Could maternal type 1 diabetes protect children from developing the disease?
A recent study published in Nature Metabolism analyzed around 2,000 mother-offspring pairs to investigate the relationship between maternal type 1 diabetes (T1D) and the epigenetic makeup of their children. In type 1 diabetes, the cells in the pancreas that make insulin—sometimes referred to as "pancreatic islet" or "pancreatic beta cells"—are killed by T-cells produced by the immune system.
In this study, researchers compared children born to mothers with T1D with those born to mothers without the disease. They found significant epigenetic differences, particularly in DNA methylation patterns (chemical modifications that influence gene activity without changing DNA sequence). These modifications appeared to provide a protective effect, reducing the risk of developing islet autoimmunity and, consequently, T1D during early childhood.
The study revealed that children born to mothers with Type 1 diabetes had certain tiny chemical tags—called methylation marks—on their DNA that were different from those in children whose mothers didn’t have diabetes. These tags don’t change the genes themselves but can turn them “on” or “off,” affecting how the body works. Many of these differences appeared in genes that help control the immune system, especially in areas of DNA known to be linked to autoimmune diseases like Type 1 diabetes. Some of the changes were found in genes that guide early growth and development as well. These differences might help explain why children of mothers with diabetes seem less likely to develop the disease themselves, possibly because these DNA changes make their immune systems less likely to attack their own cells.
The findings imply that environmental exposure to maternal T1D during pregnancy may trigger protective epigenetic programming in the child’s immune system. This supports the broader concept that maternal health conditions can shape offspring disease risk through epigenetic mechanisms. However, since the study relied on associative data from mostly European populations, further research is needed to confirm causality and test whether similar effects occur across diverse genetic backgrounds.
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