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Alcohol and Chronic Pain

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Alcohol consumption has a complex relationship with various orthopaedic diseases and pain neurophysiology. While alcohol can be an effective analgesic for some individuals in the short term, 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 and cannabis.[1]

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.[2][3]

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.[2]

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.[4][5]

Septic arthritis is another condition that can be exacerbated by alcohol abuse due to its immunosuppressive effects, which increase susceptibility to infections.[4]

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.[6][7][8][9]

Peripheral Neuropathy, with damage to the small fibres, is caused by prolonged and excessive alcohol exposure

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.[10] However interestingly, the potency of alcohol as an analgesic appears to be related to the level of alcohol abuse in the drinker.[11]

Moderate alcohol consumption is associated with a reduced likelihood of reporting chronic pain, particularly in men.[1] 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.[12]

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.[13] 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.[14][15]

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.[16][17]

Further Reading

Alcohol and Pain - Scott 2018.pdf
Alcohol Use Disorder and Pain - Edwards 2020.pdf
File:Alcohol use and the pain system - Vigorito 2024.pdf

References

  1. ↑ 1.0 1.1 Vigorito, Michael; Chang, Sulie L. (2024-01-24). "Alcohol use and the pain system". Advances in Drug and Alcohol Research (in English). 4: 12005. doi:10.3389/adar.2024.12005. ISSN 2674-0001. PMC 10880763. PMID 38389900.CS1 maint: PMC format (link)
  2. ↑ 2.0 2.1 González-Reimers, Emilio (2015). "Bone changes in alcoholic liver disease". World Journal of Hepatology (in English). 7 (9): 1258. doi:10.4254/wjh.v7.i9.1258. ISSN 1948-5182.
  3. ↑ Luo, Zhenhua; Liu, Yao; Liu, Yitong; Chen, Hui; Shi, Songtao; Liu, Yi (2017-12). "Cellular and molecular mechanisms of alcohol-induced osteopenia". Cellular and Molecular Life Sciences (in English). 74 (24): 4443–4453. doi:10.1007/s00018-017-2585-y. ISSN 1420-682X. Check date values in: |date= (help)
  4. ↑ 4.0 4.1 Al-Jarallah, Khaled F.; Shehab, Diaa Kh.; Buchanan, W.Watson (1992-12). "Rheumatic complications of alcohol abuse". Seminars in Arthritis and Rheumatism (in English). 22 (3): 162–171. doi:10.1016/0049-0172(92)90016-7. Check date values in: |date= (help)
  5. ↑ Han, Lin; Li, Runze; Lu, Jie; Ren, Wei; Ning, Chunping; Pang, Jingyuan; Sun, Jian; Wang, Yao; Sun, Wenyan; Liu, Zhen; Wang, Can (2023-05). "Association of the Quantity, Duration, and Type of Alcohol Consumption on the Development of Gouty Tophi". Arthritis Care & Research (in English). 75 (5): 1079–1087. doi:10.1002/acr.24968. ISSN 2151-464X. Check date values in: |date= (help)
  6. ↑ Liu, T.; Xu, C.; Driban, J.B.; McAlindon, T.; Eaton, C.B.; Lu, B. (2022-05). "Excessive alcohol consumption and the risk of knee osteoarthritis: a prospective study from the Osteoarthritis Initiative". Osteoarthritis and Cartilage (in English). 30 (5): 697–701. doi:10.1016/j.joca.2022.01.011. Check date values in: |date= (help)
  7. ↑ Xu, Haimuzi; Kang, Ji-Hyoun; Choi, Sung-Eun; Park, Dong-Jin; Kweon, Sun-Seog; Lee, Young-Hoon; Kim, Hye-Yeon; Lee, Jung-Kil; Shin, Min-Ho; Lee, Shin-Seok (2024-06-02). "Increased alcohol intake is associated with radiographic severity of knee and hand osteoarthritis in men". Scientific Reports (in English). 14 (1): 12648. doi:10.1038/s41598-024-63559-x. ISSN 2045-2322. PMC 11144692. PMID 38825629.CS1 maint: PMC format (link)
  8. ↑ To, Kendrick; Mak, Christopher; Zhang, Chen; Zhou, Yuhui; Filbay, Stephanie; Khan, Wasim (2021-09). "The association between alcohol consumption and osteoarthritis: a meta-analysis and meta-regression of observational studies". Rheumatology International (in English). 41 (9): 1577–1591. doi:10.1007/s00296-021-04844-0. ISSN 0172-8172. PMC 8316228. PMID 33745000. Check date values in: |date= (help)CS1 maint: PMC format (link)
  9. ↑ Kim, Seong-Kyu; Bae, Jisuk; Choe, Jung-Yoon (2021-02-12). "The relationship between alcohol consumption and knee osteoarthritis in Korean population over 50 years-old: Results from Korea National Health and Nutrition Examination Survey". Medicine (in English). 100 (6): e24746. doi:10.1097/MD.0000000000024746. ISSN 0025-7974. PMC 10545239. PMID 33578626.CS1 maint: PMC format (link)
  10. ↑ Horn-Hofmann, Claudia; Capito, Eva Susanne; Wolstein, Jörg; Lautenbacher, Stefan (2019-09). "Acute alcohol effects on conditioned pain modulation, but not temporal summation of pain". Pain (in English). 160 (9): 2063–2071. doi:10.1097/j.pain.0000000000001597. ISSN 0304-3959. Check date values in: |date= (help)
  11. ↑ Egli, Mark; Koob, George F.; Edwards, Scott (2012 Sep 11). "Alcohol dependence as a chronic pain disorder". Neuroscience and biobehavioral reviews (in English). 36 (10): 2179. doi:10.1016/j.neubiorev.2012.07.010. PMID 22975446. Check date values in: |date= (help)
  12. ↑ Karimi, Roya; Mallah, Narmeen; Nedjat, Saharnaz; Beasley, Marcus J.; Takkouche, Bahi (2022-09). "Association between alcohol consumption and chronic pain: a systematic review and meta-analysis". British Journal of Anaesthesia (in English). 129 (3): 355–365. doi:10.1016/j.bja.2022.03.010. Check date values in: |date= (help)
  13. ↑ Hung, Hao-Yuan; Chien, Wu-Chien; Chung, Chi-Hsiang; Kao, Li-Ting; Chow, Lok-Hi; Chen, Yuan-Hao; Kotlińska, Jolanta H.; Silberring, Jerzy; Huang, Eagle Yi-Kung (2021-12). "Patients with alcohol use disorder increase pain and analgesics use: A nationwide population-based cohort study". Drug and Alcohol Dependence (in English). 229: 109102. doi:10.1016/j.drugalcdep.2021.109102. Check date values in: |date= (help)
  14. ↑ Borgonetti, Vittoria; Roberts, Amanda J.; Bajo, Michal; Galeotti, Nicoletta; Roberto, Marisa (2023-09). "Chronic alcohol induced mechanical allodynia by promoting neuroinflammation: A mouse model of alcohol‐evoked neuropathic pain". British Journal of Pharmacology (in English). 180 (18): 2377–2392. doi:10.1111/bph.16091. ISSN 0007-1188. PMC 10898491. PMID 37050867. Check date values in: |date= (help)CS1 maint: PMC format (link)
  15. ↑ Avegno, Elizabeth M.; Lobell, Thomas D.; Itoga, Christy A.; Baynes, Brittni B.; Whitaker, Annie M.; Weera, Marcus M.; Edwards, Scott; Middleton, Jason W.; Gilpin, Nicholas W. (2018-09-05). "Central Amygdala Circuits Mediate Hyperalgesia in Alcohol-Dependent Rats". The Journal of Neuroscience (in English). 38 (36): 7761–7773. doi:10.1523/JNEUROSCI.0483-18.2018. ISSN 0270-6474. PMC 6125812. PMID 30054393.CS1 maint: PMC format (link)
  16. ↑ Alexander, Shevon N.; Jeong, Han S.; Szabo-Pardi, Thomas A.; Burton, Michael D. (2023-03). "Sex-specific differences in alcohol-induced pain sensitization". Neuropharmacology (in English). 225: 109354. doi:10.1016/j.neuropharm.2022.109354. Check date values in: |date= (help)
  17. ↑ Secci, Maria E.; Kelley, Leslie K.; Avegno, Elizabeth M.; Holmgren, Eleanor B.; Chen, Lily; Rein, Sydney L.; Engi, Sheila A.; Quinlan, Virginia; Wilson, Lisa; Gilpin, Nicholas W.; Wills, Tiffany A. (2024-02). "Adolescent Alcohol Exposure Produces Sex-Specific Long-term Hyperalgesia via Changes in Central Amygdala Circuit Function". Biological Psychiatry (in English). 95 (3): 207–219. doi:10.1016/j.biopsych.2023.09.006. PMC 10866691. PMID 37717844. Check date values in: |date= (help)CS1 maint: PMC format (link)
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