Oral Microbiome in Alcohol Use Disorder during inpatient treatment

People with Alcohol Use Disorder (AUD) consume large amounts of alcohol, which has the potential to disrupt oral microbiota. This dysbiosis can cause local oral disease leading to further downstream health conditions. However, little is known about the extent to which alcohol consumption amount and alcohol choice affects the oral microbiome of these individuals. Oral tongue brushings were collected from 22 participants with AUD during an inpatient treatment program at the National Institutes of Health Clinical Center. Clinical measures were collected during the treatment program including smoking history, periodontal disease status, alcohol consumption in the 90 days preceding admission (Timeline Follow Back – TLFB), alcohol choice (AC), alcohol dependence scale (ADS), DSM IV/5 mood and anxiety diagnoses, weekly CPRS scores (Comprehensive Psychological Rating Scale). Each participant's AC was grouped as one of the following: 'beer', 'beer and liquor' (referred to as B/L), 'liquor' or 'wine'. Next generation 16s rRNA gene sequencing amplifying 7 of the 9 hypervariable regions was performed on up to ten oral samples from each participant. Data were analyzed using USEARCH and QIIME2 workflows. During the first two weeks of inpatient treatment, changes in Shannon Diversity Index (SDI) were highly dependent on the AC (p<.005 and p<.002). Wine drinkers had the lowest average SDI (1.86±.03) while B/L and liquor drinkers had higher average SDI (2.26±.02 and 2.32±.03, respectively) through the course of the inpatient treatment. Smokers had a significantly higher average SDI than non-smokers (1.99±.08 vs. 2.33±.07, p<.05), but the amount of alcohol consumed prior to admission did not impact SDI. Periodontal disease status was not associated with significant changes in SDI. During the first week of the inpatient program, higher depression scores (MADRS) were associated with lower SDI (r=-.49, p<.02). In addition, initial breath alcohol content scores were also associated with lower initial SDI (r=-.49, p<.02). Contact: Jennifer J. Barb. This submission was powered by METAGENOTE (https://metagenote.niaid.nih.gov).