However, each of these studies sampled older adults who did not necessarily have chronic pain, reported low levels of baseline drinking, and whose patterns of alcohol use may not generalize to other age groups. For example, an age-related decline in alcohol use tends to begin following young adulthood (Shaw et al., 2011), and older adults have evinced a general motivation to reduce alcohol use in response to health concerns (Dawson, Goldstein, & Grant, 2013). 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. In one study, alcohol administration enhanced tolerance for a painful electric shock only in FHN subjects (Perrino et al., 2008) whereas a more comprehensive study (Ralevski et al., 2010) found that FHP subjects scoring high for neuroticism displayed greater alcohol analgesia than FHN subjects and FHP subjects with low neuroticism scores. 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.
Pain as a Situational Motivator of Alcohol Use
Prescription opioid misuse has been defined as inappropriate use of opioid medication, including aberrant drug behaviors (e.g., dose escalation, use other than as prescribed; Pergolizzi et al., 2012). Multiple reviews have concluded that a history of substance use disorder, including alcohol, is the strongest predictor of opioid misuse (Turk, Swanson, & Gatchel, 2008), and that excessive alcohol consumption appears to precede the onset of opioid misuse (Pergolizzi et al., 2012). Researchers have noted a need for integrated treatments that are informed by knowledge of reciprocal relations between pain and substance use, and initial pilot data suggest that integrated treatments may be beneficial for treating co-occurring pain and substance use disorders (Ilgen et al., 2011). Future work is needed to develop and test integrated interventions for pain and alcohol use across a range of health-care settings. For example, persons with co-occurring pain disorders who engage in treatment for AUD may benefit from taking additional measures to manage their pain during the early stages of alcohol abstinence. Similarly, patients receiving pain treatment may benefit from interventions that seek to reduce the use of alcohol for pain-coping.
Other Factors Associated with Pain and Alcohol Use
However, even a mild disorder can escalate and lead to serious problems, so early treatment is important. The effects of alcohol consumption on ischemic stroke5 are similar to those on ischemic heart disease, both in terms of the risk curve and in terms of biological pathways (Patra et al. 2010; Rehm et al. 2010a). On the other hand, alcohol consumption mainly has detrimental effects on the risk for hemorrhagic stroke, which are mediated at least in part by alcohol’s impact on hypertension. When selecting MDE, MDD, and PDD, we did not adjust for the presence of other comorbid psychiatric disorders. Furthermore, data on severity, duration, or interference with daily activities of the pain were only available for individuals who were suffering from pain up to 12-months prior to data collection. If the data were available, it would have been interesting to see if depression affected individuals with more severe or prolonged forms of chronic pain at a higher incidence, comparable to ALC individuals.
2. Pain, chronic excessive drinking and alcohol dependence
The CeA receives functionally distinct inputs from the pontine parabrachial area (PB, nociceptive information) and basolateral amygdala (BLA, sensory-affective information) that are magnified in chronic pain states (Ikeda et al., 2007; Neugebauer et al., 2003). This plasticity is driven in part by an enhancement of glutamatergic systems, most notably activation of group I metabotropic glutamate receptors (mGluR1/mGluR5; Kolber et al., 2010; Li and Neugebauer, 2004; Neugebauer et al., 2003; Ren and Neugebauer, 2010). Neugebauer (2007) speculated that the amygdala facilitates nociceptive signaling in persistent pain states. Such altered processing may orient the organism’s motivational capacity to act toward alleviating this condition via heightened arousal (Koob et al., 1976) or negative reinforcement mechanisms (Koob and Le Moal, 2008). This function of pain contrasts with the stress-induced analgesia that is typically produced by acute stressors (Butler and Finn, 2009; also see Knoll and Carlezon, 2010). Relevant to the interface with alcoholism, chronic pain-induced activation of the amygdala is accompanied by alterations in mPFC function and production of cognitive deficits (Ji et al., 2010; Ji and Neugebauer, 2011; Sun and Neugebauer, 2011).
As a multifaceted experience that is not exclusively driven by the noxious input, pain involves much more than sensory activities. In fact, much of the complexity of pain arises from the involvement of higher centers in the brain rather than periphery, thereby making pain a uniquely experienced phenomenon by each individual and, as such, a subjective experience. Such studies have revealed that functional activity in the primary and secondary somatosensory cortices are linked to the sensory-discriminative processing aspect of pain, such as sensing the intensity of pain or discriminating the site of pain (Bushnell et al., 1999; Hofbauer, Rainville, Duncan, & Bushnell, 2001). Anterior cingulate cortex, insular cortex, and prefrontal cortex are linked to affective-motivational processing aspects of pain, such as finding it to be unpleasant and bothersome even though sensory-wise it may be considered to have low intensity (Apkarian et al., 2005; Auvray, Myin, & Spence, 2010; Gu et al., 2012). Attention, expectation, and reappraisal are thought to be the most important contributing factors for the cognitive modulation of pain (Porro et al., 2002; Wiech, Ploner, & Tracey, 2008).
- Future experimental research should test whether situational pain increases craving for alcohol or subsequent alcohol consumption.
- 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.
- NIAAA also encourages research on the impact of alcohol and sleep disturbances on pain through a new funding opportunity (PA ).
- “Fibromyalgia patients in particular have a lot of psychological trauma, anxiety and catastrophizing, and allowing for the occasional drink might increase social habits and overall health.”
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. Nevertheless, laboratory studies suggest that the presence of hyperkatifeia and enhanced responsiveness to painful stimulation may not always be sufficient to increase alcohol drinking. 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).
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. We hypothesize that the sensory and emotionally based allostatic state serves as a predisposing condition, as well as a shared phenotypic characteristic of alcohol dependence, anxiety and depression, and chronic pain disorders. We suggest that full expression of these distinct disease states may depend on between-systems interactions in which how long after taking muscle relaxer can you drink alcohol the shared neural circuitry illustrated in this model influences systems exclusive to a single disorder or subset of disorders. Shared neurocircuitry and neurochemistry enables crosstalk between the diverse disorders such that changes in neural structure and function (i.e., allostatic load) arising from one disorder can affect the others. The model accounts for well-documented comorbidities between alcohol and anxiety disorders (Kushner et al., 2012), anxiety, depression and chronic pain disorders (Gerrits et al., 2012; Gureje et al., 2008) as well as alcohol dependence and pain sensitivity discussed previously.
Also, given initial evidence that persons who are alcohol dependent experience increased pain during periods of abstinence (Jochum et al., 2010), it seems reasonable to hypothesize that increased pain may precipitate relapse to drinking. Finally, given that stress-related cues have been shown to increase craving in abstinent alcoholic patients (Sinha et al., 2009), there is reason to hypothesize that pain may increase cravings for alcohol, and that persons in pain may be motivated to drink in order to alleviate those cravings (e.g., Bottlender & Soyka, 2004). 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. Negative reinforcement models of addiction posit that substance use is motivated, in part, by a desire to alleviate aversive psychological and physical states (e.g., McCarthy, Curtin, Piper, & Baker, 2010). One possibility is that pain may motivate alcohol consumption via a desire to alleviate pain-related negative affect. Negative affect is a central component of pain-processing (e.g., Wade, Dougherty, Archer, & Price, 1996), and it has been suggested that coping with negative affect may be a primary drinking motive among persons with AUD (e.g., Kuntsche et al., 2005).
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). Research has shown several benefits to moderate alcohol consumption, including decreased risk of coronary heart disease, stroke and dementia and increased physical function and quality of life. 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).
