The negative impact of alcohol on chronic pain management

Alcohol intake and withdrawal can lead to increased pain and hypersensitivity.


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Alcohol consumption is a widespread social activity that can harm health, including chronic pain. Chronic pain is a persistent condition that can last for months or even years, and its causes are varied. Several studies have shown that alcohol consumption can contribute to the development of chronic pain, and there are several mechanisms through which this can occur.

Scientists at Scripps Research in La Jolla, CA, have discovered that chronic alcohol consumption can increase pain sensitivity through two molecular mechanisms: one driven by alcohol intake and the other by alcohol withdrawal. This sheds new light on the intricate relationship between alcohol and pain.

The research, published in the British Journal of Pharmacology on April 12, 2023, also suggests potential new drug targets for treating alcohol-associated chronic pain and hypersensitivity.

Senior author Marisa Roberto, Ph.D., the Schimmel Family Chair of Molecular Medicine, and a professor of neuroscience at Scripps Research, said, “There is an urgent need to understand better the two-way street between chronic pain and alcohol dependence. Pain is a widespread symptom in patients suffering from alcohol dependence and a reason why people are driven to drink again.”

Long-term alcohol consumption can lead to chronic pain, including alcoholic neuropathy, changes in how the brain processes pain signals, and changes in immune system activation. Scripps Research conducted a study on adult mice to identify the underlying causes of alcohol-related pain. 

They found that while dependent and non-dependent animals showed elevated inflammation pathways, specific molecules were only increased in conditional mice, suggesting different molecular mechanisms drive the two types of pain. This research may help identify potential molecular targets for developing therapies for alcohol-related chronic pain conditions.

The experiment “Chronic alcohol-induced mechanical allodynia by promoting neuroinflammation: a mouse model of alcohol-evoked neuropathic pain” aimed to investigate the underlying molecular mechanisms that contribute to alcohol-related chronic pain conditions, specifically alcoholic neuropathy. 

The study aimed to compare the differences between the pain sensitivities of dependent and non-dependent mice, identify the specific inflammatory molecules associated with alcohol-induced pain, and potentially identify molecular targets that could be used to develop therapies to treat alcohol-related chronic pain.

The researchers used chronic-intermittent ethanol two-bottle choice CIE-2BC to study the effects of alcohol on mice. This method created three groups: mice that were dependent on alcohol, mice that were not dependent but drank alcohol moderately, and mice that never drank alcohol. 

They tested the mice for pain sensitivity using von Frey filaments during alcohol withdrawal and after the last drinking session. They also looked at specific proteins in the mice’s spinal cord to see if they were affected by alcohol.

The study found a significant increase in drinking in male and female dependent groups compared to non-dependent groups. During the 72-hour withdrawal period, the dependent group developed a heightened sensitivity to pain, which was reversed after drinking. Additionally, there was an increased sensitivity to pain in some of the non-dependent mice. The spinal cord tissue of both hypersensitivity and neuropathy mice showed increased expression of IBA-1 and CSF-1, while only the hypersensitivity group showed increased expression of IL-6 and ERK44/42 activation.

The study demonstrated that the CIE-2BC model of ethanol exposure causes two different types of pain conditions, depending on the type of exposure. Dependent mice showed hypersensitivity to pain during withdrawal, while about half of the non-dependent mice developed neuropathic pain related to alcohol exposure.

In conclusion, chronic pain is a complex condition with various causes, and alcohol consumption can contribute to its development and exacerbation. The mechanisms through which alcohol contributes to chronic pain include inflammation, nerve damage, sleep disorders, and worsening of pre-existing pain conditions. 

Therefore, it is important to limit alcohol consumption and seek medical advice if you are experiencing chronic pain symptoms.

The study was supported by funding from the National Institutes of Health and other organizations.

Journal Reference:

  1. Borgonetti, V., Roberts,etal. Chronic alcohol-induced mechanical allodynia by promoting neuroinflammation: A mouse model of alcohol-evoked neuropathic pain. British Journal of Pharmacology. DOI: