The role of alcohol use as a risk factor for dementia is complicated. At different times, alcohol has been seen as protective, harmful, or incidental to the risk of dementia. Each of these views is partially correct, and the entire story is not yet fully known. This article discusses some of what we do know.
In small to moderate amounts, alcohol may be neutral or even protective against cognitive decline. Several observations support the idea of alcohol as beneficial. In smaller amounts, alcohol promotes an increase in high-density lipoprotein levels (HDL). This is the “good cholesterol,” and higher HDL levels are associated with lower cardiovascular disease risk.
Alcohol, too, decreases “platelet stickiness,” which is a condition that interferes with the clotting of blood, and it improves the functioning of the endothelial cells that line the interior surface of blood vessels.
Some studies attribute the benefits of moderate alcohol consumption to a component of wine that is independent of its alcohol content: antioxidant polyphenols.
These protective chemicals, abundant in grapes, may strengthen the brain’s ability to fight off oxidative damage and may reduce the accumulation of amyloid plaques between nerve cells in the brain, one of the hallmarks of Alzheimer’s disease (AD). Oxidative damage occurs when our bodies produce very reactive molecules that can adversely interact with other molecules inside of our cells. The resulting inflammation can contribute to a number of age-related diseases.
At the other end of the spectrum, there is plenty of evidence for increased dementia risk among people who abuse alcohol. Alcohol in higher concentrations is thought to have a direct toxic effect on the lining of blood vessels, promoting vascular disease. In addition, alcohol activates a process that damages brain cells, called glutamate excitotoxicity, increases oxidative stress, and interferes with the process of new cell creation known as neurogenesis. Higher levels of alcohol consumption are linked with elevated triglycerides (a type of fat found in the blood) and raised blood pressure, with increased risk for the formation of clots inside of blood vessels (arterial thrombosis) and strokes.
If that were not sufficient cause for concern, researchers on alcohol-related brain damage also point out that thiamine deficiency frequently accompanies excessive alcohol use. Alcohol disrupts thiamine metabolism, and heavy drinkers may also neglect balanced nutrition.
Finally, intoxication may increase the risk for head injuries, themselves contributors to cognitive symptoms and dementia. A remarkable 78 percent of people with diagnosed alcoholism are found on autopsy to have brain pathology, typically including damage to frontal areas, hypothalamus, and cerebellum.
Multiple alcohol-related cognitive syndromes have been described, of which the two most important are alcohol-related dementia (ARD) and Wernicke-Korsakoff syndrome (WKS).
ARD is seen less often than AD. It accounts for only 3 to 5 percent of dementia cases overall, though it’s responsible for a higher number, as many as 10 percent, of those with the early-onset form of dementia. ARD’s symptoms include visuospatial problems (the ability to understand such things as shapes, locations, and directions), impaired working memory, slowed physical movements, and difficulties in executive function (the ability to reason and solve problems).
Compared to people with AD, those with ARD have more highly preserved language skills. Compared to AD patients, those with ARD reflect the demographics of people with alcohol use disorders and tend more often to be younger at onset, male, unmarried, and socially isolated.
In WKS, an initial severe neurological syndrome may leave in its wake the condition called alcohol amnestic disorder. This syndrome, also known as Korsakoff’s psychosis, is characterized by profound difficulty making new memories.
Halting the Progression of Cognitive Decline
In both ARD and WKS, alcohol abstinence can lead to significant improvement. Alcohol abstinence, good nutrition (which may include thiamine supplementation), adequate sleep and activity, and peer support may help someone with ARD avoid further decline. In addition, one study found beneficial effects of treatment with memantine. With such an approach, Terry might be successful in halting the progression of cognitive decline and reclaiming a more satisfying life.