We all know that fructose is the sugar in fruits, however, we can also find it naturally in honey, panela, agave syrups, maple, and even in greater or lesser amounts in vegetables or vegetables such as pumpkin or squash, onions, garlic, eggplant, zucchini, carrot, red and yellow pepper. We also find it naturally forming sucralose, a disaccharide composed of 50% fructose and 50% glucose; this type of sugar makes up many foods such as corn, peas, pickles, beets, and carrots. In fact, many of the fruits on the market, apart from having fructose, also contain glucose and sucralose, such as banana or banana, figs or figs, apricot, plum, feijoa, tangerine, mango, apple, peach among many others.
Synthetically, fructose is present in table sugar or white sugar, brown sugar, corn syrups, all sweeteners and sweeteners, maltodextrin, polyalcohols (such as erythritol, xylitol and maltitol) etc; all of these are practically in all packaged products, ultra-processed, nectars, 0 calorie drinks, diet, light, non sugars added (without added sugars), gums, light desserts among many others.
The health problem that fructose generates comes from its excessive consumption; in the 21st century we have had an increase of more than 500% compared to its consumption in the 1930s. At that time, a person on average could consume between 16 and 20 grams of fructose per day from fruits and vegetables, while currently a person on average consumes between 75-80 grams per day in the form of packaged and ultra-processed products.
To understand how fructose impacts our health, we must know how its metabolic pathway is. In figure 1 we can observe the entire route that fructose takes once it enters our body.
In addition to the negative effects that excessive fructose has on our health; it also plays a role in the relationship of emotional hunger and anxiety. The consumption in large quantities of fructose derived from sweeteners, additives and ultra-processed foods, causes an increase in hunger and the desire to eat, as fructose decreases leptin (hormone that produces satiety), increases blood ghrelin levels (hormone that is released when we are hungry), resulting in worse control of hunger and satiety, leading to the behavioral alterations observed in addiction, such as anxiety to eat.
Every time a poorly balanced diet is ingested or at night; foods rich in sugars from fruits, flours and ultra-processed foods, will stimulate the release of insulin. If the diet is not controlled, it will remain high in a sustained way, which is known as hyperinsulinemia and leads to a greater sensitivity of our body towards these groups of foods, which translates into a sharp increase in weight.
It is important to bear in mind that there are moments or physiological conditions that trigger a sharp rise in insulin (hyperinsulinemia) such as emotional stress, inflammatory processes in response to a sudden illness or a hidden infection. Therefore, hyperinsulinemia is considered a response to a stimulus that is producing hormonal imbalances in our body and that can be reversible (6).
Through our diet, fructose is absorbed in the small intestine, from there it passes our blood or portal circulation to the liver and there it is transformed into metabolic intermediaries such as acetyl CoA and uric acid. Acetyl CoA will be used to form glucose (sugar) through a process called gluconeogenesis and fatty acids (fats) lipogenesis. The uric acid, sugars and fats that have been formed in the liver will be sent to our blood where they will follow different paths. Fats (cholesterol and triglycerides) will be sent to adipose tissue or localized and visceral fat for storage, while sugars will go to our organs to be used as energy, but uric acid blocks their entry and as a consequence they will remain circulating in large amounts in the blood which stimulates the release of insulin by the pancreas. And here a vicious circle is created since the action of insulin is toopen the channels for sugar or glucose to enter the different organs but being blocked by uric acid, it will lead to what is known as insulin resistance. Through this mechanism, we can observe that patients present an increase in triglycerides, elevation of blood sugar, increase in uric acid, insulin resistance, increase in localized and/or visceral fat and non-alcoholic fatty liver, etc.
According to Hao Cheng et al., 2022 and Muriel et al., 2021, the excess of fructose in our diet also alters the composition of the microbiota and the integrity of the intestinal barrier. The change in our bacterial flora breaks the bonds that exist between the cells of the small intestine, giving way to the entry of toxins and allergens leading to what is known as leaky gut (to understand it, the intestine works as a strainer that filters, if it breaks it will give way to the entry of harmful substances for our health). Recent studies conclude that part of allergies, intolerances and diseases are generated when the barrier of our intestine is altered; clinical pictures that are resolved or improve when restoring the intestinal barrier.
In summary, chronic inflammation derived from the high consumption of fructose through our diet is related to the development of multiple diseases (Figure 2), among them, the increase in localized and/or visceral fat (overweight/obesity), cardiovascular disease, metabolic syndrome, insulin resistance, diabetes, non-alcoholic fatty liver, inflammation, different types of cancer, irritable bowel, intolerances and allergies, diseases that our society faces.
All this leads us to the conclusion that it is necessary to lower the daily consumption of fructose to balance the balance of our body, restore intestinal permeability and improve the metabolic environment. Therefore, it is important to:
- Use whole fruits 2 times a day (immediately after breakfast and lunch)
- Avoid using fruits between meals, on an empty stomach and at night
- Stop natural juices, nectars, box juices, sodas, packaged refreshments of all kinds.
- Learn to use drinks without any type of sweetener, sweetener and/or substitute.
- Check and read the ingredients of foods (even if they are organic) and choose those with a smaller number of ingredients.
- Choose foods for their quality rather than the number of calories they contain.
- The solution is not to abruptly suspend everything that contains fructose, but to start choosing better what we put into our body, always prioritizing the consumption of vegetables, fruits and proteins with moderation and balance.
- References: Andres-Hernando, A., Orlicky, D. J., Kuwabara, M., Ishimoto, T., Nakagawa, T., Johnson, R. J., & Lanaspa, M. A. (2020). Deletion of fructokinase in the liver or in the intestine reveals differential effects on sugar-induced metabolic dysfunction. Cell Metabolism, 32(1), 117–127.e3. https://doi.org/10.1016/j.cmet.2020.05.012
- Blüher, M. (2019). Obesity: Global epidemiology and pathogenesis. NatureReviews Endocrinology, 15(5), 288–298. https://doi.org/10.1038/s41574-019-0176-8
- Caliceti, C., Calabria, D., Roda, A., & Cicero, A. (2017). Fructose intake, serum uric acid, and cardiometabolic disorders: A critical review. Nutrients, 9(4), 395. https://doi.org/10.3390/nu9040395
- Carvallo, P., Carvallo, E., Barbosa-da-Silva, S., Mandarim-de-Lacerda, C. A., Hernández, A., & del-Sol, M. (2019). Metabolic Effects of Excessive Fructose Consumption. International Journal of Morphology, 37(3), 1058–1066. https://doi.org/10.4067/s0717-95022019000301058
- Cheng, H., Zhou, J., Sun, Y., Zhan, Q., & Zhang, D. (2022). High fructose diet: A risk factor for immune system dysregulation. Human Immunology, 83(6), 538–546. https://doi.org/10.1016/j.humimm.2022.03.007
- Jang, C., Hui, S., Lu, W., Cowan, A. J., Morscher, R. J., Lee, G., Liu, W., Tesz, G. J., Birnbaum, M. J., & Rabinowitz, J. D. (2018). The small intestine converts dietary fructose into glucose and organic acids. Cell Metabolism, 27(2), 351–361.e3. https://doi.org/10.1016/j.cmet.2017.12.016
- Jensen, T., Abdelmalek, M. F., Sullivan, S., Nadeau, K. J., Green, M., Roncal, C., Nakagawa, T., Kuwabara, M., Sato, Y., Kang, D.-H., Tolan, D. R., Sanchez-Lozada, L. G., Rosen, H. R., Lanaspa, M. A., Diehl, A. M., & Johnson, R. J. (2018). Fructose and sugar: A major mediator of non-alcoholic fatty liver disease. Journal of Hepatology, 68(5), 1063–1075. https://doi.org/10.1016/j.jhep.2018.01.019
- Malik, V. S., Li, Y., Pan, A., De Koning, L., Schernhammer, E., Willett, W. C., & Hu, F. B. (2019). Long-Term consumption of sugar-sweetened and artificially sweetened beverages and risk of mortality in US adults. Circulation, 139(18), 2113–2125. https://doi.org/10.1161/circulationaha.118.037401
- Muriel, P., López-Sánchez, P., & Ramos-Tovar, E. (2021). Fructose and the liver. International Journal of Molecular Sciences, 22(13), 6969. https://doi.org/10.3390/ijms22136969
- Taskinen, Packard, & Borén. (2019). Dietary fructose and the metabolic syndrome. Nutrients, 11(9), 1987. https://doi.org/10.3390/nu11091987
Author: Catherine Del Pilar Villoria Rojas
Medical Director, Natural Body Center. Research Physician Complutense University of Madrid.