Medical Experts Once Again Helping People Become Diabetic

Yet another absurdity in diabetes advice comes from the staff at Harvard Medical School and it illustrates quite nicely why we have become a nation of diabetics.

In an article entitled Sugar’s Role in Diabetes (on a web site with the laughable title Better Medicine), physician author Robert Shmerling argues that elevated blood sugar levels are the result of having diabetes, not the cause.

Improved blood sugar control may reduce the chances that certain complications of the disease will develop. But just because the disease is characterized by an elevated blood sugar level and because lowering the blood sugar level is an important goal of therapy, a high-sugar diet does not cause the illness. An elevated blood sugar level is a result of having diabetes, not the cause.

Dear Dr. Shmerling: I’ve got news for you: Elevated blood sugars are both. They are the result of diabetes and a significant cause.

In his own definition of Type 2 diabetes, Shmerling states:

…the body’s tissues become resistant to insulin, requiring more insulin than the pancreas can produce to keep the blood sugar normal (type 2 diabetes).

What does he claim causes a person’s tissues to become resistant to insulin?

He says that heredity, obesity, and medications are the culprits.

Here’s a CDC graph showing the growth of diabetes in America:


While I’m sure genetic factors play a role in determining the likelihood and the rate at which one develops Type 2 diabetes, is he really arguing that our population’s genetics have changed so dramatically during this time as to explain this rise in diabetes?

In other words, a rapid and unexplained genetic shift in the modern world’s population, not diet, is causing the incidence of diabetes to skyrocket?

Uh, ok. Sure, doc.

I would have to practice in front of a mirror so that I could say that without bursting into laughter.

And, medications? Please tell me what medications have caused such an alarming increase in diabetes over the past 50 years. The attorney general in every state in America would like the answer to that question, too.

And finally, Shmerling states that obesity causes diabetes. I knew that one would rear its head soon enough. That’s laughable from a man that states:

Assuming an elevated blood sugar level is the cause of diabetes is like assuming that coughing is the cause of pneumonia.

Let me channel Dr. Shmerling:

Assuming that obesity is the cause of diabetes is like assuming that coughing is the cause of pneumonia.

Obesity isn’t the cause of diabetes, it’s simply another result of insulin resistance and elevated glucose levels.

Shmerling seems to have forgotten that elevated insulin levels trap fat in fat cells, preventing weight loss.

In my book, Don’t Die Early, I talk about the effects of insulin on weight retention:

“It may seem unbelievable that having an elevated insulin level could prevent the body from burning fat when we’re hungry, but it’s true. Insulin is amazingly powerful at keeping fat locked into fat cells where it remains inaccessible and cannot be metabolized for energy. How powerful? Obese rats that are given insulin injections to maintain high insulin levels and then put on a starvation diet remained obese while dying of starvation. These starving, yet obese rats digested their own muscles and organs for food until they died from starvation, without losing any of their body fat.

“Yes, even though they were starving, the elevated insulin levels prevented their body from metabolizing fat from their fat cells for energy, forcing their bodies to digest their own organs and muscles for nourishment. Think about this the next time you wonder why people can’t lose their unwanted body fat even though they are not eating much. It’s very likely that the foods that they are eating are causing a large insulin response, which is keeping the fat locked into their fat cells.”

And while we’re on the subject of weight, Shmerling states:

And not all persons with diabetes are overweight — that’s another myth. For these patients, heredity and perhaps other undiscovered factors are more important.

Dr. Shmerling, let me explain the “mystery” of why some diabetics are thin and some are not. (Again, I’m quoting my own book. Sorry to be so self-serving here, but I wrote this book to help enlighten people about the causes of diabetes and other maladies affecting us today. I didn’t think Harvard Medical School staff members were part of my target audience.)

“The most surprising thing about the effect of insulin resistance and trapping fat in fat cells is that despite what I’ve just said about this effect, we cannot determine how insulin-resistant we are by how much extra fat we are carrying.

“While it’s true that an overweight person is almost certainly insulin-resistant, a thin person is no less likely so. Why is this? It’s because fat cells can become insulin resistant at different times in different people. If you’re “lucky” enough to have fat cells that become insulin resistant quickly, before they expand considerably, then you’re a thin, insulin-resistant person, subject to the same damage from elevated glucose and insulin levels as an obese insulin-resistant person.

“Everything I’ve said in this section about fat being trapped in fat cells and about a person becoming hungry every couple of hours and spending the majority of the time with elevated glucose and insulin levels can be just as true for a thin person as for an overweight person. In fact, it’s probably the thin person who is less fortunate when it comes to insulin resistance because the thin, insulin-resistant person’s diabetes will go undetected far longer, due to the false sense of security that being thin brings.”

So back to the original question, what does cause insulin resistance, the definition of Type 2 diabetes?

Why, it’s exposure to increased levels of glucose, of course!

I’ll once again quote from my own book:

“Let’s think about the amount of glucose in a healthy, non-diabetic person. In such a person, the total amount of glucose in the blood-stream during the fasting state is less than a teaspoon (which is less than 4 grams of glucose). An 80-pound, fasting, non-diabetic child has less than one-half teaspoon of glucose.

“What do you think happens when a person eats a meal that dumps ten or a hundred times the fasting amount of sugar into the bloodstream? The body simply cannot allow the blood glucose level to suddenly become 100 times the normal fasting amount. That much glucose in the bloodstream would be acutely harmful, perhaps even fatal, if not metabolized quickly. The body reacts to elevated glucose levels by doing whatever it must do to quickly metabolize the glucose. This means secreting insulin. Lots of insulin! Way more insulin than was ever necessary for a person before the advent of refined white flour, 64-ounce sodas, tortilla chips, and candy bars. 

“Over time and with frequent exposure to high levels of insulin, the cells in the body become increasingly resistant to insulin, requiring more and more insulin to accomplish the same glucose transport functions as before.”

In other words, repeated and significantly elevated glucose levels, the levels caused by our daily diet of grains, 64-oz sodas, chips, and other crap, cause insulin resistance.

What other problems do elevated glucose levels cause?

In a sad, cruel irony, elevated glucose levels damage the very components that are responsible for producing insulin: the beta cells of the pancreas.[1]

That is, elevating one’s glucose levels causes beta cell death, which causes glucose levels to rise, thus hastening beta cell death.

It’s what I call a “shit spiral.”

But in his thoughtful assessment of diabetes, Dr. Schmerling completely ignores the role that elevated glucose levels play in damaging the beta cells of the pancreas.

Oh, I forgot. Sugar doesn’t cause diabetes.

In conclusion, Shmerling states:

…the notion that a high-sugar diet causes diabetes is a medical myth that demonstrates how the effect of an illness may be mistaken for its cause.

And I submit to you, Dr. Shmerling, that by ignoring the role of excessive carbohydrate intake in the development of Type 2 diabetes, you are propagating a horribly damaging falsehood.

The advice from physicians of your ilk are a significant factor in the rise of diabetes and the decline of this nation’s health.

[1] Gleason, CE, et al. Determinants of glucose toxicity and its reversibility in pancreatic islet Beta-cell line, HIT-T15. American Journal of Physiology, Endocrinology, and Metabolism 2000;279: E997–E1002.

This is only one of many studies showing how elevated glucose levels kill pancreatic beta cells, thus hastening the onset of Type 2 diabetes.

2 thoughts on “Medical Experts Once Again Helping People Become Diabetic

  1. A sudden genetic shift is unlikely, but that doesn’t mean that diet is necessarily the primary culprit. I tend to think of the shift towards sedentary lifestyles (and, if you wish to view it through the lens of diet, the failure to modify our diets accordingly) has caused the obesity and type 2 spike. Humans have a long tradition of eating what is available *and* working very hard to get that food, and generally keep alive. The tendency to eat what is at hand hasn’t changed too much, so near as I can tell (though the foods have changed) but the need to work really hard every day has changed. We no longer have to work in the fields or walk long distances on a daily basis. That seems a bigger shift that the food that is in some ways of a lower quality (at least it’s less common for it to kill you quickly with a round of noxious food poisoning or hepatitis). We seem inclined to seek out a higher calorie diet than our work-load requires . . . I’m not sure how quickly we can evolve to desire the appropriate amount of food for this drastic lifestyle change plunked on top of thousands and thousands of years of the folks who survived were the ones who managed to find the most calories . . .

    We’re doomed, doomed I tell ya ;)

    • The work of Gary Taubes drives a pretty convincing stake (steak?) into the heart of the calories in/calories out model of weight balance. As he puts it, maintaining a constant weight to within a pound or so a year requires that caloric intake match caloric output to within 20 calories per day, which is approximately equivalent to one bite of a sandwich or a few M&M’s. He argues convincingly that there are far more people with stable weights than can be explained by an inadvertent caloric balance with this precision. I tend to think that the hormonal impact of our foods, way more than quantity, is the primary culprit. I agree that the role genetics plays in our increased obesity is likely a genetically influenced response to unfavorable eating: there are those of us that are genetically more likely to suffer diabetic-related maladies in response to an unfavorable lifestyle, just as some segments of the modern population are more susceptible to neurological issues like MS, Parkinson’s, and their ilk.

      While I readily agree that as a culture we are becoming more sedentary than ever before, I think the surge in diabetes, over the past 50 years or so, is way more dramatic than the lifestyle changes you describe. I honestly doubt that the relative quantity of laborers to sedentary workers has changed so dramatically since 1960 to produce the profound increase in obesity that we’re seeing. I’m swayed rather strongly by the parallels in dietary macronutrient changes, largely a shift away from fat and towards carbohydrates, that so closely matches the diabetes and heart disease curves.

      I agree that we’re doomed. A huge part of the problem, too, is a medical establishment that focuses so intently upon treating disease rather than preventing it and a public that’s so short sighted and complacent that they like it that way. As one physician I interviewed put it, “I very quickly learned to categorize each patient as a person who wants me to whip out my prescription pad and offer a quick fix or a person who is seriously intent upon making lifestyle changes for their benefit.”

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