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 reinforced by the just-revised “Dietary Guidelines for Americans, 2010.” (This post was originally written in early 2011.) The joint press conference promoting this Low-Fat, High-Carb, mostly plant-based Pattern of Eating, was held by the Secretaries of the USDA and HHS, both former farm state governors. It also means that you probably haven’t read or accepted the Alternative Interpretation of the Energy In – Energy Out formulation explained in Retrospective #5 in this series. (To see #5 on this blog, just scroll down, or on Face Book, click on my name and scroll through my timeline.) It flat-out refutes the Low-Fat, High-Carb WOE.
Gary Taubes, in his very good book, “Good Calories – Bad Calories,” introduced in Retrospective #4, makes the case convincingly. In #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. Obesity is a disorder of excess fat accumulation.” But why do we get hungry and eat and accumulate more fat rather than burn body fat for energy balance? What makes us hungry and eat too much and too often when we have plenty of stored body fat to use? The answer, according to Taubes, is too many dietary carbohydrates, especially sugars and highly processed carbs.
All of Taubes’s ten “certain conclusions” merit re-reading (scroll down to #4), 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 processed carbs, 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. 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. Then, the levels of both glucose and insulin in the blood decline.
Thus, one of primary functions of insulin -- glucose transport – has been fulfilled. Its function is only slightly, but significantly and progressively altered in a person with Impaired Glucose Tolerance (IGT): Insulin Resistance. These impairments are the first signs, usually undetected and overlooked, of the metabolic disorder called Pre-diabetes.
Until recently, the fasting blood glucose (FBG) test was the most common test for diagnosing Pre-diabetes. The diagnosis was sometimes confirmed with a more expensive test, the Impaired Glucose Tolerance Test (IGTT), which takes 2 to 4 hours, with blood drawn at half hour intervals. Within the last year (this was written back in 2011), however, there has been a change in protocols. Now, a test called the A1c is coming to be the norm (again, 2011).
In addition, in 1997 the “then” diagnostic standard for Type 2 Diabetes Mellitus was lowered: FBG from ≤140mg/dl to 126. In 2002, the A1c test for Type 2 Diabetes was established at 6.5%, and later at 5.7% for Pre-diabetes. Some clinicians (Richard K. Bernstein, MD: “The Diabetes Solution”) and researchers (Ralph A. DeFronzo, MD, UTHSCSA) have always used a lower standard. None of these tests are perfect; the single best indication for an individual is a series of blood glucose checks. If your blood glucose doesn’t return to “normal” two hours after you begin eating, you have Insulin Resistance. This can be done at home – no appointment required – with a meter and test strips.In the next Retrospective, we’ll examine the other major role of insulin: its regulatory role in fat metabolism. When this hormone is “out of balance,” the result is fat synthesis and accumulation. We get fat. We’ll explain how, next.
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