I’m not trying to be alarmist here. It’s just that there’s a broad misunderstanding in the patient population perhaps due to misunderstanding or reluctance to counsel patients by most clinicians: The diagnosis (Dx) of Pre-diabetes is prima facie evidence of an already failed glucose metabolism. The biomarkers used, an A1c of ≥5.7% (39mmol/mol) and/or an elevated blood sugar (≥100mg/dl or 5.6 or even 6.1mmol/L) is proof of that.
Most clinicians understand that a Dx of T2DM means that you have Insulin Resistance (IR). IR means that the uptake of glucose by the body is impaired by the inability of the hormone insulin, which accompanies glucose in the blood, to open receptor cells. This results in an elevated glucose. The body fights this dysfunctional response by sending more insulin. And as long as it sends more insulin, your blood glucose stays “Pre-diabetic.”
Here’s the misunderstanding. Your body has been successfully fighting IR by sending more insulin. And because it has been “successful” – keeping your blood glucose levels in the high-normal or even “Pre-diabetic” range – you, and ruefully in most cases your clinician, think you are not diabetic. The truth, however, is: You have IR (the definition of T2DM) and YOUR BODY is CONCEALING it from you.
Your pancreas will fight to make enough insulin to keep your blood sugar “normal,” until it fails. That failure is what constitutes a clinical diagnosis today. The failure of this late symptom of a dysfunctional glucose metabolism is after the fact. You have type 2 diabetes. Your pancreas has exhausted its ability to make enough new insulin. Either the Islet cells have died from fatigue or they so clogged with fat that they are blocked from functioning properly.
So, what should your clinician tell you or you do instead? If you have been told that you have a “slightly elevated” or “high-normal” or even a “Pre-Diabetic” blood glucose, accept that 1) you have Insulin Resistance, and 2) this is the definition of T2DM. NOW is the time to do something about it. Most clinicians will counsel you to “wait and see.” That’s because under clinical guidelines (and Medicare and other insurance rules), they can’t write you an Rx until you have been “clinically diagnosed.” But by then it’s too late. Your pancreas has already failed. It’s a fait accompli.
But up until this point your doctor has been in something of a bind. He can tell you to “diet and exercise,” but government’s idea of a “healthy diet” is to eat a “mostly plant-based” or even a Mediterranean diet. You’ve also been led to think that exercise is an effective weight loss strategy. Your doctor is also unlikely to know or believe that the diet or “lifestyle change” that will work to reverse your dysfunctional glucose metabolism is a low carb diet.
Nevertheless, losing weight is a good prescription, especially losing weight around the waist. Central obesity and belly fat are terms for visceral fat. As distinguished from subcutaneous fat, this is fat within the abdomen, around and within the organs, especially the liver and pancreas. This is why some people who are not obese have T2D. They are “skinny-fat” with a fat-clogged pancreas and probably a fatty liver (NAFLD) as well. This is very common in American children and adolescents. Losing this visceral fat can help restore function to pancreas for the obese, overweight and “skinny-fat” or viscerally obese.You got into this mess by eating far, far too many carbs. You can turn this whole thing around by eating far fewer carbs. Personally, I eat a Very Low Carb, Moderate Protein, High Fat (Healthy Saturated Fat, not the PUFA vegetable oils), also known as a LCHF or Keto diet. I also incorporate Intermittent Fasting (IF) from time to time. I’ve lost a lot of weight (170 pounds) and put my T2DM (Dx 1986) in remission. I have very good blood markers and I feel great. I did it without hunger (because fat is satiating), and without exercise. You can too.