Metabolic Hormones With Dr. Bryan Walsh Part 2

diabetic science







This is part 2 of our look at Dr. Bryan Walsh's video on metabolic hormones.  We left off speaking about looking at the markers of insulin and glucose to determine one's degree of insulin resistance, and the more insulin that is needed to maintain a given level of blood sugar, the more insulin resistance we have.

Eventually we may get to the point where we have high glucose levels but normal insulin levels, mainly due to a downregulation of our insulin secretion, which actually is a protective measure overall, but may also result from beta cell dysfunction.  We generally see blood sugar levels to up even further here, so there's still insulin resistance going on, because without insulin resistance, normal levels of insulin should produce normal glucose levels.

Finally, we may get to the point where our own insulin secretion is below normal, and once again, glucose tends to go up further with this, but this does result in a further lessening of the insulin resistance, provided that levels aren't kept artificially high.  While we do medicate normal insulin levels to bring them higher, up to toxic levels, in the case where levels are below normal and one's glucose load isn't reduced in turn to compensate, then there will be a need for raising insulin at this point.

This last point is important though, as our need for insulin is to a large degree dependent on our diet, and if we overconsume glucose sources, carbs in other words, then our need will be greater, and this is the big reason why carb restriction is so important, to lessen our need for insulin, and high insulin is the bigger culprit here, although this does tend to lower blood sugar as well.

So now we move on to insulin like growth factor 1 (IGF-1), and we also see the targets for this test, and interestingly enough, both too high and too low are a risk.  Low risk is in the range of 117-130, and both being below and above this range is high risk.

So the stimulation of IGF-1 is driven by growth hormone release by the pituitary, which in turn stimulates the liver to produce IGF-1.  IGF-1 can also be produced by the cells themselves, locally.  However, the blood test only really measures systemic IGF-1, from the liver.

So what does IGF-1 do?  Well it stimulates cellular metabolism and cellular growth.  In doing so, it stimulates glucose uptake, which is obviously important in glucose metabolism, and when low, less glucose is taken in by cells, and therefore blood sugar tends to be higher.

When IGF-1 is low, we also see cellular destruction, degeneration, malfunction, and cellular death.  This hormone also declines with age and plays a big role in the aging process.  So this is obviously an important thing not to be low in, and needs to be a lot bigger focus than it tends to be, especially with diabetics.

We generally see this too low rather than too high, and it's quite unusual for it to be too high, but what we see in this case is excess cellular growth and proliferation.  So even as important a hormone as IGF-1 is, we want it to be balanced, not too high or too low, and that's true of all hormones, including insulin by the way, which is the one we abuse the most by looking to purposely increase it well beyond healthy levels.

In diabetics, it's low IGF-1 that we need to be wary of, and low IGF-1 is typical with us.  So how does this get low?  Well, given that it's primarily produced in the liver, liver dysfunction causes an underproduction.  As diabetics, we do tend to have fattier livers than the general population, so that's certainly implicated.

So we then look at markers of liver function to determine one's liver health, however that doesn't always give us a clear picture, and one's liver markers can be within the normal range but we may still suffer from things like low IGF-1.  In the end, if this hormone is low, it doesn't really matter so much why, we need to raise it, although things that support the liver are a great idea for diabetics.

The big thing that causes fatty liver is actually excess insulin, because it increases fat production and too much of this is retained in the liver, so if your insulin levels are high and your IGF-1 levels are low, that very likely plays a role, so this is yet another important reason not to drive insulin levels to excess.

Another thing to look at is growth hormone levels, since growth hormone stimulates IGF-1, and not enough growth hormone secretion will result in not enough IGF-1 being produced.  Excessive insulin levels oppose growth hormone release by the way, as does high blood sugar as well.

Poor sleep also affects growth hormone release negatively.  Sleep is super important to health and this is one of the reasons that people taking SGLT2 inhibitors and waking up several times at night to urinate has me concerned.

Bryan also mentions the role that xenobiotics have been shown to play in decreasing both growth hormone and IGF-1, including such things as phytoestrogens as well as pesticide residues.  So we want to look to minimize these, especially phytoestrogens, and this is one of the ways that unfermented soy does us in, as well as toxins found in certain plastics.  Besides soy, there are quite a few more plant based foods that contain phytoestrogens, I really watch my intake of plant based foods for this reason actually, although soy is in a class by itself here, and I avoid that completely.

Chronic stress can also decrease these important hormones, as well as an excess of free fatty acids, and that's the biggest deal for diabetics, as our free fatty acid levels tend to be high, due in large part by the way by the excessive levels of insulin we have.  Obesity increases free fatty acid levels as well, and that's caused primarily by high insulin levels.

Diabetes in a nutshell is the disease of high insulin, at least until your pancreas finally gives out, and the list of dysfunctions that are caused by high insulin is a long one indeed, and this is why it's so important to look to keep our insulin levels in check.

I'll continue this discussion in part 3.

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