What do I mean by “incident type 2 diabetes”? The medical definition refers to the diagnosis and first intervention for the medical condition diabetes mellitus. For my purposes here (as I’ll relate later) “incident diabetes” is defined as two successive glucose readings of ≥126mg/dl or an A1C≥6.5% or treatment with a hypoglycemic medication such as Metformin. Using Metformin as a defining criterion may seem overly broad to some, but it was used in this important study in 2003 linking type 2 diabetes to CVD and CHD. Let me also remind everybody that the American Diabetes Association standard for diagnosing type 2 diabetes has changed substantially over the years and continues to be very controversial.
Until 1997, when it was changed to 126, the criterion for diagnosing type 2 was a fasting reading of 140mg/dl. In 2009, the inexpensive A1C test, which measures sugar on the surface of red blood cells over their 2-3 month lifetime, became the new standard, and the diagnosis point was lowered from 7.0% to 6.5%. The A1C blood test simulates the continuous level of glucose circulating in our blood, including the “excursions” (spikes) in postprandial blood sugar levels (after meals and snacks). This “averaging” methodology is a more accurate measure of insulin resistance (IR), especially when “challenged” by a carbohydrate load. IR is the underlying mechanism responsible for high blood sugar, and you can read a very good explanation of it in this About.com article. Shortcut: Easiest at-home test to determine IR – your waist to hip ratio.
A1Cs are also controversial. Most clinicians still follow the guidance of the American Diabetes Association and strive, thru “lifestyle intervention” and pharmacotherapy, to maintain a patient’s A1C at 7.0mg/dl, but that translates to an estimated Average Glucose (eAG) of 154mg/dl (determined with this calculator http://www.phlaunt.com/diabetes/20898027.php) and assures that the disease, and the pharmacotherapy, will be progressive. In other words, the onset of complications and co-morbidities, like cardiovascular disease, kidney disease, neuropathy and retinopathy , are inevitable. In clinical practice most practitioners are complicit. I don’t suggest overt self-interest, but the “trail of breadcrumbs” tells a cautionary tale.
Quest Diagnostics lab reports state the current A1C “reference intervals,” as published annually in Diabetes Care, the Journal of the American Diabetes Association, are a guide to the diagnosis of incident type 2 diabetes. They are:
< 5.7% Decreased risk of diabetes
5.7-6.0% Increased risk of diabetes (most prediabetics become diabetic within 10 years)
6.1-6.4% Higher risk of diabetes
≥6.5% Consistent with diabetes
A plain speaking translation of this very lax ADA testing standard for “incident type 2 diabetes” is : ≥6.5% = You’ve got Type 2 Diabetes, period; 6.1-6.4% = You’re Pre-Diabetic; 5.7-6.0% = You’ve got “impaired glucose tolerance” (IGT); and <5.7% but closing on it = you’ve got “impaired fasting glucose” (IFG). In all instances, you are Insulin Resistant (which means you are Carbohydrate Intolerant); you’ve lost and continue to lose beta cell function including the ability to make insulin. This “Natural History of Type 2 Diabetes,” explaining beta cell function and Pre-Diabetes, is described in “The Nutrition Debate #99” here. It is based on Dr. Ralph A DeFronzo’s presentation in his Banting Award Lecture at the ADA’s 2008 convention.
In the full published paper in the ADA Journal Diabetes, Dr. DeFronzo says, “In summary, our findings (40–42) demonstrate that, at the stage of IGT, individuals have lost over 80% of their β-cell function, while the results of Butler et al. (47) suggest that subjects with “pre-diabetes” have lost approximately half of their β-cell volume. In the next section, “Pre-Diabetes,” he adds, “The clinical implications of these findings for the treatment of type 2 diabetes are that the physician must intervene early, at the stage of IGT or IFG, with interventions that target pathogenic mechanisms known to promote β-cell failure.As a physician/researcher, Dr. DeFronzo cannot be faulted for advocating that “the physician must intervene early, at the stage of IGT or IFG, with interventions that target pathogenic mechanisms known to promote β-cell failure.” That’s the doc’s job! But how about the patient? The intervention that best targets the mechanism that kills beta cells is dietary. Eating carbs forces the pancreas to work. As you reduce carbohydrates, you spare your pancreas. It’s that simple, folks.