Deciphering diabetes

Heart attacks, strokes, kidney disease. Cancers of the breast, colon, lung, ovary, liver, kidney, and bladder. Liver disease, lung disease, pneumonia. and other infectious diseases. Having type 2 diabetes increases the risk of dying of those illnesses and more, according to a new compilation of 97 studies on 820,900 people. Already, an estimated 11 percent of adults have diabetes. And many of them don’t even know it. But that doesn’t tell the whole story. Experts estimate that by 2050, one out of three adults will have the disease. Among people over 65, one out of four already has diabetes. And another 35 percent of all adults (half of those over 65) have prediabetes.

The good news: Type 2 diabetes is almost entirely preventable. “People who have a healthy weight and lifestyle have a 90-percent lower risk,” says JoAnn Manson, professor of epidemiology at the Harvard School of Public Health. Here’s the latest on diabetes and how to lower your risk.

Diabetes 101

If your fasting blood sugar is higher than 125, you have diabetes. If it’s higher than 99, you have prediabetes.

It’s easy to understand why blood sugar soars in people who have type 1 diabetes. The beta-cells in their pancreas make no insulin, the hormone that acts like a key to admit blood sugar into cells, where it can be stored or burned for fuel. (One possible explanation: The body may destroy its own beta-cells in a misguided auto-immune attack.)

People who have type 2 diabetes (which accounts for 90 to 95 percent of cases) often make plenty of insulin, but the insulin doesn’t work well. “Their cells are resistant to insulin, so the body needs to pump out more of it,” explains Varman Samuel of Yale School of Medicine. “And for a while, the beta-cells can compensate,” so blood sugar levels stay under control. But in many people, the pancreas can’t keep up with the demand for insulin. “When the beta-cells poop out, you tip over into diabetes,” says Samuel. Insulin output falls short, and blood sugar climbs. “It’s as though you are listening to loud music, but you have wax in your ears,” he suggests. “So you keep turning up the volume, but you still can’t hear because the music isn’t going through. Then at some point, your speakers blow.” The question is: What sets off insulin resistance in the first place?

Insulin resistance

It’s hard to miss the first clue that explains insulin resistance. Roughly 80 percent of people with type 2 diabetes are overweight or obese, “excess body weight is by far the strongest risk factor for diabetes,” says Manson. And the “visceral” fat deep in your belly may boost the risk the most: “If we could get people to a healthy weight, it could eliminate roughly half of all cases of diabetes,” says Manson. “That’s the big picture.”

Obesity doesn’t explain why we all  no matter how fat or thin  have a greater risk of diabetes as we get older. And genes, smoking, exercise, and diet also play a role. But for most people, the trouble starts when they eat too many calories, day after day. “Any excess calories you eat are eventually turned into fat that needs to be stored,” explains Kimberly Stanhope, a molecular biologist at the University of California, Davis.

At first, the fat fits into your fat cells. “Let’s say your body is doing a good job of being able to store fat,” says Stanhope. “But once your fat cells get too large, they’re less likely to continue to take up and retain more fat.” Some obese people though, may never become insulin resistant (or diabetic) because their bodies keep making more fat cells or they’re just better at storing the fat because their fat cells can get much bigger.

However, when there’s no more “room at the inn,” the body stashes the fat wherever it can. “It’s called ectopic lipid,” says Stanhope. “Fat is stored in tissues that aren’t supposed to be storing it  like the liver, muscle, and pancreas.” Some scientists believe that misplaced fat is the key to insulin resistance. When insulin arrives at a cell, it signals a “glucose transporter” to ferry blood sugar (glucose) into the cell. Ectopic fat may block the signal, suggest studies at Yale and elsewhere.” We think the initial insult is ectopic lipid in muscle or liver or both,” says Samuel.

Excess fat can also lead to low levels of chronic inflammation, which makes matters worse. “When cells get overfat, some scientists call them ‘angry fat’ because they release inflammatory proteins,” explains Sheri Colberg, professor of human movement science at Old Dominion University in Norfolk, Virginia. In fact, some researchers contend that it’s the inflammatory proteins that keep insulin from working well.

Fatty livers and muscles

Scientists debate whether insulin resistance starts in the liver or the muscles, but one thing is clear: A fatty liver matters. Researchers at Washington University in St. Louis matched 20 obese people according to high or low levels of liver fat or high or low levels of deep belly visceral fat. “Liver fat was a better predictor of metabolic dysfunction than visceral fat,” notes study author Samuel Klein at the experimental Biology 2011 meeting in April in Washington DC.

Another sign that a fatty liver matters: It may explain why a modest drop in weight can get diabetes under control. For example, in 2005, when researchers at Yale put eight obese people with diabetes on a low-calorie diet for seven weeks, their fasting blood sugar levels returned to normal. “They lost only 18 pounds, and there was no change in muscle fat content,” explains Samuel. However, 84 percent of their liver fat disappeared. If you can cut calories, “that will melt away that liver fat,” says Samuel. “And once you do that, your liver responds much better to whatever insulin you make. It’s enough to control your glucose metabolism.”

Sugars

“Is Sugar Toxic?” asks the headline in the April 17, 2011 issue of the New York Times magazine. Unlike the starch in grains, which consists of glucose, most sugars  including table sugar (sucrose), high-fructose corn syrup, and honey  are about half-glucose and half-fructose. It’s the fructose half that has recently raised alarms.

“In animals, or at least laboratory rats and mice, it’s clear that if fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat,” wrote author Gary Taubes in The Times. But so far, at least in humans, it’s not clear that fructose causes diabetes. Nor is there presently any definitive proof that fructose causes a fatty liver.

Researchers have come close, though. In a 2009 study, Stanhope fed 32 overweight or obese people 25 percent of their calories either as fructose or glucose-sweetened beverages for 10 weeks each. Both groups gained about three pounds, but the fructose drinkers were much worse off. “They gained more visceral fat, they became more insulin resistant, their triglycerides went up, and their livers made more fat,” says Stanhope. “That suggests that we may have had an increase in liver fat.”

Stanhope’s bottom line: “There is enough data associating fructose consumption with metabolic disease  diabetes, heart disease, fatty liver, high blood triglycerides  so consume it with caution.” And since we get glucose from all carbs, but fructose only from sugars, the only way to limit fructose is to limit sugars. “I’ve had people argue with me that if people overeat, it doesn’t matter what those calories are,” says Stanhope. “Our study showed that it does matter.”

Magnesium and vitamin D

“Magnesium is understudied and underappreciated for its effect on glucose tolerance,” says Manson. In two studies, magnesium lowered blood insulin levels and the risk of diabetes. “It’s biologically plausible that magnesium would have an effect on glucose tolerance and insulin sensitivity,” notes Manson, “but more research needs to be done.” However, magnesium is looking “very promising,” she adds.

Some studies have also found a lower risk of diabetes in people who have higher levels of vitamin D. Others have not. One possible explanation for the inconsistent findings: The higher your weight, the lower the blood levels of vitamin D. Manson is leading a large, long-term trial that should help clarify the role of vitamin D in diabetes and other health problems.

The bottom line

Meanwhile, based on current research, here is the bottom line on diabetes:

 • The best way to dodge diabetes is to lose (or not to gain) extra pounds.

• Limit sweets, especially sugar-sweetened drinks. Even the naturally occurring sugars in 100- percent fruit juice may raise your risk.

• Eat leafy greens, whole grains, beans, and nuts, to boost your magnesium.

• Get the RDA for vitamin D (600 IU a day up to age 70 and 800 IU over 70) from supplements or foods fortified with vitamin D.

• Do at least 30 minutes of brisk walking or other aerobic exercise every day.

• Shoot for two to three strength training sessions a week. Each should include eight to 12 repetitions of eight to 10 exercises.