15 Mar Alcohol Accelerates Aging of Brain’s Frontal Cortex
MedicalResearch.com Interview with:
Edith V. Sullivan, Ph.D.
Department of Psychiatry & Behavioral Sciences
Stanford University School of Medicine
Stanford, CA 94305-5723
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Alcohol misuse is a major public health problem worldwide with profound health consequences on the body, brain, and function. Our research group has conducted naturalistic yet controlled studies of alcohol dependence for several decades to further our understanding of when and how alcohol misuse affects specific parts of the brain. In addition, we wanted to know how alcohol misuse interacts with the typical changes in the brain as we grow older. The studies are controlled in that we recruit healthy, non-alcohol dependence men and women from the community to undergo the same screening and neuroimaging procedures as our alcoholic recruits. The studies are quantitative because we use neuroimaging methods (Magnetic Resonance Imaging) that enable us to measure specific regions of brain structural volumes. Consistent collection of such data over the years positioned us to ask whether age and alcohol dependence interact to produce regional brain volume loss beyond the loss that occurs in normal aging.
A number of cross-sectional studies pointed to the likelihood that the effects of alcohol dependence on brain structure would be exacerbated by normal aging, which we do know from longitudinal neuroimaging studies results in shrinkage of cortical gray matter volume and thinning of the cortex. What was particularly striking about our longitudinal study of men and women with alcohol dependence was the acceleration of the aging of brain structure that was especially prominent in the frontal cortex. Critically, even those who initiated dependent drinking at an older age showed accelerated loss.
Because our study sample was large enough, we could also test whether our findings were attributable to conditions that commonly co-occur with alcohol dependence, namely, illicit drug use and hepatitis C. Although both drug use and hepatitis C infection may have exacerbated brain volume loss, these factors did not fully account for the alcoholism-aging interaction we identified.
MedicalResearch.com: What should readers take away from your report?
Response: A take-home message of our results is that old age is not protective against developing alcoholism-related brain volume deficits. Indeed, “we speculate that age-alcohol interactions notable in frontal cortex put older adults at heightened risk for age-associated neurocompromise even if alcohol misuse is initiated later in life” (Abstract).
MedicalResearch.com: What recommendations do you have for future research as a result of this work?
Response: We are continuing to follow study participants as they — and we all —continue to age and anticipate that with prolonged sobriety or perhaps low or controlled drinking that we may be able to detect at least partial recovery of focal brain volume shrinkage we have observed. Given the accelerated aging observed, such recovery may face special challenges from the inexorable march of time.
MedicalResearch.com: Is there anything else you would like to add?
Response: Note how much you drink in a week and take a day off from drinking every week.
Sullivan EV, Zahr NM, Sassoon SA, Thompson WK, Kwon D, Pohl KM, Pfefferbaum A. The Role of Aging, Drug Dependence, and Hepatitis C Comorbidity in Alcoholism Cortical Compromise. JAMA Psychiatry. Published online March 14, 2018. doi:10.1001/jamapsychiatry.2018.0021
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