The brain is damaged by alcohol. It kills off cells and alters critical parts of the brain. Excessive drinking can lead to impairment of thinking and structural brain changes. Alcohol is absorbed directly into the bloodstream through the stomach and the small intestine. Alcohol is distributed throughout water in the body, but not into fatty tissue. The liver breaks down about 90% of alcohol to other chemicals that the body can use.
Alcohol metabolism is a complex process with large individual variations related to absorption, distribution and elimination. These include genetic factors and two in particular (the ADH2 and ALDH2 alleles). These alleles are thought to relate to the development of alcohol dependence. The individual variations in the metabolism of alcohol are responsible for the different toxicity of alcohol in both the liver and other organs like the brain.
In the brain some of the damage is permanent and some appears to be reversible. The brain damage relates to lifetime alcohol consumption as well as associated medical complications. The most important of these is the nutritional vitamin deficiency state – Wernicke-Korsakoff syndrome, which is caused by thiamine deficiency but is seen most commonly in alcoholics. Impairments of brain function that are commonly seen in alcohol dependency include deficits in abstract problem solving, visual-space and verbal learning, memory function, perceptual muscle skills and even muscle function.
The brain in the frontal node may shrink in alcoholics as a whole and independent sections may be affected. Repeated experience of withdrawal from alcohol (most alcoholic patients have multiple episodes of binge drinking followed by abstinence) is also associated with impaired thinking function
The Wernicke-Korsakoff syndrome and hepatic brain disease, both commonly seen in alcoholics, also cause thinking dysfunction As more alcohol consumed and more damage is sustained the larger the free, non-usable spaces of the brain became.
Alcoholics have a reduced brain weight compared to controls and there is a correlation between the degree of brain wasting and the rate and amount of alcohol consumed over a lifetime. Three genes that are vital to encoding proteins are decreased in the frontal area of alcoholics brains. The identification of these gene changes suggests that some of the diseased changes in the brain in alcoholics could be reversible.
There does not appear to be any link between alcohol-related brain damage and Alzheimer’s disease although there is some work that suggests a relationship between alcohol and ageing. Nerve-fibre shrinkage has been documented in alcoholics. An important point to note is that this shrinkage has also been shown to be reversible in an experimental model following a prolonged period of abstinence.
Shrinkage of the cerebellum (part of the brain) is commonly associated with alcoholism – 26.8% of alcoholics with Wernicke-Korsakoff syndrome had cerebellum shrinkage. Pathological studies have shown that there is a loss of cells in other parts of the brain (reduced on average by 43%), which relates to clinical inability to completely co-ordinate muscles. There was a 36% loss of cells in the side lobes of the cerebellum that is associayed with ‘mental signs’. This is of particular interest given the recent data suggesting that the cerebellum is important in the organization of higher intellectual thinking. Korsakoff patients have a severe memory-loss syndrome with or without the classical signs of Wernicke’s encephalopathy (confusion, uncoordinated muscles and eye muscle paralysis / involuntary eye movements). New criteria for the diagnosis of Wernicke’s encephalopathy have been formulated that are more useful. Two of the following should be present: dietary deficiency, eye muscle abnormalities, cerebellar dysfunction and either an altered mental state or mild memory impairment. C Harper. The neurotoxicity of alcohol. Human & Experimental Toxicology (2007) 26, 251_257.