ITIS -- It's the Insulin, Stupid (pt 6/8)

LOOKS CAN BE DECEIVING!

We’re in the home stretch with all this insulin stuff, folks, I promise. Just two more posts after this, and we’ll be done. (I also promise to get back to the cancer series soon. I know I’ve got some readers who’ve been waiting a long time for that to be resurrected.)

Okay, I left off last time asking why chronically elevated insulin causes some people to gain body fat, but not others. I also hinted that the accumulation of adipose tissue might actually be a protective mechanism. We’ll start with the first issue, since it’s quicker to address. I also want to start with it because it is probably the zillion-dollar question in all of human metabolism in our current dietary  & cultural zeitgeist. Upon consuming the same diet—the same number of calories, possibly the same macronutrient ratios—and maybe even having the same degree of hyperinsulinemia/insulin resistance, why do only some people get fat?

And here, my friends, is my zillion-dollar answer:

I don’t know.

I don’t know if anyone knows. Most likely, there are genetic factors involved. After all, some people are tall; some are short. Some have blue eyes; some have brown eyes. In the face of chronically elevated insulin, some of us accumulate lots of adipose tissue, some don’t. (Lucky bastards…) How come some people’s bodies are so good at not accumulating excess adipose? Put more bluntly—and in terms most of us have probably said to ourselves a hundred times about friends and relatives who have never had weight problems—despite eating junk and being sedentary—Dammit, why don’t they ever get fat?!

My hunch is, maybe there are other factors that have to come together in a kind of “perfect storm” scenario to allow the accumulation of body fat. Maybe it’s chronic hyperinsulinemia and any number of the following: a sluggish thyroid; skewed omega-6/omega-3 ratio; micronutrient deficiencies (perhaps specifically iodine, selenium, magnesium, chromium, and biotin); whacked-out gut flora; heavy metal toxicity; insufficient sleep; unremitting stress; or Saturn rising in Aquarius the day they were conceived. Who knows? (Except that last one. It's not that.) In some people, elevated insulin, all by itself, is probably enough to lead to an increase in body fat. Other people’s bodies might start to accumulate fat only with a confluence of these factors. I do think genetics has a lot to do with it, though. And it’s not that any of us is “programmed” or destined to become obese; it’s that the particular polymorphisms in our genes respond to the modern diet & lifestyle by accumulating body fat more readily than other people’s. Lucky bastar…but wait!

Are those people lucky? 

Is it really a blessing to be able to consume sugar and starch all day long with seeming impunity?

I say “seeming” impunity, because, the truth is, they are not eating that stuff with impunity.

That some people manage to remain thin 

in the face of the same dietary & lifestyle inputs that make the rest of us fat does not make them immune to the myriad other effects of these inputs.

Don’t be misled by the size of these people’s bodies. They might be thin, but that doesn’t make them healthy. The medical profession has a coined a new phrase to describe these people. They are the “normal weight obese,” also known as “metabolically obese.” In my writing for Designs for Health, I referred to this phenomenon as “TOFI” – thin outside, fat inside. (A phrase I first heard from J.J. Virgin.)

Here’s an excerpt from a blog post I wrote for the company:

“That such a diverse group of clinical presentations can be tied to the hyperinsulinemia and inflammation likely induced by a carbohydrate- and grain-heavy diet low in total fat and/or high in the wrong types of fat, shows us that excess body fat is only one result of the misguided conventional dietary recommendations of the last half-century. People who sidestep the fate of gaining weight are not immune to the myriad other effects of a poor diet upon their health—and in fact, a lack of visible ‘proof’ of these effects might make it more difficult to help these patients see the connection between their dietary choices and suboptimal health.”

So let’s be clear: lack of excess adipose tissue does not automatically mean someone is healthy. Nor, as Dr. Kraft's 5-hour insulin assays demonstrated so stunningly, does it automatically mean they are totally in the clear with regard to insulin sensitivity. The accumulation of body fat is simply one symptom among many that can result from chronic hyperinsulinemia. High levels of insulin drive the growth of fat tissue—in some people. Kind of like how decades of smoking drives lung cancer—in some people. The fact is, in the face of sustained hyperinsulinemia, some people become overweight or obese. Some people develop heart disease. Some develop Alzheimer’s, or tinnitus, or infertility, or kidney damage, or vision problems. Some poor souls end up with everything!

And the ones who don’t become obese? They are what a registered nurse I know calls the “constitutionally obesity-resistant.” What a demonstrative phrase, no? Their bodies are resistant to accumulating excess adipose. We could also cell them the “constitutionally thin.” As in, seemingly no matter how much they eat, or how little they exercise, their bodies remain thin. We all know people like this. (And as much as we might love them, we hate them a little bit, too, right?) Researchers have conducted overfeeding studies, wherein they sequester subjects in a metabolic ward, monitor them to make sure they are consuming larger amounts of calories than normal, and they Just. Don’t. Gain. Weight. (Or, they gain significantly less than predicted, based on the caloric surplus they’re stuffing these folks with.) Likewise, in my own n=1 experiments, and probably among many of you, simply cutting calories did not lead to magical weight loss. Some people’s bodies like to accumulate adipose tissue, and some people’s don’t. Like I said, genetics probably play into this to some extent, as do things happening at the cellular level that have nothing to do with calories, carbs, or exercise. (More on this coming in part 8.)

BMI: Let’s Be More Intelligent Than This

So we’ve got people who are at a “normal” or “healthy” body mass index (BMI), but remember: BMI is a measure of weight in relation to height. That’s it. Nada más. It says nothing—absolutely nothing—about the composition of that weight. (That is, how much of it is fat, and how much is muscle mass, bone, organs, water, etc.) This is why people like, say, Mario Lemieux and Wayne Gretzky, in their hockey-god heydays, would probably have been classified as obese. Can you i-freaking-magine? Uh, Wayne? Mario? You guys need to eat less and move more, ‘cuz you’re just too darn heavy for how tall you are. Sorry; looks like all those speed drills and Stanley Cup playoff games aren’t enough exercise for you.

So here’s the deal: Just as people who are quite fit and athletic can be mistakenly called “obese” by the ridiculous parameter that is BMI, so, too, can people with high body fat percentages be classified as “normal” weight or possibly even underweight. And now, we come to a very interesting place. It’s time to talk about fat versus weight. Skeletal muscle tissue—metabolically active, calorically hungry skeletal muscle—is a pretty great thing to have on your body. (I will write a post sometime about why. Just trust me for now. Or, if you don't want to trust me, trust Jamie Scott, founder of the Ancestral Health Society of New Zealand.) Adipose tissue, not so much. Some adipose, yes, definitely. It’s there for a reason and you would die without it. But you don’t need fifty, a hundred, two hundred extra pounds of it.

People who are “TOFI” tend to have a high body fat percentage. They have a small body size, but they have a lot of fat, relative to someone of the same size who is leaner. Here’s an example: Let’s say we have two women who both weigh 140 pounds. One woman has 22% body fat, and the other has 40% fat. If you had to guess which of these women was metabolically healthier and at far lower risk for a multitude of gnarly issues, which would you guess? (Yes, you’re right.) We could also hazard a guess as to which one looks better naked, but that is NOT WHAT THIS IS ABOUT.

There are lots of people out there who are at a “healthy” weight, yet are at far greater risk for pretty much all of the conditions associated with insulin resistance, or diabetes in-situ. These people might have many of the hallmarks of metabolic syndrome, insulin resistance, and/or type-2 diabetes, minus being overweight. (They aren’t overweight, but they might be overfat.)

According to the modern Western beauty ideal, these folks are cruisin’ along happily. But what’s going on “under the hood,” as Robb Wolf calls it? High triglycerides? Hypoglycemia? Mood swings? Brain fog? Hypertension? Can’t go up a flight of stairs without getting winded? Can’t conceive? Can’t get it up? Yep, sure sounds like these people are doing just great, since they’re not overweight, right?

“Excess” Body Fat: Physical Cushion and Physiological “Protection?”

Finally, we come to the second big question of this post: is an increase in body fat—total fat, not just as a percentage—the body’s way of protecting itself from something worse that could happen if body fat were not increasing? After all, we know darn well not all T2 diabetics are overweight. Nor is everyone with heart disease, or Alzheimer’s, or kidney problems.

Let’s be a bit politically incorrect, shall we? In an odd way, the accumulation of body fat might be a good thing, and those among us who find ourselves a little softer & squishier than we’d like might actually be lucky. (Say what?!) It’s true. Stay with me here.

See, when someone’s body starts to accumulate fat, it’s pretty easy for them to recognize something has gone awry. Whether it’s diet, sleep, stress, physical activity, environmental "toxin" exposures, or some other factor, the evidence is clear. It’s clear in the mirror, in the pants we can no longer button, in the rings that no longer fit—that something ain’t right. On the other hand, it’s difficult for the constitutionally obesity resistant to connect their acne, erectile dysfunction, brain fog, fatigue, chronic pain, vertigo, migraines, and more, to a harmful diet & lifestyle.

I am certainly not the first person to suggest that the accumulation of adipose tissue might be a protective mechanism in the body. (I wish I was; it’s brill.)  And it’s not the only wacky-seeming thing the body does to possibly protect itself. (I wrote something similar about cancer.) The reason it might be protective is, rather than have blood glucose remain at, say, 200 or 300mg/dL for an extended period of time, the liver converts this massive pile of glucose into fatty acids (a process called de novo lipogenesis, which means “making new fat”). So, fatty acids are being created, and, with insulin elevated (thanks, in part, to a ceaseless influx of carbs), the activity of lipoprotein lipase is stimulated, so an enzyme is standing at the ready to help escort those fatty acids into adipose cells. (Or to keep them right there in the liver, resulting in fatty liver.)

You’ll recall from part 2 of this series that the effects of chronic hyperglycemia are pretty disastrous. So, rather than allowing all that glucose to remain in the bloodstream indefinitely, where it will cause a storm of glycation that can affect just about every organ and tissue we can think of, the liver takes some of that glucose out of the bloodstream, converts it into triglycerides, and the body stores these triglycerides wherever it can: our hips, bellies, thighs, upper arms, rear ends (all of which is called “subcutaneous fat,” because it’s under the skin), as well as surrounding our organs (called “visceral fat,” because it’s deeper inside us, in and around the viscera). Since chronic hyperglycemia can cause such fun and benign things as stroke, blindness, and renal failure, it makes sense that a human body would rather have some more cushioning on its frame than run the risk of these serious health complications.

So the conversion of glucose to triglyceride, and its storage as adipose tissue, is actually the body’s way of protecting against the gnarly effects of sustained hyperglycemia. Because the body has so kindly and efficiently gotten that glucose out of the blood and stored it away for safekeeping, the blood glucose remains normal. (Or, if not "normal," then, say, more like 150-185mg/dL, rather than 200+.) And here, my friends, we come to a crucial, crucial question:

Did the accumulation of adipose tissue lead to hyperglycemia & hyperinsulinemia, or did hyperglycemia & hyperinsulinemia lead to the accumulation of adipose tissue? Or, in layman’s terms, do people become T2 diabetics because they’re fat, or do they become fat because they first have dysregulated blood sugar and insulin? Like I’ve said before: which is the chicken, and which is the Cadbury crème egg?

And as I have also said before, there is no mistake that adipose tissue is an endocrine apparatus. It is not physiologically inert. It doesn’t just sit there. It secretes and absorbs things, sends and receives. So yes, once excess adipose tissue has begun to accumulate, it can wreak plenty of havoc on health all throughout the body. But what is causing it to accumulate in the first place? That is the real question. And I think, with all this insulin stuff, we have at least part of the answer. Not the whole answer, mind you, but definitely part of it. (There’s a reason this series is called “It’s the Insulin, Stupid.”)

So, we’re on the same page here, right? It seems more likely that blood sugar & insulin dysregulation come first, and the accumulation of adipose tissue is the result. As I have written ranted about before, the accumulation of excess adipose tissue—whatever we might define “excess” to be—is most often an EFFECT of underlying hormonal and metabolic disturbances, rather than their causative factor. And even though obesity is “associated” with a long list of nasty health outcomes, that does not mean obesity causes them.

There are many putative causes of obesity. Hyperinsulinemia/insulin resistance is merely one of them. (And there are many putative causes of insulin resistance. And no, it’s not all about the carbs! Even I, as a LCHF-friendly nutritionist, say that loud and clear. After all, I called this series “It’s the Insulin, Stupid,” and not “It’s the Carbs, Stupid.” Because it’s not just the carbs. Excess carbohydrate consumption is a big factor, for sure. Maybe even the biggEST. But it’s not the only one. Details in the 8^th and final installment. We’ve got one more post before that, where we’ll tackle this question: Does insulin affect "calories in and calories out?" And if so, how?

In the meantime, if you’re not already reading Dr. Jason Fung’s blog on a regular basis, what are you waiting for? Check out his latest, where you’ll get additional info on this being an insulin issue, and not necessarily a carbohydrate issue.

Continue on to part 7 of this series.

Remember: Amy Berger, M.S., NTP, is not a physician and Tuit Nutrition, LLC, is not a medical practice. The information contained on this site is not intended to diagnose, treat, cure, or prevent any medical condition.