Alcohol use disorder (AUD) is a common neuropsychiatric disorder marked by neuropsychological deficits and neurocircuitry brain damage that can lead to serious negative consequences for family, work, and personal well-being. Researchers will share their published findings on the adverse effects of AUD on the brain and its interaction with aging and postural instability at the 46th annual scientific meeting of the Research Society on Alcohol (RSA) in Bellevue, Washington.

“The neuropsychological deficits and neurocircuitry damages of AUD refer to the chronic effects of heavy drinking after the acute effects of alcohol toxicity, or drunkenness, have worn off,” said Edie Sullivan, a professor in the Department of Psychiatry and Behavioral Sciences at Stanford University School of Medicine.

Sullivan described some of the damage and related cognitive deficits that can be caused by excessive drinking: impaired executive functioning can diminish planning and forethought, and the ability to control behaviors such as drinking; weakenedepisodic memory limits the ability to remember and recall new events; and compromised spatial skills lessen the ability to assemble pieces, follow a map, or remember where one’s car is parked. Motor performance is also vulnerable to the effects of chronic drinking, undermining the ability to translate a cognitive thought or plan into a motor action, as well as postural stability while standing and walking.

“This damage to brain function and the related deficits is owing to alcohol’s impact on three principal neurocircuitries,” Sullivan added. “They are the frontocerebellar network, the frontolimbic network, and the frontostriatal network.” Sullivan will provide explanatory slides on her research at the RSA meeting on Sunday, 25 June 2023.

“These three frontal systems play a big role in AUD, as well as during normal aging,” she said. “Our longitudinal studies show that the frontal cortical regions are the last to develop during adolescence and young adulthood and show the fastest accelerating decline in normal aging,” said Sullivan. “So, when AUD and aging intersect, we find accelerated aging, especially in the frontal brain regions.”

Even if drinking is initiated later in life, older drinkers are vulnerable – if not more vulnerable – to a decline in regional brain volumes. Nevertheless, Sullivan added, problem drinkers of any age who reduce or cease consumption may see fewer adverse physical and functional effects of drinking. “Indeed, several studies report that cortical gray matter volume may show some improvement with reduction in drinking.”

AUDs are likely more prevalent than people realize, added Sullivan. “Many people have some level of AUD but less than 10 percent ever get treatment for it,” she said. “I think that our message about the prevalence of heavy drinking by older adults needs to be recognized, along with knowledge about age-alcohol interactions. Just because you are aging and perhaps retired does not make you a safe drinker.”