Chronic alcohol consumption may increase pain sensitivity through two different biochemical processes, one driven by alcohol intake and the other by alcohol withdrawal. That’s a new finding by Scripps Research scientists investigating the complex relationship between alcohol and pain.
The research, published in the British Journal of Pharmacology, also suggests potential new drug targets for the treatment of alcohol-related chronic pain and hypersensitivity.
“There is an urgent need to better understand the two-way street between chronic pain and alcohol dependence,” says senior author Marisa Roberto, PhD, Schimmel Family Chair in Molecular Medicine and professor of neuroscience at Scripps Research. “Pain is a common symptom in patients suffering from alcohol dependence, as well as a reason that drives people to drink again.”
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Alcohol use disorder (AUD), which encompasses conditions commonly called alcohol abuse, alcohol dependence and alcohol addiction, affects 29.5 million people in the US, according to the 2021 National Survey on Drug Use and Health. Over time, AUD can trigger the development of many chronic diseases, including heart disease, stroke, liver disease and some cancers.
Pain is among the many effects of long-term alcohol abuse: more than half of people with AUD experience some form of persistent pain. These include alcoholic neuropathy, which is nerve damage that causes chronic pain and other symptoms. Studies have also found that AUD is associated with changes in how the brain processes pain signals, as well as how the immune system is activated. In turn, this pain can increase alcohol consumption. Furthermore, during withdrawal, people with AUD may experience allodynia, in which noxious stimuli are perceived as painful.
Roberto and his colleagues were interested in learning the underlying causes of these different types of alcohol-related pain. In the new study, they compared three groups of adult rats: animals dependent on alcohol (heavy drinkers), animals with limited access to alcohol and not considered dependent (moderate drinkers), and those who were never given alcohol.
In dependent rats, allodynia developed during alcohol withdrawal, and subsequent alcohol access significantly reduced pain sensitivity. Separately, about half of the rats that were not dependent on alcohol also showed signs of increased pain sensitivity during alcohol withdrawal but, unlike the dependent rats, this neuropathy was not reversed by re-exposure to alcohol.
When Roberto’s group measured the levels of inflammatory proteins in the animals, they found that while inflammatory pathways were increased in dependent and non-dependent animals, specific molecules were increased only in dependent mice. This indicates that different molecular mechanisms may drive the two types of pain. It also suggests which inflammatory proteins may be useful as drug targets to combat alcohol-related pain.
“These two types of pain are very different, so it’s important to be able to distinguish between them and develop different ways to treat each type,” says first author Vittoria Borgonetti, PhD, a postdoctoral associate at Scripps Research.
Roberto’s group continues to study how these molecules can be used to diagnose or treat alcohol-related chronic pain conditions.
“Our goal is to unveil new potential molecular targets that can be used to distinguish these types of pain and potentially be used for the development of treatments,” says co-senior author Nicoletta Galeotti, PhD, former associate professor of clinical pharmacology. University of Florence.
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