Signs of biological aging have been seen in the brain and blood in alcoholism

Scientists analyzed postmortem brain and lifetime blood samples from patients with alcohol use disorder and found evidence of accelerated biological aging. A report of the work is published in the journal Alcohol: Clinical and Experimental Research.

Alcohol use disorder (AUD) is associated with increased overall morbidity and mortality. A potential reason for this could be accelerated biological aging, which is influenced by underlying pathological processes such as inflammation. Indications of such a possibility have been obtained in several scattered observations of individual biomarkers in blood and brain samples from alcohol and other substance abuse, but they have not yet been systematically analyzed.

For their work, Lea Zillich from the University of Heidelberg and colleagues from Australia, Finland, Germany, Sweden and the United States used 248 brain samples from the University of Sydney Biobank (91 from the ninth Brodmann field, 94 from the caudate nucleus and 64 from the ventral part of the corpus striatum) and also included data on 16 samples from the University of Texas collection and 17 samples from the Tampere Sudden Death Study. All were collected postmortem from adults with and without SUA without other substance abuse, severe psychiatric disorders, or neurodevelopmental disorders. 179 whole blood samples were collected in Germany from patients undergoing rehabilitation for RUA and otherwise matched healthy individuals.

Epigenetic clocks Levine (PhenoAge, more related to phenotypic age) and Horvath (more strongly reflecting chronological age), telomere length, indirect assessment of telomere length by DNA methylation (DNAmTL) and mitochondrial DNA copy number (mtDNAcn) were used as markers of biological aging. Statistical processing of the data was performed using linear regression models with adjustment for chronological age, sex, smoking and estimation of the proportion of cell types in the sample.

All biomarkers except mtDNAcn showed positive correlation with chronologic age in all samples. By epigenetic clock Levin and DNAmTL, significant signs of biological aging were observed in Brodmann's ninth field and whole blood samples; evaluation by Horvath's clock gave the opposite result for Brodmann's ninth field and similar for blood. No significant association of RUA with telomere length and mtDNAcn was recorded. Objective measurement of telomere length and DNAmTL correlated weakly in blood samples and did not correlate in brain.

The work performed was the first study to simultaneously analyze a set of diverse biomarkers of biological aging in postmortem brain samples and lifetime blood samples. It provided evidence of accelerated biological phenotypic aging in RWA as measured by the PhenoAge clock. Although a strong association was also seen with DNAmTL, this indicator had little correlation with actual telomere length, which should be considered when choosing methods for further aging studies.