Every year, the rate of Type I diabetes incidence among children under the age of 14 increases by three percent worldwide. That means that approximately 80 people per day are diagnosed with Type I diabetes, and this number is only increasing. While the exact cause of juvenile diabetes continues to elude scientists, a new study from Tel Aviv University suggests that the trigger for the condition may occur before birth.
In a recent paper published in “Diabetic Medicine,” Prof. Zvi Laron, Professor Emeritus of Pediatric Endocrinology at TAU‘s Sackler Faculty of Medicine, evidence is put forth that Type I diabetes is initiated in the uterus. According to the research, women who contract a viral infection during pregnancy and especially in winter months can transmit viruses to their genetically susceptible fetuses, which can spark the eventual development of Type I diabetes.
The “right season” for diabetes
“We knew that type 1 diabetes was associated with other autoimmune diseases like Hashimoto Thyroiditis, celiac disease, and multiple sclerosis, so we investigated the seasonality of birth months for these respective diseases in Israel and other countries,” said Prof. Laron. “We found that the seasonality of the birth of children who went on to develop these diseases did indeed differ from that of the general public,” meaning that children born in certain seasons were more susceptible to autoimmune diseases like diabetes than those born in others.
“In further studies, we found evidence that viral infections of the mother during pregnancy induced damage to the pancreas of the mother and/or the fetus, evidenced by specific antibodies including those affecting the pancreatic cells producing insulin,” Laron said.
For the study, Prof. Laron and his team of researchers from Israel, the University of Washington, and Lund University, Sweden, conducted blood tests on 107 healthy pregnant women, testing for islet cell autoantibodies — evidence of diabetes that appears years before initial symptoms do. They also tested for anti-rotavirus and anti-CoxB3 antibodies.
The researchers found a striking difference between women tested in different seasons, suggesting a link to winter epidemics. The concurrent presence of GAD65 antibodies in cord blood and their mothers indicated autoimmune damage to islet cells during pregnancy, possibly caused by cross-placental transmission of viral infections and/or antivirus antibodies. In other words, during viral epidemics of winter months, ten percent of the healthy pregnant women who had no family background of autoimmune diseases tested positive for damaging antibodies connected to the development of Type I diabetes.
Sign up for our free weekly newsletterSubscribe
Vaccination before conception
By comparing the cord blood samples of infants, which tested positive for the Type I diabetes biomarkers, to those of their mothers who tested negative for diabetes biomarkers, the researchers implied that the development of juvenile diabetes could be an in utero response by the fetus to its mother’s viral infection.
“If our hypothesis can be verified, then preventive vaccine before conception would be useful in stopping the increasing incidence of type 1 diabetes and other autoimmune diseases,” said Prof. Laron. “There is no cure for this diabetes, so true intervention would be important not only medically but also psychologically and financially, as the costs of the lifelong treatment of this chronic disease and other autoimmune diseases are great.”
Prof. Laron and his international collaborators are currently raising funds to expand their research to include nearly 1,000 women and newborns.
Prof. Zvi Laron is Professor Emeritus of Pediatric Endocrinology at TAU’s Sackler Faculty of Medicine, Director of the Endocrinology and Diabetes Research Unit at Schneider Children’s Medical Center of Israel, and Head of the World Health Organization Collaborating Center for the Study of Diabetes in Youth. Prof. Laron is internationally known for the discovery of the Laron Syndrome, also known as Laron-type Dwarfism, an autosomal recessive disorder characterized by an insensitivity to growth hormone. He conducted the research together with collaborators from the University of Washington and Lund University in Sweden.