Type 1 diabetes can be predicted in children, study suggests

Mon, 02 Mar 2015
Measuring levels of autoantibodies in the blood can predict the development of type 1 diabetes in young children, according to new research.

The study, known as "The Environmental Determinants of Diabetes in the Young" (or TEDDY) and published in Diabetologia, indicates that autoantibodies reveal whether or not the immune system is attacking insulin-producing beta cells in the pancreas, thereby causing type 1 diabetes in children.

Antibodies are proteins found in the blood. Their presence indicates that the immune system has attacked a foreign body. Autoantibodies indicate autoimmune disease. That is, they suggest that the immune system is attacking healthy, beneficial cells, such as insulin-producing beta cells. This kind of abnormal immune system behaviour is the cause of type 1 diabetes.

If the first autoantibody found in young children attacks insulin, this could indicate the presence of type 1 diabetes. Similarly, if the autoantibody targets GAD65 (a protein found inside insulin-producing beta cells), the child may be likely to develop type 1 diabetes. In some cases, autoantibodies targeting both insulin and GAD65 will be found simultaneously.

The research followed 8,600 children from Sweden, the United States, Germany, and Finland, all of whom were highly likely to develop hereditary type 1 diabetes. 6.5 per cent of them had their first autoantibody before the age of six.

Of these children, 44 per cent had an autoantibody targeting insulin, 38 per cent had GAD65 autoantibodies before two, and 14 per cent had both autoantibodies by the age of three.

The study suggests that autoantibodies can appear earlier than previously thought.

Although the kind of autoantibody was determined by the child's genetic risk factors, researchers still do not know why the immune attacks insulin-producing beta cells in the pancreas.

Ake Lernmark, lead researcher of the study, suggested that a virus may be responsible: "It is possible that there are two different diseases involved. Perhaps one virus triggers the autoantibodies against insulin and another one the autoantibodies against GAD65."
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