According to a study published in the journal Diabetes, by the University of Copenhagen, mouse mothers can protect their offspring from developing type 1 diabetes by eating a gluten-free diet.
More than 1% of the Denmark population is affected by type 1 diabetes and experiments have shown a correlation between the mother’s gluten free diet and the development of type 1 diabetes in their offspring. The experiments revealed that the diet changed the intestinal bacteria in both the mother and the pups. The intestinal flora plays an important role for the development of the immune system as well as the development of type 1 diabetes, and the study suggests that the protective effect of a gluten-free diet can be ascribed to certain intestinal bacteria. The advantage of the gluten-free diet is that the only side-effect seems to be the inconvenience of having to avoid gluten, but there is no certain evidence of the effect or side-effects.
“Preliminary tests show that a gluten-free diet in humans has a positive effect on children with newly diagnosed type 1 diabetes. We therefore hope that a gluten-free diet during pregnancy and lactation may be enough to protect high-risk children from developing diabetes later in life,” said assistant professor Camilla Hartmann Friis Hansen from the Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences.
Professor Axel Kornerup, the co-author of the study from the Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences commented on the study as follows: “Early intervention makes a lot of sense because type 1 diabetes develops early in life. We also know from existing experiments that a gluten-free diet has a beneficial effect on type 1 diabetes.
This type of research correlates to a previous study which confirmed that the gut bacteria in children with type 1 diabetes is substantially different. The study published in the journal Diabetes, demonstrated the impact of gut bacteria on their overall health and found that children with type 1 diabetes have a different gut microbiota than children who are healthy. The changes take place before they are detected in the blood through an autoimmune response and are attributed to the microbial DNA. Colonies of bacteria congregate to form what is known as the microbiome, which acts as a central regulator to influence the host organism. Previous research has associated the microbiome with different diseases; the gut microbiome, in particular, is thought to play a role in the pathogenesis of metabolic diseases such as diabetes.
Scientists from the Helmholtz Zentrum in Munich compared the composition and interaction of the gut microbiota in children who went on to develop diabetes-specific autoantibodies in their blood with data from children who were auto-antibody negative.
The bacterial metabolic pathway and their interaction in the gut varied significantly in the two groups before one group developed the typical diabetes autoantibodies. The changes could be traced back to the first months of life.
Colonies of bacteria form what is known as the microbiome, and the genetic information contained within it influences the host organism.
Professor Ziegler, the lead study author commented on the epigenetic influence and their impact on gut bacteria as follows:
“A range of external factors such as diet, hygiene or even the birth delivery mode can influence both the composition of gut bacteria and the way in which the bacteria interact. If we are able to identify those parameters that tend to indicate more negative microbiome characteristics, we can develop new approaches to preventing autoimmune processes — for example, in type 1 diabetes.”
C. H. F. Hansen, ukasz Krych, K. Buschard, S. B. Metzdorff, C. Nellemann, L. H. Hansen, D. S. Nielsen, H. Frokiaer, S. Skov, A. K. Hansen. A maternal gluten-free diet reduces inflammation and diabetes incidence in the offspring of NOD mice. Diabetes, 2014; DOI: 10.2337/db13-1612
Endesfelder, D. et al. Compromised gut microbiota networks in children with anti-islet cell autoimmunity, Diabetes. Diabetes, March 2014 DOI: 10.2337/db13-1676 1939-327X