A high-fat Western diet can increase the risk of painful disorders commonly found in people with conditions like diabetes or obesity. However, some changes in the diet can reverse or reduce the suffering.
The novel findings are published last week in the journal Nature Metabolism (Boyd et al., 2021). First authors Jacob T. Boyd, MD, Ph.D., and Peter M. LoCoco, Ph.D., of the Department of Endodontics, over the last five years, led the study team of 15 local researchers, including seven former or currently enrolled students of its Graduate School of Biomedical Sciences.
Role of a High-fat Diet in Pain Sufferings
Western diets are rich in PUFAs or omega-6 fatty acids, which are also found in fast foods, processed snacks, cakes, and fatty and processed meats, and in some vegetables, are associated with obesity and considered unhealthy. However, omega-3 fatty acids, primarily found in fish, flaxseed, walnuts, are considered healthy and serve many functions, including cardiovascular protection, promoting brain health, reducing symptoms of metabolic disorders.
Chronic pain is one of the leading causes of disability worldwide (Vos et al., 2017) and is commonly associated with comorbid disorders (Spracklen et al., 2012), such as diabetes, obesity. However, the roles of the high-fat Western diet rich in ω-6 polyunsaturated fatty acids (PUFAs) in pain conditions, either inflammatory such as arthritis, trauma, or surgery—or neuropathic pain, such as diabetes, are poorly investigated.
Study Design and Results
In the new study, Dr. Boyd and colleagues used multiple methods in both mice and humans to study the role of PUFAs in pain conditions. They found that most Western diets high in omega-6 polyunsaturated fatty acids can be a major risk factor for both inflammatory pain and neuropathic disorders.
When administered PUFAs rich food, Mice develops several markers of peripheral nerve damage indicative of peripheral neuropathy. Linoleic and arachidonic acids accumulate in the spinal nerve, with elevated phospholipase (PLA)2 activity.
The researchers demonstrated that pharmacological and molecular inhibition of PLA2G7 or diet reversal with high levels of ω-3 PUFAs reduce pain, suffering, and other abnormalities induced by high ω-6 intake.
Also, the authors found that skin levels of omega-6 fatty acids in Type 2 diabetic patients with neuropathic pain were strongly associated with reported pain levels and the need for taking analgesic drugs.
“This paper is a high-profile contribution for a huge unmet translational need”, as no treatments available to alter the nature of this neurological disease, stated José E. Cavazos, professor of neurology and director of the National Institutes of Health-designated South Texas Medical Scientist Training Program at UT Health San Antonio.
Kenneth M. Hargreaves, professor and chair of the Department of Endodontics at UT Health San Antonio, also the senior author of the paper, wrote, ‘this study exemplifies team science at its best as multiple scientists and clinicians with complementary expertise working together to make lives better.’
In an editorial, researchers Aidan McGinnis and Ru-Rong Ji at Duke University mentioned the study as ‘comprehensive and elegant’ from Boyd and colleagues.
The findings may serve as a foundation for new clinical trials and ultimately provide new avenues for the clinical treatment of neuropathies.
Boyd, J. T., P. M. LoCoco, et al. (2021). “Elevated dietary ω-6 polyunsaturated fatty acids induce reversible peripheral nerve dysfunction that exacerbates comorbid pain conditions.” Nature Metabolism 3(6): 762-773. 10.1038/s42255-021-00410-x.
Spracklen, D. V., S. R. Arnold, et al. (2012). “Observations of increased tropical rainfall preceded by air passage over forests.” Nature 489(7415): 282-285. 10.1038/nature11390.
Vos, T., A. A. Abajobir, et al. (2017). “Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016.” The Lancet 390(10100): 1211-1259. 10.1016/S0140-6736(17)32154-2.