Saturday, September 21, 2019

Retrospective #217: Type 2 Diabetic says, “I can eat whatever I want.”

I was seated next to a Type 2 diabetic acquaintance at a church supper recently. As the plates of food were passed around, I took a nice portion of ham and then (guiltily) a serving of cole slaw. I knew it was loaded with added sugar, but I also knew my other choices would be limited. I passed on the scalloped potatoes au gratin and the peas, and the bread basket, and the sweetened ice tea, each time passing the dish to my friend, who took a regular portion of each.
I didn’t say anything, but I thought to myself, how can he do this to himself? This man is somewhere in his eighties, skinny as a rail and looks healthy. Maybe the question should have been, how does he get away with eating like this? Eventually, I managed to open the subject with him. He responded by saying, “I can eat whatever I want.” He then reached down to his belt and, out of a small pouch, raised his pump controller to show me how he does it. My friend, it turns out, is an insulin-dependent Type 2 with a pump that allows him to set the amount of basal and mealtime (bolus) insulin before each meal. So, he knew what was for supper – it’s the same every year – and had given himself a “shot” via the needle imbedded under his skin. Voila! He can now “eat whatever he wants” and “cover it” with insulin.
Managing Type 2 diabetes with injected insulin has heretofore always been the last resort of pharmacotherapy. Type 2s used to be started on a course of oral pharmaceuticals and told to continue to eat a “balanced diet.” As one drug failed to achieve the desired control (A1c’s within the ADA recommended range of 7.0%), the dose was increased and/or another class of oral introduced until the patient, still eating “a balanced diet,” maxed out on three classes.
Then, the dreaded insulin injection was employed for basal (slow acting for 24-hour control) and mealtime “boluses.” Today, the introduction of new classes of orals, and the (GLP)-1 receptor agonists, and more recently the new (SGLT)-2 inhibitor drugs, that work on eliminating sugar in the blood via the kidneys, have enabled some patients to delay multiple daily insulin injections. And “the insulin pump” has replaced them all, for those who use it.
Another approach has been the introduction of injected insulin as a first course of treatment. The rationale is that if you eat a low carb diet, and inject a low dose of basal insulin once a day, you can potentially achieve better control by reducing postprandial spikes (elevated blood “sugars” after meals), thus achieving much lower A1c’s vs. the 7.0%. Better control also means the surviving beta cells of the pancreas, that produce endogenous insulin, get a rest.
An A1c of 7.0%, by the way, is equivalent to an estimated average glucose (eAG) of 154mg/dl, but an A1c of 6.0% is an eAG of 126 and an A1c of 5.0% is an eAG of 97. This improvement will surely reduce the possibility of the complications of poorly controlled diabetes: retinopathy, neuropathy, and nephropathy (translation: blindness, amputations and end-stage kidney disease). Plus, it reduces the possibility of a much greater chance of a heart attack. Any time your blood sugar is above 140, you are causing damage, and an average of 154 means it is above 140 A LOT. It is, in my opinion, bordering on criminal to counsel patients to only strive to achieve an A1c of 7.0%.
I don’t write about insulin dependent Type 2s because I know very little about it. Years ago, I read Richard K. Bernstein’s Diabetes Solution, the definitive source book on the subject (for both Type 1s and Type 2s), but promptly forgot most of the Type 1 details. His latest edition is very highly regarded among those in the know. It is the “bible” for the growing numbers of T2s as well as T1 diabetics who have discovered THE BEST WAY TO MANAGE AND CONTROL THEIR DISEASE IS TO EAT LOW CARB, with or without an insulin regimen.
But because I rely on my dietary choices (plus a daily, single low-dose Metformin) to directly limit the response of my (broken) blood sugar metabolism, I’ll bet my blood sugar is more stable, with fewer excursions, and therefore better controlled, than my friend’s (except at this particular supper: LOL). I’d even venture to wager that my A1c is lower than his. I didn’t ask him his, though. He, and his doctor apparently, are happy with whatever it is, and he was very happy to be able to say, “I can eat whatever I want.”
This column was originally written in 2014. Sadly, my friend died of “complications” (heart disease) in 2015.

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