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Refined carbohydrates

White bread,pasta,pastries

refined carbohydrate, white starch, sugar, glycemic index
Refined carbohydrates

Increased production of pro-inflammatory cytokines and insulin resistance

The Relationship between Refined Carbohydrates and Inflammation: A Focus on Fructose


Refined carbohydrates are simple sugars and processed grains that have been stripped of their natural fiber, vitamins, and minerals. Examples include white flour, white rice, and added sugars like high-fructose corn syrup (HFCS). The consumption of refined carbohydrates has been associated with an increased risk of chronic diseases, including type 2 diabetes, obesity, and cardiovascular disease, partly due to their impact on inflammation (1). This article will delve into the relationship between refined carbohydrates and inflammation, with particular emphasis on fructose, while citing relevant sources and providing references for further exploration.

Refined Carbohydrates and Inflammation

Refined carbohydrates, especially simple sugars like sucrose and HFCS, have been shown to induce inflammation through several mechanisms. First, their rapid absorption in the digestive tract can lead to rapid spikes in blood glucose and insulin levels (2). High levels of glucose and insulin can trigger the production of pro-inflammatory cytokines and oxidative stress, which contribute to inflammation (3).

Second, the consumption of refined carbohydrates can promote the formation of advanced glycation end products (AGEs) (4). AGEs are compounds formed when sugars react with proteins or lipids in the body, and their accumulation has been linked to increased inflammation, oxidative stress, and the development of chronic diseases like diabetes and atherosclerosis (5).

Fructose and Inflammation

Fructose is a simple sugar found naturally in fruits and honey and is a major component of added sugars like HFCS and sucrose. In recent years, fructose has received considerable attention due to its potential role in inflammation and chronic diseases (6).

Fructose is metabolized differently from glucose, primarily in the liver, where it can be converted into fat (triglycerides) through a process called de novo lipogenesis (7). Excessive fructose consumption can lead to increased triglyceride production, which contributes to the development of non-alcoholic fatty liver disease (NAFLD) and promotes inflammation (8).

Furthermore, fructose consumption has been shown to increase uric acid levels, which can contribute to inflammation (9). High uric acid levels can activate the NLRP3 inflammasome, a key component of the innate immune system that triggers the release of pro-inflammatory cytokines, leading to a heightened inflammatory response (10).

Another important aspect of fructose-induced inflammation is its impact on the gut microbiota. High fructose intake can alter the composition of the gut microbiota, leading to an increase in pro-inflammatory bacterial species and the production of endotoxins like lipopolysaccharide (LPS) (11). LPS can enter systemic circulation and activate immune cells, resulting in the release of pro-inflammatory cytokines and the perpetuation of inflammation (12).

Reducing Refined Carbohydrates and Fructose Intake

Reducing the consumption of refined carbohydrates and fructose can help lower inflammation and decrease the risk of developing chronic diseases. This can be achieved by:

  1. Replacing refined grains with whole grains: Whole grains, such as brown rice, whole wheat bread, and quinoa, contain more fiber, vitamins, and minerals than refined grains (13).

  2. Limiting added sugars: Reducing the intake of added sugars, such as HFCS and sucrose, can help lower fructose consumption and reduce inflammation (14).

  3. Consuming fruits in moderation: While fruits are a natural source of fructose, they also contain fiber, vitamins, and antioxidants that can help counteract the potential negative effects of fructose (15).


The relationship between refined carbohydrates, particularly fructose, and inflammation is complex and multifaceted. Excessive consumption of refined carbohydrates and fructose can contribute to inflammation through various mechanisms, including rapid spikes in blood glucose and insulin levels, the formation of AGEs, increased triglyceride production, elevated uric acid levels, and alterations in the gut microbiota. Reducing the intake of refined carbohydrates and fructose can help lower inflammation and decrease the risk of developing chronic diseases.

Further research is needed to fully understand the intricate relationship between refined carbohydrates, fructose, and inflammation, and to develop effective dietary strategies for mitigating their adverse effects on health.

  1. Hu, F. B. (2010). Are refined carbohydrates worse than saturated fat? The American Journal of Clinical Nutrition, 91(6), 1541-1542.

  2. Stanhope, K. L. (2016). Sugar consumption, metabolic disease and obesity: The state of the controversy. Critical Reviews in Clinical Laboratory Sciences, 53(1), 52-67.

  3. Lê, K. A., & Tappy, L. (2006). Metabolic effects of fructose. Current Opinion in Clinical Nutrition and Metabolic Care, 9(4), 469-475.

  4. Uribarri, J., & Tuttle, K. R. (2006). Advanced glycation end products and nephrotoxicity of high-protein diets. Clinical Journal of the American Society of Nephrology, 1(6), 1293-1299.

  5. Vlassara, H., & Uribarri, J. (2014). Advanced glycation end products (AGE) and diabetes: Cause, effect, or both? Current Diabetes Reports, 14(1), 453.

  6. Tappy, L., & Lê, K. A. (2010). Health effects of fructose and fructose-containing caloric sweeteners: where do we stand 10 years after the initial whistle blowings? Current Diabetes Reports, 10(3), 208-218.

  7. Softic, S., Cohen, D. E., & Kahn, C. R. (2016). Role of dietary fructose and hepatic de novo lipogenesis in fatty liver disease. Digestive Diseases and Sciences, 61(5), 1282-1293.

  8. Basaranoglu, M., Basaranoglu, G., & Bugianesi, E. (2015). Carbohydrate intake and nonalcoholic fatty liver disease: fructose as a weapon of mass destruction. Hepatobiliary Surgery and Nutrition, 4(2), 109-116.

  9. Johnson, R. J., Nakagawa, T., Sanchez-Lozada, L. G., Shafiu, M., Sundaram, S., Le, M., … Lanaspa, M. A. (2013). Sugar, uric acid, and the etiology of diabetes and obesity.

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