As medicine shifts its focus towards sustainable lifestyle changes to combat disease, diet is often the first criteria to be evaluated since its composition influences the health status of an individual. For example, a Western diet consisting primarily of saturated fats that contribute to the increasing levels of obesity, diabetes, and comorbidities in Western countries. Individuals who consume high amounts of saturated fats possess high amounts of broken-down circulating free fatty acids (FFAs) in their bloodstream. Recently, it has been shown that a HFD increases existing mechanical pain hypersensitivity independent of obesity. However, it is still unclear if a HFD has the pain plasticity altering machinery that can sensitize individuals to respond to subthreshold stimuli and what it could mean for clinical populations earlier in diagnosis.
Individuals consuming a Western diet over time manifest a variety of symptoms and morbidities, including meta inflammation, obesity, and diabetes. Exposure to saturated fatty acids found in a Western diet induces systemic inflammation via pro-inflammatory cytokine release such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6).
Several studies demonstrate how HFD exposure can exacerbate pre-existing conditions, such as post-operative pain and inflammatory-induced pain and can hinder recovery from injury, indicating that components of the HFD may have a direct role in pain development
A new study in mice suggests that a short-term exposure to a high-fat diet may be linked to pain sensations even in the absence of a prior injury or a preexisting condition
The study, published Sept. 1 in the journal Scientific Reports, compared the effects of eight weeks of different diets on two cohorts of mice. One group received normal chow, while the other was fed a high-fat diet in a way that did not precipitate the development of obesity or high blood sugar, both of which are conditions that can result in diabetic neuropathy and other types of pain.
The researchers found that the high-fat diet induced hyperalgesic priming, a neurological change that represents the transition from acute to chronic pain, and allodynia, which is pain resulting from stimuli that do not normally provoke pain.
Dr. Michael Burton , assistant professor of neuroscience in the School of Behavioral and Brain Sciences, and his team looked for saturated fatty acids in the blood of the mice fed the high-fat diet. They found that a type of fatty acid called palmitic acid, the most common saturated fatty acid in animals, binds to a particular receptor on nerve cells, a process that results in inflammation and mimics injury to the neurons.
The metabolites from the diet are causing inflammation before we see pathology develop.
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.
Jessica A. Tierney, Calvin D. Uong, Melissa E. Lenert, Marisa Williams, Michael D. Burton (September 1, 2022). High-fat diet causes mechanical allodynia in the absence of injury or diabetic pathology. Scientific Reports. Retrieved from : https://www.nature.com/articles/s41598-022-18281-x