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). Chronic pain produces multiple electrophysiological and molecular neuroadaptations in the CeA, a number of which are lateralized to the right CeA (e.g., Carrasquillo and Gereau, 2008; Ji and Neugebauer, 2009).
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For example, co-administration of alcohol and theophylline (i.e., an adenosine receptor antagonist) has been shown to attenuate development of hyperalgesia during withdrawal, presumably because theophylline promotes up-regulation of adenosine A1 receptors (Gatch & Selvig, 2002). 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. Primary outcomes tend to include pain threshold, which is typically defined by the time (e.g., seconds) or stimulus intensity (e.g., volts) at which participants first report pain, and pain tolerance, which represents the duration of exposure or maximum stimulus intensity that a participant is willing to endure (IASP, 1994). There is substantial evidence that alcohol consumption can cause unprovoked seizures, and researchers have identified plausible biological pathways that may underlie this relationship (Samokhvalov et al. 2010a).
Influences of Alcohol on Processes Involved in Pain Perception
- Unfortunately, the assessment of pain in patients who already have been diagnosed with varying types or combinations of types of dementia and amnesia, is especially challenging, and therefore, research and clinical treatment with these populations has been limited and inadequate (Buffum, Hutt, Chang, Craine, & Snow, 2007).
- An improved understanding of the effects of alcohol on pain, the role of pain in alcohol misuse, and potential interactions between alcohol and opioids during pain treatment hopefully will improve treatment outcomes for patients in pain.
- Thus, the availability and effectiveness of strategies for coping with pain may relate to drinking motivation in at least two ways.
- By stipulating that the allostatic state arising through actions by alcohol, trauma (stress) or injury does not depend on the temporal sequence of exposure (i.e., the insults are functionally substitutable) our model is compatible with many hypotheses.
Instead, they proposed that dysregulated corticostriatal connectivity may underlie reward-processing abnormalities in MDD. It is likely that the more prominent neuroplastic changes in these cortical regions due to direct or indirect effects of ALC may contribute to a stronger corticostriatal dysregulation and hence the higher likelihood of depression that we observed in association with ALC. Because of the interrelatedness among chronic pain disorders, depressive disorders, and alcohol abuse, and their common neural pathways, we hypothesized that in the presence of chronic pain, the burden of depression would be similar for individuals with and without a history of alcohol abuse. In other words, we expected that depressive disorders would be a high burden in patients with chronic pain, independently of whether or not they also have a diagnosis of alcohol abuse. To test this hypothesis, we leveraged a large national database 23, to compare the lifetime incidence of three depressive diagnoses in individuals with a history of alcohol abuse compared to those with no such history in the presence or absence of non-cancer chronic pain disorders. To our knowledge, all of the studies that examined prospective relations between pain and subsequent alcohol consumption were limited to samples consisting of older adults who reported low levels of baseline drinking and did not necessarily have chronic pain (Bobo et al., 2012; Brennan et al., 2011; Brennan & Soohoo, 2013).
Alcohol dependence as a chronic pain disorder
Genetic, psychological, social and environmental factors can impact how drinking alcohol how to store a urine sample 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. 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.
However, no global prevalence data on these disease categories exist because they cannot be validly assessed on a global level. Thus, these conditions are too specific to assess using verbal autopsies and other methods normally used in global-burden-of-disease studies (Lopez et al. 2006; pancreatitis can be estimated indirectly Rajaratnam et al. 2010). Nevertheless, via the prevalence of alcohol exposure the prevalence of alcohol-attributable and relative risk for the wider, unspecific liver cirrhosis and alcohol-induced disease categories (Rehm et al. 2010a). People with alcohol use disorder are unable to stop or control their alcohol consumption, even when it causes problems to their health, relationships, and work. When Roberto’s group then measured levels of inflammatory proteins in the animals, they discovered that while inflammation pathways were elevated in both dependent and non-dependent animals, specific molecules were only increased in dependent mice.
Our review of the literature identified a range of biopsychosocial factors and health-related behaviors (e.g., tobacco use, illicit drug use) that may covary with both alcohol use and pain. For example, although we noted that many studies statistically-controlled for some common sociodemographic factors (e.g., age), there was substantial variation in the number of covariates accounted for across studies. In the following section, we briefly examine a selection of biopsychosocial factors that are relevant to both pain and alcohol use. 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).
What is considered 1 drink?
Such executive system deficits are hypothesized to play a critical role in the aberrant decision-making that accompanies the transition from drug use 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). Cultural factors that are related to both differences in drinking patterns and beliefs and expectations about the effects of alcohol also influence the relationship between drinking and aggression (Bushman and Cooper 1990; Graham 2003; Leonard 2005; Room and Rossow 2001).
In addition to the well-established acute alcohol actions (reward, stimulation, and impairment) and withdrawal effects (CNS/ANS hyperexcitability, anxiety, sleep disturbances, and dysphoria) that contribute to excessive drinking and relapse, alcohol produces analgesia followed by hyperalgesia after withdrawal (Gatch, 2009). We hypothesize here that pain sensitivity, analgesic actions of alcohol and withdrawal-induced hyperalgesia also contribute to alcohol misuse and alcohol addiction. This hypothesis is supported by observations that problem drinkers are more likely to report pain conditions and heightened sensitivity to painful stimulation than the general population. Alcohol dependence also was found to be a major predictor of pain severity following serious injury (Castillo et al., 2006; Holmes et al., 2010). Other studies suggest that people who do not have drinking problems, but have a positive family history of alcoholism (FHP), are more sensitive to painful stimulation than those having no family history of alcoholism (FHN; Stewart et al., 1995). Likewise, people with chronic pain conditions are more likely to have family members with drinking problems (Goldberg et al., 1999; Katon et al., 1985).
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). To date, the lack of preclinical, or animal, models of alcoholic neuropathic pain limited the investigation of pathological mechanisms underlying the onset of neuropathic pain in people with alcohol use disorder. There is also reason to believe that expectancies for pain relief via drinking may have a potent influence on pain reporting (Pollo et al., 2001).
Most of the relevant studies found that a high percentage of heavy alcohol users with epilepsy meet the criteria of alcohol dependence. Overall, we found that the incidence of depressive disorders was the highest among ALC women and the lowest among CTRL men. The incidence of PDD was comparable in ALC men and ALC women with a history of back/neck pain or severe headaches. 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 group (ALC, 31.3% vs. CTRL, 65.1%). 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.