Despite decades of food industry propaganda blaming fat as the scapegoat, more and more research points towards sugar as being a major contributor to inflammation in the diet. Many studies have correlated sugar consumption with a variety of inflammatory conditions. Scientists are not, however, satisfied with correlations. We want mechanisms of action to be clear so we can understand and feel more confident in interventions. Researchers from Julius Maximilians University of Würzburg (JMU) provide some satisfaction in this case by linking glucose metabolism with genetic expression in Th17 immune cells.
One can hardly read a health publication these days without reading about a ketogenic diet or some other form of low carb diet. So many health benefits are claimed by the promotions. Most start with weight loss, but brain health, heart health, autoimmune conditions, yeast overgrowth, and more are touted as reasons to drop the carbs, especially the refined sugars. Many tell stories of how their health turned around on these low carb type diets. This is especially true for those who were living the Standard American Diet, high in sugar bad carbs.
On the other hand, not that many likely recognize Th17 immune cells in any general publication or comfortably roll it off the tip of their tongue. This subgroup of T cells, as part of our body’s immune system, act as regulatory cells. Yes, they help regulate other immune cells and serve as determinants of whether the immune system remains calm or gets fired up. Influencing their decisions thus influences all the various health conditions impacted by inflammation.
Researchers at JMU worked through multiple steps in how these Th17 cells absorb and utilize glucose, connecting this process with how they influenced other immune cells. Glucose, the primary form of simple sugar (carbohydrate) that floats through our bloodstream and supplies much of the energy for cell activity, must get into any cell before being used. Several glucose transporter types exist throughout our body, but Th17 depend highly on one called GLUT3.
Once glucose enters the cell, other metabolic steps change it into acetyl-coA for further burning in the mitochondrial. Here is where the connection with inflammation appears to occur. Levels of Acetyl-coA appear to influence the genes that increase inflammatory activity of the Th17 cells. The Th17 cells that are turned on by increased glucose uptake then release chemical messengers to fan the flames of other immune cells.
This mechanistic connection justifies interventions which functional MD’s like myself already employ. Encouraging our patients to pursue an anti-inflammatory nutrition lifestyle includes avoiding processed foods and limiting refined sugars. We sometimes encourage ketogenic type nutrition plans or intermittent fasting. While ketogenic or paleo diets are not great for everyone, we definitely see patient benefits from avoiding high inflammatory foods.
At the same time, we don’t want patients to develop negative attitudes towards the foods that God has provided us to enjoy. Rather than focus on what they cannot eat, we encourage them to focus on finding enjoyable AND health foods. We also point out that occasionally, celebrating with a less healthy food option is no the end of the world. Just don’t make it a habit.
Besides such simple daily interventions, researchers are also looking to chemical interventions that can interfere with this inflammatory pathway. Yes, limiting sugar would seem to be easy enough, but for some who won’t change their nutrition lifestyle or have already progressed down the inflammatory pathway, having late stage interventions in natural or pharmaceutical forms can be helpful.
Helping patients live healthier more abundant lives means applying the best of lifestyle medicine along with the best of science and necessary therapeutics. It also means stopping to appreciate a deeper understanding of the mechanisms in our cells on which we base our interventions.
Sophia M. Hochrein, Hao Wu, Miriam Eckstein, Laura Arrigoni, Josip S. Herman, Fabian Schumacher, Christian Gerecke, Mathias Rosenfeldt, Dominic Grün, Burkhard Kleuser, Georg Gasteiger, Wolfgang Kastenmüller, Bart Ghesquière, Jan Van den Bossche, E. Dale Abel, Martin Vaeth. The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming. Cell Metabolism, 2022; DOI: 10.1016/j.cmet.2022.02.015
Thanks to Science Daily:
University of Würzburg. “How sugar promotes inflammation.” ScienceDaily. ScienceDaily, 22 March 2022. <www.sciencedaily.com/releases/2022/03/220322122836.htm>.
Sanctuary Functional Medicine, under the direction of Dr Eric Potter, IFMCP MD, provides functional medicine services to Nashville, Middle Tennessee and beyond. We frequently treat patients from Kentucky, Alabama, Mississippi, Georgia, Ohio, Indiana, and more... offering the hope of healthier more abundant lives to those with chronic illness.