Titre : Hep C Compounds Alcoholism’s Effect on Brain Volume
link : Hep C Compounds Alcoholism’s Effect on Brain Volume
Hep C Compounds Alcoholism’s Effect on Brain Volume
StudyJAMA Psychiatry Published March 14, 2018
Full Text Article: The Role of Aging, Drug Dependence, and Hepatitis C Comorbidity in Alcoholism Cortical Compromise
Findings
This combined cross-sectional/longitudinal study evaluated magnetic resonance imaging data collected during 14 years in 199 control and 222 alcohol-dependent participants. Findings revealed frontally distributed cortical volume deficits in individuals with alcohol dependence, accelerated age-dependent decline, and compounded deficits with drug dependence or hepatitis C virus infection comorbidity.
Meaning
These findings raise concern for heightened risk of accelerated cortical aging with alcohol dependence even when alcohol misuse develops later in life.
In The Media
Hep C Compounds Alcoholism’s Effect on Brain VolumeIn The Media
Last Updated: March 16, 2018.
Media Source - DoctorsLounge
FRIDAY, March 16, 2018 (HealthDay News) -- Alcohol dependence has deleterious effects on frontal cortical volumes that are compounded by hepatitis C virus (HCV) infection and drug dependence, according to a study published online March 14 in JAMA Psychiatry.
Edith V. Sullivan, Ph.D., from the Stanford University School of Medicine in California, and colleagues examined cortical volume deficits using 826 structural magnetic resonance images from 222 individuals with alcohol dependence and 199 age-matched control participants. Longitudinal data were available for 116 participants with alcoholism and 96 controls.
The researchers found that participants with alcohol dependence had volume deficits in frontal, temporal, parietal, cingulate, and insular cortices; the deficits were prominent in fontal subregions and were not dependent on sex. In the frontal cortex and precentral and superior gyri, accelerated aging occurred; this could not be attributed to the amount of alcohol consumed, which was greater in younger- versus older-onset participants with alcoholism. Smaller frontal volumes were seen for alcohol plus cocaine and alcohol plus opiate groups versus drug-dependence-free alcoholism groups. Greater deficits were seen in those with versus those without HCV infection in frontal, precentral, superior, and orbital volumes; in uninfected participants with alcoholism, total frontal, insular, parietal, temporal, and precentral volume deficits persisted compared with control participants with known HCV status.
"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," the authors write.
Abstract/Full Text
Edith V. Sullivan, Ph.D., from the Stanford University School of Medicine in California, and colleagues examined cortical volume deficits using 826 structural magnetic resonance images from 222 individuals with alcohol dependence and 199 age-matched control participants. Longitudinal data were available for 116 participants with alcoholism and 96 controls.
The researchers found that participants with alcohol dependence had volume deficits in frontal, temporal, parietal, cingulate, and insular cortices; the deficits were prominent in fontal subregions and were not dependent on sex. In the frontal cortex and precentral and superior gyri, accelerated aging occurred; this could not be attributed to the amount of alcohol consumed, which was greater in younger- versus older-onset participants with alcoholism. Smaller frontal volumes were seen for alcohol plus cocaine and alcohol plus opiate groups versus drug-dependence-free alcoholism groups. Greater deficits were seen in those with versus those without HCV infection in frontal, precentral, superior, and orbital volumes; in uninfected participants with alcoholism, total frontal, insular, parietal, temporal, and precentral volume deficits persisted compared with control participants with known HCV status.
"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," the authors write.
Abstract/Full Text
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