The afflicted are often obese, but not always // Fat cells ensure survival, but can spew toxins too // A bodily defense—inflammation— only accelerates the crisis.
An Epidemic of Excess
Most Americans—including many physicians —seem not to have noticed, but type 2 diabetes has reached pandemic proportions. (Don’t be fooled by the conventional notion of pandemic diseases as explosive infections that burn across the planet killing millions.) According to a study published in the Journal of the American Medical Association in October 2003, approximately one of three children born today in the United States is at risk of developing the disease. Many won’t know they’re sick, at least for a while. But soon enough, the symptoms will be all too evident, with rapid weight gain or loss, extreme thirst, increasing hunger, slow-healing wounds and constant fatigue. If the condition is uncontrolled, it may spiral into devastating complications: rotting teeth and gums, heart disease, kidney failure, blindness, lost limbs and early death. Of the 200 million diabetics worldwide, at least 90% have type 2.
As the pandemic has spread, research has begun zeroing in on the causes, but no one yet understands exactly why a disease that dates to earliest history is only now threatening so many lives. “It must be something new, some new factor,” says Paul W. Ewald, a biologist from the University of Louisville who specializes in the evolution of infectious diseases. But what?
Most experts, including those at the Centers for Disease Control and Prevention (CDC), think the “something new” is our diet, because the correlation between obesity and diabetes is undeniable. But not all type 2 diabetics are fat. Indeed, people suffering from lipodystrophy, the almost total absence of fatty tissue, have a risk of developing type 2 diabetes that’s just as pronounced as it is for the obese. So the road between fat and diabetes isn’t a straight one, and there are some surprising stops along the way.
Diabetes comes in two basic versions. Type 1, which used to be known as insulin-dependent or juvenile diabetes, was invariably fatal until the advent of insulin injections. This version of the disease involves autoimmune destruction of the beta cells in the islets of Langerhans in the pancreas, which produce the hormone insulin. (By the time blood sugars have begun to rise, 80% to 90% of the beta cells may already have been destroyed.) With too little insulin, the body cannot process glucose and other nutrients into energy to feed the organs and muscle tissue. Unused glucose builds up in the blood and causes tissue damage while muscles starve.
In type 2, the course of the disease is much slower. Type 2 diabetes doesn’t destroy insulin production in the same way as type 1, although, for reasons not yet known, type 2 does damage beta cells and reduce insulin production. But the principal problem is insulin resistance—the body is unable to use insulin in the bloodstream to convert glucose into energy. Glucose builds up, just as in type 1, to similarly dire effect. But type 2 diabetics also have other potentially devastating problems—obesity, high blood pressure and abnormal blood fat levels, all of which combine to increase the risk of heart disease and stroke.
In simple terms, the body of an insulin-resistant person has run out of places to store fat. The normal repository is fat cells, and there are plenty of those—typically between 25 billion and 50 billion, some subcutaneous (beneath the skin) and some visceral (under the peritoneal membrane in the abdominal cavity). The body must either build more fat cells or store the additional fat in existing cells.