Yes, I know: Insulin is essential for life. People who don't produce enough insulin have to take insulin shots to stay alive. And by carefully matching their food with their insulin, they can live long and happy lives, albeit lives that are more difficult than those of people who don't need extra insulin.
However, controlling diabetes through diet and insulin -- even with the "artifical pancreas" that does some of the calculations for the patient -- is not enough for most people. We want a cure. Both type 1 and type 2: We want a cure.
What is a cure? Different people define cure differently. Some sellers of the "miracle cures" that you can find on the Internet seem to define cure as having lower blood glucose levels than you had when you started. Some people define cure as not taking any drugs, even though you might have to go on a strict low-carb diet in order to do so. Dr Richard Bernstein defines cure as having a normal glucose tolerance test. I agree with him.
There's certainly no lack of studies of insulin. I just searched PubMed, which showed almost 13,000 articles with insulin in the title published so far in 2015, and more than 30,000 papers about diabetes.
But we still don't have a cure.
Is it possible that because insulin is so important for diabetes, and essential for controlling it, it's drawing attention and research funding away from other compounds that might be less important for control but more important for prevention or cure?
Don't ask me what these compounds would be. If I knew I'd be famous. But some people feel that hormones like glucagon play a big role, and more and more are studying this hormone (about 1300 papers in 2015). How about somatostatin (621 articles), which inhibits the release of both insulin and glucagon, as well as having effects on other hormone systems?
It wasn't that long ago that we didn't know about leptin (identified in 1990s), which plays a large role in obesity. Could there be other yet-undiscovered hormones out there that would be the key to preventing diabetes and maybe even reversing it once it's manifest? Could the focus on the essential-for-life hormone insulin be blinding us to the effects if other, more obscure hormones?
I'm probably wrong, but it never hurts to wonder.
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Welcome back!
ReplyDeleteYes to a degree I agree. The other side of the coin is that insulin is a "master hormone" along with leptin and T3 and not only has direct effects, not only on glucose but fat metabolism and food partitioning, but indirect effects on a lot of other stuff.
My problem has been a lack of Phase 1 insulin since early childhood, but now in my sixties my Phase 2 insulin response is still good. Do I not make it, store it or release it? Maybe it's actually a problem with incretins which fail to order its release. Conversely maybe it's the glucagon that doesn't shut off when it should - and there are a whole bunch of things such as cortisol, epinephrine and norepinephrine that act alongside glucagon and counter to insulin to *increase* BG.
In truly normal people the balance between these is exquisite and BG is very tightly controlled. When BG goes out of spec insulin gets the blame but it may be only one player.
Insulin resistance is an adaptive response when it varies between different tissues (physiological IR) for food partitioning - sending glucose one way and fats and ketones another - and still adaptive when it is whole body and used to rapidly store a glut of food. After which it should shut down, and only when it becomes chronic does it become a problem because the stored food (body fat) and dietary fat become unavailable to metabolise.
Looking at how IR is switched on and off would be useful.
OTOH claiming insulin is not a factor at all, or even that it DEcreases obesity, like certain obesity researchers, is distinctly unhelpful. Claiming that it is not involved in diabetes at all would be another foot-shooting exercise.
Yes, type 2 is a complex situation, with many hormones involved. Apparently almost everyone with classic T2 lacks the phase 1 response, but as long as phase 2 is strong, no one will notice. I think no one knows *why* the phase 1 response is faulty, but when I was in a clinical study of salsalte, my phase 1 response was restored to about 70% of normal. This suggests inflammation.
ReplyDeleteInteresting! My mother took that or one of its derivatives for Crohn's but it didn't offset the effects of steroids. She died "nondiabetic" despite postprandial BG between 11 and 15 because her A1c was "only" 6.4, so that's all right then, she never became a Statistic!
ReplyDeleteMy postprandial BG always spiked around the 1 hour mark, hers was around 2 hours when mine was back approaching normal, but then she was 94 at the time.
Over time I've met a small but significant number of people with the same phenomenon - Reactive Hypoglycemia and diabetes *symptoms* starting in childhood but with slow progression - only about half went on to become *diagnosed* diabetic, the rest remained "prediabetic" but in all cases acting as if they were already diabetic, ie. low carb, kicked the IR into touch and allowed the remaining insulin to be more effective. Some of them also, like me, had diabetes and CVD in their family which suggests a genetic basis.
Yes, to the genetic basis. Any chance one of the MODYs runs in your family?
DeleteClose but no banana! The distribution of disease is more complex than that though there are obviously similarities in the symptoms/metabolism. Mainly the actual diabetes is only in males, the fat people score better on tests than us skinnies, and it skips people and generations.
ReplyDeleteOne of the other sufferers of Reactive Hypoglycemia starting in childhood was convinced as a child that old people lost limbs in the same way trees dropped their leaves in fall as there were so many diabetics in her family. Not all of them were obese either. Hang around diabetes newsgroups/forums long enough and you see plenty of similar stories, suggesting a whole bunch of different genes may lead to the same outcome.
And I know someone who was convinced as a child that when boys grew up, they turned into women. That was because it was WWII, and there were no adult men around.
ReplyDeleteHahahaha!
ReplyDeleteWhen I was little I was convinced hard (fish) roes came from male fish and soft roes from female fish because my father and I preferred the former, and my mother preferred the latter. I only discovered heterosexuality some time later . . .
. . . so many dietary (and other) experts seem to make the same mistakes in logic.