September 17, 2015

ITIS -- It's the Insulin, Stupid (pt 1 of 8)






As you can imagine, I spend a lot of time educating myself about health, nutrition, and food. Whether I’m reading papers in the scientific and medical literature, keeping up with posts by intelligent bloggers, or learning more about human anatomy and physiology, a good portion of my week is devoted to ensuring that, as a nutritionist and blogger, I know what I’m talking about, and I provide my clients and readers with reliable information. There’s so much hashing and rehashing of old news in this field, and you can’t walk five feet without bumping into a dead horse that’s been beaten over and over—and over—again. So it isn’t often that something comes along that really blows my mind. (Like this. I am still fascinated by this.) Once in a while, something that’s actually very simple, and which should be totally obvious, blows my mind, if only because it makes me think about things in ways Id never considered before.

With the help of some very cool people in the low-carb, high-fat (LCHF) world, I have been introduced to a new concept—well, new to me, but certainly not “new” at all—and I’d like to share it with you. There’s a lot to talk about, but the overall theme boils down to this: by focusing almost exclusively on blood glucose, the medical and nutrition professions have been missing the boat on a much larger, much more insidious problem: insulin.

As you know, blood glucose and insulin are intimately related. It’s hard to discuss one without the other. But when was the last time your basic bloodwork panel included a measurement of your insulin levels? Have you ever had a doctor look at anything but your fasting glucose and maybe your A1c if (s)he was concerned about your blood sugar management? (Never mind that the A1c isn’t even included in a typical blood panel. You often have to specifically request it.) If you’ve ever been the victim of experienced an oral glucose tolerance test (OGTT), did your doctor measure your insulin levels, or only your blood glucose?

With a single-minded focus on glucose, glucose, glucose, we have distracted ourselves from what is really driving the ship in type 2 diabetes (T2D), metabolic syndrome, Alzheimers disease, and many more conditions that we’ll explore in detail in part 2 of this series. Hence, the title of this post.


A New Rediscovered Perspective


The suffix “--itis” is used to indicate inflammation. Arthritis? Inflammation of the joints. Tonsillitis? Inflammation of the tonsils. Bronchitis? Inflammation of the bronchial tubes. You get my point. But here, let’s use ITIS as an abbreviation to keep us grounded in the subject at hand: it’s the insulin, stupid.

The brilliant doctor who deserves credit for this reawakening to the importance of insulin over glucose, is Joseph Kraft. I am convinced that Dr. Kraft is worthy of a spot on the ever-growing list of health and nutrition pioneers who were way ahead of their time, and who were intelligent, insightful, and courageous enough to see things from a perspective quite different from those of their colleagues and the prevailing wisdom of their time. These people—all of whom are/were MDs or PhDs—were mocked, ridiculed, scorned, and darn near made laughingstocks, whether in academia, industry, medicine, or the public eye, but their work has since been vindicated time and again: John Yudkin, Robert AtkinsGerald Reaven, Mary Enig, Fred Kummerow, Otto Warburg, and Thomas Seyfried. And those are just the ones I can think of off the top of my head!

So yeah. Dr. Kraft saw something happening among thousands upon thousands of patients and study participants. What he saw was something different from what others were seeing, mostly because they weren’t looking for it. What he saw was something big.

Before we talk about what, exactly, Dr. Kraft saw, I’d like to give credit where credit is due and express my sincere thanks to Ivor Cummins, the man behind the little-known and ridiculously under-appreciated blog, The Fat Emperor. Ivor stumbled upon Dr. Kraft’s work a while back and has been sharing his critical messages far and wide. (I feel almost like Ivor is at the helm of the Titanic, and he can see the iceberg way ahead of time. He’s flailing his arms and shouting like mad to get the captain to turn the ship around, but everyone’s too busy partying to notice. The industrialized world is already sinking to the bottom of the ocean when it comes to disastrous dietary advice, but it’s never too late. Maybe, just maybe, by getting this information out as much as we can, we can toss a few people—and doctors!—some life jackets.) Also, if I’m not mistaken, Ivor found this Kraft stuff via Grant Schofield, a professor of public health in New Zealand, who has been trying to bring Dr. Kraft’s message to the forefront since 2013.

Ivor is the one who’s spearheading the revival of Dr. Kraft’s findings, but he’s enlisted the help of two quite awesome LCHF & keto-friendly MDs: Theodore Naiman, whose practice is in Seattle, and Jeffry Gerber, a.k.a. “Denver’s Diet Doctor.” He is also shining a well-deserved spotlight on the work of Dr. Kenneth Brookler, who was among the first physicians to recognize the importance of Kraft’s work. (More on him in part 2.)

Okay. Now that we’ve gotten through the preliminaries, let’s jump into this.

We’ll start with the key idea, and then break it down into the details.

The way type-2 diabetes (T2D) is typically diagnosed means that several thousand, if not several million, people with raging carbohydrate intolerance fly under the radar.

T2D is typically diagnosed through a combination of elevated fasting blood glucose (FBG), elevated hemoglobin A1c, and “failure” upon administration of an OGTT. And no one would argue that chronically elevated glucose and a high A1c do not indicate a diabetic state. But it’s not the only game in town, folks.

How could millions of people with diabetic profiles be missed? With all our fancy-schmancy diagnostic tools—not to mention pharmaceutical companies champing at the bit to increase their customer base and medicate as many people as humanly possible [for better or worse], how is it that so many can be misdiagnosed, or not diagnosed at all? Well, it works like this:

In many cases, A1c and fasting blood glucose are the last things to rise. If your A1c and FBG are elevated, then your pancreas has already been working overtime for a while, most likely years, but quite possibly decades. See, FBG will only be elevated after a significant amount of your bodys tissues are already insulin resistant. If they were not insulin resistant—that is, if they were sensitive to the presence of insulin, then fasting BG wouldn’t be high. The cells would respond to insulin by taking the glucose in in a timely manner. This would keep your A1c in the normal range as well, since we understand A1c to be a general indicator of your average blood glucose during the past 3-4 months. So if these numbers are high, your cells have already lost the ability to respond effectively to insulin.

When it comes to identifying diabetics, pre-diabetics, and those at risk for developing diabetes in the near future, the thing that Dr. Kraft found—and that no one else seemed to care much about—is that IT’S THE INSULIN, STUPID. Kraft administered over 10,000 oral glucose tolerance tests, but in addition to measuring blood glucose, he measured insulin levels as well. And instead of doing the standard OGTT, which concludes after just two hours, Dr. Kraft extended his tests for five hours. This allowed him to see how long it took people’s glucose and insulin levels to return to normal. This is a much bigger deal than it might seem.

What Kraft discovered was so astounding, yet so simple, and so logical, that he ended up writing a book about it. (A book that pretty much no one had ever heard of until Ivor started publicizing all this. I haven’t read it yet, myself, but you can bet your sweet patootie I’ll have a review of it after I do.)


No, really, it’s the insulin


Here’s the gist of what he discovered: some people will do an OGTT and their glucose and insulin levels are just peachy. Great! No problem. However, these metabolic ninjas are a very, very small minority of the population. The vast majority of people Kraft tested were hyperinsulinemic to some degree, even though their blood glucose was “normal.” Here’s how this works: Over the course of the OGTT with insulin assay, Kraft was able to see that thousands of people’s blood glucose returned to normal nice & quickly only because of dangerously elevated insulin. Being that his tests ran for five hours, rather than two, Kraft could see there were a few different patterns underlying this phenomenon, but all of them indicated abnormally elevated insulin.

Dr. Naiman has put together some handy graphics that illustrate the basics. He has given me permission to reproduce them here, so we can talk about what these patterns mean:


  • Pattern 1: This is the aforementioned metabolic ninja. In response to a carbohydrate load, the insulin level rises quickly, but moderately, and it comes back down relatively quickly. By about 3 hours later, they’re back to baseline.
  • Pattern 2: In response to a carbohydrate load, the insulin level rises quickly, and it rises higher than that for the “normal” person in pattern 1. And besides just rising higher, it also takes longer to come back down, not returning to baseline until about 4-5 hours after. Insulin is elevated higher than normal, and it remains elevated for a prolonged amount of time. This pattern indicates hyperinsulinemia.
  • Pattern 3: In response to a carbohydrate load, the insulin rises even higher than the already hyperinsulinemic example in pattern 2, but it doesn’t reach its peak until later. This is a delayed peak, and it takes even longer to come back to baseline. (And don’t forget that this person’s baseline insulin is actually elevated anyway, so their “normal” is already higher than a healthy person’s.) It goes without saying that this pattern also represents hyperinsulinemia, but it’s even worse than pattern 2.
  • Pattern 4: In this pattern, the baseline insulin level is already dramatically elevated. This person’s cells are awash in insulin all the time, not just in response to a carbohydrate load. Upon consuming a bolus of carbohydrate, this person’s insulin level skyrockets, it takes a very long time to come back down, and even when it does finally come down, it only comes down to the baseline, which, as I just said, is abnormally elevated. This person is—to use the scientific term—in deep hyperinsulinemic doo-doo.

 In fact, all three patterns that indicate hyperinsulinemia are in deep doo-doo; the only difference is how deep.

What’s pattern 5? Good question. In pattern 5, there’s very little insulin in the blood, and even after a carbohydrate load, the insulin level hardly budges. This suggests type-1 diabetes, which is NOT WHAT I’M TALKING ABOUT HERE. Please know that when I say “diabetes” throughout this post, I am referring only to type 2.

Okay. Back to patterns 2-4. Using the hyperinsulinemia as a defining signature, Dr. Kraft called all of these troublesome responses “occult diabetes,” or diabetes in situ. (Plain English: hidden diabetes. We can also think of it as diabetes brewing under the surface. Its not the same as “pre-diabetes, since that diagnosis requires blood glucose to already be slightly elevated. This is like pre-pre-diabetes.) According to Dr. Kraft’s data (graciously provided by Ivor), 8138 people out of 10,829—that’s over 75%—with a normal OGTT exhibited one of the hyperinsulinemic patterns. Moreover, 93% of the total 10,829 had normal fasting BG. Do you see the problem here? Extrapolating these numbers to the population as a whole, when we use only fasting BG and an OGTT to diagnose diabetes, we miss millions of folks who have diabetes in situ. Out of Kraft’s 10,829 subjects through the years, only 2,223 (20%) with a normal OGTT exhibited the pattern 1/metabolic ninja response. Twenty percent. One-fifth. That means approximately four-fifths (80%!!) of the population has some degree of hyperinsulinemia, or diabetes in-situ. Four out of five people! (Minus a few who have type 1 diabetes.) They are diabetic; it is only thanks to prolonged elevated insulin that their glucose levels remain normal. But let there be no mistake: they are diabetic. (Or, if you insist on total linguistic precision, they are carbohydrate intolerant and hyperinsulinemic, and they will likely be diabetic soon; all that’s left to do is wait until their FBG and A1c are high enough for an MD to give the official diagnosis. But even if they remain in a hyperinsulinemic state without an eventual rise in FBG & A1c, which is totally possible, they are still in serious physiological trouble. More on this next time.)

You can see this represented visually, with thanks once again to Dr. Naiman:



So the fasting BG is normal, and due to sky-high insulin, the A1c might be normal, too. But how long will that be the case? The higher levels of insulin and the delayed return to baseline upon ingestion of a carbohydrate bolus suggests that patterns 2-4 are already somewhat insulin resistant. That is, cells have to be bathed in more insulin, for a longer period of time, before they respond by sucking some glucose out of the bloodstream. How long will it be before the cells stop sucking the glucose out of the blood, and the BG is elevated constantly? How long before this situation finally results—which it will, eventually—in elevated fasting BG, and elevated A1c? Months? Years? Decades? I don’t know, and I don’t know if anyone knows, for sure. But this will happen at some point—provided the affected individual continues with the same diet and lifestyle practices that created this situation in the first place. But do remember: A1c and fasting BG are the last things that will rise indicating carbohydrate intolerance. (In part 2, we’ll look at some other blood markers that might help us keep better tabs on how our insulin sensitivity is holding up.)

Check out this graphic Ivor put together, based on Kraft’s data. 

(Click here for a larger version.)


As you can see, an elevated fasting blood glucose identified only 25% of people who had hidden diabetes/diabetes in-situ. OGTTs identified only about 40% of people with diabetes, while in fact, closer to 78% of people with a “normal” OGTT result had diabetes in-situ. Employing Kraft’s 5-hour OGTT with insulin assay seems a much more effective way of identifying those who already have hidden diabetes, as well as those at high risk. (Even if you’re not comfortable calling hyperinsulinemia hidden diabetes/diabetes in-situ, and you’d rather reserve the diabetes diagnosis only for people whose A1c and fasting BG are elevated, I’m sure you can still see the clinical utility in employing Kraft’s strategy. If you wanted to prevent as many as possible cases of full-blown regular ol’ hyperglycemic diabetes, then you would use elevated insulin as an early warning sign, and you would take it as a loud & clear message to change your diet & lifestyle, or recommend changes to your patients/clients. At the risk of giving them any ideas, I have to say, if I ran a pharmaceutical company, this would be music to my ears, because we could use Kraft’s test to identify millions of potential new lifelong customers for insulin-lowering drugs. Of course, we could also tell them to go on a freaking low-carb diet, but then we wouldn’t make any money selling our drugs, so mum’s the word on that! If anything, though, you have to think that Kraft's insulin assay might be what finally wakes the conventional medical establishment up to the idea that MORE INSULIN IS THE LAST THING MOST T2 DIABETICS NEED. They are not suffering from an insulin deficiency.)


If your A1c and fasting glucose are normal,
are you in the clear?


If your A1c and fasting BG are “normal,” ask yourself why they’re normal. Should they be normal? Is it logical that theyre normal? If youre eating a low-ish carbohydrate diet, exercising regularly to maintain the insulin sensitivity of your muscle cells, getting sufficient sleep, and taking time to relax, decompress, and reduce your stress levels, then okay, yeah. Your numbers are probably normal because everything’s trucking along just fine. But if you’ve spent several years eating a lot of junk, being sedentary, stressed to the max, and barely getting through the day as a sleep-deprived zombie, then you might very well fall under one of Dr. Kraft’s hyperinsulinemic patterns. There’s really only one reason why your numbers aren't elevated. So, congratulations, you have diabetes in-situ. You (and likely also your doctor) have been fooled into thinking everything’s been hunky-dory all these years, because your A1c and fasting BG were normal. (Mind you, though, not everything was normal. Most likely, over the years, your triglycerides were creeping up, your HDL was sinking down, and your lipoprotein particle size was shifting toward an unfavorable pattern, but your doctor didn't know anything about particle size testing, nor did they have any clue these issues are related to carbohydrate intolerance, and, rather than advise you to adopt a low-carb diet, [s]he likely told you to avoid butter, egg yolks, and red meat.)

But those glucose markers are normal only because something metabolically insidious is brewing under the surface. By secreting inordinate amounts of insulin, your body is doing its best to prevent the damage that would accrue with chronically elevated glucose. But it can only do this for so long before things really go awry.  

In part 2, we’ll look at what happens when things do go awry, and we’ll explore some of the consequences of elevated glucose and insulin. Some of them will be old news to you, but some will be surprising.

Whew! Quite a long post, I know. Thanks for hanging in there!

In the meantime, if you’d like to explore this diabetes in-situ thing further—and who wouldn’t?—I encourage you to check out the video where Ivor interviewed Dr. Kraft, so you can hear things directly from the source. It’s mostly the two men talking, which is fascinating all by itself, but there are also a couple of great slides explaining the different patterns of hyperinsulinemia Kraft identified: Kraft – Father of the Insulin Assay

Also, I’d be remiss if I didn’t acknowledge the awesome work Dr. Jason Fung is doing in explaining the role of insulin in exacerbating, rather than ameliorating, the pathology of type 2 diabetes. Great video here: The Two Big Lies of Type 2 Diabetes.



**Continue to part 2 in this insulin series:  http://www.tuitnutrition.com/2015/09/its-the-insulin-2.html






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.

24 comments:

  1. Thanks, Amy, for helping get out Dr. Kraft's message. I was quite blown away when I watched the interview with him, and am looking forward to learning more.

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    1. :) Me too, haha! The more I learn, the less I know...

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  2. Great Post! I'm looking forward to the next installment. I have a hereditary form of PCOS, which causes me to be highly insulin resistant. My 14 year old daughter is the same--her BMI is 18%, so clearly obesity is NOT the cause of the PCOS/Metabolic syndrome (and I was thin with severe symptoms at her age, too).

    I had a great endocrinologist who routinely measured my fasting insulin and C-peptide and recommended both a low carb diet and Metformin (resulting in reversal of PCOS symptoms which is how my daughter came to be ;o).

    Now we get our medical care through Kaiser HMO. You would think they would want to track insulin levels in two individuals (my daughter and me) whom they are treating for severe insulin resistance, but NOPE. "We don't test insulin levels because they don't tell us anything we need to know." Sigh . . .

    The true problem is that if all that population was recognized to have "diabetes in situ" things would be WORSE, not better, because more people would be told to eat more carbs and limit fat, and that a pill can be used to cover a bad diet. Until the foundation is laid for the benefit of carbohydrate limitation and the safety of real fats, identifying all those people doesn't accomplish much. I know it sounds cynical, but I believe that's true.

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    1. Oy! Right...there are plenty of health issues that have hyperinsulinemia as their underlying cause -- in LEAN people as well as the overweight. As this "obesity ---> diabetes" connection is a personal pet peeve of mine, I'm going to talk about the issue of weight just a tiny bit in part 2, and it will be a big focus in part 3. It's really a shame that the medical establishment hasn't caught on to this yet. There's a very automatic reaction to assume someone who is thinner is healthier than someone who's chubby, but what's going on *inside* often tells a very different story. Sounds like your endo knew what (s)he was doing, though. Maybe all hope is not lost!

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  3. Thank you. Great post. Anything that helps to get this understanding through the 'diabetes fog' is very helpful.

    I am exceedingly IR, undoubtedly due to the injected insulin I've been prescribed over the last 12 years. Wish I could sue....

    Seeing Jason Fung's presentation on Youtube was a lightbulb moment. I am trying (on my own, as the UK Medical system is a wasteland when it comes to Ketogenic dieting or fasting. I've been trying Keto but the merest sniff of carb sends my BG into orbit, so I suspect extended fasting may be my only option. Bit scared to do it without support though. I've done 2 x 4 days & a nine-day fast. Would have gone longer than that but got very weak so had to break it. That may have been a transition thing to just go to bed and allow it to pass, but I didn't know who to ask.

    It's very frustrating......

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    1. I've been learning a lot from Dr. Fung, myself. It really gives me hope when there are more and more MDs embracing lower-carb approaches. (Even if not keto or super LCHF.) Honestly, I don't know how most of them can deny what's as plain as day all around us. I've never done an extended fast. Longest was about 3 days, and it was sort of unintentional. (Wacky story there!) I think you'll do great. Not sure you would need to do a long fast, but if you want to try one, I would recommend listening to the interview Jimmy Moore did with Dr. Fung today: https://vimeo.com/139612930 Lots of good tips about salt, broth, electrolytes, exercise, etc.

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    2. There's a group on FaceBook that may interest you called "Principia Lenta" that is basically a support group for fasting with ketosis. I may not have explained it well, but it's a closed group so you have to ask to join. They're very supportive, though, which is immensely helpful if you have no real-life support.

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    3. I watched Jimmy's interview with Jason Fung and it was very good. He did a good one with Andreas Eenfeldt too. Basically, the point is, high insulin leads to IR and that leads to high sugars, and you can't treat hyperinsulinemia with more insulin. It's so glaringly obvious but medicine and Pharma always has to do everything the wrong way around. Sigh.

      Thanks Denise. Yes I have come across Principia Lenta, although not joined yet. I am in the Principia Carnivora group though. I am awaiting a ketone monitor so when that arrives I will be able to dive into fasting. I have been off the insulin for a month and it does look as though my BG is trending very slowly downwards. I would probably not be able to get into proper ketosis until my levels are a lot nearer normal. At the moment I am trying a 3 days on, 3 days off protocol between fasting and zero carb.

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  4. Fantastic job by AB, bringing to light Joseph Kraft's work on insulin testing to diagnose diabetes. It is surreal to see a clearly well intentioned health (I swore I will never use the m-word again, medicine...) specialist come down hard on the stubborness of his colleagues in the m-word world. As well noted by Joe Kraft, knowledge and progress on health issues will not come via blindfolded docs, but by enlightenment of the public. Prodigious health writers such as AB have a huge responsibility to help get this going.

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    1. Obrigada meu amigo! You're right -- the majority of healthcare professionals out there just don't "get it," and it could take decades more before they do. It's up to us to do this as a grassroots education movement.

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    1. :) We could say I'm just returning the favor, considering everything I've learned from you!

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  6. Thank you very much, Amy. As always, you give us a very thought-provoking blog. You are so right – “it’s the insulin, stupid.” Nevertheless, it is generally assumed that it is pigging out on sugars and starches that causes type-2 diabetes, not insulin. As you point out from your insightful research, there may be untold numbers of people who live in a dangerous pre-diabetic state (or diabetes in situ?) with unrecognized elevated insulin levels.

    This extremely important revelation of the magnitude of unrecognized high insulin levels in the general population, absent overt diabetes, begs the question of why? It is assumed to be due to insulin resistance. Might there be other causes? For example, we have been concerned about the effect of magnesium deficiency on insulin sensitivity/resistance. Carol Dean writes in the 2003 edition of The Miracle of Magnesium, that magnesium deficiency significantly increases the harmful effects of type-2 diabetes. In magnesium deficiency, “cells cannot accept glucose from the insulin because the body’s cells require magnesium to open their door to the glucose that is delivered by insulin.” You have two more installments on this subject, Amy, so you may have already covered this matter.

    We are also very pleased by another most important point you made. It was that “more insulin is the last thing most type-2 diabetics need.” This was in reference to use of insulin injections for treatment of insulin resistance. The reason that this extremely important truth is generally lost to medical and nutritional sciences is because of their lack of acquaintance (or interest) with the biochemistry and functions of the lipid mediator endpoints of the EFAs. The latter information is critical to an understanding of the relationship between diet and human health/disease.

    A brief description of why more insulin is detrimental is as follows: High insulin levels stimulate the enzyme delta-5 desaturase, which in turn stimulates the synthesis of arachidonic acid. In the absence of sufficient dietary omega-3 fatty acids (which is the usual situation with the modern American diet) to counter the increased arachidonic acid formed, proinflammatory prostaglandins from arachidonic acid add to the body’s burden of and damage from chronic inflammation. This might be classed as a harmful unintended consequence.

    Looking forward to your next installments A & F

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    1. Great points, as always. I wasn't going to talk about nutrient deficiencies or the EFA pathways, but maybe I'll tackle that at some point in the future. There are definitely nutrients that play a role in proper glucose handling & insulin signaling. Chromium, obviously, and yes, magnesium. And Mg deficiency is *rampant* in America. (Same with chromium, actually.) I didn't know Mg was required for proper functioning of the insulin receptor, but I knew Mg plays at least some role in CHO metabolism, since it's required for no less than 6 steps of glycolysis.

      What you've said about the role of insulin in the EFA pathway is new to me. (Guess I need to read that chapter in your book in detail!) D-5-D is required for the n-3 pathway as well as the n-6, so in a way, a rise in insulin would be good for the n-3 pathway, but I can see how in today's hugely skewed n-6/n-3 ratio, in the absence of adequate n-3, chronically elevated insulin would lean things heavily toward the inflammatory side.

      In some ways, this all so incredibly complex, yet, when we look at the underlying biochemistry, it's actually very simple!

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    2. Thank you Alice & Fred! I always love your comments and shared knowledge.

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  7. When the very foundation of the Western diet - the three staples, flour, sugar, and milk - are denatured, stripped of some or all of their essential nutrients, it's no wonder diabetes and other diseases are rampant. Denatured, fractionated food robs the body of far more than it gives. It is 'pseudo-food', a hologram, tasting, smelling and looking like food, yet not providing the body with the nutritional elements needed for its digestion and assimilation into the body. Unlike complete, unprocessed, unmeddled-with food it becomes harmful rather than beneficial.....

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    1. Absolutely true! And even the "fortified" grains are only fortified with a handful of vitamins & minerals -- just the ones deemed important enough by the powers that be. Micronutrient deficiencies are *rampant* in the U.S. Regarding ones that may play at least some causal role (however small) in the tsunami of T2 diabetes, insulin resistance, metabolic syndrome, right off the top of my head, I would say chromium and magnesium. No doubt in my mind.

      And you're right -- it's not just that many of the "foods" (and I use the term loosely!) most commonly consumed in the U.S. are nutritionally empty; it's actually *worse* than that. They *steal* nutrients from the rest of the body just to be processed/metabolized! For example, magnesium is required in at least 6 steps of glycolysis. (As I mentioned in a comment above.) So all the empty sugar we eat actually siphons off magnesium from somewhere else just to be oxidized. (Same with chromium...we need that for proper function of the insulin receptor...or maybe it's the glucose transporters...I don't remember which, at the moment, but chromium is sometimes referred to as the "glucose tolerance factor.") So these foods aren't merely devoid of beneficial things, themselves; that would leave them simply as neutral. The truth is, they're full-on negative.

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  8. Diabetes runs in my husband's family. His dad had a major stroke at the age of 59 and is disabled in an assisted living facility. I've been on my husband for years about his diet, low cholesterol but high triglycerides. Just this last spring at almost 50 his A1C and fasting blood sugar finally showed up as elevated. His insulin has never been tested. This makes so much sense but I'm still having problems getting him off the sugar and carbs!! Very frustrating as I worry about his health. His sister is 7 years younger and has been officially diagnosed as a diabetic for several years. I got Dr. Kraft's book to read and I'm going to print this article off for him. Thanks for all you do, I really enjoy your articles. :)

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    1. Thank *you!* Really, I'm just glad people have the patience to read my super-long posts. :) I hope you can talk some sense into your husband. Sounds like he has the family history working against him, but I firmly believe that we are in control of our health destinies, to the extent that we are willing to take responsibility. When other things seem okay, triglycerides often tell the tale.

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  9. Nice to see this topic being discussed, hyperinsulinemia is indeed the driving force behind diabetes. This is only the first step though, recognizing this disorder as primary, and using insulin testing to diagnose it, the much bigger issue is what we need to do about it. We accept that T2DM is a disorder of insulin resistance, we know that insulin resistance is primarily caused by too much insulin, and thanks in part to the work of Dr. Kraft we see these high insulin levels with us.

    So the primary goal needs to be to reduce insulin resistance, and to do that we need to make reducing insulin levels a prime target. Actually what we really need to do is to reduce glucagon levels, but high insulin levels play a big role in raising glucagon, and high glucagon is the cause of high blood sugar by the way. Reducing insulin levels though is just one strategy in reducing glucagon, but it's an important one.

    So what do we do instead? Well we look to increase insulin, in effect improving the symptoms of diabetes in the short term but worsening the disease itself over time. This is the colossal mistake that we make. So we do owe a debt to Joseph Kraft for his great efforts at exposing this fallacy, the fallacy that we don't have enough insulin, however they just will say well we have a relative deficiency.

    Conventional thinking about diabetes is so broken, even the idea that this excess glucose should be in our cells but isn't is totally wrong, this is a problem of excess supply, we need to focus on reducing this excess supply, instead of increasing cellular toxicity dramatically by looking to override the cellular protective mechanisms that are blocking these excess nutrients.

    So it all starts by looking to measure our insulin levels and look to normalize them as we would want to do with any hormone actually, except where insulin is concerned we don't care about worsening hormonal imbalance, in fact we make that the goal.

    Thanks for the article and we need more stuff like this out there.

    Cheers
    Ken Stephens
    http://understandingtype2diabetes.com

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  10. I have read through all eight parts and am confused. I'm 66. In the late 90's my fasting blood sugar started going up to the 90's a lot of the time. I have always and still do have high HDL, low LDL, never high triglycerides, very low HS CRP and perfect blood pressure but do battle weight and have autoimmune thyroid disease and have taken Armour thyroid for years. In 2008 I requested a fasting insulin test when I had a couple of fasting blood sugars just over 100. "normal" was 6-27 and my insulin was 4.2. In 2011 I requested a 3 hour glucose tolerance test. All insulin levels were bottom of normal and actually went down to below normal during the test but the blood sugar results had to be wrong because they started in the 80's and went up and down to 70's and 60's during the test! Doctors said it was "interesting" but it was never questioned and I stopped worrying about it. The one time A1C was taken around then it was 5.4. A doctor also did a GAD test which was negative. Now I had an H1C of 6 and C peptide that was a bit below normal. Was a bit more careful with carbs and A1C went down to 5.7 but doctor started me on Byduren shot in his office and I was intimidated when I questioned the safety of this. I have gone on a very low carb diet and refuse to take the drug but have not been back yet for another A1C. After several weeks with the low carb, ketones in urine, calories are also lower and I should lose weight but NOTHING has happened. However, I'm now having some morning fasting glucose levels as low as 92 (They started out at 115-118). Mostly after meal spikes are staying below 130 and going back down to around 110 3 hours after eating. But thing is I have never in at least 8 years had high insulin or C-Peptide - always a bit below normal. And other than a bit of weight BMI of 26.3 - I have no other indicators for metabolic syndrome yet this is what I'm told. why don't I lose weight and how come after probably 8 years plus with low insulin levels and no doubt blood sugar spikes and such I have nothing wrong. He even sent me for a cardiac calcium scan and I had ZERO calcium in the arteries! I don't know if I ever had high insulin levels! I also think the Byduren trash idea was totally ridiculous now and not sure if I will end up having to find yet another doctor.

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    1. Is there a question in here somewhere? It may have gotten lost. If you're asking why you haven't lost weight, despite being in ketosis, I have two suggestions:
      1. Read the series I recently wrote on stubborn fat loss: http://www.tuitnutrition.com/2015/11/why-not-losing-weight-1.html

      2. Look into Jason Seib's AltShift diet. Lots of people are having good results when they weren't successful on other approaches, including LCHF/keto: http://altshiftdiet.com/

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