It also suggests which inflammatory proteins may be useful as drug targets to combat alcohol-related pain. Researchers have suggested that motivation to consume alcohol for pain-coping may increase when alternative coping strategies have failed (Lawton & Simpson, 2009). Thus, the availability and effectiveness of strategies for coping with pain may relate to drinking motivation in at least two ways. First, the employment of more adaptive approaches to pain-coping may depend on the degree to which an individual believes that consuming alcohol will sufficiently diminish pain reactivity.
NIAAA also encourages research on the impact of alcohol and sleep disturbances on pain through a new funding opportunity (PA ). These efforts, among others, should shed light on how alcohol affects pain and vice versa and could have implications for both treating AUD and managing chronic pain. Opioid analgesics commonly are prescribed to treat physical pain and often are misused to cope with emotional pain. Used separately, alcohol and opioids can cause overdose deaths by suppressing areas in the brain stem that control breathing.
Future research should test whether engagement of effective pain-coping strategies (e.g., in the context of pain treatment) decreases motivation to drink alcohol over time. Recurrent pain is highly prevalent among treatment seeking problem drinkers (Boissoneault, Lewis, & Nixon, 2018; Sheu et al., 2008), and alcoholism is considered a risk factor, both for the development of chronic pain in patients who suffer from AUD, and for relapse in those attempting to remain abstinent. But despite numerous reports on the associations between chronic pain and AUD, the underlying mechanisms involved in linking them remain elusive. AUD may share common neural pathways with chronic pain, which may facilitate pain affecting alcohol use patterns, or facilitate modulatory effects of alcohol on pain processing, thereby precipitating the risk of chronic pain development. It is influenced by a host of familial, biological, environmental, and socioeconomic mediators that affect drinking behavior and susceptibility to pain disorders.
Experimental Investigations of Pain and Alcohol Consumption
It is estimated that 50% to 60% of the total variance in risk for AUD is accounted for by variation in genetic factors (Rietschel & Treutlein, 2013). Twin studies and studies of the offspring of individuals with AUD have shown that family history of AUD mediates the risk of AUD. But controversy exists regarding whether family history is a risk factor through genetic mechanisms, or through environmental mechanisms (e.g., growing up in a household with parents with AUD), or through the interaction of genes and environment. Alcohol Use Disorder and pain are complex conditions having multiple additional etiological impacts reviewed elsewhere (Oscar-Berman et al., 2014; Zale et al., 2015).
George F Koob
Increased pain in the context of alcohol abstinence may be of particular relevance for persons with co-occurring chronic pain and AUD. The fear-avoidance model of chronic pain posits that persons who experience chronic or recurrent pain may be hypervigilant to perceived increases in pain (Leeuw et al., 2007), which suggests that persons with chronic pain may be especially sensitive to hyperalgesia during the early stages of alcohol abstinence. Hyperalgesic responses have been observed during withdrawal from other substances (e.g., nicotine), and researchers have proposed that increased pain may precede relapse (e.g., Ditre et al., 2011). Thus, increased pain in the context of alcohol abstinence and withdrawal may have important clinical implications for the treatment of AUD among persons who experience chronic pain. Chronic pain syndromes have the propensity to trigger the risk of initiating alcohol abuse, or triggering relapse in individuals who had attained abstinence. Characterization of the interrelatedness of alcoholism and pain allows for early detection and treatment of patients at risk for developing chronic pain conditions, and for preemptive interventional approaches to reduce the risk of consequent alcohol abuse.
- Dysregulation of pain neurocircuitry and neurochemistry has been increasingly recognized as playing a critical role in a diverse spectrum of diseases including migraine, fibromyalgia, depression, and PTSD.
- For example, in a study of older adult (ages 55–65) problem drinkers and healthy controls, the drinkers were more likely to report more severe pain, greater pain interference, and more frequent use of alcohol to manage pain (Brennan et al., 2005).
- Chronic Pain refers to the participants with a history of both pain diagnoses (chronic back/neck and frequent/severe headaches).
- For example, ecological momentary assessment (EMA) may provide an optimal method for assessing such covariation in near-real-time.
- The acute effects of alcohol consumption on injury risk are mediated by how regularly the individual drinks.
Alcohol Use Disorder and Chronic Pain: An Overlooked Epidemic
Future work in this area should test relations between pain and subsequent patterns of alcohol consumption using representative samples drawn from the general population, treatment-seeking chronic pain patients, and persons seeking treatment for AUD. For example, longitudinal studies may test whether persons with chronic pain are at greater risk for the development or persistence of AUD. Given evidence that pain may motivate alcohol consumption, researchers have hypothesized that recurring pain may increase alcohol consumption over time (Egli et al., 2012), and further research is needed to identify pain-related factors that may contribute to this transition (e.g., pain frequency, pain duration, affective disturbance). Additionally, researchers have suggested that persons who utilize effective pain coping strategies may experience reduced pain and pain-related distress, which, in turn, could result in decreased motivation to use substances (Ditre, Heckman, Butts, & Brandon, 2010).
The three depressive diagnoses were combined into one factor (Depression) to represent the participants with a history of any depressive disorder (MDE, MDD, or PDD). Chronic Pain refers to the participants with a history of both pain diagnoses (chronic back/neck and frequent/severe headaches). Since previous research has shown that the immune system is activated in response to peripheral alcohol neuropathy, the researchers also examined the activation of the immune response in non-dependent mice with neuropathic pain. Although the links between alcohol use and pain are increasingly appreciated, significant gaps in understanding remain and systematic study of alcohol/pain interactions at all levels, including basic, preclinical, translational, and interventional, is needed. Nearly half of all US adults report drinking alcohol at least once per month (Schiller, Lucas, & Peregoy, 2012), and up to 30% of adults in the general population have met diagnostic criteria for AUD at some point in their can police dogs smell nicotine vapes lifetime (Hasin, Stinson, Ogburn, & Grant, 2007).
Our sample included only individuals who had responded to CPES questions related to chronic pain, depressive disorders, and alcohol abuse, and met the CPES inclusion/exclusion criteria. Demographic information for the total sample and the chronic pain group is included for descriptive purposes. Family history of AUD also could be a mediating risk factor for comorbid affective disorders in pain patients. In a study on the relationship between fibromyalgia and familial history of depression and AUD in first-degree relatives (Katz & Kravitz, 1996), patients who had both fibromyalgia and depression also had higher odds of AUD in their first-degree relatives.
Impaired cognition can modulate the cognitive-evaluative dimension of pain experiences, both as a reinforcing factor for alcohol-seeking behavior (as alcohol is known to alleviate pain) and also in how pain is perceived. Additionally, physiological cues accompanying alcohol consumption can influence drinkers through modulating their expectancy. This may be the main enabling factor in developing chronic pain through reinforcement in susceptible individuals, and a behavioral model of chronic pain (the operant model; (Fordyce, 1976; Sharp, 2001)), suggests that positive and negative reinforcement of acute pain behaviors may lead to the development of chronic pain. It should be noted that this model does not rule out or ignore the role of biological factors in the development of chronic pain, but instead emphasizes the significance of reinforcement and learning in the development and maintenance of chronic pain (Gatzounis, Schrooten, Crombez, & Vlaeyen, 2012). For instance, it is likely that dopamine release in the mesocorticolimbic dopamine system (precipitated by consuming alcohol) is responsible for relief from acute pain.