Moderate Alcohol Intake Associated with Less Chronic Pain, Depression
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. Initial results derived from human laboratory studies suggest that alcohol may confer acute analgesic effects.
Of the study participants, more than half reported use of opioid medication, which carries serious risks when combined with alcohol. A doctor will take a thorough health history and have you complete questionnaires related to alcohol intake to help diagnose these conditions. This condition can be acute, affecting people for a short period of time before resolving, or chronic, lasting for a longer period of time. Researchers have not determined if this is caused by the effects of alcohol on the brain or is the result of thiamine deficiency. In the meantime, while chronic pain should always be evaluated by a medical professional, there are many options for medication/opioid-based treatment, drawing on complementary and alternative approaches. The researchers found that there was a significant increase in drinking behavior in the group of mice that were dependent on alcohol compared to the non-dependent group.
What causes alcohol-related neurologic disease?
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. 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). Most of the relevant studies found that a high percentage of heavy alcohol users with epilepsy meet the criteria of alcohol dependence. We also explored the breakdown of incidence by sex, and the results are presented in Figure 3.
Substance-related disorders: A review of prevalence and correlates among patients with chronic pain
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. 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. 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.
Neural dysregulation, alcohol dependence and chronic pain
Remission of alcohol abuse could also complicate the treatment of chronic pain disorders, as it might increase the chances of depression remission in ALC patients with comorbid depression 45. Studies utilizing representative population-based and clinical samples are needed to generate prevalence estimates that account for varying definitions of pain (e.g., chronic pain duration, type of pain condition) and alcohol use (e.g., amount consumed, AUD). Future research would benefit from a more detailed and consistent approach to the quantification and operationalization of self-reported alcohol consumption. Future research should also attempt to differentiate between lifetime abstainers and those who abstain later in life (e.g., due to illness that prohibits alcohol use or recovery from AUD), as pain-related outcomes may vary as a function of alcohol exposure.
NIDA had no role in the study design, collection, analysis or interpretation of the data, writing the manuscript, or the decision to submit the paper for publication.
- 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.
- Those same cortical regions are part of the depression neurocircuitry, but additionally, the ventral striatum, another reward system structure, has been reported to play a central role in depressive disorders 19.
- However, what starts out as something that seems like a solution often becomes part of the problem and can even make chronic pain worse.
Prevalence and Factors Common to Pain and Alcohol Use
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.
These regions feed into the rostral ventromedial medulla, which includes the midline nucleus raphe and periaqueductal gray matter that have neural pathways to the spinal dorsal horn. Together, they form the descending pain modulatory system from the brain to the spinal cord and can modulate nociceptive processing by providing a substrate for cortical and subcortical structures to exert their influence. We review the neural bases of pain and the influence of AUD on processes involved in pain perception. We propose potential mechanisms involved in the development of chronic pain in AUD, and we consider implications for pain management in recovery from AUD.
We then proceed by proposing some potential mechanisms involved in the development of chronic pain in AUD. In fact, chronic pain and alcohol consumption often combine to create a vicious circle wherein people with chronic pain drink to feel less uncomfortable, but drinking ultimately increases their pain. Pain is a widespread symptom in patients suffering from alcohol dependence and it’s also a reason why people are driven to drink more. Additionally, we found that the onset of MDE in ALC group was younger than the CTRL group, whether or not they had chronic/severe back pain. Regarding the age of onset of the various conditions, we found that the onset of MDE in the ALC group was younger than in the CTRL group, whether or not either group experienced pain. We looked at the temporal relations between the ages of onset of each of the depressive disorders to determine if onset of ALC, preceded onset of MDE, MDD, or PDD.
Ischemic diseases are all conditions that are related to the formation of blood clots, which prevent adequate blood flow to certain tissues. Jürgen Rehm, Ph.D., received a salary and infrastructure support from the Ontario Ministry of Health and Long-Term Care. Their aim is to uncover Buddhist Teachings to Overcome Addiction with Vimalasara fresh molecular targets that can differentiate between different types of pain and could eventually be employed to create new treatments. This indicates that the inflammatory pathways involved are different and could potentially lead to the development of targeted therapies in the future. By determining the minimum force required to elicit a withdrawal response, the researchers could assess the severity of allodynia. This work was supported in part by grant R21DA awarded to Joseph W. Ditre by the National Institute on Drug Abuse.
