Alcohol consumption and premature aging. A critical review.
Research conducted during the past ten years has demonstrated that alcoholics resemble yet older nonalcoholics on a variety of behavioral, radiological, electrophysiological, and regional blood flow measures of brain function. These similarities have led to speculation that excessive alcohol consumption causes a premature aging of the brain that, in turn, is responsible for the characteristic structural and functional changes seen in detoxified alcoholics. In this chapter, we discuss some of the conceptual and methodological problems associated with what has become known as the premature-aging hypothesis and review a series of recent studies that have used neuropsychological, computerized-tomography, and evoked-potential techniques to test its validity. We conclude that there is very little compelling empirical support for this intriguing hypothesis and suggest that the neurobehavioral changes seen in alcoholics are merely the reflection of a diffusely distributed pattern of brain damage.
D000368:Aged; D000375:Aging / Q000187:drug effects*; D000437:Alcoholism / Q000503:physiopathology*; D001921:Brain / Q000503:physiopathology; D001925:Brain Damage, Chronic / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects; D003072:Cognition Disorders / Q000503:physiopathology; D004569:Electroencephalography; D005071:Evoked Potentials / Q000187:drug effects; D006801:Humans; D008875:Middle Aged; D011581:Psychological Tests; D011930:Reaction Time / Q000187:drug effects; D019966:Substance-Related Disorders / Q000503:physiopathology*; D009435:Synaptic Transmission / Q000187:drug effects*; D014057:Tomography, X-Ray Computed