Finally, management of chronic pain in AUD patients cannot be optimized without considering the reciprocal risks and benefits of the treatment choices on exacerbating drinking patterns or increasing the risk of relapse. Opioids in particular may not be appropriate for managing pain in individuals with AUD, as they probably engage the same brain reward pathways as in AUD. Indeed, there is evidence for the involvement of the endogenous cannabinoid system in the pharmacological and behavioral effects of alcohol (Perra et al., 2005). However, gabapentin, a GABA analogue anticonvulsant medication that also is used to treat pain, has been shown to have the benefit of reducing cravings and to significantly delay relapse in individuals with AUD (Brower et al., 2008). Given the analgesic effects of alcohol on pain, pervasiveness of alcohol use as a pain management strategy has proven to be substantial among individuals exhibiting pain.

Pain and Recovery from AUD

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.

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.

Dysfunctional Descending Pain Pathways.

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.

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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.

• Early theories explaining pain in terms of direct dedicated pathways for nociception began to be questioned by paradoxical observations such as the observation of less than severe pain or no pain in soldiers with extensive wounds 151.
• When levels of inflammatory proteins were measured, the researchers discovered that while inflammation pathways were elevated in both dependent and non-dependent mice, specific molecules were only increased in dependent mice.
• When a person stops chronic heavy alcohol use, withdrawal symptoms often cause pain sensitivity to increase.
• The amygdala—consisting of 3 nuclear groups, the basolateral amygdaloid complex (BLA), central nucleus (CeA), and cortical-like group (Co)—is well suited for the integration of sensory/perceptual and affective/emotional information.

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Roberto’s group is why alcohol worsens chronic pain 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.

It is the latter integrative function that transforms nociceptive information from a basic sensory experience (Melzack’s sensory-discrimination dimension) to a constructed perception that is experienced as pain 66, 72. The onset of chronic pain may precede memory problems, and chronic pain has been shown to increase the risk of dementia in older adults (Whitlock et al., 2017). Unfortunately, the assessment of pain in patients who already have been diagnosed with varying types or combinations of types of dementia and amnesia, is especially challenging, and therefore, research and clinical treatment with these populations has been limited and inadequate (Buffum, Hutt, Chang, Craine, & Snow, 2007).

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.

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.

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.

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).

• Because the NFR is moderately positively correlated with verbal reports of pain this measure is also used as an indicator of nociceptive-pain 14.
• 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).
• For instance, it is likely that dopamine release in the mesocorticolimbic dopamine system (precipitated by consuming alcohol) is responsible for relief from acute pain.
• This indicates that the inflammatory pathways involved are different and could potentially lead to the development of targeted therapies in the future.
• 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.

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.

The hidden risks of alcohol use for pain relief

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).