From the Journals

Alcohol dependence may accelerate aging, frontal cortical deficits

 

Key clinical point: Older alcohol-dependent patients are at greater risk of functional compromise, even if their excessive drinking starts later in life.

Major finding: Individuals with alcohol use disorder show significantly greater deficits in the precentral and superior frontal cortex, compared with age-matched controls.

Data source: Longitudinal study of 116 participants with alcohol dependence and 96 age-matched controls.

Disclosures: The U.S. National Institute on Alcohol Abuse and Alcoholism, and the Moldow Women’s Hope and Heal Fund supported the study. No conflicts of interest were declared.

Source: Sullivan EV et al. JAMA Psychiatry. 2018 Mar 14. doi: 10.1001/jamapsychiatry.2018.0021.

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Study’s evidence ‘compelling’
George F. Koob, PhD

With an aging population that is also showing significant increases in alcohol use and misuse, studies of the interaction between alcohol and aging and the brain are highly significant. The most compelling finding of this study is the impact of that interaction on the frontal cortex volume, because of the key role this region of the brain plays in executive function.

Deficits in frontal cortical volume associated with aging are hypothesized to also result in impulsivity and compulsivity, which opens up the possibility of greater vulnerability to alcohol use disorder later in life. So as excessive alcohol consumption contributes to this aging process, this aging process also might contribute to excessive drinking in the elderly as a form of self-medication of the negative emotional states associated with aging.

“The study ... 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,” wrote George F. Koob, PhD.

Given this, it is critical that strategies be explored and implemented aimed at addressing the misuse of alcohol by older drinkers. “As Yoda might say, ‘Protect their brains, we must.’ ”

George F. Koob, PhD, is affiliated with the National Institute on Alcohol Abuse and Alcoholism at the National Institutes of Health, Rockville, Md. These comments are taken from an editorial (JAMA Psychiatry. 2018 March 14. doi: 10.1001/jamapsychiatry.2018.0009). No conflicts of interest were declared.


 

FROM JAMA PSYCHIATRY

Alcoholism compounds age-associated volume deficits in the frontal cortex, independent of the additional effects of drug dependence or hepatitis C infection, suggests new research published March 14 in JAMA Psychiatry.

Edith V. Sullivan, PhD, and her coauthors reported the results of a 14-year longitudinal study that used magnetic resonance imaging to examine the brains of 116 participants with alcohol dependence and 96 age-matched controls.

They found that participants with alcohol dependence as defined by the DSM-IV had significantly greater gray matter volume deficits in their frontal, temporal, parietal, cingulate and insular cortices, compared with controls – most prominently in the frontal subregions – with the only exception being the occipital lobe. When age was taken into account, age-related volume deficits were seen in the control group in five of the six cortical regions, but the alcoholism group showed a significantly greater deficit in the precentral and superior frontal cortex.

An illustration of the brain Epifantsev/Thinkstock
There was also a correlation trend between total lifetime alcohol consumption and smaller age-adjusted frontal cortical volumes, while participants with later-onset alcoholism also had smaller age-adjusted frontal cortical volumes compared with earlier-onset.

Dr. Sullivan, of the department of psychiatry and behavioral sciences at Stanford (Calif.) University, and her coauthors said the presence of age-alcoholism interactions puts older alcohol-dependent individuals at greater risk of age-associated functional compromise, even if their excessive drinking starts later in life.

More than half of individuals in the alcoholism group (54.5%) also reported drug dependence. The imaging showed that participants with alcohol use disorder who also reported opiate or cocaine use had smaller frontal cortex volumes compared with those who were not drug users. However, the non–drug-dependent participants in the group still showed deficits in precentral, supplementary motor and medial cortices volumes, compared with controls.

“These findings in alcohol-dependent and control participants, examined 1 to 8 times or more during intervals of 1 week to 12.5 years, representing, to our knowledge, the largest and longest-studied group to date, support our study hypotheses regarding alcoholism-associated accelerated aging and cortical volume deficits independent of drug dependence or HCV infection comorbidity,” the authors wrote.

“We observed a selectivity of frontal cortex to age-alcoholism interaction beyond normal aging effects and independent of deficits related to drug dependence.”

The study also showed a correlation between hepatitis C infection, alcoholism, and smaller frontal cortex volumes in those with both, compared with those with alcoholism alone and compared with controls. “Thus, HCV infection, while having focal effects on frontal brain systems, targeted frontally based systems also vulnerable to chronic and extensive alcohol consumption,” the authors wrote. “Whether the compounded untoward effects of alcoholism and HCV infection on brain structure can be ameliorated with successful treatment of the infection remains to be determined.”

Dr. Sullivan and her coauthors cited several limitations. For example, non–alcohol-dependent or HCV-infected comparison groups were not available for analysis.

The study was supported by the National Institute on Alcohol Abuse and Alcoholism, and the Moldow Women’s Hope and Heal Fund. No conflicts of interest were declared.

SOURCE: Sullivan EV et al. JAMA Psychiatry. 2018 Mar 14. doi: 10.1001/jamapsychiatry.2018.0021.

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