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.
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