Chronic Pain and Hazardous Alcohol Consumption Are Associated with Mitochondrial DNA Damage in People Living with HIV

1. Michael D. Ho, 1. Shannon R. Gilstrap, BS., 1. Joanna M. Hobson, BS., 4. Michael A. Owens, PhD, 1Dyan M. White, 3. Melissa J. Sammy, PhD, PhD, 2,3. Scott W. Ballinger, PhD, & 1. Burel R. Goodin, PhD Department of Psychology, University of Alabama at Birmingham (UAB), 1300 University Blvd, Birmingham, AL 35294

Background: People living with HIV (PLWH) demonstrate a high prevalence rate of widespread chronic pain. Chronic pain is associated with substantial functional impairment in PLWH, which is exacerbated by substance use/abuse. PLWH and chronic pain may be more susceptible to alcohol use disorders resulting from the use of alcohol as a coping mechanism for their pain. HIV, chronic pain, and alcohol consumption each promote oxidative stress, which can lead to damage of mitochondria. Excessive mitochondrial damage can have grave implications for cellular energy production. The purpose of this study was to examine whether chronic pain and hazardous alcohol consumption were associated with mitochondrial DNA (mtDNA) damage following acute painful stressors in PLWH. 

Methods: Participants included 23 PLWH and chronic pain and 21 PLWH without chronic pain, who were recruited from an HIV Clinic at a major medical campus. Participants completed a battery of acute painful stressors that included thermal and mechanical noxious stimuli. Blood was drawn before and after exposure to the acute painful stressors to assess change in mtDNA damage. Further, participants self-reported hazardous alcohol use was measured via the 3-item Alcohol Use Disorders Identification Test (AUDIT-C).

Results: Results revealed a statistical trend for the interaction between chronic pain status (with versus without) and hazardous alcohol consumption status (hazardous vs. not hazardous) in relation to mtDNA damage following exposure to acute painful stressors (p = .078). Specifically, PLWH and chronic pain who reported hazardous alcohol consumption demonstrated greater mtDNA damage in response to the acute painful stressors (p = .041) than did PLWH without chronic pain who denied hazardous alcohol consumption (p = .646).

Discussion/Implication: This study provides novel evidence that the combination of chronic pain and hazardous alcohol use may promote mtDNA damage in response to acute injuries and stress for PLWH. 

Additional Abstract Information

Presenter: Michael Ho

Institution: University of Alabama at Birmingham

Type: Poster

Subject: Psychology

Status: Approved

Time and Location

Session: Poster 10
Date/Time: Wed 1:30pm-2:30pm
Session Number: 6597