The Nutrition Debate #10: Carbohydrates, Insulin and Pre-diabetes

Why do we get fat? We eat too much and don’t exercise enough, you say. Well, if you do, you’ve got company; that’s the conventional wisdom. It was most recently reinforced by the release on 1/31/11 of the “revised” “Dietary Guidelines for Americans, 2010.” This was at a joint press conference held by the Secretaries of the USDA and the HHS, both former farm state governors. It also means that you probably haven’t read, or certainly haven’t accepted, the Alternative Interpretation of the Energy In – Energy Out formulation explained in Installment #5 in this series. (To see previously published installments, go to http://danbrown-thenutritiondebate.blogspot.com.) It flat-out refutes the Lipid Hypothesis.

Gary Taubes, in his serious and rather heavy read, “Good Calories – Bad Calories,” introduced in Installment #4, makes the case convincingly. In number 5 of his “certain conclusions” in the Epilogue of that book (p. 454), he states, “Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior” (emphasis added by me). The “obesity is a disorder of excess fat accumulation” is not a tautology; the operative word here is “disorder.” Why do we accumulate (synthesize and store) fat rather than break down and burn (catabolize and oxidize) the fat calories we eat? What drives our hunger to the point of eating too much and too often? The answer, according to Taubes, is carbohydrates.

All of Taubes’s ten “certain conclusions” merit rereading now and again (see Installment #4 in the archives), but his last two speak directly to these questions: 9) “By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be;” and 10) “By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.”

The mechanism at work here is the effect that all carbohydrates exert on the hormone insulin. That includes all sugars and all starches, regardless of their glycemic index or glycemic load. When carbs are eaten by a healthy person with normal glucose metabolism and regulation, in the initial response the enzyme amylase in saliva in the mouth triggers a quick burst of ready-made insulin previously produced by the pancreas. The digestive process continues in the stomach where acids assist in starting to break down all the sugars and starches. Then, in the small intestine, additional enzymatic action further breaks down the sugars and starches to simple glucose, which are then absorbed through the wall of the small intestine and into the bloodstream. In a healthy person, with normal insulin sensitivity and non-impaired glucose response, the additional insulin, produced by the pancreas in response to elevated glucose levels in the blood, slowly “mops up” the glucose (takes it to the muscles, etc.) over a one to two hour period and then, with glucose, declines in level in the blood.

Thus, the primary function of insulin -- glucose transport – has been fulfilled. Its function is only slightly, but significantly and progressively altered in a person with impaired glucose tolerance and/or insulin resistance. These impairments are the first signs, often undetected and overlooked, of the metabolic disorder called pre-diabetes.

Until recently, the fasting blood glucose test was the most common test for diagnosing pre-diabetes. The diagnosis was confirmed with a more difficult and expensive test, called the Impaired Glucose Tolerance Test (IGTT), which takes 2 to 4 hours, with blood drawn at half hour intervals. Within the last year, however, there has been a change in protocols, and now a test called the Hb A1c, or simply the A1c, is becoming the norm.

In addition, the diagnostic standard for Type 2 Diabetes Mellitus has been lowered, from 7.0 to 6.5, and to 6.0 for pre-diabetes. Some physicians set a much lower standard. Dr. Richard K. Bernstein, himself a Type 1 diabetic and a pioneer in blood test monitoring to achieve “normal” blood sugars, uses an A1c of 5.8 to diagnose full-blown Type 2 diabetes. None of these tests are perfect; the single best indication for an individual is a series of blood glucose checks after eating, that is, post-prandial. This can be done at home on your own schedule, no appointment required. Just eat to the meter.

In the next installment, we’ll examine the other major role of insulin: its regulatory role in fat metabolism. When the regulation of this hormone is out of balance, the result is fat synthesis and accumulation. We get fat. We’ll explain next.

© Dan Brown 2/6/11