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Type 2 Diabetes
Are We Closer to Knowing "Why?"

by Wayne Clark

Diabetes was described as early as 1552 BC, but it wasn’t until the late 1800’s that it was linked to the pancreas, and not until 1936 that it was classified into two different types. Today, the cause of Type 2 diabetes, the most common form, is still an open question. Still, scientists are closing in on a more thorough understanding of what Dr. J. Denis McGarry, former Professor of Internal Medicine and Biochemistry at the University of Texas, Southwestern Medical Center, once described as “the enormous complexity of a disease process in which almost every aspect of the body’s metabolism goes awry.”

What causes Type 2 diabetes is an important question, not least because people with diabetes want to know why they have it. The questions only go on from there: Could it have been prevented? Can it be reversed? Are my children at risk? Does obesity cause diabetes, or does diabetes cause obesity? Does insulin resistance (the reduced ability of muscle, fat, and other cells to respond to insulin) harm the insulin-producing beta cells of the pancreas, or is insulin resistance the result of damaged beta cells?

These “chicken and egg” questions are at the heart of current investigations into the cause of Type 2 diabetes. What is immediately apparent is that diabetes is more than a disease; it is a disease process. It begins long before it becomes evident, as much as 15 years before the appearance of any signs or symptoms. More and more, in fact, it is obvious that it begins at conception.

“It’s widely felt that genetics plays a role in why some people can be subjected to the obesifying environment in which we live and not develop diabetes, and others can become equally obese and develop it,” says David E. Cummings, MD, Associate Professor of Medicine at Seattle VA Puget Sound Health Care System. “It largely has to do with the health of their beta cells.”

There is an undeniable association between obesity and diabetes. In one study, 30% of people newly diagnosed with diabetes had a body-mass index (BMI) of 25–30 kg/m2, and 60% had a BMI greater than 30 kg/m2. A BMI of 25–30 is considered overweight, and a BMI above 30 is considered obese.

Genetic mapping has found a number of genes that are associated with diabetes, and others associated with obesity. Recently, a gene locus was identified that influences the risk of diabetes primarily by increasing fat mass. A study of the Pima Indians of Arizona found an exact match between the locations of an obesity susceptibility gene and a diabetes susceptibility gene. These are the first, but likely not the last, indications that diabetes and obesity may be “co-inherited.”

Generally, obesity is believed to be a genetic predisposition, though one that can be compensated for by behavior. As evidence, Dr. Cummings points to studies of identical twins in which both will become obese even if raised in different environments, and studies of fraternal twins (who are not genetically identical) in which one will become obese and one not, even though raised in the same environment. These studies and others demonstrate, he says, that 70% to 80% of obesity has a genetic basis.

“The fallacy of the ‘willpower’ argument,” Dr. Cummings says, “is the genetic basis of obesity. It is possible to modify lifestyle and achieve a 5% to 10% reduction in weight, and this should be encouraged, but the biological set-points are difficult to change.”

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