Insight into The Prediabetes Epidemic

A recent headline blares that fully one third of people in the U.S. have "prediabetes." This sounds dire, because the implication is that it is only a matter of time until one third of the population has full-fledged diabetes.

In fact, it is highly unlikely that will ever happen. The incidence of full-fledged diabetes has remained around 9% in the entire population for decades and most of the small recent rise in diagnoses is attributable to the lowering of the blood sugar level at which diabetes is supposed diagnosed that happened in 1998.

Though the name makes it sound like prediabetes and diabetes are two stages of one condition, research that has studied the patterns in which the disease develops--makes it clear that they are not. (Details HERE.)

A diagnosis of prediabetes means only that a person's blood sugar has been tested and found to lie in a specific range, one that stretches from the top of normal to the lower bound of the range defined as diabetic. But there are two major--completely unrelated--reasons why people's blood sugar might rise into that prediabetic range. The first, and most common reason, is that they have developed insulin resistance.

Insulin resistance describes people who need to use more than normal amounts of insulin to counteract the blood-sugar-raising effects of the carbohydrates they eat. Where a normal person might be able to keep their blood sugars rising after eating 40 grams of sugar and starch by secreting two units of insulin, an insulin resistant person might need to secrete 20 units to keep blood sugars from rising after eating the same amount of food.

A surge in insulin resistance in the general population appears to be what is driving the increase in diagnoses of prediabetes.

The other, and much more serious, reason people's blood sugar rises into the prediabetic range is that their beta cells don't work properly, and are having trouble secreting insulin. In that case, a person who needs to secrete two units to keep their blood sugar normal after eating can only make one unit, when they need two. Or if they are also insulin resistant, they may be making only ten when they need that twenty.

However, it turns out that most people who become insulin resistant over time will grow new beta cells which though they don't secrete enough insulin to keep their blood sugar normal, keep it from rising into the very high range defined as diabetes.

The people who do become diabetic are those who can't grow new beta cells because their beta cells were already in poor shape. In fact, evidence is accumulating that while people who develop Type 2 diabetes often are insulin resistant, as are so many other people in the general population, it is the fact taht their insulin-producing beta cells are defective, not their insulin resistance, that causes them to progress from "pre-" to full-fledged diabetes. (Details HERE.)

This finding is confirmed by the finding that the most common gene defect found in people of Western European heritage who have developed Type 2 diabetes is TCF7L2, a gene that causes defective insulin production--not insulin resistance. This has turned out to be true of almost EVERY gene that has been associated with Type 2 diabetes. (Details HERE.)

Exactly what causes insulin resistance is not well understood. Too much of the research into this question has started at the wrong end. Researchers who think they know the answer--for years they were sure that it was eating fat that caused insulin resistance--engineer what they call mouse models of diabetes. These are mice chosen specifically because they become insulin resistant when they eat high fat diets. Unfortunately, the genes that make this happen in these mice bear no relationship to the genes found in humans who have Type 2 diabetes--who almost never become insulin resistant when they eat fat.

That's because in humans eating carbohydrates appears to be what raises insulin resistance. Eating starches and sugars raises blood fats--the triglycerides which may increase insulin resistance. But more significantly, fructose has an even stronger impact on insulin resistance. Eating fructose causes fat to be deposited in the liver, and it turns out that the more of this intracellular liver fat you have, the more insulin resistant you are likely to be. Even worse, once that fat is deposited, it is almost impossible to remove no matter what you eat.

So the increase in insulin resistance in the general population has a lot to do with the huge increase in their intake of fructose due to the huge amounts of high fructose corn syrup we've been getting in processed foods since the late 1970s.

Other causes for the increase in insulin resistance are the widespread use of SSRI antidepressants, large scale exposure to the herbicide Atrazine, and high blood levels of the plastic, Bisphenol-A. There are others. (Details HERE.)

If you have been diagnosed with prediabetes your chances of progressing to full-fledged diabetes are highest if your one hour glucose tolerance test result is over 155 mg/dl (8.6 mmol/L),(see the study HERE for details) if you have diabetic relatives, if you have taken any of the pharmaceutical drugs known to damage the beta cell, such as Zyprexa, if you have an autoimmune condition, and, ironically, if you aren't obese at diagnosis. The thinner you are when you are found to have abnormally high blood sugars, the more likely it is that failing beta cells is causing your elevated readings rather than increased insulin resistance.

Prediabetes, even when it does not progress to full-fledged diabetes, is not a benign condition. It does damage the body, and though this damage is often subtle--it causes small changes in the growth of blood vessels in the retina and kidneys, for example--the real danger lurking for people with prediabetes is heart disease. The risk of heart attack is much higher in people with prediabetic blood sugars than in those with normal blood sugars.

So if you have been diagnosed with prediabetes you should do all you can to lower your blood sugars to normal, since it is the blood sugars, not the insulin resistance that damage your organs.

The research makes it clear that what correlates most strongly with the risk of heart attack is how high your blood sugar goes after meals, not the fasting blood sugars which are, all too often, the only sugars doctors tell you to measure.

People whose blood sugars are over 155 mg/dl (8.6 mmol/L) an hour after eating have a higher risk for heart disease. (Details HERE.)

The experience of the online diabetes community suggests that if you keep your blood sugars under this level--many of us shoot for under 140 mg/dl (7.7 mmol/L) to be safe--you will do fine, no matter what your diagnosis, or even what the cause is of your diabetes. It appears to be the high concentrations of glucose in the blood that cause organ damage, not the underlying condition.

So use the simple strategy you'll find explained HERE to find out what foods you can eat safely without pushing your blood sugars into the danger zone.

The cheap, generic drug, Metformin is also highly recommended for people who are insulin resistant. It seems to block the process by which the liver deposits more liver fat, changes the way that muscles burn glucose to one that lowers insulin resistance, and lowers blood sugar.

Metformin's only significant side effects, observed after decades of use, appear to be that it decreases your chance of having a heart attack and also lowers your risk of developing various cancers. (Details HERE.) If only other drugs had those kinds of side effects!