Type 1 diabetes (previously known as juvenile diabetes) is an autoimmune disease that attacks and destroys insulin-producing cells in a person’s pancreas making it so the body is unable to produce insulin. It affects 5 to 10 percent of those people diagnosed with diabetes, and it increases the chance of cardiovascular disease, blindness, kidney damage, and nerve damage. Until recently researchers have conducted exhaustive studies hoping to find an elusive and defective gene that caused the problem, but recent discoveries suggest researchers have been on the wrong track.
Garry Fathman, MD, Professor of Immunology and Rheumatology, and his colleagues at Stanford Research Center learned in a recently released study“what triggers that immune response apparently has less to do with having a distinct set of gene variants than how the behavior of genes may differ in people with the disease.” Because numerous studies have used twins, Fathman described the situation as “reminiscent of the 1988 movie ‘Twins,’ starring Arnold Schwarzenegger and Danny DeVito. They may have started out identical, but something diverged, somewhere.” Fatham and his team also looked at the difference in genes between the twin who got diabetes and the twin who didn’t get diabetes.
Over the course of Fathman’s seven year study, he learned that “many genes never previously identified as germane to the disease process – seemed to participate in coordinated zigzags of swooping and soaring expression over time.” Ultimately, they learned it is genes behaving badly that provides an early warning sign for pre-diabetics. “We need to know that people are on their way to diabetes before they get hyperglycemic or, better, even before their insulin-producing pancreas cells have taken a hit,” announced Fathman. Learning this information, “plus, [knowing] the newly identified genes in these clusters with orchestrated, disease-associated activity changes, may, in their own right, point the way to new therapies.”