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For Better Gut Health, Cut Sugar!

The key to good health is in your gut!

A recent study on mice sheds light on how sugar intake may impact our gut microbiome, the risk of diabetes, and unwanted weight gain.

Most of us recognize that a high-fat, high-sugar, “Western-style” diet can lead to obesity. This study, published in Cell, suggests that there are more than extra calories that are doing damage to the gut.? According to Ivalo Ivanov, Ph.D., an associate professor of microbiology & immunology at Columbia University's Vagelos College of Physicians and Surgeons, “The gut microbiome is indispensable for an animal's nutrition.”To reach this conclusion, Ivanov and colleagues examined the initial impact of a high-fat, high-sugar diet on the gut microbiome in mice.

Your Gut on Sugar

A type of immune cell known as Th17 protects against diseases like diabetes. It also protects against weight gain. These immune cells protect our bodies from absorbing fats that lead to disease. Th17 cells create molecules that reduce the absorption of unhealthy lipids and reduce inflammation in the intestine. It’s important to protect these cells.

After a month of the unhealthy, Western-style diet, the animals in Ivanov’s study showed signs of metabolic syndrome. This included weight gain, insulin resistance, and glucose intolerance. Additionally, their microbiomes drastically changed. The number of healthy bacteria decreased, and bad bacteria increased. Specifically, filamentous bacteria decreased. Filamentous bacteria are vital to the animal’s health because they impact Th17 cells.

Fat or Sugar?

Ivanov and his team discovered that sugar -- not fat -- caused issues with filamentous bacteria.?Filamentous bacteria and the protective Th17 cells decreased due to sugar intake.

According to Ivanov, "When we fed mice a sugar-free, high-fat diet, they retained the intestinal Th17 cells and were completely protected from developing obesity and pre-diabetes, even though they ate the same number of calories."However, not every mouse in the study was impacted by removing sugar. In mice that don’t have filamentous bacteria, a beneficial effect wasn’t seen when sugar was taken out of their diets. The animals became heavy and developed diabetes.?After supplementing filamentous bacteria in mice without it, Th17 cells regenerated to protect against metabolic syndrome despite a high-fat diet.

Bacteria in people may be different from filamentous bacteria in mice, but Ivanov believes supplementing with other bacteria may have similar protective effects. He states, "For optimal health, it is important to modify your diet and improve your microbiome, or intestinal immune system. For example, by increasing Th17 cell-inducing bacteria." Giving the mice Th17 cells offered protection and could be therapeutic in humans.

Ivanov notes that popular diets advising sugar reduction may only work in individuals with certain bacteria in their microbiota. Certain probiotics could be beneficial in those cases.

His study stressed that a complicated relationship between diet, the microbiome, and the immune system is at play. It can impact the development of obesity, type 2 diabetes, metabolic syndrome, and other chronic conditions.

How can you protect your microbiome?

  1. Reduce added sugars in your diet, especially from ultra-processed food.

  2. Include fiber-rich foods to diversify gut bacteria. Beans, lentils, whole grains, fruits, and vegetables are essential.

  3. Avoid extreme diets that eliminate healthy carbs, such as a keto diet.

  4. Choose healthy fats such as avocado, canola oil, corn oil, olive oil, nuts, and seeds.

  5. Discuss the pros and cons of probiotics with your healthcare provider.

By Lisa Andrews, MEd, RD, LD Reference:

Kawano, Y., Edwards, M., Huang, Y., Bilate, A. M., Araujo, L. P., Tanoue, T., Atarashi, K., Ladinsky, M. S., Reiner, S. L., Wang, H. H., Mucida, D., Honda, K., & Ivanov, I. I. (2022). Microbiota imbalance induced by dietary sugar disrupts immune-mediated protection from metabolic syndrome. Cell, 2022. https://doi.org/10.1016/j.cell.2022.08.005