A New Paradigm of Insulin Resistance

wabmester

Dr Jason Fung explains insulin resistance! No idea if he's right, but it sounds pretty good.

http://www.dietdoctor.com/a-new-paradigm-of-insulin-resistance

Dragonwolf

But this does not necessarily mean that the door is jammed. Instead, perhaps the cell is already overflowing with glucose and therefore more glucose cannot go in.

Imagine the cell to be a subway car. When the door opens, the passengers on the outside (glucose in the blood) march in a nice orderly manner into the empty subway car (cell). Normally, it doesn’t really require much of a push to get this glucose into the cell (insulin gives the push).

But during insulin resistance, the problem is not that the door does not open. The problem, instead is that the subway car (cell) is already overflowing with passengers (glucose). Now the glucose outside the cell simply can’t get in and is left crowded on the platform.

Insulin tries to push the glucose into the cell like the Japanese Subway Pushers, but they simply can’t do it because it’s full. So, it looks like the cell is resistant to the effects of the insulin, but really the problem is that the cell is already overflowing. So, the knee jerk reaction is to manufacture more insulin (pushers) to help push glucose into the cell. Which works, but only for a while.

So, the cell is not in a state of ‘internal starvation’. Instead, the cell is overflowing with glucose. Glucose starts spilling into the blood, which looks like gluconeogenesis has not been stopped consistent with insulin resistance. But what happens to fat production?

In the classic model of insulin resistance, the paradox was that DNL was enhanced, not decreased which looked a lot like heightened insulin sensitivity instead of resistance. But in the overflow model, the DNL would be enhanced because the cell is trying to rid itself of the excess glucose by producing extra fat. The cell is overflowing and not in an ‘internal starvation’ mode.

While this makes sense, it also doesn't really jive with my experience dealing with hyperinsulinemia and insulin resistance, at least on the surface (I'll explain in a minute). This does, however, make a lot more sense than the lock and key model and basically saying that the locks and/or keys are just broken (so let's pump you full of more keys to get the locks open).

It never did make sense to me to do something like prescribe Byetta to someone who's suffering from both insulin resistance and hyperinsulinemia already. Your insulin isn't working right, so let's force your pancreas to make even more, because surely throwing more insulin at your receptors is going to make them work!

However, his conclusion does agree:

The answer then seems obvious – it’s a matter of too much glucose and too much insulin. In other words, it was the insulin itself that caused the insulin resistance. We don’t need to chase shadows looking for some mysterious cause of insulin resistance.

Once we understand that excessive glucose and excessive insulin is the cause of the insulin resistance, then we can now devise a rational treatment. Reduce insulin and reduce glucose. Once you reverse the insulin resistance, you cure the type 2 diabetes.

From my personal experience, this..."revelation"...will open up a new can of worms regarding the exact circumstances by which excess insulin comes about in cases where glucose isn't necessarily in excess (though it may change the definition of "excess glucose" from what it currently is). (I put "revelation" in quotes, because his model actually does seem painfully obvious and makes so much more sense than the conventional one.)

Where things get really fun is how this state of insulin resistance triggers ghrelin release and inhibits leptin. In my experience, there's very much something that's telling the body that it's starving while in that cycle. It could be the cycle of extremes, itself, doing it. I'm not sure. What I do know, though, is that before going low carb and while having big trouble with my insulin levels, I felt like I was literally starving on 2000+ calories a day, but when I'm able to keep my insulin (and by extension, glucose, though my glucose never measured above about 125 even after meals) down, that hunger is no longer present and my body is content.

That dysfunctional state, though, I often describe as basically a starving-storage loop. The body is, for whatever reason, saying both "need more fuel!" and "we're full!" simultaneously, resulting in feeling constantly hungry, but gaining fat at the same time. What's triggering what part? I don't know. Hopefully, Dr. Fung's research will lead him (or someone) to uncovering those mysteries.

canadjineh

Thanks Wab & Dragon.... very interesting. It does make sense too, let's hope more research is done but not the kind sponsored by Diabetes meds, lol.