In the last article, we looked at the two main characteristics which are supposed to define type 2 diabetes and we discussed the fact that one of them, a lack of insulin, is generally not a characteristic. I suppose though, to be fair, since some type 2 diabetics do have a an absolute deficiency of insulin, in other words they aren’t capable of making even a normal amount, then we can say that we either have this or insulin resistance and that would be true I guess.
Now some people may say that although we may not have an absolute insulin deficiency, we may have a relative insulin deficiency, given that our pancreas cannot make enough insulin to obtain normal blood sugar. However, it’s a very open question whether that’s even something we ever want, for reasons we’ll discuss in more detail later, but for now the pancreas is not supposed to be secreting these huge amounts of insulin anyway, so having a lesser ability to do that is at the very least not something that is causing the disease.
So this leaves us with insulin resistance, which is a huge topic actually and one I’ll only be able to touch on here, but that’s the idea, to introduce you to these concepts and look at them in more depth later.
However, this isn’t your average introduction to insulin resistance, as we want to start out by asking whether insulin resistance is the disease or whether it, like excess insulin secretion, is merely a compensatory mechanism by the body to try to deal with the disease.
I think to a certain degree it is actually, and there is a lot of confusion out there as to what should and should not be uptaken by the cells. It is assumed that, for instance, if there’s excess glucose in the blood then that glucose should be in the cells and insulin therefore isn’t doing its job.
It might be the case though that the cells have already reached their capacity for glucose uptake and they’ve decided any more would be toxic, so they reject more and the way they do it is through insulin resistance.
So how can this happen? Non diabetics can eat the same diet and not have high blood sugar. What we tend to forget here, and this is very noteworthy, is that a lot of the extra glucose in our blood does not come from our diet at all, not from digesting food, but instead from the liver.
Now the liver is supposed to kick in extra glucose when our blood sugar gets low, but in diabetics, it delivers this extra glucose all the time, not just when you’re low, but when you are high as well. This is the primary breakdown behind type 2 diabetes actually.
So now we have too much glucose in the blood, and extra insulin is required to deal with it, but extra insulin over time causes more and more insulin resistance, including in the liver as well, which becomes more and more prone to elevate our blood sugar as high insulin takes its toll over time.
As insulin resistance progresses, it gets harder and harder to control your blood sugar. We often pay too much attention to blood sugar levels and if we’re looking to keep insulin levels up over time, that will tend to worsen and worsen the diabetes, and make it harder and harder to control.
This is the main reason why, with standard treatment, diabetics do get worse and worse over the years. So we do get worse and worse insulin resistance and diabetes is indeed generally progressive but a lot of this worsening is by our own hands, because we don’t pay enough attention to how we may be impacting insulin resistance over time, in spite of some very good science telling us that this should definitely be a concern.
In the next post I’ll talk about the third factor in type 2 diabetes, glucagon, which is actually the biggest one of the three.