Alcohol Intake, Withdrawal Lead To Increased Hypersensitivity, Pain: Study
Researchers have identified the molecular mechanisms by which chronic alcohol consumption leads to increased hypersensitivity and pain.
Scripps Research scientists suggest that in people with chronic alcohol consumption, two different molecular mechanisms driven by intake and withdrawal can intensify the pain.
"There is an urgent need to better understand the two-way street between chronic pain and alcohol dependence," said Marisa Roberto, senior author and a professor of neuroscience at Scripps Research. "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)
It is a medical condition caused by alcohol abuse wherein people resort to drinking even when it causes problems, emotional distress or physical harm.
Signs of alcohol use disorder:
- Strong urge to drink alcohol
- Irritability when not drinking
- Giving up activities to drink alcohol
- Wants to cut down on the quantity but turns unsuccessful
- Need more quantity of alcohol to feel the effect
- Experience withdrawal symptoms
The condition is sometimes called alcoholism or alcohol dependence and requires medical and psychological treatments to control it.
AUD affects 29.5 million people in the U.S., according to a 2021 national survey on drug use and health. It can cause several health issues in the long run, including cardiovascular diseases, liver diseases, stroke and certain types of cancers.
Another long-term issue that affects more than half of AUD patients is persistent pain caused by nerve damage, also known as alcoholic neuropathy.
Earlier studies have shown that AUD causes changes in how the brain processes pain signals and how immune system activation occurs.
The researchers decided to determine the underlying causes of alcohol-related pain in a study conducted on three groups of adult mice. They evaluated mice that were dependent on alcohol, those that had limited access to alcohol but were not considered dependent, and those that were never given alcohol.
During alcohol withdrawal, the mice that were dependent developed allodynia - the pain caused by a stimulus that does not normally provoke pain. However, they had decreased pain sensitivity when they got access to alcohol.
The mice that had limited access to alcohol showed signs of increased pain sensitivity during alcohol withdrawal. But they did not show a reversal of neuropathy when they had re-exposure to alcohol.
Scientists then found specific molecules that were increased in dependent mice and determined that these inflammatory proteins could be used as drug targets to combat alcohol-related pain.
The findings of the study were published in the British Journal of Pharmacology.
"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," said co-senior author Nicoletta Galeotti, an associate professor of preclinical pharmacology at the University of Florence.