The effects of alcoholism and addiction reach far beyond the person afflicted with the disease.
Steven Schandler, a senior professor in the department of psychology at the Crean College of Health and Behavioral Sciences, discusses the factors that influence ACOAs or adult children of alcoholics.
Completing his fourth decade at Chapman University, Steven Schandler is the senior Professor of Psychology and Director of the Cognitive Psychophysiology and Addiction Research Laboratories at Chapman University. He received his M.A. in 1974 and Ph.D. in 1976 from the University of Southern California. With over three decades of funding from the National Institutes of Health, the Department of Veterans Affairs and the Alcohol Beverage Medical Rresearch foundation, Professor Schandler has directed a program that examines the interplay of brain and behavior in humans. As a cognitive psychophysiologist, Professor Schandler uses behavioral, physiological, and brain imaging measures to evaluate the brain’s ability to process information while healthy and after deterioration or damage due to aging, substance abuse, or injury. Professor Schandler is a recipient of the Hua-Cheng Wang/Fradkin Distinguished Professorship and twice recipient of the Valerie Scudder Award for outstanding faculty achievement in scholarship and teaching.
Steven Schandler – The Genetics of Addiction
Forty years of studies of the alcoholic family have shown that adults who were born to alcoholic parents, termed Adult Children of Alcoholics or ACOA, display the greatest risk for alcoholism up to 14 times greater than adults who are children of nonalcoholic parents. This increased susceptibility to alcoholism is most associated with alcohol use by the birth father and reflects an inherited, genetic-based risk factor.
ACOAs display the highest incidence of attention disorders of any clinical group. Information processing and functional brain imaging studies show that the attention disruptions displayed by ACOAs represent hyperarousal of brain areas associated with orienting and attention mechanisms. This results in a reduced ability to select and encode relevant from irrelevant information. The greater the information processing demand, the greater the potential for overload of the ACOA’s attentional systems. This finding has led to the theory that when ACOAs consume alcohol, the pharmacokinetics of alcohol depress activity in brain attention systems, resulting in normalization of attention and orienting.
ACOAs reliably report an alcohol-related ‘boost’ in their thinking skills, suggesting that ACOAs are at high risk for alcoholism because their initial experience of an alcohol-related assist in information processing reinforces its continued use. Within this model, the ACOA is disposed to alcohol consumption as a form of self-medication. In the absence of alternative drug or behavioral prophylaxis, this would explain both the ACOA’s risk for alcohol abuse and their resistance to its treatment.
While this may appear as bad news for the children of alcoholic parents, it must be stressed that, as with many diseases, the probability of expressing risk is a combination of inherited, social and environmental factors. While ACOAs may possess an inherited risk for alcohol abuse, they also display a high rate of abstinence.