Some of the detrimental effects of heavy alcohol use on brain function are similar to those observed with Alzheimer's disease (AD). Although alcohol use may be a risk factor for AD, it is difficult to study this relationship because of similarities between alcoholic dementia and AD and because standard diagnostic criteria for alcoholic dementia have not yet been developed. Similar biological mechanisms may be involved in the effects of AD and alcohol abuse on the brain. Epidemiologic studies have investigated the relationship between alcohol use and AD but have not provided strong evidence to suggest that alcohol use influences the risk of developing AD. Further research is needed before the effect of alcohol use on AD is understood fully. KEY WORDS: Alzheimer's disease; chronic AODE (effects of alcohol or other drugs); AODR (alcohol or other drug-related) dementia; risk factors; cognitive and memory disorder; cholinergic receptors; drug interaction; alcoholic beverage; nicotine; diagnostic criteria; disease course; survey of research
Alzheimer's disease (AD) is a degenative brain disorder characterized by a progressive loss of memory and other detrimental cognitive changes as well as lowered life expectancy (Morris 1999). It is the leading cause of dementia in the United States. Aside from the substantial personal costs, AD is a major economic burden on health care and social services (Ernst and Hay 1994; Leon et al. 1998). Estimates of the number of people with AD in the United States in 1997 ranged from 1 million to more than 4 million, and these figures are expected to quadruple within 50 years unless effective interventions are developed (Brookmeyer et al. 1998). The risk of AD increases exponentially with age (Kawas and Katzman 1999); consequently, as the population ages, the importance of AD as a public health concern grows, as does the need for research on the cause of AD and on strategies for its prevention and treatment.
Studying factors that influence the risk of developing AD may lead to the identification of those at high risk for developing it, strategies for prevention or intervention, and clues to the cause of the disease. Both genetic and environmental factors have been implicated in the development of AD (Kawas and Katzman 1999), but the cause of AD remains unknown, and no cure or universally effective treatment has yet been developed.
Alcohol consumption is one possible risk factor for AD. Alcoholism is associated with extensive cognitive problems (Evert and Oscar-Berman 1995), including alcoholic dementia (Smith and Atkinson 1997). Because alcohol's effects on cognition, brain disorders, and brain chemistry share some features with AD's effects on these three areas, it is plausible that alcohol use might also increase the risk of developing AD (Tyas 1996). Investigating whether and to what degree alcohol use is related to AD is made more difficult by the challenges of diagnosing and distinguishing alcoholic dementia and AD. Such studies are important, however, because alcohol use is a common but preventable exposure, an association between alcohol and AD is biologically plausible, and knowledge of the effect of alcohol on AD may provide clues to the cause of AD.
This article briefly reviews biological evidence suggesting that alcohol use may be associated with AD. It also focuses on the evidence from epidemiologic studies that link people's consumption of alcohol to whether they develop AD, considers the influence of tobacco use on the relationship between alcohol use and AD, and examines the epidemiologic evidence of the connection between alcohol consumption and types of cognitive impairment other than AD.
EFFECTS OF ALCOHOL USE
ON BRAIN DISORDERS AND COGNITION
Heavy alcohol consumption has both immediate and long-term detrimental effects on the brain and neuropsychological functioning (Delin and Lee 1992; Evert and Oscar-Berman 1995). Heavy drinking accelerates shrinkage, or atrophy, of the brain, which in turn is a critical determinant of neurodegenerative changes and cognitive decline in aging (Meyer et al. …