5 Foods to Avoid When Reducing Inflammation

It is estimated that 5 to 7 percent of people in the Western world suffer from some type of chronic inflammatory disease.[1] According to a study conducted by the Rand Corporation in 2014, 3 out of 5 people die due to chronic diseases associated with inflammation.[2] Inflammation related diseases have become one of the greatest health risks society faces today.

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While many medications and treatments exist to reduce inflammation, there are everyday ways to avoid the occurrence of inflammation. One of the biggest sources of inflammation is found in the foods that we eat. Many foods have been found to increase inflammation in the body. Here are five such foods to avoid.

Sugar and High-Fructose Corn Syrup

There are more reasons to cut sugar from your diet than just losing a few inches around the waist. Sugar and high-fructose corn syrup have been linked to many chronic diseases, but they are also associated with increased inflammation.[3]

Studies show an increased risk of developing rheumatoid arthritis in women who consume sugar-sweetened soda.[4] Sucrose, the chief component of sugar, was also shown to counteract the health effects of fish oil in decreasing inflammation. [5] In other words, eating sugar is not only a cause of inflammation, but it cancels out the health benefits that come with your efforts at eating well.

 

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Artificial Trans Fats

Who doesn’t like french fries or potato chips? But before you take that bite, beware—those fried delectables are saturated in trans fats. Trans fats are oils that have undergone the process of hydrogenation either to preserve shelf life or due to exposure to high temperatures as in the case of fried food. While they taste great, studies have shown they significantly contribute to vascular inflammation.[6]

 

Processed Meat

While tasty and high in protein, meat carries with it advanced glycation end products (AGE). These are harmful compounds that are formed when protein or fat undergo a process called glycation, where they combine with sugar in the bloodstream. AGEs have also been found to accumulate in meats that have been exposed to high temperatures like those that have been grilled. As good as that BBQ tastes, the AGE found in the meat may be causing inflammation according to studies.[7]

 

Refined Carbohydrates

All you pasta lovers out there may want to think twice before getting that second helping of noodles. According to research out of Queen’s University, Ontario, processed carbohydrates like those found in refined flours may create an inflammatory microbiota in the upper gastrointestinal tract.[8] This insight came about while studying the diets of ancestral hominids, who maintained a relatively low carbohydrate diet, consisting mainly of potatoes and fruits. The carbohydrates in our ancestors diets also tended to be less processed, than those found in our foods today.

 

Vegetable and Seed Oils

Surprising to some, vegetables sources can also contribute to inflammation. However, before you toss out those carrot sticks, note that this is only referring to oils derived from vegetables and seeds such as corn, soy, or sunflower oil. These oils are referred to as poly-unsaturated fats and until recently were considered a heart healthy alternative to traditional fats derived from milk and animal products. This is due to their ability to reduce cholesterol. However, recent research has shown that cholesterol can be beneficial if sugar intake is curbed. Vegetable seed oils are high in Omega-6 fatty acids, not the healthier Omega-3 fatty acids found in other oils such as olive oil. Research suggests that high intake of Omega-6  fatty acids can actually increase chronic inflammation.[9]


Dr. Craig Chappell is a triple board-certified physician, located in Utah. With all this extra training Dr. Chappell has a breadth and depth of experience that many other doctors do not.





[1]El-Gabalawy, H., Guenther, Lyn C., and Bernstein, Charles, N. (2010). Epidemiology of Immune-Mediated Inflammatory Diseases: Incidence, Prevalence, Natural History, and Comorbidities. The Journal of Rheumatology Supplement. May 2010, 85 2-10.

[2] Pahwa, Roma, and Ishwarlal Jialal. “Chronic Inflammation.” StatPearls [Internet]., U.S. National Library of Medicine, 4 June 2019, www.ncbi.nlm.nih.gov/books/NBK493173/.

[3] Ma, Tao, et al. “Sucrose Counteracts the Anti-Inflammatory Effect of Fish Oil in Adipose Tissue and Increases Obesity Development in Mice.” PloS One, Public Library of Science, May 20AD, www.ncbi.nlm.nih.gov/pubmed/21738749.

[4] Hu, Yang, et al. “Sugar-Sweetened Soda Consumption and Risk of Developing Rheumatoid Arthritis in Women.” The American Journal of Clinical Nutrition, American Society for Nutrition, Sept. 2014, www.ncbi.nlm.nih.gov/pubmed/25030783.

[5] Ma, Tao, et al. “Sucrose Counteracts the Anti-Inflammatory Effect of Fish Oil in Adipose Tissue and Increases Obesity Development in Mice.” PloS One, Public Library of Science, June 2011, www.ncbi.nlm.nih.gov/pubmed/21738749.

[6] Iwata, Naomi G, et al. “Trans Fatty Acids Induce Vascular Inflammation and Reduce Vascular Nitric Oxide Production in Endothelial Cells.” PloS One, Public Library of Science, Dec. 2011, www.ncbi.nlm.nih.gov/pubmed/22216328.

[7] Basta, Giuseppina, et al. “Advanced Glycation End Products and Vascular Inflammation: Implications for Accelerated Atherosclerosis in Diabetes.” Cardiovascular Research, U.S. National Library of Medicine, 1 Sept. 2004, www.ncbi.nlm.nih.gov/pubmed/15306213.

[8] Spreadbury, Ian. “Comparison with Ancestral Diets Suggests Dense Acellular Carbohydrates Promote an Inflammatory Microbiota, and May Be the Primary Dietary Cause of Leptin Resistance and Obesity.” Diabetes, Metabolic Syndrome and Obesity : Targets and Therapy, Dove Medical Press, July 2012, www.ncbi.nlm.nih.gov/pubmed/22826636.

[9] Johnson, Guy H, and Kevin Fritsche. “Effect of Dietary Linoleic Acid on Markers of Inflammation in Healthy Persons: a Systematic Review of Randomized Controlled Trials.” Journal of the Academy of Nutrition and Dietetics, Centre for Reviews and Dissemination (UK), July 2012, www.ncbi.nlm.nih.gov/pubmed/22889633.