Scientists are narrowing in on checklists of both errant genes and the environmental factors that could trigger those genes to more accurately assess type 1 diabetes risk and help children and their families avoid it.
"The next five years is the time to put the puzzle together," says Dr. Jin-Xiong She, director of the Center for Biotechnology and Genomic Medicine at the Medical College of Georgia at Augusta University and Georgia Research Alliance Eminent Scholar in Genomic Medicine.
She is talking about the TEDDY – The Environmental Determinants of Diabetes in the Young – study that started in 2003 at MCG and five other clinical centers across four countries and is following nearly 9,000 children and their families. She is principal investigator for studies in Georgia and Florida. TEDDY also has clinical centers in Colorado, Washington, Finland, Sweden and Germany.
"This will enable us to continue working with families, collecting and analyzing samples and data, for the next five years," says She, who recently received a $3 million grant from the National Institutes of Health to continue his part of the studies in two of the most populous and fastest-growing states in the nation.
He's optimistic that the unprecedented, prospective study documenting how genes and environment collide to cause a condition that typically surfaces in youth and destroys the insulin-producing beta cells in the pancreas, will enable prevention of the condition that affects about 1 in 300 by age 18, according to the NIH.
Today there is no proven way to prevent type 1 diabetes, which hits at the heart of what TEDDY is about, she said. Two peak ages ranges for type 1 diabetes are 2-4 and 12-15 and since TEDDY began, parents have been keeping exhaustive diaries on everything from a well-baby visit to the doctor to vaccinations to over-the-counter drugs the children take.
They also collect nail, stool and blood samples throughout the 15-years each child is being followed. Scientists have been analyzing it all, including the water children drink, which can vary from one metropolis to the next. The international scope of the study is enabling identification of even regional differences that may be factors in disease development.
The massive data that continues to be generated by some 9,000 TEDDY families is yielding previously unknown high-risk genes and environmental factors that will ultimately lead to those genetic and environmental checklists.
"How to predict risk is an important question, but the main question of TEDDY is what can we do about that risk?" She says. Ideally that will mean keeping the immune system of high-risk children from ever making autoantibodies against their insulin producing cells. That means screening should start early, probably within the first year of life, She says, possibly even as one of the blood tests done for newborns.
Next year, TEDDY participants start turning 15; right now, the average age is about 11. TEDDY investigators project about 450 children will be persistently autoantibody positive as they reach adolescence. TEDDY investigators would like to follow those children at least into adulthood.
The Georgia-Florida TEDDY contingent She leads includes about 600 children. To date 22 children have developed type 1 diabetes and another 58 are autoantibody positive. He suspects by the end of the next five years, about half those children will also have the disease.
Autoantibodies are evidence that the child's immune system has started to target the child's insulin producing cells. It's the attack and eventual destruction of the beta cells by the immune system that leave children dependent on insulin therapy the rest of their lives. To date about 12% of TEDDY children had autoantibodies by age 10 and nearly 8% have multiple antibodies.