Chronic alcohol consumption may increase pain sensitivity through two distinct biochemical processes, one driven by alcohol intake and the other by alcohol withdrawal.
That is one new conclusion reached by Scripps Research scientists investigating the complex relationships between alcohol and pain.
The research, published in the British Journal of Pharmacology, also suggests potential new drug targets for treating alcohol-associated chronic pain and hypersensitivity.
“There is an urgent need to better understand the two-way street between chronic pain and alcohol dependence. Pain is both a widespread symptom in patients suffering from alcohol dependence, as well as a reason why people are driven to drink again,” said senior author Ms. Marisa Roberto, PhD, the Schimmel Family Chair of Molecular Medicine, and a professor of neuroscience at Scripps Research.
Alcohol use disorder (AUD), which encompasses the 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. AUD can trigger the development of numerous chronic diseases, including heart disease, stroke, liver disease, and some cancers.
According to the statement, “Among the many impacts of long-term alcohol consumption is pain: more than half of people with AUD experience persistent pain of some type. This includes 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 changes in how immune system activation occurs. In turn, this pain can lead to increased alcohol consumption.
Moreover, during withdrawal, people with AUD can experience allodynia, in which a harmless stimulus is perceived as painful.
Method of research
In the new study, the researchers compared three groups of adult mice, animals that were dependent on alcohol (excessive drinkers), animals that had limited access to alcohol and were not considered dependent (moderate drinkers), and those that had never been given alcohol.
According to the statement, “In dependent mice, allodynia developed during alcohol withdrawal, and subsequent alcohol access significantly decreased pain sensitivity. Separately, about half of the mice that were not dependent on alcohol also showed signs of increased pain sensitivity during alcohol withdrawal but, unlike the dependent mice, this neuropathy was not reversed by re-exposure to alcohol.”
“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,” as per the reports.
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 vary greatly, which is why it is important to be able to distinguish between them and develop different ways to treat each type,” says first author Ms. Vittoria Borgonetti, PhD, a postdoctoral associate at Scripps Research.
“Our goal is to unveil new potential molecular targets that can be used to distinguish these types of pain and potentially be used in the future for the development of therapies,” commented co-senior author Ms. Nicoletta Galeotti, PhD, associate professor of preclinical pharmacology at the University of Florence.
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