If you feel that you sometimes drink too much alcohol, or your drinking is causing problems, or if your family is concerned about your drinking, talk with your health care provider. Other ways to get help include talking with a mental health professional or seeking help from a support group such as Alcoholics Anonymous or a similar type of self-help group. Alcohol withdrawal syndrome occurs when someone who has been drinking excessive amounts of alcohol for an extended period of time suddenly stops drinking or reduces their intake. Females can be more susceptible than males to many of the negative consequences of alcohol use, such as nerve damage, as they may begin to see effects from a lower amount of alcohol consumption. Psychotherapy be extremely beneficial in dealing with chronic pain’s mental and emotional aspects. Because physical and emotional pain are related and activate one another, addressing depression, sadness, frustration, irritability, anger, anxiety, and fear has multi-level benefits.
Analgesia, hyperalgesia and alcohol dependence
Approximately 15 million Americans suffer from alcohol abuse or dependence (National Survey on Drug Use and Health 2015 (“National survey on drug use and health – SAMHSA,” 2015), and an estimated 116 million American adults suffer from chronic pain (Egli, Koob, & Edwards, 2012; Grant et al., 2004). Bidirectional associations between alcohol use disorder (AUD) and chronic pain syndromes also have been reported (Apkarian, Bushnell, Treede, & Zubieta, 2005; Apkarian et al., 2013; Brennan, Schutte, & Moos, 2005; Egli et al., 2012; Zale, Maisto, & Ditre, 2015). The prevalence of AUD is increased in adult patients suffering from chronic pain conditions, partly due to its analgesic properties (Hoffmann, Olofsson, Salen, & Wickstrom, 1995), which may be heightened among individuals with alcohol dependence (Cutter, Maloof, Kurtz, & Jones, 1976). Egli and colleagues (Egli et al., 2012) have even proposed that alcohol dependence itself may stem from aberrant neurobiological substrates of pain, and have conceptualized alcohol dependence as a chronic pain disorder. Understanding the complex relationship between alcohol and pain is an important area of research for the National Institute on Alcohol Abuse and Alcoholism (NIAAA).
Overview of Pain and Alcohol
Potential mechanisms of the acute pain inhibitory effects of alcohol include activation of the endogenous opioid system and response expectancies. Acute alcohol administration has been shown to stimulate the release of endogenous opioids (Mitchell et al., 2012), which may contribute to reduced pain perception. Support for the role of endogenous opioids in alcohol-induced analgesia is further supported by animal studies, which consistently demonstrate that acute pain-inhibitory effects of alcohol can be attenuated via administration of opioid antagonists (e.g., Campbell, Taylor, & Tizabi, 2007). 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).
2. Pain, chronic excessive drinking and alcohol dependence
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).
Listen to relatives, friends or co-workers when they ask you to examine your drinking habits or to seek help. In a 2019 study, researchers showed that quitting alcohol had a positive effect on most people’s mental well-being. But according to the Centers for Disease Control and Prevention (CDC), drinking less or not at all may help you avoid neurological harm. Thus, the researchers estimated that within 1 year, more than 350 deaths were attributed to drinking by others, and more than 10 million Australians (or 70 percent of all adults) were negatively affected by a stranger’s drinking (Laslett et al. 2010).
The model also acknowledges the role of genetic influences, such as those discussed previously, on the initial homeostatic responses, as well as the parameters involved in the development of allostatic load. Dysregulation of pain neurocircuitry and neurochemistry has been increasingly recognized as playing a critical role in a diverse spectrum of diseases including migraine, fibromyalgia, depression, and PTSD. Evidence presented here supports the hypothesis that alcohol dependence is among the pathologies arising from aberrant neurobiological substrates of pain. In this review, we explore the possible influence of alcohol analgesia and hyperalgesia in promoting alcohol misuse and dependence. We examine evidence that neuroanatomical sites involved in the negative emotional states of alcohol dependence also play an important role in pain transmission and may be functionally altered under chronic pain conditions.
The incidence of depressive disorders was significantly higher in ALC cohort even in the absence of any chronic pain disorders. In the presence of chronic back/neck problems, ALC individuals still had significantly higher incidence of MDD, MDE, and PDD compared to CTRL individuals. Differences between the ALC and CTRL cohorts remained significant for MDE and PDD with respect to severe/frequent headaches, but not for MDD. As Table 1 indicates, the majority of individuals in both the ALC and CTRL cohorts reported no history of chronic pain (ALC, 69.1%; CTRL, 74.3%). However, chronic back/neck problems were reported at a higher rate (ALC, 18.3% vs. CTRL, 11.5%) and at an earlier onset (ALC, 25.1 years vs. CTRL, 28.1 years) in the ALC cohort. In comparison, absence of a history of depressive disorders was less common in the ALC group compared to the CTRL solution-focused therapy worksheets pdf group (ALC, 31.3% vs. CTRL, 65.1%).
- Although this finding is consistent with evidence of abstinence-induced hyperalgesia derived from animal models, additional research among humans is sorely needed.
- 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.
- In this sense, it has been suggested that addiction could be considered a type of chronic emotional pain syndrome (Koob and Le Moal, 2006, p. 449).
- Chronic alcohol intoxication and withdrawal, intense and/or untreated injury, or intense and/or unresolved trauma are each capable of increasing allostatic load (indicated by the dashed arrow) to the extent that a dysfunctional state emerges (symbolized by the lower inner oval) characterized by persistent hyperkatifeia and hyperalgesia.
For example, early animal studies on the relationship between alcohol dependence and withdrawal and subsequent self-administration generally yielded equivocal findings most likely because reinforcing effects of alcohol were not established prior to dependence induction (see Heilig et al., 2010; Roberts et al., 2000). Alcohol use (quantity and frequency) and withdrawal history is predicted to be an important determinant of whether allostatic-like negative emotional states induced by chronic pain or stress affect drinking and contribute to the development and maintenance of alcohol dependence. Despite these limitations, our findings may have important implications for understanding the underlying factors contributing to depressive disorders in chronic pain patients.
Alcohol’s Effects on the Body
Importantly, almost 38% of current problem drinkers reported using alcohol to manage pain, whereas in contrast, only 15% of nonproblem-drinking men and 13% of nonproblem-drinking women did so. Among the problem drinkers who experienced moderate to severe pain, almost 57% of men and 59% of women reported using alcohol for pain management, compared to 21% of nonproblem-drinking men and women with the same level of pain. Genetic, psychological, social and environmental factors can impact how drinking alcohol affects your body and behavior. Theories suggest that for certain people drinking has a different and stronger impact that can lead to alcohol use disorder. In addition, about 40 to 60 percent of people who experience chronic alcohol misuse also experience alcohol-related myopathy. The molecular and biochemical mechanisms by which chronic alcohol consumption leads to the development of cancers of various organs are not fully understood.
It is important to note that given the same amount of drinking, the increase in the risk for mortality from these diseases is greater than the increase in risk for morbidity, especially at lower levels of consumption. This finding suggests that continued alcohol consumption, even in low doses, after the onset of liver or pancreas disease, increases the risk of severe consequences. Recently, the Monograph Working Group of the International Agency for Research on Cancer concluded that there was sufficient evidence for the carcinogenicity of alcohol in animals and classified alcoholic beverages as carcinogenic to humans (Baan et al. 2007). In particular, the group confirmed, or newly established, the causal link between alcohol consumption and cancer of the oral cavity, pharynx, larynx, esophagus, liver, colorectum, and female breast. For all sites where alcohol’s causal role in cancer is established, there is evidence of a dose-response relationship, with relative risk rising linearly with an increasing volume of alcohol consumption (Corrao et al. 2004). They also found increased levels of IL-6 and activation of ERK44/42 in mice with alcohol withdrawal-related allodynia, but not in mice with alcohol-induced neuropathic pain.
These epidemiological results are consistent with the findings of biological studies that—based on alcohol’s effects on blood lipids and blood clotting—also predict beneficial effects of regular moderate drinking but detrimental effects of irregular heavy drinking (Puddey et al. 1999; Rehm et al. 2003). The current review integrated two lines of empirical inquiry (i.e., the effects of alcohol on pain and the effects of pain on alcohol use), with evidence derived from a broad range of epidemiological, clinical, and experimental research. Taken together, these data suggest that pain and alcohol may interact in a bi-directional manner, possibly resulting in greater pain and increased alcohol consumption over time. Bi-directional arrows are used to acknowledge that reciprocal influences may occur across associations between pain and alcohol use, and dashed lines are used to illustrate the modest causal evidence derived from the current literature. Dashed, bi-directional lines between moderate and excessive alcohol consumption acknowledge that alcohol use patterns may change (i.e., increase or decrease) over time. Potential mechanisms by which pain may serve as a motivator of alcohol use include negative and positive reinforcement, lack of alternative strategies for pain-coping, and overlapping neural systems that process stress and reward.