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.
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 Healing Fund. No conflicts of interest were declared.
SOURCE: Sullivan EV et al. JAMA Psychiatry. 2018 Mar 14. doi: 10.1001/jamapsychiatry.2018.0021 .
