Taken together, these data suggest that pain and alcohol may interact in a bi-directional manner, possibly resulting in greater pain and increased alcohol consumption over time. Bi-directional arrows are used to acknowledge that reciprocal influences may occur across associations between pain and alcohol use, and dashed lines are used to illustrate the modest causal evidence derived from the current literature. Dashed, bi-directional lines between moderate and excessive alcohol consumption acknowledge that alcohol use patterns may change (i.e., increase or decrease) over time.
Longitudinal Associations between Pain and Alcohol Use
- We propose potential mechanisms involved in the development of chronic pain in AUD, and we consider implications for pain management in recovery from AUD.
- This dynamic can present unique challenges for recovering individuals suffering from acute and/or chronic pain, as well as for the physicians responsible for treating both conditions.
- Additionally, the study sheds light on the pathways involved in alcohol withdrawal-related allodynia and alcohol-induced neuropathic pain.
- Human laboratory pain models allow researchers to mimic signs and symptoms of painful medical conditions without causing lasting damage.
- For more information about alcohol and cancer, please visit the National Cancer Institute’s webpage «Alcohol and Cancer Risk» (last accessed June 6, 2024).
Regarding ratings of discomfort versus intensity of pain, alcohol alleviates discomfort at lower doses and to a greater extent than intensity, suggesting the effect of alcohol may vary across components of pain. In addition, pain is influenced by alcohol dose and blood alcohol concentration (BAC), with the magnitude of the analgesic effects increasing at higher BACs (Cutter et al., 1976; Gustafson & Kallmen, 1988; Horn-Hofmann et al., 2015; Stewart, Finn, & Pihl, 1995; Thompson, Oram, Correll, Tsermentseli, & Stubbs, 2017). Studies also have shown that alcohol has less of an impact on pain as the BAC drops, due to metabolism, excretion, or evaporation (Duarte, McNeill, Drummond, & Tiplady, 2008; Horn-Hofmann et al., 2015; Zacny, Camarillo, Sadeghi, & Black, 1998). In other words, the analgesic effects of alcohol decrease over the time since the last drink.
A prescription for double trouble: how drinking alcohol fuels chronic pain.
Similarly, the model predicts that intense and/or untreated injury increases allostatic load through similar neural mechanisms enhancing vulnerability to alcohol dependence by affecting relevant alcohol actions upon dysregulated neural circuits. As illustrated in the model, intense and unresolved trauma is also predicted to contribute to allostatic load in this system to influence vulnerability to chronic pain disorders and alcohol dependence. The model also acknowledges the role of genetic influences, such as those discussed previously, on the initial homeostatic responses, as well as the parameters involved in the development of allostatic load.
Protracted exposure to dependence-inducing alcohol concentrations followed by repeated withdrawals also heightens sensitivity to mechanical stimulation through CRF1-receptor dependent mechanisms (Edwards et al., 2012). This suggests that emotional pain (hyperkatifeia) and sensory pain (hyperalgesia) resulting from allostatic-like dysregulation of overlapping pain and addiction pathways could contribute to excessive alcohol use (Fig. 2). In this sense, it has been suggested that addiction could be considered a type of chronic emotional pain syndrome (Koob and Le Moal, 2006, p. 449). One of the important risk factors for relapse to drinking and for the development of AUD and other substance use disorders, is impulsivity.
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Journal of Pain
For example, the dysregulation of brain reward circuitry may play a role in the interrelatedness of depression, chronic pain, and alcohol abuse 6. Alcohol use disorder (AUD) and chronic pain are enduring and devastating conditions that share an intersecting epidemiology and neurobiology. Chronic alcohol use itself can produce a characteristic painful neuropathy, while the regular analgesic use of alcohol in the context of nociceptive sensitization and heightened affective pain sensitivity may promote negative reinforcement mechanisms that underlie AUD maintenance and progression. The goal of this review was to provide a broad translational framework that communicates research findings spanning preclinical and clinical studies, including a review of genetic, molecular, behavioral, and social mechanisms that facilitate interactions between persistent pain and alcohol use.
Understanding how alcohol misuse causes pain is complicated by the fact that pain is not only a symptom of alcohol misuse but also a frequent cause of increased alcohol use. 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). «Alcohol increases gamma-aminobutyric acid Cannabis Marijuana National Institute on Drug Abuse NIDA (GABA) in the brain, which is why we could be seeing some of the psychiatric effects. Even though alcohol helped some fibromyalgia patients, it didn’t have the same level of effect,» says Scott. In a 2019 study, researchers showed that quitting alcohol had a positive effect on most people’s mental well-being. But according to the Centers for Disease Control and Prevention (CDC), drinking less or not at all may help you avoid neurological harm.
Under normal, homeostatic conditions (symbolized by the upper inner oval), alcohol intoxication produces emotional and sensory pain though a compensatory opponent response (i.e., withdrawal) to an initial rewarding and analgesic action. Emotional and sensory pain comprise the initial response to trauma and injury that may be followed by a compensatory analgesic/euphoric response when terminated. When the initiating condition is not resolved (i.e., chronic alcohol intoxication and withdrawal, untreated injury) homeostasis can no longer be sustained. Neural circuits become dysregulated (indicated by the dashed arrow) resulting in an allostatic state (symbolized by the lower inner oval) characterized by persistent hyperkatifeia and hyperalgesia. According to the model, chronic alcohol intoxication and withdrawal increases allostatic load and results in hyperkatifeia and hyperalgesia. Vulnerability to develop chronic pain disorders following intense and/or untreated injury is increased because the ability to restore physiologic stability is compromised by dysregulated neural circuits.
Overall, we found that the incidence of depressive disorders was the highest among ALC women and the lowest among CTRL men. However, PDD was higher in ALC women than in ALC men, in both groups with no history of chronic pain. The incidence of PDD was comparable in ALC men and ALC women with a history of back/neck pain or severe headaches. The incidence of depressive disorders was significantly higher in ALC cohort even in the absence of any chronic pain disorders. In the presence of chronic back/neck problems, ALC individuals still had significantly higher incidence of MDD, MDE, and PDD compared to CTRL individuals.
The prefrontal cortex, amygdala, and nucleus accumbens are all essential components of the alcoholism/addiction circuitry (Volkow & McLellan, 2016). Approximately 15 million Americans suffer from alcohol abuse or dependence (National Survey on Drug Use and Health 2015 (“National survey on drug use and health – SAMHSA,” 2015), and an estimated 116 million American adults suffer from chronic pain (Egli, Koob, & Edwards, 2012; Grant et al., 2004). Bidirectional associations between alcohol use disorder (AUD) and chronic pain syndromes also have been reported (Apkarian, Bushnell, Treede, & Zubieta, 2005; Apkarian et al., 2013; Brennan, Schutte, & Moos, 2005; Egli et al., 2012; Zale, Maisto, & Ditre, 2015).