A new study led by Scripps Research has found that chronic alcohol consumption can make people more sensitive to pain through two different molecular mechanisms – one related to alcohol intake and the other to alcohol withdrawal. These findings could help develop new treatments for alcohol-associated chronic pain and hypersensitivity.
“There is an urgent need to better understand the two-way street between chronic pain and alcohol dependence,” said senior author Marisa Roberto, a professor of Molecular Medicine and Neuroscience at Scripps. “Pain is both a widespread symptom in patients suffering from alcohol dependence, as well as a reason why people are driven to drink again.”
Alcohol use disorder (AUD) encompasses various conditions such as alcohol abuse and alcohol addiction and affects over 29.5 million people in the United States. Extended alcohol use can trigger a variety of chronic diseases, including cardiovascular disease, liver disease, and certain cancers. Moreover, over half of people with AUD struggle with persistent pain of some type, such as alcoholic neuropathy, in which nerve damage causes chronic pain.
Previous research has found that AUD is linked to changes in how the brain processes pain signals and how the activation of immune responses occurs. In addition, during withdrawal, people with AUD often experience a condition called allodynia, in which harmless stimuli are perceived as painful.
To clarify the underlying causes of these various types of alcohol-related pain, the experts conducted a series of experiments on three groups of mice: alcohol-dependent mice (excessive drinkers), mice that had limited access to alcohol and were not considered dependent (moderate drinkers), and mice that had never consumed alcohol.
The experiments revealed that, in dependent mice, allodynia developed during withdrawal, but subsequent alcohol consumption significantly lowered pain sensitivity. Nearly half of the mice which were not dependent also exhibited increased pain sensitivity during alcohol withdrawal, but unlike their dependent counterparts, this neuropathy was not reversed by re-exposure to alcohol.
By measuring levels of inflammatory proteins in the mice, the researchers found that, although inflammation pathways were elevated in both dependent and non-dependent animals, certain molecules were only increased in the first group, suggesting that different molecular mechanisms may trigger the two types of pain. These findings may clarify which inflammatory proteins could 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,” explained lead author Vittoria Borgonetti, a postdoctoral fellow in Molecular and Cellular Neuroscience at Scripps.
“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,” concluded co-senior author Nicoletta Galeotti, an associate professor of Preclinical Pharmacology at the University of Florence.
The study is published in the British Journal of Pharmacology.
By Andrei Ionescu, Earth.com Staff Writer
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