Chronic pain affects an estimated 116 million American adults and costs the nation up to $635 billion each year (Committee on Advancing Pain Research, Care, and Education; Institute of Medicine, 2011). Approximately 18 million Americans suffer from alcohol abuse or dependence, contributing to 100,000 deaths and $185 billion in costs annually (Grant et al., 2004a). Although the relationship between pain and opiate misuse has been extensively studied, considerably less attention has been devoted to the study of pain and alcohol use despite evidence that alcohol ingestion can acutely reduce pain. In addition, associations between chronic pain conditions and alcohol problems have been reported with episodes of alcohol abuse antedating chronic pain in some people and alcohol dependence emerging after the onset of chronic pain in others (Katon et al., 1985). In light of the great public health impact of both alcohol dependence and chronic pain, a mechanistic understanding of this relationship is important for preventing and treating both problems.
Alcohol use (quantity and frequency) and withdrawal history is predicted to be an important determinant of whether allostatic-like negative emotional states induced by chronic pain or stress affect drinking and contribute to the development and maintenance of alcohol dependence. Chronic pain, depressive disorders, and alcohol abuse are widespread health conditions with a high risk for comorbidity 1,2,3,4,5. Chronic pain may contribute to the risk of depression and alcohol abuse, and the associations can be bi-directional 4,7,8,9,10.
Pain and Recovery from AUD
They propose that the use of alcohol for analgesia rapidly gives way to acute tolerance, triggering the need for higher levels of alcohol consumption. Attempts at abstinence lead to alcohol withdrawal syndrome and hyperalgesia, increasing the risk of relapse. Chronic neurobiological changes lead to preoccupation with pain and cravings for alcohol, further entrenching both conditions. To stimulate research in this area, the authors review methodologies to improve the assessment of pain in AUD studies, including self-report and psychophysical methods. Further, they discuss pharmacotherapies and psychotherapies that may target both conditions, potentially improving both AUD and chronic pain outcomes simultaneously.
In the case of a hemorrhagic stroke, rupture of a blood vessel and bleeding into the brain occurs, which prevents normal blood supply to other brain regions. Even some of the non-dependent mice — 40% of non-dependent male mice and 50% of non-dependent female mice — showed allodynia compared to the alcohol-naïve control group. Research is needed to understand the overlaps in pathophysiology and provide better treatment to patients living with both conditions. PsychiatryOnline subscription options offer access to the DSM-5-TR® library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development. GABA is a neurotransmitter in the central nervous system responsible for reducing the activity of neurons.
- When alcohol is administered to rats in a liquid diet for 10 days, analgesic effects peak within 2–4 days and subside with continued administration until pain responses return to baseline levels by day 10 (Gatch, 2009).
- For example, it may be that a history of alcohol abuse (and perhaps additional forms of addictive behaviors) may play a pivotal role in explaining depressive disorders in at least a subset of individuals suffering from chronic pain disorders.
- There is substantial evidence that alcohol consumption can cause unprovoked seizures, and researchers have identified plausible biological pathways that may underlie this relationship (Samokhvalov et al. 2010a).
- This may account for the lack of statistical significance for the difference between the ALC and CTRL groups in age of onset of depressive disorders.
- Prolonged and excessive alcohol exposure itself generates a small fiber peripheral neuropathy in both rodents and humans (Mellion et al., 2011).
Genetic influences on pain, alcohol analgesia and alcohol dependence
Alcohol use disorder (AUD), which encompasses the conditions commonly called alcohol abuse, alcohol dependence and alcohol addiction, affects 29.5 million people in the U.S. according to the 2021 National Survey on Drug Use and Health. Over time, AUD can trigger the development of numerous chronic diseases, including heart disease, stroke, liver disease and some cancers. Initial results derived from human laboratory studies suggest that alcohol may confer acute analgesic effects.
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. We also consider recent evidence that will shape future investigations into novel treatment mechanisms for pain in individuals suffering from AUD. As noted in previous sections, alcohol has been shown to have acute analgesic effects (e.g., Perrino et al., 2008). Therefore, it is possible that some individuals may hold expectancies for pain relief via alcohol consumption.
Neural dysregulation, alcohol dependence and chronic pain
Thus, for example, a glass of wine often contains more than 5 fluid ounces and therefore may correspond to one and a half or even two standard drinks. Jürgen Rehm, Ph.D., received a salary and infrastructure support from the Ontario Ministry of Health and Long-Term Care. This indicates that the inflammatory pathways involved are different and could potentially lead to the development of targeted therapies in the future. If you’re taking medications to manage your pain, talk to your doctor or pharmacist about any reactions that may result from mixing them with alcohol. Pain perception is a subjective, complex, and distributed process that involves multiple structures involved in sensory, emotional, and cognitive processing that interact together concurrently to form the perceived pain experience (Chapman, 2005).
The most important disease conditions in this group are alcohol use disorders (AUDs), which include alcohol dependence and harmful use or alcohol abuse.3 AUDs are less fatal than other chronic disease conditions but are linked to considerable disability (Samokhvalov et al. 2010d). Overall, even though AUDs in themselves do not rank high as a cause of death globally, they are the fourth-most disabling disease category in low- to middle-income countries and the third-most disabling disease category in high-income countries (WHO 2008). Thus, AUDs account for 18.4 million years of life lost to disability (YLDs), or 3.5 percent of all YLDs, in low- and middle-income countries and for 3.9 million YLDs, or 5.7 percent of all YLDs, in high-income countries. However, AUDs do not affect all population subgroups equally; for example, they mainly affect men, globally representing the second-most disabling disease and injury condition for men. In contrast, AUDs are not among the 10 most important causes of disabling disease and injury in women (WHO 2008). This may account for the lack of statistical significance for the difference between the ALC and CTRL groups in age of onset of depressive disorders.
The experience of physical pain also has been reported to be elevated in alcohol dependent patients having high levels of impulsivity, with physical pain being an independent correlate of both subjectively reported and objectively measured levels of impulsivity (Jakubczyk, Brower, et al., 2016). In particular, there seems to be a role for an attention dimension of impulsivity that represents heightened distractibility and compromised do people snort ambien cognitive control, both in AUD (Jakubczyk, Brower, et al., 2016) and in opioid analgesic misuse in chronic pain patients (Marino et al., 2013). In other words, a high level of distractibility, together with poor cognitive control, would indicate that a person has a more difficult time cognitively regulating pain perception, as well as lower control over increasing the likelihood that s/he would engage in substance use rather than attempting to engage in self-control behavior.
