Chronic pain affects an estimated 116 million American adults and costs the nation up to $635 billion each year (Committee on Advancing Pain Research, Care, and Education; Institute of Medicine, 2011). Approximately 18 million Americans suffer from alcohol abuse or dependence, contributing to 100,000 deaths and $185 billion in costs annually (Grant et al., 2004a). Although the relationship between pain and opiate misuse has been extensively studied, considerably less attention has been devoted to the study of pain and alcohol use despite evidence that alcohol ingestion can acutely reduce pain. In addition, associations between chronic pain conditions and alcohol problems have been reported with episodes of alcohol abuse antedating chronic pain in some people and alcohol dependence emerging after the onset of chronic pain in others (Katon et al., 1985). In light of the great public health impact of both alcohol dependence and chronic pain, a mechanistic understanding of this relationship is important for preventing and treating both problems. Because pain has a negative impact on alcohol overconsumption among individuals in treatment for AUD, researchers have investigated whether addressing pain within the context of treatment for alcohol or substance use disorders may be beneficial for drinking outcomes.
Early-life stress produces muscle hyperalgesia and nociceptor sensitization in the adult rat
Even some of the non-dependent mice — 40% of non-dependent male mice and 50% of non-dependent female mice — showed allodynia compared to the alcohol-naïve control group. 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. Pain perception is a subjective, complex, and distributed process that involves multiple structures involved in sensory, emotional, and cognitive processing that interact together concurrently to form the perceived pain experience (Chapman, 2005). Therefore, effective measurement of pain perception can be challenging (Chapman, 2005; Rosier, Iadarola, & Coghill, 2002; Younger, McCue, & Mackey, 2009). Despite this challenge, there are a number of validated for assessments of pain intensity and for evaluating multiple dimensions of the pain experience, as well as overall functioning, that rely on subjective perceptions of pain apart from physiologic or neurologic measurements (Younger et al., 2009).
In contrast, AUDs are not among the 10 most important causes of disabling disease and injury in women (WHO 2008). We also reviewed evidence that persons seeking treatment for AUD demonstrated hyperalgesia to a pain induction task during the initial stages of alcohol abstinence (Jochum et al., 2010). Although this finding is consistent with evidence of abstinence-induced hyperalgesia derived from animal models, additional research among humans is sorely needed.
Chronic pain: a review of its epidemiology and associated factors in population-based studies
We found that there were no significantly different temporal patterns in onset of any of the depressive disorders relative to ALC onset. The comparability between ages of onset of alcohol abuse and depressive disorders may be suggestive of overlapping genetic predispositions for these disorders 34. Pain sensitivity and alcohol analgesia are enhanced in alcohol dependent patients and FHP individuals and may also be altered in animal models of genetic vulnerability for alcohol dependence. Studies in rodents selectively bred for differences in alcohol preference also provide partial evidence alcohol preference and pain response covary (Chester et al., 2002; Kampov-Polevoy et al., 1996; but see Kimpel et al., 2003). Given the possibility of a genetic link between pain processing and alcohol dependence, we suggest possible candidates having the potential to influence neurotransmitter systems involved in alcohol dependence and pain.
2. Pain, chronic excessive drinking and alcohol dependence
AUD patients with pain also are likely to report current opioid use (Witkiewitz & Vowles, 2018). But despite numerous reports on the associations between chronic pain and AUD, the underlying mechanisms involved in linking them remain elusive. AUD may share common neural pathways with chronic pain, which may facilitate pain affecting alcohol use patterns, or facilitate modulatory effects of alcohol on pain processing, thereby precipitating the risk of chronic pain development.
- Most of the relevant studies found that a high percentage of heavy alcohol users with epilepsy meet the criteria of alcohol dependence.
- Future experimental research should test whether situational pain increases craving for alcohol or subsequent alcohol consumption.
- In light of the great public health impact of both alcohol dependence and chronic pain, a mechanistic understanding of this relationship is important for preventing and treating both problems.
Future research should test whether engagement of effective pain-coping strategies (e.g., in the context of pain treatment) decreases motivation to drink alcohol over time. Extended periods of alcohol exposure induce pain symptoms and exacerbate chronic pain arising from other sources. Alcoholism is typically accompanied by the emergence of negative emotional states that constitute a motivational withdrawal syndrome when access to alcohol is disrupted (Gilpin and Koob, 2008; Koob, 2003). Chronic alcohol use impacts several peripheral and central nervous system actions, and while it has long been observed that oral alcohol administration increases human pain thresholds, withdrawal from chronic use often increases pain sensitivity as one component of a larger alcohol withdrawal syndrome (Jochum et al., 2010).
Such executive system deficits are hypothesized to play a critical role in the aberrant decision-making that accompanies the transition from drug use Crack Detox Symptoms, Timeline, Medications And Treatment to dependence (George and Koob, 2010), and by this mechanism individuals suffering from chronic pain may be more susceptible to alcohol misuse and poor pain management. Both average volume of alcohol consumption and the level of drinking before the event have been shown to affect suicide risk (Borges and Loera 2010). There also is a clear link between alcohol consumption and aggression, including, but not limited to, homicides (Rehm et al. 2003b). Several causal pathways have been identified that play a role in this link, including biological pathways acting via alcohol’s effect on receptors for the brain signaling molecules (i.e., neurotransmitters) serotonin and γ-aminobutyric acid or via alcohol’s effects on cognitive functioning (Rehm et al. 2003b).
We begin by providing an overview of the background and terminology relevant to the study of both pain and alcohol, reviewing data regarding the co-occurrence of pain and alcohol use disorder, and discussing potential confounds and relevant third variables. We then review studies examining both the effects of alcohol on pain and the effects of pain on alcohol use, and integrate these findings to conceptualize a series of reciprocal interrelations between pain and alcohol. Despite these limitations, our findings may have important implications for understanding the underlying factors contributing to depressive disorders in chronic pain patients. For example, it may be that a history of alcohol abuse (and perhaps additional forms of addictive behaviors) may play a pivotal role in explaining depressive disorders in at least a subset of individuals suffering from chronic pain disorders. Moreover, the presence of chronic pain disorders may delay seeking treatment for ALC, because depression or any other mood disorders stemming from alcohol abuse could be concealed by the presence of chronic pain 43. Since physical pain is thought to be a potential predictor for relapse in individuals who are in recovery, it may be essential to approach treatment of pain as a strategy to also reduce the risk of relapse 44.