For example, rats show a greater consumption of alcohol over water immediately after an expected highly preferred reward is omitted or reduced to a less preferred value 136–138. Interestingly, reward loss also induces a reduced sensitivity to nociceptive-pain (hypoalgesia) which appears to reflect activation of a compensatory opioid and cannabinoid system to modulate physical and psychological pain as a component of homeostatic and allostatic modifications 74. It is clear that low or moderate amounts of consumed alcohol also exerts clinically relevant hypoalgesic effects in controlled experimental studies with people and animals 50, 55, 56, 139. Similar effects of alcohol and endogenous opioids on nociceptive-pain suggest an intersection of neural circuits, more specifically the opioid-mediated regulation of GABA neurotransmission 109, 140. The possible involvement of alcohol’s effect on inflammation and inflammatory cytokines acting on µ-opioid receptor regulation also needs further investigation 141. Neuro-immune interaction in defensive action, homeostatic recovery, and maintenance is incompletely understood.
About this pain and alcohol addiction research news
- 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.
- These individuals would be in a situation that is analogous to what has been described for opioid analgesic misuse risk in chronic, low-back pain patients who had been prescribed opioid analgesics (Marino et al., 2013).
- Mixing opioids and alcohol can be particularly dangerous since both substances suppress respiration and can cause a person to stop breathing.
- Treatment with steroidal and non-steroidal anti-inflammatory drugs for early musculoskeletal pain conditions have hypoalgesic efficacy, however early anti-inflammatory treatment interfered with a protective effect of acute inflammatory responses against the development of chronic pain in the long-term 26.
In fact, much of the complexity of pain arises from the involvement of higher centers in the brain rather than periphery, thereby making pain a uniquely experienced phenomenon by each individual and, as such, a subjective experience. Such studies have revealed that functional activity in the primary and secondary somatosensory cortices are linked to the sensory-discriminative processing aspect of pain, such as sensing the intensity of pain or discriminating the site of pain (Bushnell et al., 1999; Hofbauer, Rainville, Duncan, & Bushnell, 2001). Anterior cingulate cortex, insular cortex, and prefrontal cortex are linked to affective-motivational processing aspects of pain, such as finding it to be unpleasant and bothersome even though sensory-wise it may be considered to have low intensity (Apkarian et al., 2005; Auvray, Myin, & Spence, 2010; Gu et al., 2012). Attention, expectation, and reappraisal are thought to be the most important contributing factors for the cognitive modulation of pain (Porro et al., 2002; Wiech, Ploner, & Tracey, 2008).
Nociception and nociceptive-pain
Acceptance and Commitment Therapy (ACT) and Dialectical Behavior Therapy (DBT) are evidence-based approaches that incorporate mindfulness practices. ACT emphasizes building psychological flexibility and emphasizes values-congruent practices, while DBT emphasizes the development of emotional regulation and distress tolerance skills. These approaches transform our relationship with our thoughts, emotions, and physical sensations, including pain. This can change the quality of our experience in ways that change the subjective experience of pain as well as the suffering precipitated by it. The researchers found that there was a significant increase in drinking behavior in the group of mice that were dependent on alcohol compared to the non-dependent group.
An important recent study (Vitus et al. 2022) examined alcohol analgesia in chronic jaw pain sufferers at this exposure level (around 0.08 g/dL), which also corresponds to the legal driving limit in several jurisdictions. The major research question explored was whether the efficacy of alcohol to relieve pain might be altered in individuals with a history of chronic pain. Paradoxically, while acute alcohol drinking reduces sensitivity to pain repeated administration of alcohol, like opioids and other analgesic drugs, results in greater sensitivity to physical nociceptive-pain-inducing stimuli (hyperalgesia). Evidence of opioid-induced hyperalgesia after chronic exposure to opioids is well established in preclinical studies and is observed in clinical populations particularly individuals with opioid use disorder 124, 142. Chronic alcohol consumption results in neural alterations that are also seen in chronic pain—a decrease in inhibitory GABA activity along with hyperglutamatergic activity 109, 143, 144. As a multifaceted experience that is not exclusively driven by the noxious input, pain involves much more than sensory activities.
At the Intersection of Alcohol Use Disorder and Chronic Pain
Roberto’s group is continuing studies on how these molecules might be used to diagnose or treat alcohol-related chronic pain conditions. It’s a common misconception that alcohol is an effective painkiller, when in reality alcohol has no direct pain-relieving value. Alcohol doesn’t directly alleviate pain symptoms; it affects the central nervous system so pain is not perceived to be as bad. The greatest pain-reducing effects of alcohol occur when it’s consumed at doses exceeding moderate daily guidelines. Drinking in moderation is defined as limiting alcohol to two drinks a day for men and one drink a day for women. Roberto’s group is continuing studies on how these molecules might be used to diagnose or treat alcohol-related chronic pain conditions.
A prescription for double trouble: how drinking alcohol fuels chronic pain.
Protocols using intermittent chronic alcohol exposure in rodents have been used successfully as reliable and valid animal models of drug and alcohol dependence. Preclinical studies on chronic pain and AUD provide new insight into the reciprocal influences between the common morbidity of pain and alcohol dependence and potential treatment strategies 45. Alcohol can also have robust dose-dependent analgesic properties in healthy human volunteers experiencing experimentally induced nociceptive-pain 50, 51. Although experimental nociceptive-pain differs in many ways with clinical pain, there is evidence that the analgesic properties of alcohol may support self-medication behaviors of pain sufferers. Experimental induction of a moderate but clinically significant acute pain (capsaicin plus heat) increased the urge and intention to drink alcohol in healthy undergraduate students reporting frequent drinking experiences 52. Several studies have reported an association between moderate alcohol use and reduced pain especially in men 51, 53, 54.
Influences of Alcohol on Processes Involved in Pain Perception
Herein, we begin with a review of the neural bases of pain, and we discuss the influence of alcohol on processes involved in pain perception. We then proceed by proposing some potential mechanisms involved in the development of chronic pain in AUD. We found significant escalation of drinking in the dependent group in male and female compared with the non-dependent group. The dependent group developed strong mechanical allodynia during 72 h of withdrawal, which was completely reversed immediately after the voluntary drinking.
- Moreover, recent research suggests that as many as 28 percent of people experiencing chronic pain turn to alcohol to alleviate their suffering.
- The CeA also forms a circuit referred to as the extended amygdala hypothesized to be involved in evaluating the affective value of sensory stimuli.
- Neuro-immune interaction in defensive action, homeostatic recovery, and maintenance is incompletely understood.
- Placebo reduction of nociceptive processing at the level of the spinal cord shows the role of cognition in modulating nociceptive-pain at the level of sensory-discrimination dimension 153.
- 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.
Rather than dismissing such reports as “all in their heads” they should be treated as no less real than any other percept. The extent to which alcohol use, misuse and addiction contributes to ambiguity and disambiguation in the pain system and integrative neural networks may be a fertile area for investigation. 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).
Separately, about half of the mice that were not dependent on alcohol also showed signs of increased pain sensitivity during alcohol withdrawal but, unlike the dependent mice, this neuropathy was not reversed by re-exposure to alcohol. These molecular modulators of nociceptive processing occur at all levels of the pain system including the peripheral nervous system (peripheral nociceptor terminals, dorsal root ganglion) and central nervous system (spinal cord, supraspinal brain circuits) 38. Alcohol can alter these processes by producing dysbiosis of the gut microbiome which then impacts on peripheral nociceptors and the gut-brain communication through several pathways including through the vagus nerve 39, 40. The ability of nociceptors to detect pathogens and modulate the experience of pain through bidirectional neuroimmune integration reflects the broader ability of sensory neurons to interact with the microbiome, including symbiotic (or commensal) microbiota to form a microbiota-gut-brain axis (for review see 35). A role of symbiotic microbes in the causal mediation of nociceptive-pain has been confirmed by the experimental construction of axenic or “germ-free” mice made free from all microorganisms by preventing natural colonization by microorganisms. Behavioral measures of nociception in germ-free mice indicated reduced nociceptor sensitization to experimentally induced inflammatory signals which was reversed with restoration of microbiota using fecal transplants from conventional mice.
One of the important risk factors for relapse to drinking and for the development of AUD and other substance use disorders, is impulsivity. Impulsivity is multidimensional construct referring to a predisposition for individuals to react quickly in response to an internal or external stimulus, without consideration of the possible negative consequences (Lejuez et al., 2010). While not a prominent trait in chronic pain patients, impulsivity may be especially relevant to individuals with AUD who suffer from chronic pain. These individuals would be in a situation that is analogous to what has been described for opioid analgesic misuse risk in chronic, low-back pain patients who had been prescribed opioid analgesics (Marino et al., 2013). 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 cognitive control, both in AUD (Jakubczyk, Brower, et al., 2016) and in opioid analgesic misuse in chronic pain patients (Marino et al., 2013).
This heightened emotional state has a parallel in the pain system in the form of the transition from alcohol-induced analgesia to alcohol-induced hyperalgesia and chronic pain 109. For example, Gatch and Lal 46 showed that alcohol administered to rats acutely (i.p.) induces hypoalgesia (dose-dependently) and when given chronically in a liquid diet. Although the hypoalgesic effect of chronic alcohol shows tolerance, withdrawal of alcohol induces hyperalgesia that is reversed by re-administration of alcohol. Withdrawal-induced hyperalgesia and mechanical allodynia is also seen when alcohol is given as a chronic intermittent ethanol vapor although the effects are moderated by several factors including amount of alcohol exposure and sex 47–49.
Supraspinal structures involved in affective-motivational aspects of pain
Yes, alcohol can cause nerve damage and lead to chronic inflammation, increasing the risk of chronic pain. Alcohol may have temporary, short-term, pain-relieving effects, but it also can have detrimental, long-term effects and actually worsen chronic pain. It not only affects pain directly but can also interact with pain medications, impact sleep, increase stress, and reduce our quality of life. 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.
Research suggests that alcohol has a pain-dampening effect and can relieve hyperalgesia — increased sensitivity to pain — even at nonintoxicating doses. 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. If you use alcohol to relieve your pain, it is important to learn about possible adverse health effects. Affect, mood, and emotion are subjective terms that are not consistently differentiated from one another. Affect is more typically defined as a broad range of subjective experiences that vary in terms of valence (positive to negative) and level of arousal. Emotion and mood are considered distinct phenomena, with the former typically short in duration and directed at a stimulus source.
The Reframe app equips you with the knowledge and skills you need to not only survive drinking less, but to thrive while you navigate the journey. Our daily research-backed readings teach you the neuroscience of alcohol, and our in-app Toolkit provides the resources why alcohol worsens chronic pain and activities you need to navigate each challenge. 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. Lithium chloride (LiCl) is a compound commonly used to establish conditioned taste aversions in preclinical studies using animals. It’s been a long week, and you finally settle in on the couch with a glass of wine, hoping to unwind.
