October 27, 2015

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


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 8th 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.

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.


  1. GREAT post! One factor not considered is the factor of time. On our family's third generation of insulin resistance and PCOS I can see the effect of time. Photos of my mom as a kid and teen--very thin. By her mid twenties she became significantly obese. I was very thin until my late twenties, when I started fertility treatments to try to conceive. Obesity followed. I ate a very high glycemic diet in those days as it was considered "healthy" for a woman wanting to conceive.

    Now I am watching my 14 year old with insulin resistance and PCOS. She is very thin and her BMI is 18%, and some physicians have said that PCOS is "not a problem" unless you are trying to conceive. They don't take into consideration the metabolic underpinnings of the syndrome. That's why I insist on treatment NOW, before there is time for long standing hyperglycemia to cause the body to take protective measures. Hopefully her body will never have to make her obese to escape the effects of too much insulin.

    I've seen women with PCOS insist they don't have insulin metabolism issues because they are thin. Clearly they and their doctors are missing a piece of the puzzle. I often translate this in my head to think "you're not obese YET".

    1. PCOS isn't a problem unless you want to conceive? Well, I guess rheumatoid arthritis isn't a problem unless you want to button a shirt... ;D Hehheh...those wacky modern doctors; they just crack me up!

      As for the slim PCOS patients not being obese "yet," I agree -- most likely, the weight will come on, *eventually,* but even for those in whom it doesn't, what are the *other* consequences of dysregulated insulin and sex hormones? Irregular & painful periods? Facial hair? Acne? Hypertension? Yeah, sounds like a real party.

      It's interesting that your daughter has confirmed PCOS but is so slender. Stefani Ruper has written a lot about this -- the myriad different types of PCOS. I guess the thing is, it's a *syndrome,* with a cluster of symptoms, and is probably diagnosed via differential diagnosis (i.e., ruling out most other possibilities, basically process of elimination), not necessarily an actual "disease," with a single blood test that gives you a definite confirmation. (As in, say, identifying that someone has been infected with giardia.)

      As for the factor of time, yes. Even looking back at myself when I was younger, I was much slimmer than I thought I was in college. (If you'd asked me back then, I would most definitely have classified myself as overweight, and my goal in life was probably to lose 20 pounds, But now, of course, looking back at the very few pictures I'd allowed to have taken of me, I was gorgeous and not at all chubby. Not "skinny," certainly -- just don't have the genes for that -- but not the scale-tipping hippopotamus I *thought* I was.) And back then, I *lived* on lower-fat carbs. Breakfast cereal was my staple food, along with bagels, pasta and pretzels. That was over 15 years ago. Clearly, my insulin sensitivity was much higher then than it is now. I can only assume that the metabolic groundwork I was unknowingly laying all those years is the reason why I no longer have the "luxury" of eating those things without significant weight gain. As they say, "Youth is wasted on the young."

    2. My daughter would not have been diagnosed if I didn't recognize the signs and symptoms. Her doctor was reluctant to test her because she thought that there was no way my thin daughter could have PCOS. When the results came back, she called me personally to tell me I was right. My daughter's testosterone levels were through the roof--higher than my highest high ever was, blood glucose and insulin levels were high for her age and size. The question in my mind is how many other thin girls are NOT diagnosed. They are thrown on BCP's to regulate periods and treat acne, and don't find out there's a real problem until they try to get pregnant a decade later. And my poor daughter had to sit through the first pediatric endocrinologist (who had all the signs of PCOS herself!) telling her that the best way to treat PCOS was to lose weight. I wanted to slug this doctor for suggesting that to a THIN 13 year old--what was she thinking???? It was the only suggestion she had! Another doctor covering for my daughter's pediatrician said "she can't have PCOS, she's thin." How many cases are these Pedi's missing entirely???

  2. Hello Amy - nice posts - thanks for the reading material.

    Just in case you hadn't caught this brilliant piece yet - http://tinyurl.com/q8qmsha

    have a good one.

    1. Thanks for the heads up. Oh, lord. Apparently these people missed the studies that show *higher* cholesterol is protective later in life - not just for Alz, but for all-cause mortality. And that being said, the E4s do seem to get a raw deal no matter what they do. I'm not willing to say for sure that *everyone* (including E4s) benefits from higher cholesterol as they age, but many do. I know one group that benefits from old folks reducing their cholesterol -- statin drug manufacturers. :-/

  3. I had wondered whether the fat gain is some kind of protection mechanism, so it was good to see you put this subject into words. I've come across overweight people who have no problem with their cholesterol and not on any medications. They are eating a diet rich in carbs and processed foods, yet it has not impacted their lipid profile.
    It makes me wonder if the skinny on the outside, fat on the inside people are actually suffering because of this lack of protection mechanism, ie elevated levels of insulin will manifest itself in a much more harmful way such as heart disease, kidney damage etc.
    It would be interesting to do a long term study of "constitutionally thin" people against those who gain fat easily and see if there is a trend in terms of symptoms/blood work changes following a long term high carb/sugar diet.

    1. " They are eating a diet rich in carbs and processed foods, yet it has not impacted their lipid profile" Depends on what you consider "impacting" the lipid profile. They may have a lowish total cholesterol and low LDL, but sky high triglycerides and HDL's in the toilet. Most doctors wouldn't bat an eye at that profile, they'd think it's perfectly fine because total and LDL are low. And most patients blindly accept the conventional wisdom. "My doctor says my cholesterol is great." That's all they know.

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  5. Just love the content and style Amy , very much enjoyed the 'ITIS' series and looking forward to the one's on cancer.

    1. Thanks, Stuart. I've been having a bad day, and seeing your comment was probably the high point. :)
      The cancer series has been in full swing since last November. It's been a while since I've added to it, because there were things I was more excited to write about, but I'll get back to it in a few weeks. If you didn't know it was already up and running, you can check out the first post here, and each one ends with a link to the next installment: http://www.tuitnutrition.com/2014/11/metabolic-theory-cancer-intro.html

  6. This is an AWESOME series of posts!

    I discovered Joseph Kraft through Ivor Cummin's' interview on The Fat Emperor and realised he is yet another Person Of Clue which doctors have never heard of, along with John Yudkin, Peter Cleave, Weston A Price etc.

    "Diabetes in situ" exactly describes what happened to me, and a significant number of people in my family.

    There's a bimodal distribution in one side of the family: my mother lived to be 95, her cousins 88 and 91, her own mother 90. Mostly they die of CVD, basically from being completely worn out.

    Her brother died at 70 - massive heart attack. One of her uncles was the only known diagnosed diabetic - skinny and poorly controlled even on insulin, he underwent several amputations. Genealogical research has shown a number of other diabetics and a bunch of other people, mainly males, who died young of CVD (also a surprising number of children who, like my siblings, died before or soon after (premature) birth). I have no doubt they were all sufferers of "diabetes in situ".

    Most interesting is that some of the fatter folks had much better outcomes than us skinnies. My late aunt (88) oh actually my mother's cousin, was told at 80 she had the blood pressure of a 30 year old. When I was 30 I already had the BP of an 80 year old. Her slimmer fitter more active sister was the one who had the gallstones, dyslipidemia, hypertension and other metabolic defects - just like me.

    I suspect the reason is that the fatties were able to stash their lipids in fat cells, whereas us skinnies left them rattling around in the blood along with the high BG and high insulin. I've seen this variously called Metabolic Obesity, Skinny Fat and even Lipodystrophy Lite.

  7. part 2

    I think IR is an adaptive mechanism for the rapid storage of a glut of food - BUT this only works if the IR genes are then switched off so the stored fat can be metabolised. This is what modern "low fat" diets, especially when most of the fats remaining are Omega 6s, fail to do. IR also works at different tissues to partition food, but when it becomes chronic this also fails.

    In retrospect all my symptoms, going back to early childhood, were symptoms of diabetes and conditions "common in diabetics" but because I was skinny and obviously not Type 1, the decision was made to claim that they were either psychiatric in origin, or completely made up. I have never had a proper Phase 1 insulin response so my postprandial BG leapt up at the 1 hour mark, by which time the Phase 2 insulin had started to come online and knocked it down. By three or four hours the insulin had failed to shut off and my BG went through the floor, causing release not only of glucagon but also cortisol, epinephrine and norepinephrine. Probably IR between the pancreatic alpha and beta cells is a factor. This cycling between hyperglycemia and hypoglycemia with hyperinsulinemia went on most of my life. I've since met a small but significant number of people with the exact same syndrome - Reactive Hypoglycemia - from whom I learned the mechanism. Now doctors are not permitted to diagnose this and anyone who "claims" to suffer from RH must be diagnosed with a "neurotic condition" called Idiopathic Postprandial Syndrome - so doctors now have no knowledge of the mechanism and therefore no clue how to treat the condition.

    About half these cases have gone on to be diagnosed diabetic: the rest have remained "prediabetic" but IN ALL CASES by acting as if they were already diabetic and eating LCHF they have stopped the progression and reversed most of the symptoms. Hence diabetes in situ.

    Yet strangely I remained at low normal weight, UNTIL I met a dietician. She was intent on removing every scrap of fat from my diet and replacing it with more carbs, and when this had the expected effect of making my dyslipidemia even worse, raising my BP further and causing me to gain weight I was naturally accused of "failing to comply" with the diet. After all, avoiding cognitive dissonance is far more important than health!

    Eventually I met a half clueful doctor who gave me a GTT and told me I "just had a touch of prediabetes" - and gave me exactly the same high carb low fat diet I was already desperately trying to follow. I was specifically told that "we" don't like our patients testing their BG. So obviously I went straight out and bought a glucometer.

    In only a few weeks I had my BG nailed by low carbing, my BP came down significantly, my HDL DOUBLED and my trigs fell to 1/10 of what they were. Obviously the IR went away - trigs/HDL is a good surrogate for IR, CVD risk and also small dense LDL: mine went from nearly 7 to under 1 (UK numbers). Oh and I lost the 15 kg I had gained.

    1. Oh my gosh, Chris...sounds like you've been through the wringer! Good on you for finding LCHF and "correcting" things on your own. It's really a shame how ignorant many healthcare providers are. These are the "experts" we trust to steer us in the right direction, and sadly, so many of them are absolutely *clueless* when it comes to the very basics about human physiology and metabolism. That's why I try to write my blog in an educational way -- translate the textbook stuff into plain English we can all understand and make sense of. Because when we understand how the human body actually works, the types of foods we should be eating is fairly easy to understand. Maybe it's still difficult to pass up the donuts and cheesecake, but at least we understand the physiological consequences if we choose to indulge.

      It's madness what you went through -- especially with the dietitian! When it comes to getting ourselves well and *staying* that way to the best of our individual bodies' capacity, we're largely on our own. Conventional doctors and nutritionists have completely missed the boat.

  8. part 3

    I have maintained this for over a decade now. As a result I have now been told there was never anything wrong with me. Thus cognitive dissonance is not engaged. I have no doubt I could have done this any time in the previous five decades, which was WHY I was never told how to achieve it, and nor were any of my relatives. After all "everyone knows" that diabetes is caused by being fat, and being fat is caused by eating fat . . . and CVD is caused by "cholesterol" which is also caused by eating fat. Low fat diets are only an abject failure because people fail to adhere to them. Everyone who has the same result as me (or even better) is "just an anecdote" and everyone from you to Ron Krauss and Jeff Volek et al. are just "cranks on the internet". Oh and Aseem Malhotra, the latest in a long line!

    What is really scary is how totally not alone I am in all this. Worse still when I die (soon) from CVD this will never be blamed on the fifty years of high carb eating, high BG, high insulin, high IR, crap lipids etc. but on the last decade of "not eating enough starch".

    1. Haha, yes, all the "anecdotes!" I love Malhotra -- he seems to be getting far more mainstream press in the UK than any LCHF researchers and MDs ever get in the US. There are so many people who think they're "eating right" or think they'll be protected because they're following doctor's orders, but then how come they just get sicker and sicker? (If not more and more overweight?)

      Thanks for all the great comments, Chris! Glad you're liking these posts.

  9. Whn my mother was young there were no "epidemics" of obesity or diabetes (or a lot of other conditions) and "everyone knew" that to lose weight you cut starches, and that diabetics ate a low carb diet.

    This was still true when I was young. I'm realising now that when my generation dies out there will be no-one left who remembers a time when low fat was NOT standard operating procedure.

    One of our doctors was the size of a small building. She told me patronisingly that "everyone has to eat carbs or you have no energy" and that "diabetes in always progressive, it's the nature of the disease!"

    Strangely when she discovered she was "prediabetic" she decided to lose weight. I had hoped she had discovered low carb but no, she was doing 5:2. Anything to keep shovelling those "essential" carbs down her neck. Obvuously she had diabetes in situ for years.

    The doctor who is a "diabetes specialist" told me she expected that by now I would be fully diabetic and on "at least two" drugs. Many (most?) diabetics are told to eat a low fat diet and expect to be on insulin within five - ten years. Since ACCORD many well controlled diabetics are told to "stop it at once" and increase their A1c, and many doctors now deregister their diabetics, even Type 1s on occasion, if they achieve A1c below 6%.

    Quote from a nurse "if you test your blood you will damage your fingers and then you won't be able to read Braille when you go blind!" There's just soooo much wrong with that statement I don't know where to start!

    Most dieticians here are overweight too. Yet they give Malhotra no end of stick. His main job is fixing their mistakes! Soon perhaps he will be operating on them.

    I see things moving in both directions at once. There are thousands of patients making huge improvements in their health - but there need to be MILLIONS to make a difference. There are probably now several dozen clueful doctors and dieticians - but there need to be thousands. There's an increasing mountain of evidence on PubMed, not a little of which backs up and develops stuff that was known in the past and since ignored - but it is concealed from doctors by what is ironically called "Evidence Based Medicine". Currently it looks as if The Establishment is fighting back - after all telling people to eat the most profitable diet and then prescribing the most profitable drugs as an antidote is a Big Win for everyone, except the patients.

    All power to you and the other bloggers for your work in disseminating Clue.

  10. Well I made it this far and I am very impressed. I had to find my own way to 6 by the way and 7 and 8 don't seem to be up but this an excellent presentation.

    I actually eat just one full meal a day and one snack and have found that regimen to be by far the best approach for me. We eat way too habitually and it's also very habit forming, if the body gets accustomed to a certain amount of feedings it will coerce you, or rather the hormones that drive this will :)

    T2 is really all about broken signaling and you have done a nice job looking at the two main influencers here, insulin and glucagon. I feel that diabetes comes down to just one of them though, glucagon. We owe a huge debt to Roger Unger here, I've referred to him on my site as the Einstein of diabetes research, and I don't feel that's an exaggeration. We would probably still be in the dark ages if not for his breakthrough work, although come to think of it just about everyone is indeed stuck back in the dark ages, at least when it comes to the practice of treating this disease. They prefer the dark though as too much light exposes their ineptitude.

    The big question from here is, what do we do about this? I brought this up in a comment earlier but now that we're at least getting to the end, it does need to be asked. This is way bigger than just being handicapped as far as glucose tolerance goes. We know that's just a symptom not a cause. I'm all for dietary management but at the same time we can't fool ourselves into thinking this is a solution, it's just a compensatory mechanism, in spite of it often being a necessary one.

    I've moved away from focusing on insulin so much over the last while, especially lately, glucagon is obviously the problem and excess insulin clearly plays a big role in its over secretion over time, and especially its role in lipogenesis and lipotoxicity. So reducing insulin is needed, but we also need to repair the damage so to speak, and also address other issues that may be going on, other means of broken signaling. I think fat plays a big role in this, especially the accumulation of fat in cells, we crow with pride when we can clear some glucose out of the blood but don't realize that this actually does harm, but what's even more significant is the fact that insulin drives both fat and glucose into the blood.

    So the two damaging mechanisms here are, guess what, glucotoxicity and lipotoxicity. We're back to excess insulin now with a vengeance, but again, reducing the insult is just part of it.

    Conventional medicine on the other hand just wants to escalate our insulin toxicity, good night!

    Anyway this comment is long enough, thanks for the very good article and thanks for helping spread the truth about all of this! :)

    1. Thanks for the insightful comments, Ken. Are you a physician? You sound like one. (And a knowledgeable one, at that.) You are correct -- parts 7 & 8 haven't been posted yet. Still writing them. ;-) Part 7 is still looking at body weight/body fat regulation in relation to insulin, but the 8th and final installment will address what you've mentioned here -- the *other* interventions that are likely necessary to correct/reverse insulin resistance, besides just a low-carb diet and possibly fasting/reducing feeding frequency. There's a lot more to it than that. It would be nice if it were as simple as going to a LCHF diet, wouldn't it? And that works very well for many people out there. Some don't even need to go full-on low-carb, but can very impressively improve & normalize their blood markers simply by adopting a Paleo or Primal diet, but not one that is expressly very low in carbohydrate. Other people need a multi-pronged approach, depending on the severity and complexity of their IR.

    2. I'm not a physician, just a diabetic looking to learn more about our disease, and there's lots to learn. Someone gave me a link to this and I tell people the same thing on my site and I've been trying to wake people up to this for quite a while now. This isn't a popular view of course, the idea that the conventional approach to diabetes has it so wrong. A lot of diabetics seem to have some real limitations on how far outside the box they will go, they may say well these people are clueless where it comes to diet but aside from that they are doctors so they must otherwise know what they are doing. I've never had that problem though :)

      I haven't read the last 2 parts yet but I am looking forward to it, I came back here to see if they were up yet.

      Without peeking, I think that while diet can obviously be very helpful, it of course doesn't get at the root of the problem, although it can limit the damage. So there are some positive changes that we can make, the usual lifestyle things, and with some of us that may be enough, although this is still a managed state and not necessarily a resolved one. When we compare diabetics with non diabetics though on the same diet there are some things that are wrong here and it's not the usual suspects, it's a disease of hormonal imbalance and there's definitely more to it than just the excess of the pancreatic hormones, or we'd be cured when we just normalize them for a while.

      I do horribly on low carb by the way and let me tell you that's made things more challenging and interesting, so when diet doesn't help and there's no way I'm touching any of their meds, well you're pretty much left to your own resources. So it's not that my diet is unrestricted but strangely enough I ended up back to what I was eating when my A1C was in the 11's, which I actually do best on now in conjunction with the stuff I take, so that's as close as taking diet right out of the picture as you can get I guess :)

      So getting back to the real pathology, this really comes down to controlling hepatic glucose production and glucagon obviously plays a big part in that, I think leptin resistance is big as well and we know what happens from that, leptin also regulates glucagon, there's lots left to think about that's for sure :) I've also had some success with things that increase AMPK, in particular with berberine and gynostemma, working on controlling lipogenesis, I think that bergamot is great for this by the way, along with the bunch of other things I take. Keep up the great work and it takes a lot to impress me but this really has :)

  11. Love these posts! Ty for writing! If I hadn't started reading and thinking, I'm sure I would be dead by now. Truly no exaggeration. New book out by Doug McGuff called Primal Prescription (foreword by MSission) is an awesome read and helps explain why there are so few doctors willing and able to investigate and recommend new protocols. Thank God for the Internet and smart, caring and generous writers such as yourself. Xo. Ann

    1. Thanks, Ann! Page views have dropped dramatically between the first post and number six here, so it's nice to know there are still people out there reading it and finding it helpful. :)

  12. Strong work Amy. The answer lies between the communication signals of adiponectin and leptin. Look there and you'll see what I've been seeing for 10 years.

    1. Thanks for reading! The learning is absolutely endless. I know very little about leptin & adiponectin. When you have even the smallest appreciation for how complex this all is, "eat less, move more" and "calories in, calories out" become almost laughably simplistic and inadequate.

  13. Regarding BMI, this has been a peeve of mine for a long time. I was in the Air Force too, and when I was at Officer Training School in '86 I was badgered about my weight. I was 5' 9.5" 190ish and quite lean and muscular. But they blindly looked at their height vs. weight charts (essentially BMI in a slightly different form) and told me I needed to lose some weight. I was a bit flabbergasted, to say the least.

    That continued when I got to navigator training a few months later. I had to bite my tongue as I stood in front of my squadron commander in my blues being told that I needed to lose weight, despite very obviously being very fit. He lectured me about how I should become a runner like him. Hated that guy. I did drop a few pounds as a result of not doing much weight lifting, so I kept them off my back. But it was my first look at a blind and stupid bureaucracy, and some pinheads like that commander who enabled it.

    They (the bureaucrats in the Pentagon) got better about it later in my career, as I'm sure you're aware of with your time in service. (I eventually went thru pilot training and retired as an O-5, after about 22 years.)

    Someone finally opened their eyes to the obvious and realized that some folks didn't fit the mold and should be tested for actual body composition instead being berated for being "overweight"; duh. In the meantime a lot of good people had to tell folks like me that there was nothing they could do about the rules even though they were beyond stupid (I was one of them later; ugh). I'm sure that some even got drummed out for their ostensible overweight condition. Although there were also a lot of actually overweight senior officers and NCOs who weren't affected. Gotta love that fair and even treatment and universality of rules, eh?

    Anyway, that always hits a nerve with me, if you couldn't tell. :-)

    Love your blog and I'm still working my way thru (and I still have to read your AD book, which is on my Kindle, waiting for me). Keep up the great work.

    1. Nobody takes issue with BMI more than I do! (Hence why I write about it so much and so forcefully.) I literally starved myself down to my "max weight" to pass the MEPS before going to basic training. It was *ridiculous,* because I had run a friggin' marathon and worked out a ton, so it's not exactly like I was out of shape. (If anything, that was my final wakeup call that exercise is NOT really all that great for fat loss. For cardiovascular conditioning, sure, but not for improving body comp.) Don't even get me started. The funny thing is, the military as a whole, I think, is starting to see that the country's dietary guidelines are GARBAGE, because there are so few young kids who meet the standards anymore, be it for weight or fitness. When so many millions of *kids* are overweight or obese, even the people who are conventional all the way have to start questioning what the heck is going on.

      I really liked some aspects of the military, but there are others that I don't miss for a second. Dumbass rules about height & weight charts are certainly one. ;-)

      Thanks for reading!

    2. BTW -- what did you fly? (I was an airborne linguist...Rivet Joint/RC-135, but we worked in many other [smaller] platforms in Iraq.)

    3. I spent about 3 yrs as a navigator on the KC-135 before going to pilot training. I was a pilot on the KC-10 (tanker and airlift) and also did some time as a instructor pilot for new pilots in the T-1; 3 years in beautiful Del Rio, TX :-)

      And I spent about 7 years at Scott AFB working in the TACC - Tanker Airlift Control Center.