Alcohol Use Disorder and Chronic Pain: An Overlooked Epidemic

Chronic Pain and Alcohol Abuse

There is also evidence that pain-inhibitory effects of alcohol tend to be reduced among mice with lower concentrations of opioid receptors, and augmented among mice with greater concentrations of opioid receptors (Yirmiya & Taylor, 1989). Finally, there is some evidence that analgesic properties of alcohol may be partially mediated by availability of benzodiazepine receptors (Gatch, 1999). 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.

Conversely, there is some prospective evidence that older adults who endorse more severe pain or a greater number of painful conditions may ultimately go on to reduce their alcohol consumption (Bobo, Greek, Klepinger, & Herting, 2012; Brennan et al., 2011; Brennan & Soohoo, 2013). However, each of these studies sampled older adults who did not necessarily have chronic pain, reported low levels of baseline drinking, and whose patterns of alcohol use may not generalize to other age groups. For example, an age-related decline in alcohol use tends to begin following young adulthood (Shaw et al., 2011), and older adults have evinced a general motivation to reduce alcohol use in response to health concerns (Dawson, Goldstein, & Grant, 2013).

Sex-specific differences in alcohol-induced pain sensitization

Chronic Pain and Alcohol Abuse

Similarly, in a study of community-dwelling older adults, the prevalence of moderate-to-severe past-month pain among problem drinkers (43%) was greater than that observed among non-problem drinkers (30%; Brennan, Schutte, & Moos, 2005). Considering that alcohol use is contraindicated for use of prescription analgesics (FDA, 1998), it is possible that rates of heavy drinking may have been suppressed among some samples, perhaps because patients who use pain medications may be reluctant to report concurrent use of alcohol (e.g., Kim et al., 2013). The analgesic effects of alcohol on pain perception have been measured in a variety of ways, including examining pain threshold, tolerance, and pain ratings (e.g., intensity).

  1. 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.
  2. The current review extends previous work by examining associations between pain and various levels of alcohol consumption (including low-to-moderate levels of drinking), and by identifying psychosocial mechanisms that may underlie these relations.
  3. A doctor will take a thorough health history and have you complete questionnaires related to alcohol intake to help diagnose these conditions.
  4. Alcohol use disorder (AUD) and chronic pain are enduring and devastating conditions that share an intersecting epidemiology and neurobiology.
  5. Additionally, people with alcohol use disorder experience allodynia during alcohol withdrawal.

Effects of Alcohol on People Other Than the Drinker

Likewise, people with chronic pain conditions are more likely to have family members with drinking problems (Goldberg et al., 1999; Katon et al., 1985). Another facet of this relationship is revealed in studies showing that people experiencing chronic pain turn to alcohol presumably for relief (e.g., Brennan et al., 2005; Riley and King, 2009). Dysfunction in the brain reward system seems to be considered as the prominent shared pathological link among these conditions 38. However, it is not clear why despite the overlap between neural pathways underlying chronic pain and alcohol abuse, as Effects of Alcohol on Each Part of the Body well as the high comorbidity of both of those conditions with depression, the burden of depressive disorders is greater in people with ALC.

Alcoholic neuropathy

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.

Alcohol-related neurologic disease refers to a range of conditions caused by alcohol intake that affect the nerves and nervous system. Neurologic disorders can include fetal alcohol syndrome, dementia, and alcoholic neuropathy. The effects of alcohol consumption on ischemic stroke5 are similar to those on ischemic heart disease, both in terms of the risk curve and in terms of biological pathways (Patra et al. 2010; Rehm et al. 2010a). On the other hand, alcohol consumption mainly has detrimental effects on the risk for hemorrhagic stroke, which are mediated at least in part by alcohol’s impact on hypertension. It’s not unusual for people with chronic pain to consume alcohol to self-medicate—to drink to help sand down the sharp edges of their pain and turn down the volume of their discomfort.

If the data were available, it would have been interesting to see if depression affected individuals with more severe or prolonged forms of chronic pain at a higher incidence, comparable to ALC individuals. Table 2 provides results of the regression analyses for each depressive disorder, comparing differences between the ALC and CTRL cohorts with and without chronic pain conditions. Moreover, recent research suggests that as many as 28 percent of people experiencing chronic pain turn to alcohol to alleviate their suffering. Despite this, using alcohol to alleviate pain places people at risk for a number of harmful health consequences.

Shared neurocircuitry and neurochemistry enables crosstalk between the diverse disorders such that changes in neural structure and function (i.e., allostatic load) arising from one disorder can affect the others. The model accounts for well-documented comorbidities between alcohol and anxiety disorders (Kushner et al., 2012), anxiety, depression and chronic pain disorders (Gerrits et al., 2012; Gureje et al., 2008) as well as alcohol dependence and pain sensitivity discussed previously. It also predicts that drugs (such as CRF-1 receptor antagonists) acting upon the shared neurocircuits would likely be effective for treating alcohol dependence and pain disorders whereas other pharmacotherapies targeting disorder-specific mechanisms would be effective for one disorder, but not the others. The model also explains observed functional substitutability of acute alcohol withdrawal episodes and restraint stress in provoking social anxiety (Breese et al., 2005). A model of how alcohol intoxication and withdrawal, trauma (stress) and injury transition to the corresponding disease states of alcohol dependence, anxiety disorders/depression, and chronic pain through actions upon an overlapping set of neural circuits (symbolized by the outer oval).

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. People with alcohol use disorder are unable to stop or control their alcohol consumption, even when it causes problems to their health, relationships, and work. Researchers have suggested that motivation to consume alcohol for pain-coping may increase when alternative coping strategies have failed (Lawton & Simpson, 2009).

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