A recent methylome-wide association study (MWAS) clarified its scope, revealing that its findings are based on a subset of 13,970 participants from the larger 15,188-person TruAge dataset. The study identified 1,266 significant methylation changes associated with alcohol consumption, implicating the gene SLC7A11 in mitigating alcohol-related oxidative stress. With rising anxiety over health burdens linked to addiction and mental wellness, these insights signal crucial therapeutic pathways for addressing alcohol use disorders.
“Excessive alcohol consumption is linked to a variety of negative health consequences including, but not limited to, several types of cancers, liver and other organ damage, and cognitive impairment.”
“the biological mechanisms linking alcohol consumption to health outcomes and disease are not fully understood, but likely involve epigenetic mediation of both environmental and genetic risk factors.”
“we conducted the largest and most comprehensive methylome-wide association study (MWAS) of alcohol using a cohort of 13,970 participants.”
“We identified 1,266 methylome-wide significant (p < 9.42×10-08) findings in whole blood.”
“Data for this study come from 15,188 participants who took the TruDiagnostic TruAge test. Specifically, participants provided self-obtained blood spots for epigenetic testing and completed a survey on their personal history, health, and lifestyle.”
“Differentially Methylated Regions. Differentially methylation regions (DMRs) were identified using the comb-p algorithm in Enmix.”
“In all MWASs, a p-value threshold of 9.42×10-08 was used to determine methylome-wide significance.”
“Enrichment analyses were conducted to evaluate the overlap and specificity of MWAS findings across different cell types.”
“The majority of participants were male (58%) and identified as European American (77.8%).”
“SLC7A11 may prevent alcohol-induced oxidative stress damage in brain and liver cells.”
“Alcohol consumption is known to trigger the UPR.”
“A theme that emerged in the pathway analyses was Rho GTPase signaling. This finding is consistent with recent work by our group showing differentially expressed genes in Rho GTPase pathways are related to AUD in a single-nuclei transcriptomic study in the nucleus accumbens of human postmortem brain tissue.”
