In the Journals

Alcohol misuse may accelerate cortical aging in older adults

Edith V. Sullivan

Longitudinal study findings showed that frontal cortical volume shortages in adults with alcohol dependence accelerated age-dependent decline, and the negative effect is compounded by drug dependence or hepatitis C virus infection comorbidity.

These results indicate an increased risk for faster cortical aging associated with alcohol use disorder regardless of whether an individual develops alcohol misuse later in life, according to researchers.

“Alcohol misuse is a major public health problem worldwide with profound health consequences on the body, brain and function,” Edith V. Sullivan, PhD, department of psychiatry and behavioral sciences, Stanford University School of Medicine, told Healio Psychiatry. “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.”

Researchers assessed cross-sectional, longitudinal data to determine the relationship between age and alcoholism, as well as analyze the link between drug dependence and HCV infection comorbidities and cortical volume shortages in patients with alcohol use disorder. They acquired 826 brain MRIs from 222 individuals with alcohol dependence and 199 age-matched controls. The investigators also examined longitudinal data from 116 participants with alcohol dependence and 96 age-matched control participants.

Frontal cortical volume shortages in adults with alcohol dependence accelerated age-dependent decline, and the negative effect is compounded by drug dependence or hepatitis C virus infection comorbidity, according to study findings.
Source:Shutterstock.com

Analysis revealed that adults with alcohol use disorder had volume insufficiencies mainly in the frontal (P < .001), temporal (P = .002), parietal (P < .001), cingulate (P = .002) and insular (P < .001) cortices, that were independent of sex. Data showed that accelerated aging appeared in frontal cortex (P < .02) and precentral (P < .05) and superior gyri (P < .05); however, it was not attributable to how much alcohol was consumed. Younger-onset participants with alcohol use disorder consumed more alcohol than older-onset participants (P < .001).

Overall, 54.5% of participants with alcohol dependence were also drug-dependent, and researchers assessed drug subgroups, including cocaine, cannabis, amphetamines and opiates, compared with drug-dependence–free alcoholism and control groups. People with alcohol dependence who used cocaine (P = .04) and opiates (P = .04) showed smaller frontal volumes than those in the alcoholism group who were not dependent on drugs; however, deficits in precentral (P = .01), supplementary motor (P = .01) and medial (P = .01) volumes persisted in alcohol-dependent participants who were not dependent on drugs compared with participants in the control group.

Adults with HCV experienced greater shortages in frontal (P = .01), precentral (P = .03), superior (P = .03) and orbital (P = .03) volumes than uninfected adults. However, total frontal (P = .02), insular (P = .003), parietal (P = .03), temporal (P = .005) and precentral (P = .01) volume shortages remained in alcohol-dependent participants without HCV compared with controls with HCV.

“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. Even those who initiated dependent drinking at an older age showed accelerated loss,” Sullivan told Healio Psychiatry. “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. A take-home message of our results is that old age is not protective against developing alcoholism-related brain volume deficits.”

In a related editorial, George F. Koob, PhD, of the National Institute on Alcohol Abuse and Alcoholism, NIH, wrote, “The study by Sullivan et al provides compelling evidence that alcohol misuse during later adulthood could confer a greater risk of deficits in frontal lobe function beyond the deficits that typically occur with aging. Given the rapidly growing aging population in the United States, it is critical that we improve and implement strategies to address alcohol misuse among older drinkers.” – by Savannah Demko

Disclosures: The authors report no relevant financial disclosures. Koob reports no relevant financial disclosures.

Edith V. Sullivan
 

Longitudinal study findings showed that frontal cortical volume shortages in adults with alcohol dependence accelerated age-dependent decline, and the negative effect is compounded by drug dependence or hepatitis C virus infection comorbidity.

These results indicate an increased risk for faster cortical aging associated with alcohol use disorder regardless of whether an individual develops alcohol misuse later in life, according to researchers.

“Alcohol misuse is a major public health problem worldwide with profound health consequences on the body, brain and function,” Edith V. Sullivan, PhD, department of psychiatry and behavioral sciences, Stanford University School of Medicine, told Healio Psychiatry. “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.”

Researchers assessed cross-sectional, longitudinal data to determine the relationship between age and alcoholism, as well as analyze the link between drug dependence and HCV infection comorbidities and cortical volume shortages in patients with alcohol use disorder. They acquired 826 brain MRIs from 222 individuals with alcohol dependence and 199 age-matched controls. The investigators also examined longitudinal data from 116 participants with alcohol dependence and 96 age-matched control participants.

Frontal cortical volume shortages in adults with alcohol dependence accelerated age-dependent decline, and the negative effect is compounded by drug dependence or hepatitis C virus infection comorbidity, according to study findings.
Source:Shutterstock.com

Analysis revealed that adults with alcohol use disorder had volume insufficiencies mainly in the frontal (P < .001), temporal (P = .002), parietal (P < .001), cingulate (P = .002) and insular (P < .001) cortices, that were independent of sex. Data showed that accelerated aging appeared in frontal cortex (P < .02) and precentral (P < .05) and superior gyri (P < .05); however, it was not attributable to how much alcohol was consumed. Younger-onset participants with alcohol use disorder consumed more alcohol than older-onset participants (P < .001).

Overall, 54.5% of participants with alcohol dependence were also drug-dependent, and researchers assessed drug subgroups, including cocaine, cannabis, amphetamines and opiates, compared with drug-dependence–free alcoholism and control groups. People with alcohol dependence who used cocaine (P = .04) and opiates (P = .04) showed smaller frontal volumes than those in the alcoholism group who were not dependent on drugs; however, deficits in precentral (P = .01), supplementary motor (P = .01) and medial (P = .01) volumes persisted in alcohol-dependent participants who were not dependent on drugs compared with participants in the control group.

Adults with HCV experienced greater shortages in frontal (P = .01), precentral (P = .03), superior (P = .03) and orbital (P = .03) volumes than uninfected adults. However, total frontal (P = .02), insular (P = .003), parietal (P = .03), temporal (P = .005) and precentral (P = .01) volume shortages remained in alcohol-dependent participants without HCV compared with controls with HCV.

“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. Even those who initiated dependent drinking at an older age showed accelerated loss,” Sullivan told Healio Psychiatry. “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. A take-home message of our results is that old age is not protective against developing alcoholism-related brain volume deficits.”

In a related editorial, George F. Koob, PhD, of the National Institute on Alcohol Abuse and Alcoholism, NIH, wrote, “The study by Sullivan et al provides compelling evidence that alcohol misuse during later adulthood could confer a greater risk of deficits in frontal lobe function beyond the deficits that typically occur with aging. Given the rapidly growing aging population in the United States, it is critical that we improve and implement strategies to address alcohol misuse among older drinkers.” – by Savannah Demko

Disclosures: The authors report no relevant financial disclosures. Koob reports no relevant financial disclosures.