Question: “Does eating sugar cause diabetes?” Original answer: “No!” Updated answer “…Maybe…” After years of research we know that just simply consuming sugary foods does not cause diabetes, at least not type 1 diabetes (T1D).
Type 1 occurs because the immune system has incorrectly decided to attack the cells in the pancreas that produce insulin (beta cells). How this happens is an area of intense research. While these rogue immune cells are attacking the beta cells in the pancreas, the interesting issue is that other cells in the pancreas that produce other hormones are not damaged. The damage is a targeted event against insulin producing cells.
The cells responsible for the attack include T cells, B cells, macrophages and others. These cells migrate to the pancreas and take up residence in the islets. These cells establish localized inflammation that prevents insulin from being produced. There continues to be debate as to whether the beta cells are killed by the inflammation or are simply shut down. The latter would be better because the cells could be revived.
There are genetic factors associated with this process but studies show that genetics alone cannot account for the surprisingly growing number of type 1 patients that are being seen.
This creates the question of how do environmental factors play in to disease development and now the issue of “sugar” comes in to play.
Americans are eating more “sugary” foods, often whether they want to or not. Food manufacturers are including more sugar in prepared foods; people like the taste of sugar. Certain types of sugars, high fructose corn syrup for example, are used as food preservatives.
1) Glycosylation, the process where cells put small “sugar” molecules on proteins as the proteins are being synthesized by the body. This is a completely normal process. The glycosylation issue is tricky at the moment. My research group has discovered that in type 1 diabetes certain proteins in the body are glycosylated differently if a person has type 1 diabetes when compared to someone who does not have diabetes. This suggests that certain enzymes in diabetics function differently than in non-diabetics. What is important here is that the differently glycosylated proteins occur on a specific type of immune cell that my laboratory also showed attacks the islets during type 1 diabetes. Whether the intake of “sugar” affects this process isn’t known yet.
2) The Gut Microbiome: gut microbiota is the technical term for the bacteria that live normally in the gut. Where diet can impact disease is by influencing the gut-microbiome. The microbiome is made up of the different types of bacteria. Those bacteria are important for digesting food properly, but it has now been shown that those bacteria heavily influence the immune system. When a person consumes certain types of foods, the microbiome responds in a particular way; some of the bacteria thrive and other bacteria die off. This changes the overall makeup of the microbiome and the immune system also changes. Some foods promote healthy bacteria that help to control inflammation and other foods promote bacteria that promote inflammation.
Going back to the original statements about type 1 diabetes, there are genetic factors that are required. A person will not develop diabetes just because she ate a candy bar. In fact, sugars are an important part of the diet. Glucose is a major energy source for all cells; brain cells cannot survive without glucose. Current research shows that for a person to develop type 1 diabetes that person needs to have a specific combination of genes, a specific type of immune system and now we believe a specific combination of environmental events, including diet. The problem is that more sugar in dietary habits over the years may be promoting diabetes in people who are susceptible. If diet, sugar intake, were lower, even though an individual has some predisposition to diabetes, they might not develop the disease.
Also it is reasonable that the changes in the microbiome and changes in glycosylation of proteins is pushing individuals who were low or very low risk up to high risk and then development of diabetes.
David H. Wagner, PhD
Director of Help a Diabetic Child Foundation
Associate Professor and Head, Immunology Section
Department of Medicine and The Webb-Waring Center
The University of Colorado Anschutz Medical Campus