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

Well, here we are, folks! The 8^th and final installment of the crazy journey that began way back when we looked at Dr. Joseph Kraft’s 5-hour glucose tolerance tests with insulin assay. You remember those, right? The ones that suggested far more people are in the early stages of diabetes and insulin resistance than anyone ever would have guessed, based on their “normal” fasting glucose and hemoglobin A1c results.

In case anyone’s stumbling upon this series for the first time, here are links to the seven posts that preceded this one:

• Part 1: Introduction to insulin resistance and the work of Dr. Kraft: What is diabetes in-situ?
• Part 2: Health consequences of hyperinsulinemia & hyperglycemia unrelated to body weight.
• Part 3: Deep-dive into the pancreas and the balancing act between insulin and GLUCAGON.
• Part 4: The role of insulin in the gain & loss of body fat.
• Part 5: More on insulin & the regulation of body fat—how do different eating patterns (such as intermittent fasting and carbohydrate reduction) affect insulin, and what does that mean for body fat and energy levels?
• Part 6: The concept of “normal weight obesity” or TOFI—thin outside, fat inside, and what this means for overall health. (Summary: “thin” doesn’t automatically mean healthy.) Also: how come some people don’t become overweight when they’re insulin resistant?
• Part 7: “Calories in, calories out” and “eat less, move more.” Are these sound bytes the least bit helpful? In a word, no. If you have even the smallest appreciation for the complexity of the biochemical regulation of human metabolism, in general, and body fat, in particular, then you will agree that these phrases are laughably simplistic and one step shy of being completely meaningless.

Okay! Let’s get down to business.

Having covered some of the gnarly health conditions and debilitating downstream effects of insulin resistance (IR), hyperinsulinemia, and hyperglycemia—which can affect your eyes, your ears, your brain, your kidneys, your heart & blood vessels, your nerves, and your man parts or lady bits, not to mention make you the three Fs: fat, fatigued, and foggy-headed—it’s time to address perhaps the most important questions of all...

What causes insulin resistance, 
and what can we do about it?

Insulin resistance served up
for breakfast?
Maybe not…

Let’s take care of the low-hanging fruit first. Here’s what does not cause IR: consuming carbohydrates, per se. As I have mentioned in past posts, I called this series “It’s the Insulin, Stupid,” and not “It’s the Carbs, Stupid.” Because it’s not just the carbs. Exceeding your own individual level of carbohydrate tolerance is a big factor in this, for sure. But it’s not the only one, and I don’t even know if, by itself, it’s sufficient to cause IR. Like I said in part 6, it’s more likely that a confluence of factors is required before the “wheels start to fall off the wagon,” as Robb Wolf likes to say. Maybe just eating tons of carbs isn’t enough to induce IR. Maybe IR only creeps up when regularly gorging on carbs is combined with a high omega-6 intake, long-term inadequate sleep and poor stress management, a sluggish thyroid, heavy metal toxicity, exposure to environmental “obesogens” and endocrine disruptors, micronutrient deficiencies (vitamin J, anyone?), Mercury in retrograde, and/or factors we don’t even know about yet.

Anyone who’s been reading this blog for any length of time knows I am most definitely a proponent of low-carb and ketogenic diets. (But I am also a firm believer in individualization and there being no one-size-fits-all approach when it comes to feeding ourselves.) So maybe it’s surprising to hear me say that I truly believe eating lots of sugar & starch is not the only way to induce IR. (And no, this has absolutely nothing to do with the Kitavans. As I have written about many times, the Kitavans likely remain lean and free of chronic degenerative illness on their high-starch and fruit diet because they are the Kitavans, and they are evolutionarily/dietarily conditioned to thrive on that type of diet. This does not mean that everyone else, everywhere else on the planet, will do equally well on the same diet. I will quote myself here, because I think it’s one of the most important things I’ve written in the history of this blog: “Human beings can thrive on a wide variety of diets. But that does not mean that all humans can thrive on all diets.” [Never mind that the Kitavans don’t consume venti caramel macchiatos, chocolate-frosted breakfast cereal, bottomless baskets of breadsticks, sugary granola, and other fare that has become the norm in the U.S. The Kitavan version of a “high-carb diet” is a world apart from that of the U.S.]) So, no, the Kitavans are not proof that eating a high-carbohydrate diet is safe for all other population groups. What the Kitavans do prove is that, at least in some populations, in the absence of several other potential contributors to insulin resistance, a high intake of whole, unprocessed, nutrient-rich carbohydrate foods does not cause IR or other forms of metabolic dysfunction. (Let me reiterate: They are not proof that donuts, bagels, soda, and 64-oz slushies do not contribute whatsoever to metabolic illness.)

I swear, if I hear one more freaking thing about the Kitavans…

I have already mentioned some other issues that might be at play when it comes to the development of IR. There are many more, some of which are under our control, and some of which are not. If/when necessary, we can all find ways to better manage stress, get more sleep, build more muscle, maintain adequate vitamin & mineral stores, and even—with the guidance of a knowledgeable physician or clinical nutritionist—chelate or “detoxify” heavy metal buildups, optimize thyroid function, and address other hormonal imbalances that might be affecting glucose & insulin disposal. We can also tinker with our gut flora, but to be honest with you, I don’t think anyone knows enough just yet about what constitutes a “healthy” microbiome, and it's possible people loading up on resistant starch and probiotics could end up doing themselves more harm than good.

All that being said, there are yet other factors that might contribute to the development of IR—factors we have zero control over. If any of you are familiar with the research of Weston Price, DDS, then you know that the diet of our parents—and our grandparents, and maybe even their parents—influence our own physical development, and we have no reason to suspect they don’t also influence our physiological or endocrinological development. That is, maybe our carbohydrate tolerance, or our caffeine tolerance, or FODMAP sensitivity, or liver detoxification capacity, or methylation efficiency, or whatever else, is out of our hands. We can manipulate all of these things to some extent, but overall, some of the wacky things our bodies do might simply be the hand we’re dealt. We already know for sure that maternal hyperglycemia can predispose offspring to some pretty serious health issues down the road. Maybe it doesn’t outright cause them, but it certainly makes them harder to avoid, particularly in the context of the modern American diet and lifestyle. (For an updated but equally impactful version of Dr. Price’s findings, I recommend the book Deep Nutrition. Be warned, though: reading these works may lead you to start scrutinizing the faces of strangers—particularly children—and jump to conclusions about their ancestors’ dietary habits. Happens to a lot of us!)

I could go on and on (and on!) regarding my theories on why some people tolerate carbohydrate, or stress, or short sleep, better than others—and why some of us tolerate these things just fine when we’re young, but less so as we age—but let’s stay on message here.

Having acknowledged that there are several routes to the same destination of insulin resistance, I will defer to the experts to explain the details on the multiple inputs that are currently hypothesized to contribute to IR. The people at Meridian Valley Lab have put together a fantastic 3-part video lecture series on the causes of insulin resistance, how to test for it, and how to treat/reverse it. As it relates to this post, regarding the causes and what to do about them, you’ll want to watch parts I and III. (Part II looks at the glucose & insulin assays the lab uses to assess IR, and they are pretty much the same ones Dr. Kraft used. It is worth watching, for reasons I’ll get to in a minute. If nothing else, it’s worth it just to hear the speaker say that the result that puzzles them—the one they almost never see and can barely make sense of—is likely due to someone following a low-carb diet. [Approximately 30 minutes into the video.])

• Part I: Foundations of Insulin Resistance
• Part II: Insulin Resistance Assessment, Testing and Monitoring
• Part III: Insulin Resistance Treatment Strategies

Part I will give you an appreciation for how far beyond “carbz” this all goes. Part III presents several answers to the “what to do about it” question.

Now back to part II. Part II provides answers to the question you might have after reading all these posts and being skeer’d of developing insulin resistance, and maybe being especially skeer’d of developing any of the conditions associated with IR, such as Alzheimer’s or cardiovascular disease. This question, in particular, is driven by what we saw way back in the first post in this series, with Dr. Kraft’s insulin assays. Remember: Dr. Kraft showed that, in many people with normal glucose tolerance, normal fasting glucose, and normal A1c, hyperinsulinemia, or “diabetes in-situ” was lurking behind the scenes. As I explained, the reason those measurements were normal is because of sky-high insulin, which, as we saw in the second post in this series, has very serious implications for health all on its own, apart from anything going on with blood glucose.

What should we be on the lookout for
in our various & sundry bodily fluids?

So what is this burning question? (And do they make a cream for it?)  The question is, until insulin assays become standard protocol at your annual physical, or until testing insulin at home is as simple as using a handheld glucometer, what other markers can we keep an eye on in order to make sure we don’t have a date with disaster?

I don’t have any groundbreaking answers for you. Most of them are pretty old news if you read other blogs and listen to podcasts about this stuff. (If you don’t, then, congratulations. You are not the gigantic nerd I am, and you are probably way too busy having fun and living life to immerse yourself in this stuff like I do.) Okay, back to what matters: if we can’t measure insulin directly (many doctors don’t want to, even some of the LCHF-friendly ones), what else can we look at to see how we’re doing?

Pretty much the usual suspects: If your glucose & A1c are elevated, then you’ll know you’re already in dangerous territory. Beyond that, there’s triglycerides, blood pressure, HDL, LDL particle size (but not necessarily number), C-peptide, uric acid, and fructosamine. (Possibly also CRP or hs-CRP [C-reactive protein and high-sensitivity C-reactive protein, respectively], which are markers of inflammation. I think they can be surrogate indicators of IR as well, since chronically elevated insulin is pretty damn inflammatory.)

For more on the markers to watch, and what are currently believed to be the optimal ranges, part II of the video lectures is your best bet. (You don’t have to watch part I first. I recommend watching all of them in order, but each part stands alone just fine.)

I’m sorry if this post is a somewhat anti-climactic end to what has otherwise been a pretty good ride. I guess I just feel the videos explain the nuances better than I can, and there’s no point in reinventing the wheel.

HOWEVER, just so I don’t leave you completely disappointed, allow me to share some thoughts on the strategies that might help us protect ourselves from the horrible outcomes detailed in part 2, or, if we already have some of those issues, how we might stop them from progressing, and possibly even reverse or cure them.

Can insulin resistance be reversed?
Can it be cured?

Those two words are quite interesting: reverse, and cure. Can insulin resistance be reversed? Dr. Fung seems to think so. He routinely uses that word in his videos and tweets.

@TheSugarFreeMan Certainly. I suspect insulin resistance is reversible in 95% of people given the right approach.

— Dr. Jason Fung (@drjasonfung) November 8, 2015

Can it be cured? Probably not, but really, it’s just semantics. Dr. Fung has taken some harsh criticism, even among the LCHF community, regarding his claims of “curing” type 2 diabetes (and, for our purposes here, we can lump IR together with T2D). Is it cured, or is it merely managed?

Well, it’s managed, in the sense that an alcoholic who’s been sober for 20 years isn’t “cured” of alcoholism, but as long as they avoid the triggering element, there’s no problem. If they were to start drinking again, then boom: problem. It probably works the same way with eating excess carbs, or chronically undersleeping, or being stressed out, or exposed to environmental obesogens, or whatever other factors are contributing to someone’s insulin resistance. Avoid the triggering factors, and you avoid the problem. For example: If you go swimming in the ocean and get stung by a jellyfish, then take medication to counteract the poison, you are cured. But are you “cured” in the sense that you are immune to any and all future jellyfish stings? Are you impervious to jellyfish stings henceforth? No, of course not. Dr. Fung gave a similar example regarding antibiotics: If you develop a bacterial infection and take antibiotics, when the pathogenic organisms are gone, you are cured of the infection. But that doesn’t mean you are immune to getting infected again if you come into contact with the organism again.

I suspect it’s the same with frequently exceeding your individual carbohydrate tolerance and playing fast & loose with the other contributing factors: you are “in the clear” as long as you continue to avoid the triggering substances and/or behaviors. But that doesn’t mean IR isn’t reversed. Like alcoholism, by sticking to certain behaviors and avoiding others, we manage the condition. We keep it in check. And there’s nothing wrong with that. The fact that someone is an alcoholic is irrelevant if they abstain from alcohol. The fact that someone had a past diagnosis of T2D or insulin resistance is irrelevant if they control their diet and lifestyle, right now and going forward. For some people, maybe that means an ultra-low-carb diet. For others, maybe it means a moderate-carb diet as long as they’re getting good sleep and have time to relax and do lots of walking. Maybe it means berberine and chromium supplements, or occasional fasting.

So yes, I think we can “cure” T2D and IR, provided we keep on top of the things we think may have contributed to developing those conditions in the first place. And you know what? The nifty thing about all this is that we can keep on top of things. Even if we start to slide—maybe an 80/20 diet drifts precariously toward 60/40, or you’ve been gunning for a promotion at work or maybe are the parent of a newborn, and your stress levels are at an all-time high, while your quality sleep is at an all-time low—whatever the interfering circumstances, we can get back on track as soon as we choose to. Many of the presumed causes of IR are firmly within our control, and when we start to see or feel things getting out of whack—or objective lab values tell us they’re out of whack—we can take corrective measures immediately. It might take a few weeks or months for the effects of those measures to be reflected in the bloodwork, but we can take control as soon as we decide to. (Kind of like gaining weight: we don’t have to wait until we’re 50, 100, or 200 pounds overweight before we do something about it. You’d probably notice if you gained 20 or 30 pounds, and you can start doing something about it before it becomes 50 or 150.)

If I want to be a real stickler for semantics (and I usually do), then I guess we really are better off saying insulin resistance/T2D is “managed,” rather than cured. Or perhaps a better word is remission: “Thanks to a reduced-carbohydrate diet, more sleep, weightlifting, occasional fasting, and appropriate supplements, my type-2 diabetes is in remission.” I think that sounds pretty great, actually.

So no, none of us is “immune” to diabetes or insulin resistance. Frankly, just by being 21^st Century inhabitants of industrialized nations, I’d say we’re all “at risk.” Those of us who have never been officially diagnosed with T2D or insulin resistance are at just as much risk as those “in remission,” right? If they screw up their diet & lifestyle, those things come back, and if we screw up our diets & lifestyles, there’s a good chance we’ll develop those things, too. (Or, if not T2D, then maybe heart disease, or a stroke, or PCOS, or BPH, or one of the myriad other manifestations of insulin resistance that are not diagnosed via elevated blood glucose.)

Of course, the funny thing about this is, conventional doctors and dietitians will insist that IR & T2D are progressive and irreversible. They will say it’s not possible to put T2D into “remission,” because people only ever get worse and worse; no one ever gets better. But that’s only because those practitioners have never seen it stopped in its tracks, let alone reversed. Why not? Because they prescribe insulin and a high-carb, low-fat diet, to be eaten in the form of several small meals per day. (As we showed in part 5, this is an absolute metabolic disaster.) Like we covered in part 1, giving insulin to individuals who are hyperinsulinemic (most T2 diabetics) is pouring fuel on the fire. T2D is not an insulin deficiency, and in many ways, more insulin actually makes things worse. So, yes, IR is abso-tively, posi-lutely reversible. It does NOT need to be progressive, and tailspin into an unmanageable sh*tstorm of neuropathy, kidney failure, blindness, and amputation. Knowledgeable MDs, such as Ted Naiman, Rakesh “Rocky” Patel, Jeff Gerber, and Andreas Eenfeldt, reverse diabetes in their clinics all the time. They get their patients off medication, rather than on ever-increasing amounts of increasing numbers of drugs, and they do it with a low-carb high-fat diet, intermittent fasting, lifestyle recommendations, targeted supplementation, and, when necessary, yes, pharmaceutical medication. 

For the note I’d like to close on, I came across a comment on someone else’s blog recently that I thought was pretty awesome. My apologies for not remembering where I saw it, but the gist was something like this: we should stop using the phrase “pre-diabetes” and call it what it is: stage-1 diabetes. Don’t you agree that calling metabolic syndrome and pre-diabetes “stage 1 diabetes” would scare the shit out of wake people up? Hearing that they ARE DIABETIC, albeit in the early phase, would probably have people leaving doctors’ offices far more determined to do something about it than if they were simply told that their blood glucose, A1c, triglycerides, CRP, and uric acid are “kinda on the high-ish side,” and their HDL is “kinda on the low-ish side,” but they’re not diabetic yet, so just keep an eye on things. [AYFKM?!] Now, granted, if their physician is a total moron not well-versed in the science of carbohydrate reduction and ancestral health, they might walk away with nothing more than a semi-useless platitude about eating less and moving more—with emphasis that eating less pertains only to high-fat foods, because you absolutely must—MUST!—be sure to eat lots of whole grains. But we can hope that, in the age of the internet and social media, in looking for information to help dig themselves out of the hole they’re in, those stage-1 diabetics might stumble across the low-carb, Paleo, and/or Primal communities, and it just might save their lives.

And that, my friends, is the end of this brief foray into insulin! It’s time for me to work on some posts I’ve had on the backburner for a while. (Topics include: why fat loss doesn’t always happen like magic on a low-carb diet; the difference between being “in ketosis” and being fat-adapted, and why people need to STOP FREAKING OUT ABOUT THE COLOR OF THEIR KETOSTIX; and, of course, the cancer series.)

Do you have any questions about anything you’ve read here? Is there something I missed but you were hoping I’d cover? I can guarantee you I don’t have all the answers, and if there were some other aspect of this that I thought was essential to address (without turning this blog into a graduate seminar in biochemistry [like this one]), I’d have written about it. But I’m happy to take requests. If there are additional topics related to this that you’d like me to write about, let me know in the comments, or contact me directly at tuitnutrition [at] gmail [dot] com. Or you can send me a tweet! @TuitNutrition  

In the meantime, check out this post by Georgia Ede, MD. It's a fantastic primer on all this for newbies, and would be a great thing to show people in your life who are curious about this stuff.

P.S. Regarding tracking bloodwork: I’m not a doctor (and I don’t even play one on TV), but if I were one, I would try to avoid becoming alarmed based on any one-time snapshot. I think it’s more important to pay attention to how things are trending over time. This is especially true when it comes to prescribing side-effect riddled medication. This is completely different from the current standard of care, which would have everyone with a total cholesterol over 200mg/dL on statins (which we know are disasters), and similarly demands that other drugs be prescribed for other single measurements that are out of the normal range. Obviously, many of us in the LCHF/Paleo worlds are better educated in some of this stuff than the average patient. But we’re not immune to freaking out if something in our bloodwork surprises us. SO: what I said above, about keeping an eye on trigs, HDL, CRP, etc.? The same thing holds true. Don’t get overly alarmed if one or two things seem out of whack, particularly if they’ve been fine in the past and you haven’t made any dramatic changes (for the worse) to your diet & lifestyle. Some of the markers we keep an eye on—fasting glucose and blood pressure, for example—can be affected by things that happen just days—and sometimes minutes—before the blood is drawn. Did you get stuck in a traffic jam on the way to the lab or doctor’s office? Your BG could easily be 20 points higher than it would otherwise be. Did you have an intense workout the night before, or do you have a mild infection somewhere, or have you had dental work recently? Any of those things can temporarily elevate serum cholesterol. So yes, we should keep an eye on these things, but we should keep an eye on how they’re moving over time, and not scare ourselves silly over one marker at one point in time.

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.