We’ve really covered a lot of ground in this series so far, although there’s quite a few FAQs to still work though in the article we’re looking at. I’m not looking to repeat myself so if you want the full picture here I’d suggest you read this series in its entirely if possible, and some of these FAQs would involve rehashing some of the material we’ve already covered, and the series is long enough as it is.
The next one concerns the question of whether steroids can give you diabetes, and Dr. Hite points out that this would not be the case on its own, and that’s certainly correct. He does speak of it doing so with people who have already lost some function in their pancreas, but we know the truth is that with type 2 diabetes the pancreas is too active, both the beta and alpha cells actually.
Steroids do affect blood sugar to be sure, but it’s not by way of increasing insulin resistance as Dr. Hite mentions, this stuff actually improves insulin sensitivity if anything, by reducing inflammation, which does increase insulin resistance.
Controlling inflammation is important though in managing diabetes and this means all inflammation, but especially the inflammation caused by excessive insulin levels.
The reason why steroids increase our blood sugar is because that’s just what they do, and their two main functions are to decrease inflammation and to raise blood sugar. This is the case with naturally secreted cortisol and the prescription stuff. In a non diabetic, who doesn’t have high glucagon levels to go along with this, another hormone that raises blood sugar a lot, one may see a little higher blood sugar from steroids but nothing to be concerned about.
Diabetics though need to be cautious with these things and take the excursions in blood sugar that occur with this medication into account in choosing their treatment options. However, higher blood sugar is a chronic problem, not an acute one, and should one need this medication, going up for a short while won’t really matter much in the grand scheme of things.
Next, we deal with the curious issue of bariatric surgery improving diabetes, to the point where it’s even touted as a cure. He mentions GLP-1 but it’s actually the other incretin hormone, GIP, that is most likely involved here. Bariatric surgery by the way deals with the stomach, not the intestines, where GLP-1 is secreted. GIP though is secreted by the stomach, as is glucagon, and stomach secreted glucagon seems to be pretty significant indeed, although we do need to learn more about how to control it without this drastic surgery.
A defect in stomach secreted glucagon may also explain how eating can raise it up so much in spite of the higher insulin levels that are accompanied by eating. This was one of the discoveries of Dr. Unger, who we spoke a little about in past episodes, as he wondered why removing the pancreas still produced high blood sugar, and it turned out that it as glucagon from the stomach that was doing it.
Among the interesting possibilities here is the role that h pylori infection may play in this, which has been shown to increase glucagon, and that’s something a lot of people have. This alone probably wouldn’t be enough to do that much, but if someone is already diabetic, it may play a fairly big role.
H pylori also influences other hormones, including raising leptin levels, and high leptin levels and leptin resistance are implicated in diabetes, and in particular, in failing to regulate glucagon levels properly.
We then move on to a discussion about the complications of high blood sugar, and he mentions glycation, and when that topic comes up I always make sure to mention that there are two sides to this, reducing the stressors, in this case looking to control high blood sugar, and also strengthening the body against such things, by taking certain things that do this, such as benfotiamine and ALA.
People usually wait until they get the damage to get on this train, and only the people fortunate enough to be familiar with natural treatment of microvascular damage, but this is something we all should be looking to actively prevent.
The question comes up as to whether an A1C of 6, which would be a pre-diabetic A1C, would not be better than an A1C of 7, and he answers that we don’t want to risk hypoglycemia while striving for these targets, which is indeed wise. A lot of people achieve this target without any presctription medication or risk of hypoglycemia at all though, so it’s not the case that we need to take on these risks, and anything that is going to risk hypoglycemia may not provide lasting benefits anyway, and you’ll end up struggling to stay below 7 and then 8 and so on in time.
It’s worth pointing out here though that there are a group of people who do inject insulin and do manage their blood sugar very well, with low risks, and these people combine modest doses of insulin with ketogenic diets, extremely low carb ones in fact.
These diets downregulate insulin production below normal, not in a dangerous way though, just a bit below, and then when insulin is added this can lower blood sugar further, taking someone to perfectly normal blood sugar without increasing insulin at a level which likely would be harmful.
I’m not advocating this by the way and this appeals to people who have a very low risk tolerance, they want their A1C to be in the low to mid 5’s, and while people often can achieve this with diet alone, these folks do inject a bit to help themselves along, and I don’t see anything too wrong with that.
In the end, how one progresses will tell the tale, and once you start needing more insulin to achieve the same effect, the jig is up, your insulin resistance is increasing, but by the accounts of the people I’ve observed doing this, this is generally not the case, thus far for them anyway.
So using insulin is really all about staying away from hyperinsulinemia, which is insulin levels not just a tad higher than normal but quite a bit higher, double normal for instance or higher, and this just isn’t healthy for anyone, especially a type 2 diabetic. So insulin can be used but care must be exercised for sure, and what we’re out to avoid is making insulin resistance worse on purpose.