Jerry Silva's body was not designed for life in the early 21st century. A 44-year-old financial analyst from Sherborn, Massachusetts, Silva spends most of his time behind a desk tracking high-tech stocks. It's a life far removed from that of his Mexican forebears, who spent their days hoeing maize fields and fishing near Guadalajara. Silva has more than enough to eat, whereas his ancestors often went hungry. The significance of that difference in lifestyle became painfully apparent last January, when he was diagnosed with diabetes. The disease, closely linked with not eating the right foods and sitting around too much, is beginning to look something like a pandemic as millions of people around the world confront a central irony of the modern world: A lifestyle of abundance can be deadly.

BIOCHEMICAL IMBALANCE: Type 2 diabetes develops slowly and relentlessly as insulin-producing cells in the pancreas malfunction, causing insulin levels to drop. Without insulin, the body cannot process all the glucose from the carbohydrates and other sugars in food. Nearly one out of five type 2 diabetics needs daily injections. That amounts to 3 million Americans, a number that is steadily rising.

On this planet 194 million people have diabetes, double the number of 25 years ago. In another 25 years the number is expected to double again. But those numbers represent only people who reach such high blood-sugar levels that diagnosis is clear and certain. Recent research suggests that the plague may be many times worse, affecting a much larger group of people who are slowly but surely developing a resistance to insulin in their bodies and who could be categorized as prediabetic. Long before such people are officially diagnosed, their eyesight, their hearts, and other organs come under attack. In this country, there are 41 million known prediabetics and 18 million diabetics, about one in every five Americans.


The tangible consequences of this growing epidemic are staggering. Each year in the United States 40,000 diabetics get kidney disease, up to 24,000 go blind, and 82,000 have amputations—a toe, foot, or leg—because of vascular failure. Recently, researchers have found alarming links between diabetes and neurodegenerative afflictions such as Alzheimer's disease. Diabetes and insulin resistance may cause depression, decreased cognitive function, and harmful alterations in brain structure. Diabetes can cut up to 20 years off the human life span and costs the United States at least $130 billion annually.

Globally, the number of diabetics and prediabetics is in the hundreds of millions and skyrocketing as nations in Asia, Latin America, and Africa modernize. In Africa today, overweight and obese children outnumber the hungry three to one. Those most at risk are people whose recent ancestors led subsistence lives. "We're sitting on a time bomb here," says Francine Kaufman, a physician-researcher at Children's Hospital in Los Angeles and a past president of the American Diabetes Association. "The problem is spreading around the globe, and it's getting worse."

Why this is happening and the molecular mechanics of how it is happening are among the most intensively studied areas in medical research, and definitive answers have yet to emerge. "We have theories and ideas, but nothing concrete about the exact genetics of insulin resistance," says Gerald Reaven of Stanford, a pioneer researcher of type 2 diabetes, which afflicts 95 percent of all people with diabetes. Type 2 usually appears later in life, but in the last two decades type 2 diabetes has quadrupled in children and adolescents, in lockstep with increasing weight gain. Type 1, which typically occurs when the pancreas shuts down and no longer makes insulin, strikes relatively early in life.

The frequency and growth of diabetes has not gone unnoticed by pharmaceutical companies—at least 20 firms are feverishly searching for remedies, and at least 40 new drugs are being tested. Yet none of those drugs will become a cure. "And many will fail," says Reaven.

Like diabetes, prediabetes is diagnosed when fasting blood-glucose levels rise above normal—100 to 126 milligrams per deciliter. The rise usually comes with weight gain, but not always. Too many french fries, servings of mashed potatoes, sugary sodas, and loaves of white-flour bread can result in insulin resistance, the underlying defect in both pre- and full-blown diabetics. It crops up when cells begin to resist absorbing glucose. Every type 2 diabetic and prediabetic is insulin resistant, which stimulates the pancreas to churn out even more insulin. This stresses pancreatic cells until they eventually shut down partially or completely, forcing patients to inject insulin.

AROUND-THE-CLOCK INSULIN: A portable pump is the most advanced means for delivering insulin. Typically, a pump can be programmed to release a low, steady dose of insulin throughout the day as well as a high dose before a meal. Spikes in blood-glucose levels exacerbate the health complications from diabetes, which can be fatal. Adults with diabetes are two to four times more likely to die of heart disease or stroke than adults without diabetes.

Resistance to insulin can arise by simply eating too much and by not exercising enough. When a patient's blood-sugar levels rise, a physician may offer amazingly effective advice: "Lose five percent of your body weight and keep it off." Even in the half or so of all diabetes cases that seem to be related to genes that have programmed a person's cells to need less fuel, exercise and moderate diet changes can work wonders if the progress of insulin resistance is noticed soon enough during regular checkups.

Prediabetes happens slowly and insidiously. Cells gradually become resistant to insulin, which is produced in the body to process glucose levels that rise in the blood after a meal. Insulin can open up a cell's outer membrane like a key in a door lock and set in motion the machinery that feeds the cell glucose, which is converted to energy. The human body works best when the supply of fuel equals the exact energy needs of its cells.

Nonetheless, our bodies are designed to compensate for times when food is scarce by taking advantage of times when it is abundant. One method is to turn excess glucose into fat, which can be stored for leaner times. On the ancient savannas, this manifested itself when hunters killed a wildebeest, and everyone gorged for a few days, storing the excess food in fat cells. Another method is for cells to throttle back the processing of glucose during lean times by becoming insulin resistant, which blocks insulin from entering the cell and in essence rations the supply of glucose to last longer while also creating a powerful hunger impulse to drive people to find food. Researchers in the 1960s theorized that modern people prone to obesity and diabetes might have inherited these two ancient methods of coping with feast and famine.

In 1962 James Neel suggested that early hunter-gatherers possessed a "thrifty gene" that helped them survive by speeding up the accumulation of fat when food was available. The closer a person is to the time when his or her ancestors were hunter-gatherers, says Allison Goldfine, a physician and investigator at the Joslin Diabetes Center at Harvard University, "the higher the rates of weight gain." In 1966 George Cahill offered a different scenario for the thrifty gene, conjecturing that this gene is actually for insulin resistance. This notion is supported by the high numbers of diabetics and prediabetics who have insulin resistance running in their families. Moreover, while all diabetics are insulin resistant, not all of them are fat. Both theories may help explain the explosion of diabetes in our time.

Evolutionists suggest that some people are less prone to diabetes, even if they grow fat, because their ancestors had steady and abundant supplies of food. This allowed them to evolve away from needing a thrifty gene. Called the fertile crescent theory after a part of the world where agriculture appeared early, the notion is supported by lower instances of diabetes in people whose ancestors came from the Middle East and Europe. Still, Goldfine points out that there is much variability among people with and without the disease—some are skinny and diabetic, and some are grossly obese but not diabetic. No theory yet accounts for all possibilities.