Association between alcohol consumption and chronic pain: a systematic review and meta-analysis

Chronic Pain and Alcohol Abuse

Chronic pain syndromes have the propensity to trigger the risk of initiating alcohol abuse, or triggering relapse in individuals who had attained abstinence. Characterization of the interrelatedness of alcoholism and pain allows for early detection and treatment of patients at risk for developing chronic pain conditions, and for preemptive interventional approaches to reduce the risk of consequent alcohol abuse. Because pain can be a significant risk factor for relapse in those recovering from AUD, there is an urgent need to understand the links between AUD and development of chronic pain. As mainly central rather than peripheral mechanisms are thought to be involved in the chronification of pain, identifying structural and functional differences in the brain in relation to AUD is key to recognizing links between the two conditions. 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.

Not only does early and protracted abstinence induce a type of pain characteristic of early recovery, but it also has the tendency to exacerbate dysregulated nociception (Egli et al., 2012). In cases where pain among AUD individuals results from a comorbid condition (e.g., cancer, neuralgia, fibromyalgia), abstinence of any duration can reveal the presence and intensity of pain that was previously being masked by the analgesic effects of alcohol. This dynamic can present unique challenges for recovering individuals suffering from acute and/or chronic pain, as well as for the physicians responsible for treating both conditions. Overall, the effects of alcohol consumption on cardiovascular disease are detrimental in all societies with large proportions of heavy-drinking occasions, which is true for most societies globally (Rehm et al. 2003a). For example, studies in Lithuania (Chenet et al. 2001) found that cardiovascular deaths increased on weekends, when heavy drinking is more common. Also, when overall consumption was reduced in the former Soviet Union (a country with a high proportion of heavy-drinking occasions) between 1984 and 1994, the death rate from cardiovascular disease declined, indicating that alcohol consumption had an overall detrimental effect on this disease category (Leon et al. 1997).

Interrelations between Pain and Alcohol: An Integrative Review

The individuals in the ALC cohort were slightly younger, and had more men, and fewer Asians than the CTRL cohort. While the overall distribution of education levels was similar between the two cohorts, there were fewer individuals in the ALC cohort who had 16 years or more education. 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. Another family history study on prepubertal children suggested that the risk of prepubertal onset of major depressive disorder in families with a high aggregation of affective disorders is higher when there also is a high prevalence of AUD in the families (Puig-Antich et al., 1989).

Pain catastrophizing predicts alcohol craving in heavy drinkers independent of pain intensity

By doing so, we increased the numbers of subjects in all three cohorts of no pain, chronic back/neck problems, and frequent/severe headaches. Accordingly, we found that the ages of onset of MDE, MDD and even PDD were consistently younger in the ALC cohort independently of the presence or absence of the chronic pain disorders compared to the control cohort. Despite numerous reports on multi-directional associations between chronic pain disorders and depression or alcohol abuse 1,2,6,7,9,15,16,17, it is not clear if depressive disorders carry a different burden for those with and without a history of alcohol abuse in the presence of chronic pain. Consideration of the brain reward system may help to clarify the links among chronic pain, depression, and alcohol abuse by showing their overlapping neuroanatomy. For example, the dysregulation of brain reward circuitry may play a role in the interrelatedness of depression, chronic pain, and alcohol abuse 6. Alcohol use disorder (AUD) and chronic pain are enduring and devastating conditions that share an intersecting epidemiology and neurobiology.

We found that independently of the presence or absence of chronic back/neck pain, the age of onset of MDE was significantly younger in the ALC individuals, but it was comparable to the age of ALC onset. The age of onset of MDD was younger in the ALC cohort in the No Pain group compared to the CTRL cohort, but the difference in the back/neck problems cohort didn’t remain significant after correction for multiple comparisons. There were no significant differences between the age of ALC onset and any of the depressive diagnoses as confirmed by pair-wise t-test comparisons for each disorder. There were no significant differences in the age of onset of MDE, MDD, or PDD between the ALC and CTRL cohorts with frequent/severe headaches, which may in part be due to a sample size issue (see Discussion). Our sample included only individuals who had responded to CPES questions related to chronic pain, depressive disorders, and alcohol abuse, and met the CPES inclusion/exclusion criteria. Demographic information for the total sample and the chronic pain group is included for descriptive purposes.

How does alcohol cause pain?

Chronic Pain and Alcohol Abuse

“This study has uniquely shown that alcohol dependence is not required to worsen pain outcomes and that even moderate drinking can lead to pain pathology, and thus consumption of ethanol is a poor strategy for dealing with pain,” Dr. Nothem told MNT. According to the National Survey on Drug Use and Health, 29.5 million people aged 12 years and older had alcohol use disorder — also known as alcohol abuse, alcohol dependence, or alcohol addiction — in 2021. The investigators found that, of the problem drinkers, approximately 43% of men and 44% of women reported experiencing moderate to severe pain, but in nonproblem drinkers, only 28% of men and 33% of women reported that level of pain. Likewise, pain interfered with daily activities ‘moderately’ to ‘extremely’ among 34% of men and 29% of women with drinking problems, compared to 16% and 19% of the men and women without drinking problems.

Regarding ratings of discomfort versus intensity of pain, alcohol alleviates discomfort at lower doses and to a greater extent than intensity, suggesting the effect of alcohol may vary across components of pain. In addition, pain is influenced by alcohol dose and blood alcohol concentration (BAC), with the magnitude of the analgesic effects increasing at higher BACs (Cutter et al., 1976; Gustafson & Kallmen, 1988; Horn-Hofmann et al., 2015; Stewart, Finn, & Pihl, 1995; Thompson, Oram, Correll, Tsermentseli, & Stubbs, 2017). Studies also have shown that alcohol has less of an impact on pain as the BAC drops, due to metabolism, excretion, or evaporation (Duarte, McNeill, Drummond, & Tiplady, 2008; Horn-Hofmann et al., 2015; Zacny, Camarillo, Sadeghi, & Black, 1998). In other words, the analgesic effects of alcohol decrease over the time since the last drink. We also found a higher burden of MDE among ALC women compared to ALC men and CTRL men and women. Understanding the similarities and differences between the ALC and CTRL cohorts in depressive disorders is particularly intriguing because alcohol abuse is more prevalent in men than in women 31, while chronic pain disorders and depressive disorders tend to have a higher prevalence in women 32.

Neural dysregulation, alcohol dependence and chronic pain

This finding was surprising given that the hippocampus is a brain region in which new neurons can grow both in adult humans and in adult mice (Mutso et al., 2012). Recent comprehensive reviews of studies evaluating working memory and long-term memory in chronic pain patients reported that the patients commonly complained about poor memory, and that there was a moderate decline in both working memory and long-term memory in chronic pain patients (Berryman et al., 2013; Mazza, Frot, & Rey, 2018). While based on these studies, it seems reasonable to conclude that chronic pain causes memory problems, it is also likely that chronic pain and memory problems may how much did steve harwell drink occur in parallel due to damage in brain structures (such as hippocampus) shared between the two, and caused by something else, without either necessarily causing the other. The prefrontal cortex, amygdala, and nucleus accumbens are all essential components of the alcoholism/addiction circuitry (Volkow & McLellan, 2016).

Co-administration of L-type calcium channel blockers and alcohol has also been shown to reduce hyperalgesia during alcohol abstinence, possibly because L-type calcium channel blockers prevent up-regulation of L-type calcium channels that would otherwise occur in the context of chronic alcohol administration (Gatch, 2009). Despite consistent evidence from the animal literature, and well-documented historical use of alcohol as an anesthetic (e.g., Shealy & Cady, 2002), only a few experimental studies have been conducted among humans to test the causal effects of acute alcohol administration on laboratory pain reactivity. Human laboratory pain models allow researchers to mimic signs and symptoms of painful medical conditions without causing lasting damage. Common paradigms include mechanical pressure, electrical stimulation, and exposure to thermal stimuli.

  1. Used separately, alcohol and opioids can cause overdose deaths by suppressing areas in the brain stem that control breathing.
  2. In the alcohol-dependent mice, allodynia (in which a harmless stimulus is perceived as painful) developed during alcohol withdrawal, and subsequent alcohol intake significantly decreased pain sensitivity.
  3. The interrelationship between chronic pain and AUD resides in the intersection of etiological influences, mental experiences, and neurobiological processes.
  4. Regarding ratings of discomfort versus intensity of pain, alcohol alleviates discomfort at lower doses and to a greater extent than intensity, suggesting the effect of alcohol may vary across components of pain.
  5. Chronic neurobiological changes lead to preoccupation with pain and cravings for alcohol, further entrenching both conditions.
  6. However, PDD was higher in ALC women than in ALC men, in both groups with no history of chronic pain.

As part of the National Institutes of Health Helping to End Addiction Long-Term (HEAL) initiative, NIAAA is encouraging studies to develop and validate biomarkers of comorbid alcohol misuse and chronic pain and that address alcohol misuse in the context of chronic pain management. NIAAA also encourages research on the impact of alcohol and sleep disturbances on pain through a new funding opportunity (PA ). These efforts, among others, should shed light on how alcohol affects pain and vice versa and could have implications for both treating AUD and managing chronic pain. Opioid analgesics commonly are prescribed to treat physical pain and often are misused to cope with emotional pain.

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