Research proposes common link between autism, diabetes

A review of the genetic and biochemical abnormalities associated with autism reveals a possible link between the widely diagnosed neurological disorder and Type 2 diabetes, another medical disorder on the rise in recent decades.

"It appears that both Type 2 diabetes and autism have a common underlying mechanism - impaired glucose tolerance and hyperinsulinemia," said Rice University biochemist Michael Stern, author of the opinion paper, which appears online in this month's issue of Frontiers in Cellular Endocrinology.

Hyperinsulinemia, often a precursor to insulin resistance, is a condition characterized by excess levels of insulin in the bloodstream. Insulin resistance is often associated with both obesity and Type 2 diabetes.

"It will be very easy for clinicians to test my hypothesis," said Stern, professor of biochemistry and cell biology at Rice. "They could do this by putting autistic children on low-carbohydrate diets that minimize insulin secretion and see if their symptoms improve."

Stern said the new finding also suggests that glucose tolerance in pregnant women may need to be addressed more seriously than it is now.

Stern said he first realized there could be a common link between Type 2 diabetes and autism a few years ago, but he assumed someone else had already thought of the idea.

Stern's lab, which is located at Rice's BioScience Research Collaborative, specializes in investigating the genetic interactions associated with genetic diseases like neurofibromatosis, a disorder in which patients are several times more likely to be afflicted with autism and autism spectrum disorders (ASD) like Asperger's syndrome.

Autism and ASD are neurological disorders that have a strong but poorly understood genetic basis. The U.S. Centers for Disease Control and Prevention estimates that about nine out of 1,000 U.S. children are diagnosed with ASD.

Stern said at least four genes associated with increased frequency in autism are known to produce proteins that play key roles in a biochemical pathway known as PI3K/Tor. Stern said he had been studying a form of abnormal function in the synapses of fruit flies that was remarkably similar to abnormalities observed in rats and mice with defects in a different pathway known as mGluR-mediated long-term depression.

"I had also spent a lot of time thinking about insulin signaling because another project in my lab is an endocrinology project in which we're studying how key proteins involved in insulin signaling affect the timing of metamorphosis in fruit flies," Stern said.

From his studies in both areas, Stern knew two things: PI3K/Tor was the major pathway for insulin signals within cells, and insulin could affect synapses in a remarkably similar way to the mGluR defects associated with autism.

"When I read that the incidence of autism was increasing, and combined that with the fact that the incidence of Type 2 diabetes is also increasing, it seemed reasonable that each increase could have the same ultimate cause - the increase in hyperinsulinemia in the general population," Stern said. "I didn't do anything with this notion for a few years because it seemed so obvious that I figured everyone already knew this hypothesis, or had tested it and found it was not true."