Alcohol-related liver disease also contributes to neurological disturbances associated with heavy drinking (Tarter et al. 1993). The risk of alcoholic liver damage depends on factors such as the drinker’s nutrition, gender, and quantity and pattern of alcohol consumption. Recent research (Tarter et al. 1993) has focused on biological factors involved in protecting liver cells during metabolism; in some alcoholics, these protective mechanisms appear to be impaired. One condition associated with advanced liver disease, including alcoholic liver disease, is hepatic encephalopathy (also called portal-systemic encephalopathy [PSE]). PSE is a progressive metabolic liver disorder that affects intellectual functioning. Alcoholics with PSE have livers so damaged by cirrhosis that the flow of venous blood into the liver is obstructed, allowing toxic substances and metabolic by-products to enter the bloodstream. These toxins, which can include ammonia and manganese, circulate to the brain, where they interfere with the actions of neurotransmitters. The effects of PSE can be reversed to some extent with liver transplantation.
