the brain, lowering dementia risk. Sleep deprivation, at its extreme, produces symptoms indistiguishable from dementia. More research into the glymphatic system may help explain these observations.) The slightly increased risk of dementia in teetotalers is not considered a reason to begin drinking for someone who prefers to abstain.
Understanding alcoholic beverages
Knowledge and awareness are keys to moderation in alcohol consumption. The alcohol in beer and wine comes from fermentation of sugars. Alcohol in whiskey, vodka and other spirits comes from distillation and the process produces additional chemicals which are like alcohol, but more toxic. The percentage of alcohol in beers, wines and spirits can vary widely. As a rough guide, standard drinks like a 12 oz. beer (typically 5% alcohol), a 5 oz. glass of wine (12%alcohol) and a 1.5oz. shot glass of distilled liquor (40% alcohol) contain roughly the same amount of alcohol – 12-14 gms. Label reading is important since the percentage of alcohol can vary significantly among different beers and wines. A 12 oz. craft beer may be the equivalent of 1.4 drinks because of a 7% alcohol content.
The risk of dementia begins to climb after about 60gm/week for men and 40gm/week for women on a regular basis – about 5-6 servings. It takes about an hour to metabolize 150 mgm of alcohol/per kilogram of body weight, which translates to about 1 oz. of 90 proof whiskey for a man of average weight. Take in more over that hour and the excess alcohol circulates in the blood and begins dissolving membranes in the brain, and mental effects appear. As alcohol is cleared from the body recovery occurs in the brain and the mental symptoms resolve. With chronic, repetitive, excessive exposure, some changes fail to reverse and dementia is the result.
If you are concerned about alcohol “stealing away your brain,” and want to rethink drinking, there is much useful information for you at the link below.
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