Alcohol and Chronic Pain

Alcohol consumption has a complex bidirectional relationship with various orthopaedic diseases and pain neurophysiology. While alcohol can be an effective analgesic for some individuals in the short term and pain can motivate alcohol use, long-term consumption is not only a risk factor for multiple diseases, but it can also paradoxically exacerbate pain states analogous to that seen in chronic use of other agents like opioids, nicotine, and cannabis. It can also cause alcoholic neuropathy in almost half of those with alcohol dependence which is often painful.
== Risk Factors ==
Risk factors for alcohol use disorder include lower socioeconomic status, obesity, anxiety and depression, family history of alcohol use disorder, other substance use disorders, and nicotine use.Bonica's Management of Pain 5th Edition. Chapter 21: Pain Psychology Evaluation. Individuals with Alcohol Use Disorder have higher rates of chronic pain.
== Assessment ==
Other than simply asking, alcohol use can be further assessed using the validated AUDIT tool (Alcohol Use Disorders Identification Test) which is a 10-item questionnaire. Scores above 8 are associated with poor health outcomes.
== Associated Medical Diseases ==
Alcohol consumption is associated with several medical diseases. 
Osteoporosis has a well established link to alcohol consumption. This is primarily due to the toxic effects of ethanol on bone remodeling, which inhibits bone synthesis and increases bone resorption.
Osteonecrosis, particularly of the femoral head, is another significant orthopaedic complication linked to alcohol consumption. This condition results from the interruption of blood supply to the bone, leading to bone death and subsequent joint collapse.
Gout is also associated with alcohol consumption, especially with the intake of beer and spirits. Alcohol can increase uric acid levels, leading to the formation of urate crystals in joints, which causes inflammation and pain.
Septic arthritis is another condition that can be exacerbated by alcohol abuse due to its immunosuppressive effects, which increase susceptibility to infections.
Osteoarthritis (OA) has a complex relationship with alcohol. Some studies suggest that excessive alcohol consumption is associated with an increased risk of knee and hip OA, while other studies indicate a potential protective effect of moderate alcohol consumption against OA. However, the evidence remains conflicting and warrants further investigation.
Peripheral Neuropathy, with damage to the small fibres, is caused by prolonged and excessive alcohol exposure. Consider B1 and B6 deficiencies (See Nutritional Peripheral Neuropathies and Alcoholic Neuropathy)
== Pain Neurophysiology ==
Alcohol has complex effects on pain neurophysiology, which can be both analgesic and hyperalgesic depending on the context and duration of exposure.
Acute alcohol consumption has been shown to enhance endogenous pain inhibition mechanisms. Specifically, it boosts conditioned pain modulation (CPM) without affecting temporal summation of pain (TSP). This suggests that the analgesic effects of alcohol may be primarily driven by the enhancement of endogenous pain inhibitory pathways. However interestingly, the potency of alcohol as an analgesic appears to be related to the level of alcohol abuse in the drinker.
Moderate alcohol consumption is associated with a reduced likelihood of reporting chronic pain, particularly in men. A systematic review and meta-analysis found that any alcohol consumption was related to lower odds of chronic pain, with a pooled odds ratio (OR) of 0.76 (95% CI, 0.61-0.95). This association was non-linear, indicating that moderate consumption might be more beneficial than either abstinence or heavy drinking.
Chronic alcohol consumption, however, can lead to tolerance of the analgesic effect and even mechanical allodynia and hyperalgesia. This is particularly in the case of alcohol use disorder (AUD). A nationwide cohort study demonstrated that patients with AUD had a higher adjusted hazard ratio (aHR) for developing pain disorders (aHR = 1.290, 95% CI: 1.045-1.591) and required more analgesics. This suggests that while moderate alcohol consumption might have a protective effect, chronic heavy use exacerbates pain conditions. Withdrawal of alcohol induces hyperalgesia that is reversed by re-initiating alcohol consumption.
There are several potential pathways for the hyperalgesic effect including through neuroinflammatory pathways and changes in central pain processing. For example chronic alcohol exposure reduces GABA activity, increases glutamate activity, and also alters cell signaling in the central nucleus of the amygdala (CeA) and its projections to the periaqueductal gray (PAG), which are critical for descending pain modulation. 
Furthermore, sex-specific differences have been observed in alcohol-induced pain sensitization. Short-term ethanol exposure can induce mechanical and thermal sensitivity, particularly in female mice, through peripheral and central immune and glial activation. Chronic adolescent alcohol exposure also produces long-term hyperalgesia via changes in central amygdala circuit function, with notable sex differences in the effects.
==Further Reading==
== References ==
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