Detecting Sugar in Baby Food

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Common diseases are often in the news. When the discussion turns to diabetes, most people think of age-related diabetes, the medical term for which is type 2 diabetes. Type 1 diabetes, which occurs already in infants and children, is far less well known. The patients, some of whom are still very young, will spend the rest of their lives injecting insulin several times a day. Roughly 10 percent of diabetes sufferers in Germany have this type of diabetes. Every year, around 2000 children contract type 1 diabetes.

Since the discovery in the 1970s of a group of antibodies referred to as islet cell autoantibodies, which attack parts of the insulin producing cells, medical science has assumed that type 1 diabetes is an autoimmune disease. Subsequently, researchers have focused on asking how the autoimmune destruction of the insulin producing cells in the pancreas comes about. They suspect that a combination of genetic factors and external influences is to blame.

At what stage of life does the disease affect patients, who is more commonly affected (genetics) and can the disease be diagnosed before the onset of clinical symptoms – these are all questions pertaining to the search for triggers of this serious illness. Research work in Germany, and especially in the context of the German BABYDIAB study, has delivered some seminal findings. When it was initiated in 1989, the BABYDIAB study was the world’s first study to follow the natural course of type 1 diabetes from birth onwards in children at risk, i.e., children whose parents have type 1 diabetes. Among their most important findings, they determined that autoimmunity against islet cells starts already in the first two years of life, and that children with a genetic predisposition to type 1 diabetes are 10 times more likely to acquire islet autoimmunity. They also found that children with early islet autoantibodies are highly likely to contract type 1 diabetes during infancy. In view of this, the search for triggers concentrated on factors which have an influence during early childhood. Food is the most prominent of these factors.

The BABYDIAB study was able to demonstrate for the first time that children who are fed on solid food at an early stage have a significantly higher risk of islet autoimmunity. A survey of the BABYDIAB parents revealed that 5 percent of the children were given solid food when they were less than four months old, contrary to the recommendations of the Research Institute of Child Nutrition. Frequently, the food in question was baby milk thickened with gluten-containing grain flakes. In comparison to children fed exclusively on milk during their first four months, these children were four times as likely to develop islet autoantibodies and type 1 diabetes. Children with diabetes risk genes had an especially strong reaction to the early administration of gluten and developed complete islet autoimmunity. Very similar results were achieved by the American DAISY study, which commenced about four years later than the BABYDIAB study.

Gluten is a protein contained by most grains and has already been identified as the trigger of a chronic disease of the small intestine’s mucous membrane, known as “coeliac disease”. Curiously, the children of the BABYDIAB study exhibit a high predisposition not only to type 1 diabetes, but also to coeliac disease. These findings raised a number of questions, which prompted the Research Group on Diabetes in Munich to establish a study programme on the role of gluten and early children’s nutrition in the genesis of type 1 diabetes. Can islet autoimmunity and type 1 diabetes be prevented by a glutenfree diet? And is gluten really the nutritional factor which triggers diabetes? With these and other questions in mind, the interventional study BABYDIÄT started work in 2001. The aim was to prevent the occurrence of islet autoimmunity through the systematic administration of gluten-containing food in the sixth or twelfth month. One hundred and fifty infants were treated, all of whom had both first-degree relatives with type 1 diabetes and the diabetes risk gene, so that the children had a diabetes risk of 20 percent. Half of the families were instructed to eat gluten-free food for the first twelve months, while the other half was supposed to give the infant gluten only after the sixth month. The progress of these children has since been followed for an average of 2.8 years, and a first evaluation of the results is scheduled for the end of 2009. Besides preventing islet autoimmunity, an examination was made, using the children’s stool samples, of how solid food and especially gluten altered the intestinal flora and the frequency of gastro-intestinal disease. A very positive side- A shared meal brings even infants together Illustration: BABYDIAB study effect of BABYDIÄT is that mothers breastfeed longer and smoke less thanks to their participation in the study. In other words, they are living a healthier, more conscious life, which will have a positive overall effect on the development of their children. The question also arose whether the elimination of gluten from the diets of children with several islet autoantibodies could prevent the onset of type 1 diabetes. In order to find out, children who had already been fed with gluten-containing food and who had a high risk of developing type 1 diabetes because of their islet autoantibodies were given a gluten-free diet for one year. Afterwards, the children were given a normal glutencontaining diet again. This experiment revealed that the one-year gluten-free diet did not protect the children from further development of islet immunity or type 1 diabetes. The conclusion of this study is that children with already existing islet autoimmunity cannot be protected from the progress of the disease by means of a short-term gluten-free diet. Parallel to the interventional studies on children, studies were also conducted on mice with a 90 percent chance of developing a type of diabetes very similar to the human type 1 diabetes. The aim of these studies was firstly to find out whether it was possible to protect the animals from autoimmune diabetes by omitting gluten-containing grains such as wheat or barley from their diet. It was ascertained that the mice that were deprived of wheat and barley contracted diabetes much less frequently.

In a second experiment, the researchers asked whether renewed feeding of wheat or an isolated wheat protein increased the mice’s diabetes risk once again. The answer they found was that feeding wheat in a small quantity increased the rate of diabetes in the mice, but not the feeding of isolated wheat proteins such as gluten, albumin and globulin or other products such as fruit and potatoes. The conclusion that may be drawn from these experiments is that the dosing of grain content influenced the development of autoimmune diabetes in mice. However, the strongest diabetes triggering effect was observed with very low doses.

Up to now, it has not been explained why the immune system attacks the body’s own insulin. It is conceivable that insulin antibodies result from a cross reaction with food proteins. The infant’s still premature immune system is confronted by food antigens already in its first few months of life. At this time, the intestine has a much higher permeability to larger molecules, which means that an interaction between the intestinerelated immune system and food components is possible. Some children thus had types of insulin autoantibodies which were with very high probability activated by the intestine-related immune system. Interestingly, these antibodies also exhibited a reaction against cow milk. But further tests revealed that these antibodies played no direct role in the progression of diabetes in the children. It has therefore yet to be clarified what role is played by these insulin autoantibodies in the genesis of type 1 diabetes. The findings gathered up to now have led to the design of the TEDDY (The Environmental Determinants of Diabetes in the Young) study, the world’s largest research consortium, which is looking at the influence of early childhood nutrition as well as other environmental factors on the genesis of type 1 diabetes.

In this study, over 7000 children from the U.S.A., Finland, Sweden and the Federal Republic of Germany, who have a heightened genetic risk of type 1 diabetes from birth on, will undergo regular checkups at short intervals. In the framework of the TEDDY study, it will be possible to test whether previous findings can be confirmed in other countries with different nutritional habits.

Dr. Sandra Hummel, M. Sc. Maren Pflüger and Prof. Dr. med. Anette-G. Ziegler work at the Institute for Diabetes Research at the TU Munich.