When researchers first began to study the effects of alcohol on the brain, they observed structural brain changes in alcoholics similar to those seen in nonalcoholic subjects as a result of normal chronological aging. These observations gave rise to the “premature aging hypothesis.” Two versions of the hypothesis exist, each with different propositions concerning the period in an alcoholic’s life during which premature aging begins (for reviews, see Ellis and Oscar-Berman 1989; Evert and Oscar-Berman 1995). According to the accelerated aging version of the hypothesis, aging starts to accelerate at whatever age problem drinking begins. This version predicts that young alcoholics will become old before their time and that neuropsychological and brain changes in alcoholics will mimic those found in chronologically older nonalcoholics. According to the increased vulnerability version of the premature aging hypothesis, vulnerability to alcohol-related brain damage is hastened only in people over age 50, in whom the normal manifestations of aging already have begun. This version suggests that because of the increased vulnerability of their brains to alcohol-related damage, older alcoholics will suffer more age-related symptoms and impairment than their nonalcoholic peers and younger alcoholics.
