A New Look at Insulin, Glucagon & the Pancreas (a.k.a. ITIS part 9)

“Contrary to popular belief, insulin is not needed for glucose uptake and utilization in man.” (Source)

What? Insulin is not needed for glucose uptake? Did I just blow your mind a little?  If so, hang on to your hat. Lots more of that to come.

As I mentioned in my previous post on the personal fat threshold concept, what I enjoy most about writing my blog is that I get to share with you the fascinating and surprising things I learn. And one thing I can say with certainty is, the more I learn, the less I know. It seems like I barely hit publish on a new blog post before coming across a bunch of papers that teach me even more about the subject in question, or make me rethink what I wrote about it in the past.

One subject I’ve learned more about since I last wrote about it is insulin. If you’re new here, I recommend digging into my 8-part series on insulin. If I do say so myself, it’s some of the most important and educational stuff I’ve written.  But you don’t need to have read that to understand today’s post.

If you’re accustomed to thinking about insulin as a “blood sugar hormone,” you’re about to have your world turned upside down.  What I’ve learned about insulin over the past couple of years makes me think that lowering blood glucose might be one of the least important and impressive things it does.

Another very long post coming your way here, so grab a coffee or some pork rinds, and happy reading!

Before you dive in, though, I recommend scrolling way down to the bottom of this post where it says “End.” You might want to spend a while reading the whole thing, or you might not…that will help you decide. 

More Than You Ever Wanted to Know About Protein & Gluconeogenesis

My dear readers, the website/blog update has run into some snags. Rather than continuing to keep you waiting, though, I’m going to publish new posts and I’ll worry about transitioning them over later on. And since it’s been a few months since I last posted anything of substance, I’ve decided to drop this enormous, enormous post on you to make up for that lost time—and it might take you equally long to read it. Sorry about that, but hey, I haven’t written anything meaningful since May, so, depending on your point of view, this post is either a gift or a punishment. As I’ve said in the past, if you’re an insomniac or a cubicle dweller with lots of time to kill, you’re welcome. (The rest of you, go get yourself a cup of coffee or tea, come back, and get comfy.)

I’ve been meaning to write this post for over a year, but it’s such a big topic and so much can go wrong that the thought of tackling it all was enough to make me not write it. But it’s gotten to the point that I’m tired enough of seeing the same questions asked and the same myths propagated over and over on various keto and low carb forums that I’ve decided this needs to be done, no matter how painful I might find it. Because seeing nonsense and fearmongering regarding the role of protein in low carb or ketogenic diets is even more painful. So if finally managing to organize my thoughts into some kind of coherent prose means I never have to read the phrase, “too much protein turns into sugar” ever again, it will be worth it.

So that’s what’s on tap today, kids: Gluconeogenesis.

That’s right, friends, it’s time to do some myth-busting surrounding the whacked-out notion that protein—lean protein, in particular (like a skinless chicken breast, or tuna canned in water)—is the metabolic equivalent of chocolate cake. (Or cotton candy, or gummy bears, or any other insanely sugary thing that might raise your blood glucose and insulin far more than protein does.) 

ITIS -- It's the Insulin, Stupid (pt 4/8)

“Insulin is vital for lipogenesis. Its role as a lipogenic hormone is underplayed, but we know that without insulin, you can’t get fat.”
                                        --Dr. Roger Unger

Having raved about Dr. Unger’s lecture in the previous insulin post, obviously, I think he’s pretty brilliant. That being said, chronically elevated insulin isn’t the only mechanism by which people accumulate excess adipose tissue. (For the newbies out there, “accumulating excess adipose tissue” is the fancy way to say “get fat.”) I prefer to use the word adipose instead of fat, because I am trying to make a distinction between dietary fat that we consume in food, and the body fat that we all love to hate so much on our bellies, hips, thighs, and elsewhere. Even if they both occur in the form of triglycerides, I still want to keep them separate, since eating dietary fat does not automatically result in said fat depositing itself on our rear ends or forming second and third chins.

Apart from insulin, there are several other things that contribute to the regulation of body weight, and, perhaps more important, the composition of that weight. And I’m not ignoring those. Sometime in the next few weeks, I’ll be writing a post about the myriad other reasons someone might not be losing weight on a low-carb diet (unrelated to this insulin series). For our purposes right now, though, we’ll stick with insulin. Because even if there are other factors playing a role in excess adiposity, when we look at changes that have occurred to the food supply and the general dietary guidelines from various government and professional medical/health organizations during the last several decades, systemic hyperinsulinemia is probably one of the largest influences, if not the single largest.

In tackling the role of insulin on the accumulation of adipose tissue, first we need to explore just a few more things about insulin’s biochemical & physiological roles. After that, we’ll see how it all plays out in the real world—that is, in the body.

ITIS -- It's the Insulin, Stupid (Pt 3/8)

If you made it through the encyclopedic posts that were part 1 and part 2 of this series on insulin, and you’ve come back for more, thank you! It is one of my biggest flaws as a writer: brevity is not my strong suit. (But at least I admit I have a problem. That’s the first step, right?) This post is no exception. In fact, it's probably longer than the first 2. So go grab a cuppa joe, or tea, or whatever you like, and hunker down for a nice, long read.

Okay. So I left off last time pointing out that, in covering the effects of elevated insulin and glucose on the cardiovascular system, reproductive function, the brain, kidneys, eyes, and inner ear & balance mechanisms, I had not said one word about obesity. I hope we’re all on the same page and can agree that insulin resistance is not something limited to people who are carrying around a few—or a couple hundred—extra pounds. Obviously, there are millions of non-overweight people who are infertile, have heart disease, kidney disease, vision problems, dementia, and more. (I have written about this before. One of my personal favorite posts on this entire blog is the one where I explained that obesity is simply one more effect of metabolic derangement, rather than its cause. I also wrote about this topic for Designs for Health.)

Nevertheless, we’d be missing a substantial piece of the insulin puzzle if we didn’t talk about the role of insulin in regulating body weight. Before we get to that, however, we first need to look at the actual functions of insulin, as well as the pancreas. It is an unfortunate byproduct of our epidemic of “diabesity” that we automatically think of blood glucose when we hear the word insulin. And there’s no doubt insulin does have an important role in regulating—or, more specifically, lowering—blood glucose (BG). But that’s not insulin’s only function. In fact, I would argue it’s not even the primary function. We will get to weight, I promise. But just like we did in the cancer series, we’ve got to trudge through a lot of biochemical weeds before we get to the good stuff. So here goes.

Time for a brief extremely verbose endocrinology lesson.