Wednesday, March 12, 2014

The Nutrition Debate #191: Insulin-Dependent Type 2s

Okay, this is going to be an opinion piece. I admit to bias, but I will strive to present the subject in a factual way. That being said, I am not a doctor, and I have no formal medical/scientific training. I am a type 2 diabetic with almost 28 years of personal experience, all of which gives me certain bona fides (and contributes to my bias). In fact, the revelation that my pharmacist was an insulin-dependent type 2 diabetic, and had died prematurely some years ago, was the impetus for me to start writing “The Nutrition Debate.” I view his death as a tragedy and totally unnecessary.

First, a little background about insulin and diabetes. There are basically two types of diabetes: Type 1 and Type 2. Type 1 is an autoimmune disease. The onset usually occurs in childhood, permanently destroying the body’s ability to make insulin, a key hormone produced by the pancreas. Until the discovery of man-made insulin in 1922, most Type 1s didn’t live long. The only medical treatment was a strict medical “ketogenic diet” in which the patient’s food intake was 90%+ fat.

Type 2 diabetes, formerly called “adult onset diabetes” but now found in children (scary read here), is a disorder of metabolic disregulation resulting from insulin-resistance at the cellular level. The pancreas thus overworks to produce insulin. It is diagnosed by testing blood glucose since one of insulin’s key duties is the transport of glucose, the molecules that originate in food as complex carbohydrates and simple sugars. If the cells are resistant to insulin, glucose can’t get into the cells and the level of glucose in the blood rises. Hence, the diagnosis of type 2 diabetes is made with an elevated fasting blood glucose or an elevated A1c test (a 3-month “average” of circulating glucose as measured on red blood cells).

Type 2 diabetes is often suspected in overweight and obese individuals. Why? Because insulin stores fat.  When we consume carbohydrates, the body chooses wisely to use the exogenous “sugars” of foods (that all convert to glucose) that we catch or gather (or buy) as its primary energy source. It conserves energy in the form of body fat for use when those foods are not available – think winter and very early spring. So, when we eat foods that include carbs, we will burn sugar for energy and not body fat. It’s a brilliant design, anthropologically thinking, since fat is a very good storage vehicle. It is more than twice as dense in energy value (9 calories per gram vs. 4 calories for either protein or “sugar”).

When a doctor determines a patient is a type 2 diabetic, the conventional medical treatment is to 1) council weight loss via diet and exercise (lifestyle changes), and 2) prescribe an oral medication to help. If the patient is not successful in losing weight, which is, after all, an effect – not a cause – of type 2 diabetes, the doctor adds another oral med and then maybe a 3rd to the “cocktail.” More recently, injectable medications (GLP-1s) are sometimes prescribed. Traditionally, though, insulin injection has been reserved by most patients and their doctors as a “last resort” due to stigma.

Many (this suggests it is 26%) patients who are treated using the conventional treatment standards for blood glucose control, which are much too lax, will eventually progress to becoming insulin-dependent type 2s. Conventional treatment standards don’t call for the dramatic diet changes that can stop the progression of the disease.  The medical community acknowledges this. They consider type 2 diabetes a progressive disease, with a decrease of 10 years in the expected lifespan for T2 adults and 15 years for T2 children, compared to non-diabetics. See this link to a paper in the journal of the ADA.

Alternatively, some doctors today (and others, for many years, like Richard K. Bernstein) have developed a protocol to prescribe insulin as a first treatment upon diagnosis of type 2 diabetes. The thinking is that 1) it will spare the pancreas from further destruction of the beta cells that create insulin, and 2) it will result in much, much better glucose control.

Normalized glucose control is essential to reduce the complications of long-term elevated blood glucose levels: peripheral neuropathy (nerve and microvascular damage), commonly resulting in gangrene and amputations of limbs; retinopathy (damage to the blood vessels of the retina, resulting in blindness); and nephropathy, resulting in end-stage kidney disease.

Insulin therapy for type 2 diabetics usually begins with a regimen called “basal” insulin, injected once or twice a day. To this is added “meal time” insulin in which you, the patient, estimate the amount of carbohydrate you will eat at a meal and then inject an appropriate dose 20 minutes or so before sitting down to each meal. Some people now wear an “insulin pump” in which a needle, embedded under the skin, injects an amount that you determine by making an adjustment on the pump.

Dr. Bernstein, who is a type 1 diabetic himself, says that everyone is entitled to “normal blood sugar.” His own A1c’s are in the 4s, which is truly remarkable, but he has studied this subject, in the very real sense of the word, for half a century. He “eats to the meter,” because he has to, as a type 1; his body makes no insulin - he must inject it! And he manages his type 1 very well by eating small numbers of carbohydrates and consequently only needing to inject small amounts of insulin.

If you are a type 2, what does this suggest for you? If your pancreas still makes insulin, couldn’t you do the same? Eat small amounts of carbohydrates and only need to use small amounts of your body’s precious supply of insulin? And by avoiding glucose spikes, protecting your beta cells from further destruction.  I say you can. Eat fewer carbohydrates. Reduce your body’s reliance on your weakened pancreas to avoid the comorbid complications of heart attack, stroke and Alzheimer’s. Preserve and protect your feet, your vision, and your kidneys. Reclaim your life expectancy.

No comments:

Post a Comment