Posted on Nov 25, 2022, 3 p.m.
Most experts agree that nerve damage and pain that is observed in those with obesity or diabetes is related to their metabolic state. A new study published in Scientific Reports from the University of Texas-Dallas is challenging this notion, suggesting that the act of indulging in fattening food alone may be the driving factor behind pain in some people. Findings add to the growing evidence supporting the avoidance of a high-fat diet (HFD).
“This study indicates you don’t need obesity to trigger pain; you don’t need diabetes; you don’t need a pathology or injury at all,” said co-author Dr. Michael Burton, assistant professor of neuroscience in the university’s School of Behavioral and Brain Sciences. “Eating a high-fat diet for a short period of time is enough — a diet similar to what almost all of us in the U.S. eat at some point.”
For most people in America, the standard diet (Western Diets) is rich in processed foods, fats, and fried foods, these choices are known gateways to a lengthy list of chronic diseases as well as obesity. Eating these types of fattening foods, that lead to high amounts of free fatty acids circulating in their bloodstream, may even exacerbate pre-existing conditions and hinder recovery from injury.
In this animal study, the researchers compared the effects of different diets on mice over eight weeks, with one group receiving normal food while the other was on an HFD that would not induce obesity or diabetes since both can result from disease-state-related pain like diabetic neuropathy. (These groups of animals were also compared to diabetic and obese mice)
While examining blood samples for saturated fats, it was revealed that the most common form of saturated fat found in the HFD mice was palmitic acid, and it binds to certain nerve cell receptors that lead to inflammation and mimics nerve damage. This finding suggests that if a way can be found to stop this binding process it could be used as a possible intervention.
“The metabolites from the diet are causing inflammation before we see pathology develop,” Burton said. “Diet itself caused markers of neuronal injury.” “Now that we see that it’s the sensory neurons that are affected, how is it happening? We discovered that if you take away the receptor that the palmitic acid binds to, you don’t see that sensitizing effect on those neurons. That suggests there’s a way to block it pharmacologically,” says Burton.
“The mechanism behind this transition is important because it is the presence of chronic pain — from whatever source — that is fueling the opioid epidemic,” he said. “If we figure out a way to prevent that transition from acute to chronic, it could do a lot of good.”
The researchers suggest that their findings indicate that healthcare professionals should take into account the dangerous effects of eating fattening foods for anyone reporting experiencing pain, not just those with obesity or those at risk for diabetes. This study reveals that there may be more clues/answers hiding in how a patient reached a specific point of pain than the endpoint or a disease state itself.
“The biggest reason we do research like this is because we want to understand our physiology completely,” he said. “Now, when a patient goes to a clinician, they treat a symptom, based off of an underlying disease or condition. Maybe we need to pay more attention to how the patient got there: Does the patient have diabetes-induced or obesity-induced inflammation; has a terrible diet sensitized them to pain more than they realized? That would be a paradigm shift.”
As with anything you read on the internet, this article should not be construed as medical advice; please talk to your doctor or primary care provider before changing your wellness routine. This article is not intended to provide a medical diagnosis, recommendation, treatment, or endorsement.
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