2023-04-25 16:23:04
Chronic alcohol use makes us more sensitive to pain through two different molecular mechanisms: one driven by alcohol intake and one driven by withdrawal. This is one of the conclusions reached by scientists at the Scripps Research Institute (USA) about the complex links between alcohol and pain. The results of the research have been published in the British Journal of Pharmacology.
“There is an urgent need to better understand the relationship between chronic pain and alcohol dependence,” says lead author Marisa Roberto. “Pain is both a widespread symptom in patients suffering from alcohol dependence, and a reason that drives people to drink again.”
Alcohol use disorder (ADD), which encompasses the disorders commonly referred to as alcohol abuse, alcohol dependence, and alcohol addiction. Over time, excessive alcohol consumption can trigger the development of numerous chronic diseases, including heart disease, stroke, liver disease, and some types of cancer.
Among the many long-term impacts of alcohol use is pain: more than half of people with eating disorders experience persistent pain of some kind. This includes alcoholic neuropathy, which is nerve damage that causes chronic pain and other symptoms.
Studies have also found that ED is associated with changes in the way the brain processes pain signals, as well as changes in the way the immune system is activated. In turn, this pain can lead to increased alcohol consumption. Additionally, during withdrawal, alcoholics may experience allodynia, in which a harmless stimulus is perceived as painful.
In the new study, three groups of adult mice were compared: animals that were alcohol-dependent (heavy drinkers), animals with limited access to alcohol and not considered dependent (moderate drinkers), and those that had never been given alcohol.
In the dependent mice, allodynia developed during alcohol withdrawal, and subsequent access to alcohol significantly decreased pain sensitivity. On the other hand, approximately half of the non-alcohol-dependent mice also showed signs of increased pain sensitivity during withdrawal, but, unlike the dependent mice, this neuropathy was not reversed by re-exposure to alcohol.
When the levels of inflammatory proteins in the animals were measured, it was found that while the inflammatory pathways were elevated in both the dependent and non-dependent animals, some specific molecules were only increased in the dependent mice. This indicates that the two types of pain may be due to different molecular mechanisms. It also suggests which inflammatory proteins may be useful as drug targets to combat alcohol-related pain.
Half of the mice that were not alcohol dependent also showed signs of increased pain sensitivity during withdrawal.
“These two types of pain vary enormously, so it’s important to be able to tell them apart and develop different ways to treat each type,” says first author Dr. Vittoria Borgonetti.
This group continues to study how these molecules could be used to diagnose or treat alcohol-related chronic pain.
“Our goal is to uncover new potential molecular targets that can distinguish these types of pain and that can be used in the future for the development of therapies,” concludes co-lead author Nicoletta Galeotti, from the University of Florence, Italy.
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