That suspicion might seem counterintuitive given that diabetes dogma holds that being overweight tugs the body toward producing large amounts of insulin (as in type 2), not too little insulin. But some contend that the stress of producing all that extra insulin can burn out the insulin-producing beta cells of the pancreas and push a child whose beta cells are already under attack into developing type 1 diabetes. This idea, called the accelerator or overload hypothesis, proposes that “if you have a kid who is chubby, that extra adiposity is going to challenge the pancreatic beta cells,” says Rebecca Lipton, an emeritus professor at the University of Chicago.* “In a child who has already started the autoimmune process, those beta cells are just going to fail more quickly, because they are being forced to put out more insulin than in a thin child.”
Overweight makes a logical perpetrator. People are packing on the pounds in rich countries and poor ones. Of course, investigators want to do more than just to explain the rise of type 1 diabetes; they want to prevent it. Unfortunately, if excess weight is a major contributor to the problem, that task will not be easy. No one, so far, has been able to slow the global obesity epidemic. (By 2048, according to researchers from Johns Hopkins University, all American adults will be at least overweight if present trends continue.) Until societies can ensure that most children (not to mention adults) are more physically active, eat healthfully and maintain a normal weight, diabetes researchers will be in the position of detectives who, having solved a murder, realize they can do nothing to prevent the next one.
*Erratum (2/17/12): Rebecca Lipton is incorrectly identified as an emeritus professor. She is a retired associate professor.