The Nutrition Debate #196: The Diagnostic Power of A1c vs. Fasting Glucose

There have been scads of scientific papers published on this subject. I promise not to cite any of them in this piece. Instead, I will offer the example of two people’s A1c’s and fasting glucoses to illustrate the wisdom of using A1c rather than fasting glucose in diagnosing incipient or “incident T2DM.”

Until a few years ago the ADA official criterion for diagnosing T2DM was 2 consecutive fasting glucose tests (on separate office visits) of 126mg/dl. At the time of the introduction of the 126 value, the ADA also guided physicians that a fasting value of 100-125mg/dl was to be considered “pre-diabetic.” A “normal” fasting glucose was then 70-100mg/dl.

The A1c became increasingly the diagnostic tool of choice in 2009, although the fasting glucose test, while seriously flawed, particularly for middle aged women, is still widely used. But first, what is the A1c test? Officially, the hg A1c (hemoglobin A1c), is a measurement (percent) of the glucose on the surface of red blood cells that are continuously circulating in your body. Since red blood cells live about 2 to 3 months before they die and your bone marrow replaces them, the test is then a measurement of the level of glucose circulating in your body 24/7 during that time period. It’s like wearing a “monitor.”

The idea is that the A1c test will thus captures the postprandial spikes (called “excursions”) that your blood sugar takes after eating. Everyone’s blood sugar surges after eating. As food digests, to the extent that there are carbohydrates in the food, they will break down to glucose and will be transported, by insulin secreted in the pancreas for the purpose, to the cells. That is how your body gets the (sugar) “energy” from food to, and hopefully into, your cells. In people with a “normal” metabolic process, the sugar moves from the blood into the cell and, after a couple of hours, when all the carbs have been digested, then circulated and “taken up,” the level of glucose (and insulin) in the blood returns to where it began.

However, in people whose metabolism has developed a specific “dysregulation” called “insulin resistance,” the surface of the destination cell resists the up-take of insulin (and the glucose it’s transporting), and the level of both insulin and glucose in the blood remains “elevated” (and you get hungry and tired and lack energy, literally. So, these people, who are developing insulin resistance, will have a higher A1c, corresponding to the higher blood glucose and insulin that is circulating for hours/days and the worst (and increasingly common) case, continuously, so long as you regularly eat carbs.

So, insulin resistance is the mechanism that starts T2DM. I describe the “history” of T2DM here. It leads to your pancreas making more insulin to overcome the resistance, eventually wearing out the beta cells where it is made. The longer and the more your insulin resistance persists, the more your pancreas’ ability to make insulin will be lost, forever.

Now, the two examples I promised you: Person #1 is the email correspondent referred to in The Nutrition Debate #195. He was diagnosed a type 2 diabetic about 9 months ago (he doesn’t say “how” exactly: A1c, or fasting glucose, or both); in response, he changed his diet (“just stopped eating bread, potatoes, pasta and ice cream”). Now, I’m thinking, that’s not an “extreme” or “very low carb” diet. The result: nine months later he had “lost 20 pounds” and his “A1c (was) totally normal (5.7) and fasting glucose (was) at 100-105 over 3 blood works.” To be clear, he is still a type 2 diabetic. He still has insulin resistance, and probably a slightly damaged pancreas, but he has learned how to control his blood glucose, and thus his diabetes, through a moderately low carbohydrate diet. His A1c, at 5.7%, is “borderline.” You could say (this is something of a “conceit”) that his diabetes is “in remission,” but it will be so only so long as he stays “moderately low carb.”

Person #2 (lab tests read to me over the phone): fasting glucose 100; A1c test = 5.0mg/dl. (Interestingly, the range on this lab test, performed by the VA, was 70 to 110mg/dl. vs.70-100 on Quest, and other labs. Hmmmm… Is this the “new normal” to reflect not what is “normal” but the trend toward a higher population average as we lemmings follow our government’s dietary advice? But I digress.) Note: this “patient” has the same blood glucose value (+/-100mg/dl), but a “normal” A1c (for a 70yo male) of 5.0mg/dl. This person eats a typical American “balanced diet,” between 40 and 60% carbohydrate, and is not diabetic or even pre-diabetic, whereas the other person definitely is, even though their fasting glucoses are the same.

Thus, the A1c test is what differentiates #1 (controlled diabetic) from #2 (non-diabetic). And #1 has learned to control his diabetes through diet alone. That’s what keeps his A1c in the clinically “non-diabetic” range, so long as he stays moderately low carb. I hope this is instructive, for all the “pre-diabetics” and “newly diagnosed type 2s” out there. Watch what you eat!