by Sharon J. Proctor, Ph.D.
Photograpy by Marina Dodis

"You have diabetes." This year 60,000 Canadians and 800,000 Americans will hear these words. They'll join an estimated 200 million people worldwide who already have it, including Mary Tyler Moore, Halle Barry, Elizabeth Taylor, Arthur Ashe, and Billy Jean King. Even Elvis Presley had it. If not controlled, diabetes can lead to coma, blindness, heart disease, stroke, amputation, kidney failure, and death. Why are there so many people with diabetes? SFU's Diane Finegood is scientific director of the Institute of Nutrition, Metabolism and Diabetes, one of 13 national virtual institutes of the Canadian Institutes of Health Research. She's been asking questions - and finding answers.

Finegood is a professor in the school of kinesiology. Recognized internationally for her groundbreaking diabetes research, she's in great demand on the research circuit, often attending conferences, visiting labs, and presenting papers. She's in her office today, seated at a small round wooden table. "Diabetes is about having high levels of sugar in the blood," she explains. "The problem is, sugar in high concentrations is toxic to cells. It can cause serious damage to body tissues."

Carbohydrates are an important source of fuel for the body. During digestion they're broken down mainly into a simple sugar called glucose. When glucose enters the bloodstream, the pancreas goes into red alert. It secretes insulin into the blood, which tells the liver and muscles to immediately remove glucose from the blood and to use or store it. If these tissues consistently fail to remove the sugar from the blood, you have diabetes. There are many different kinds of diabetes, with different causes and treatments. Finegood's focus is the two most common ones: Type 1 and Type 2.

She's concentrating on a group of cells in the pancreas called beta-cells. Fortunately laboratory rats genetically predisposed to Type 1 or Type 2 have yielded masses of details on the rates of beta-cell growth, rates of insulin secretion, and other physiological events. Finegood's approach is to develop mathematical models that describe the known events - then use the models to gain new information.

Her models resemble a bathtub scenario. "Imagine you're sitting in a bathtub and you want to add more water," she says. "So you turn on the tap. Now let some water escape out the drain at the same time. To keep the tub water at your ideal level, you need to add water at a certain rate. Our mathematical models of diabetes involve similar relationships, such as the rate sugar enters the bloodstream, how fast it disappears, and the rate beta-cells form.

Type 1 diabetes and a garbage strike

Type 1 is the so-called juvenile onset or insulin-dependent diabetes. It's an autoimmune disease, in which the victim's own antibodies destroy the insulin-secreting beta-cells in the pancreas. It affects mostly children or young adults. People with Type 1 need daily insulin injections to survive. (Mary Tyler Moore and Halle Barry have Type 1.) Before insulin injections, Type 1 victims soon died. Today, they can live normal lives. The question is, why does one's own immune system attack beta-cells that are located inside the pancreas?

Their math model of beta-cell formation led Finegood and her team to a startling discovery. "We discovered that a lot of beta-cells suddenly die right around the time in a rat's life when diabetes begins. Not only that, this mass cell-death takes place in both normal and diabetes-prone rats."

It's called programmed cell death, or apoptosis, and is the body's way of keeping tissues healthy. Unnecessary or older cells commit suicide, shrink, and get eaten by other cells. New cells immediately replace them. (When cells fail to die, the result can be cancer.)

"We began to think there might be a link between this wave of normal cell death and the onset of Type 1 diabetes," recalls Finegood. "So we did further research and modelling. We found that the rate of cell death is the same in both diabetic and healthy animals, but there are more dead beta-cells in the diabetic pancreas. For some reason, the diabetic's dead cells aren't immediately removed.

"Type 1 diabetes may be like a garbage strike," she explains. "Normally you put your garbage out, neatly packed in a plastic bag, and it's taken away. Then comes the strike. No one removes the bag. Over the next several days the food inside rots, the bag breaks, and the crows and raccoons arrive. Suppose, in the Type 1 diabetic, the dead beta-cells in the pancreas don't get removed immediately. Suppose they decay and spill their contents, causing inflammation. That would expose them to the immune system, which may see them as Ôforeign' and eventually attack living beta-cells."

In 1999, the Juvenile Diabetes Research Foundation awarded Diane Finegood $2.7 million to set up a national network of top researchers. The goal: to determine how to prevent beta-cell death.

Type 2 diabetes and sand rats

Type 2 is known as adult-onset or non-insulin-dependent diabetes. Here the culprit is not just the beta-cells in the pancreas. They start out working fine. Type 2 diabetes results when the muscles, liver, and other tissues stop reacting to insulin. They become "insulin resistant." The pancreas tries to compensate by producing additional insulin, but in some people compensation is insufficient. The blood sugar stays high. The problem is, if the sugar increase is not treated, the beta-cells die or become dysfunctional over time and the pancreas stops producing insulin.

Type 2 diabetes is associated with both genetics and lifestyle - junk food, obesity, and lack of exercise. Some patients require insulin injections. Some can control their diabetes with medication. Still others can "cure" it with increased exercise and a diet change. "The sand rat (Psammomys obesus) is a good illustration of Type 2," says Finegood. (She's referring to a gerbil native to the deserts of Libya, Egypt, Palestine, and Arabia, which has a sparse diet of mostly saltbush plants.) "If you catch a wild sand rat, set it up comfortably in a lab, and feed it the traditional lab diet, it develops Type 2 diabetes.

"In our Type 2 studies we developed math models based on laboratory-rat strains that get Type 2. We want to learn why the insulin-secreting beta-cells die. We know they're quite fragile compared to other cells. Also, Type 2 diabetics have half the normal number of beta-cells. Our results suggest that something is actually killing the beta-cells in the pancreas. It could be the high blood sugar levels. Or it could be fat, for most Type 2 patients have increased fatty acids in their blood, which can also kill cells. There may be different causes in different people.

A lesson from the past

According to scientists we are built exactly like the Paleolithic hunter-gatherers who lived 100,000 years ago. Indeed, 99 percent of human existence has involved being physically active and eating little food - and then only wild foods. In other words, our bodies aren't designed for a life of remote controls, video games, Internet, cars, greasy burgers, French fries, soft drinks, pasta, and other conveniences. Too much food and lack of exercise are major contributors to the modern epidemic of Type 2 diabetes.

So how do we avoid getting it?

Many experts suggest we mimic aspects of our ancestors' lives. "The average office worker walks 4,000 to 5,000 steps a day," says Finegood. "We probably need 10,000 steps per day for good health. Each 2,000 steps burns 100 calories. To avoid large spikes in blood sugar, we should spread out our eating and control the composition of our food. Unrefined foods, for instance, are digested slowly, which means their component sugars are slow to enter the blood." aq

>> Find out how Diane Finegood went From Gifted Child to International Diabetes Expert.

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