A recent study conducted at the McGill University Health Centre (MUHC) has revealed a significant correlation between parental diabetes and the risk of children developing type 1 diabetes. Specifically, children born to mothers who experienced gestational diabetes during pregnancy were found to be 94 percent more likely to be diagnosed with type 1 diabetes compared to those whose mothers did not have diabetes. Moreover, the risk for children with fathers who have type 2 diabetes was identified to be 77 percent higher. The findings emphasize the potential link between maternal type 2 diabetes and the development of type 1 diabetes in offspring.
Dr. Kaberi Dasgupta, Senior Scientist in the Metabolic Disorders and Complications Program at The Institute, highlighted the alarming statistic that a quarter of children diagnosed with type 1 diabetes in Canada do so late, often presenting with diabetic ketoacidosis—a serious and preventable condition. He underscored the necessity of identifying accessible risk factors that can expedite the detection of type 1 diabetes, particularly since population-wide or genetic screenings have not yet been established as cost-effective solutions.
Co-first author Dr. Isabella Albanese, who was an endocrinology fellow at The Institute when the study was conducted and is now a physician at MUHC and an Assistant Professor at McGill University, stated, “Our findings underscore the importance of including family history—not only of type 1 diabetes but also maternal gestational diabetes and paternal type 2 diabetes—in routine assessments.” She noted that such measures empower families and healthcare providers to pursue timely assessments and monitoring.
Additionally, Dr. Dasgupta remarked on the intriguing connections found between different forms of diabetes. Despite their distinct biological causes, the relationships support a broader understanding that factors leading to excess weight and insulin resistance—typically associated with type 2 diabetes—may also elevate the risk of type 1 diabetes in individuals with immune systems predisposed to attacking insulin-producing cells.
The study's findings are akin to a 2019 investigation carried out in China, which reported a 66 percent higher risk of type 1 diabetes in children born to mothers with gestational diabetes. Researchers of the Canadian study posited that economic, dietary, and lifestyle factors contributing to parental obesity and gestational diabetes could also influence the likelihood of obesity in their children. This highlights the multifactorial nature of the condition.
Laura Rendon, another co-first author of the study, discussed the potential mechanisms contributing to these findings. She pointed out that families often share lifestyle and eating habits, increasing the risk for the children. In addition, high blood sugar levels in parents may result in biological changes that enhance their children’s likelihood of developing type 1 diabetes. This aspect is particularly personal for Rendon, as she lives with type 1 diabetes herself, giving her research a meaningful drive.
What is diabetes?
Diabetes is a health condition characterized by elevated glucose or blood sugar levels. In type 1 diabetes, the immune system compromises the insulin-producing cells in the pancreas, resulting in insufficient insulin to regulate blood sugar effectively. Conversely, in cases of gestational diabetes and type 2 diabetes, the body fails to respond appropriately to insulin. These conditions are often linked to factors such as excess weight, low physical activity, and genetic predispositions.
Dr. Dasgupta further elaborated on the nature of these diabetes types, stating, “What is interesting is that type 1 diabetes is a disease of lack of the hormone insulin, while gestational diabetes and type 2 diabetes stem mostly from the body’s resistance to the hormone.” He speculated that genetic, environmental, and behavioral contributors that lead to insulin resistance might, in certain cases, trigger the immune reactions responsible for the onset of type 1 diabetes.
