The overall goal of this project is to determine the ways in which alcohol use and aging interact to produce effects on sleep and to assess the impact of this interaction. Research performed in the initial years of this grant demonstrated significant finding concerning age, nocturnal breathing and EEG sleep features of alcoholics. Mild-moderate obstructive sleep apnea occurred in 16% of a sample of 77 subjects, well above the norms for age, and was more severe in older subjects. After detoxification, sleep was still markedly abnormal with poor sleep efficiency, lighter sleep stages, shortened REM latency, and increased phasic activity in the first REM period. Age but not depressive indices correlated with phasic REM sleep measures. Alcohol given to normal volunteers at bedtime produced impairments in sleep architecture in the first half of the night that was only partly corrected by increased sleep efficiency and deeper sleep in the second half of the night. Computerized EEG delta wave counts after alcohol dosing demonstrated flattening of delta wave production rather than the normal decline of delta across the night. Studies of habitual alcohol use in patients seen in a large sleep center demonstrated increased periodic leg movements, especially in older patients, and evidence of circadian dysregulation in sleep apneics manifested by decreased REM sleep in naps. For the continuation years of this grant, four studies are planned to clarify the interaction between alcohol use, sleep disruption, and aging and to identify specific underlying factors that contribute to the interaction. A larger sample of 125 alcoholics will be assessed clinically and polysomnographically to determine more precisely the prevalence of sleep apnea in this population and the contribution of age, sex, body-mass index, smoking and sleep/wake schedule disturbance to the severity of apnea. Twenty apneic alcoholics identified with the initial assessment will be reassessed clinically and with polysomnography 3 and 12 months after initial evaluation to assess the course of apnea in these subjects and the impact of relapse or continued sobriety. In normal controls and in non-alcoholic apneics, the acute effects of 2 doses of ethanol on nocturnal respiration and EEG sleep measures will be assessed with the goal of determining the extent to which age, sex, body-mass index, smoking history, and sleep-wake patterns contribute to the exacerbation of apnea and the disruption of sleep architecture with alcohol use. Finally, motor vehicle accidents and driving violations will be assessed in large samples of alcoholics and sleep apneics to determine the interaction of alcohol se, sleep apnea, and aging in contributing to these highly significant social consequences of the behavioral morbidity associated with sleep apnea.
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