Combining Laboratory and Ecological Momentary Assessment-based Methods to Determine Age-related Differences in the Relationship Between Alcohol Use, Pain, and Inflammation

About This Grant

PROJECT ABSTRACT Pain and problematic alcohol use have substantial public health consequences and co-occur at high rates. Pain-related alcohol use is common and concerning; although alcohol use may provide short-term relief from pain, it may also worsen pain and alcohol use consequences over time. Understanding the factors that underlie whether physical pain leads to alcohol can inform intervention efforts that address both pain and problematic alcohol use. This project will help understand (1) potential pathways from pain to alcohol use and (2) factors that impact the pain-alcohol relationship over time. Specifically, this project combines laboratory-based pain induction and ecological momentary assessment (EMA – i.e., daily text-message surveys) to investigate two hypotheses of pain-related alcohol use. First, we hypothesize that pain increases negative affect (e.g., anxiety, anger), which then leads to alcohol use (i.e., a mediation effect). Second, we hypothesize that pain-related alcohol use is most prevalent among people with low capacity to modulate their experience of pain (i.e., pain modulatory capacity) and high impulsivity (i.e., moderation effects). To test these hypotheses, we will recruit 225 community adults (aged 25-80). At a baseline laboratory appointment, we will assess individual differences (e.g., negative emotionality, impulsivity), systemic inflammation (via circulating cytokines), and pain modulatory capacity during laboratory pain induction. After baseline, participants will complete a 30-day EMA protocol consisting of five daily assessments via smartphone app. Each smartphone survey will assess substance use, pain, craving, and negative affect. Leveraging these data, we will first test whether the pain-alcohol relationship is mediated by negative affect in daily life (Aim 1). We will also test whether the pain-alcohol relationship is stronger among people with lower pain modulatory capacity and higher impulsivity (Aim 2). Finally, we propose that pain-related alcohol use cannot be fully understood without considering biological age. Age is related to increased pain and chronic pain conditions; decreased negative affect, impulsivity, and pain modulatory capacity; and increased sensitivity to alcohol. Age is also associated with greater inflammation, and the two have similar associations with key facets of pain and alcohol use. It is unclear whether inflammation and aging are independent risk factors for pain and pain-related alcohol use. Thus, we will examine whether effects tested in Aims 1 and 2 vary as a function of age, and whether age and inflammation independently affect pain- related alcohol use (Aim 3). Findings across all aims will determine whether modifiable risk factors are promising intervention targets and whether the relevance of these factors varies as a function of age or inflammation.