What happens to the carbs – part II

My interest in nutrition began many years ago as part of my over-riding interest in cardiovascular disease. This means that, unlike many other people, I backed into this area with no great interest in the effect of food on health. For most doctors nutrition takes up about an hour of the medical degree course. We are pretty much given to understand that it is of little medical significance. Eat a balanced diet…end of. I also paid nutrition about that much heed.

However, because of the power and influence of the diet/heart hypothesis I felt the need to understand more about this whole area, and how the system of digestion and metabolism actually worked. At first my interest was purely to find out if there was any clear and consistent association between diet and cardiovascular disease (which I shall call heart disease from now on, as it is simplest to do so).

Like many others, before and since, I could not find any such association. Nor could I find any biochemical or physiological reason why saturated fat, in particular, could cause heart disease. That issue, of course, represents a long and winding road that I am not going down here.

However it did not take long before I became side tracked by the very powerful and consistent association between heart disease and diabetes. People with diabetes have far higher rates of heart disease than people who do not. In the case of women with diabetes, the increase in risk hovers around five times the rate of non-diabetics. So it became clear that I would need to understand diabetes, if I was going to fully understand heart disease.

This led me into the looking at the underlying causes of diabetes (type II). At first it seemed blatantly obvious that type II diabetes was primarily due to insulin resistance (it is far less clear now). In its simplest form, insulin resistance means that you need a higher level of insulin to drive down blood sugar levels, because something is ‘resisting’ its effects. Of course, like everything else, it is rather more complex than this, but I will leave it at that for now.

It also became clear that you can have mild/moderate insulin resistance for many years before you develop frank diabetes. Confronted with resistance to its effects, the body simply increases insulin production to keep blood sugar within the normal range. In this state, sometimes called ‘pre-diabetes’ you do not actually have a high blood sugar, especially not in the fasting state. This, of course was when most blood sugar level measurements were taken. Yes guys, look for a metabolic condition when it isn’t actually visible …very sensible.

However, mild to moderate insulin resistance, even if blood sugar levels are not consistently raised, is not benign. It is associated with a whole series of other metabolic abnormalities such as: central obesity, raised VLDL/triglycerides, low HDL, high blood pressure, high levels of blood clotting factors – to name but a few. In addition you can also find higher sugar levels, and higher insulin levels in the post-prandial state (after eating). Most importantly, to my mind, mild to moderate insulin resistance is also associated with a far higher rate of heart disease.

In the early days, ‘pre-diabetes’ came under many different monikers. Just to give you four:

  • Reaven’s syndrome
  • Syndrome X
  • Insulin resistance syndrome
  • Metabolic syndrome

This caused a lot of initial confusion, but once I chased them all down, it because clear that these different names were simply describing the same phenomenon, which is probably best described as insulin resistance syndrome. Although this title carries its own problems.

The next question, of course, is what causes the insulin resistance? The wisdom was, and remains, that it is caused primarily by obesity. This was based on the observation that, as people got fatter, the risk of diabetes increased almost exponentially. One paper I read many years ago stated that younger obese women had around forty times the risk of diabetes, compared to women of normal weight. That is what you call a strong association. Perhaps causation may even be whispered?

In short, if you added together what was clear about diabetes and insulin resistance, you got a model of type II diabetes which looked pretty much like this:

  • You eat too much food
  • You put on weight
  • As you put on weight you become more and more insulin resistant
  • At first you will develop insulin resistance syndrome
  • If you keep putting on weight you will become so insulin resistant that you will develop frank type II diabetes

I call this the ‘blowing up a balloon’ theory of diabetes. As a balloon expands you have to blow harder and harder to overcome the resistance. As you get fatter and fatter you need more and more insulin to force fats into fat cells. As with many things in medicine this is a nice simple story. It is also very easy to understand, and it is tantalisingly close to being correct

As always, however, when presented with a model like this, my immediate reaction is to try and smash it to bits with contradictory evidence. I figure that any theory that can withstand repeated assault is likely to be correct. On the other hand.

I started by looking at the extremes, as I always do. Beginning with the most obese group people on the planet earth, namely Sumo wrestlers. I wanted to know how many of them have diabetes, and it did not take long to discover that, whilst in training, none of them have diabetes.

I then searched for the opposite end of the spectrum. Were there people with no adipose tissue, and how many of them had diabetes? Surprisingly, there is one such group, the least obese people on earth. They are those with Beradinelli-Siep lipodystrophy. This is a genetic abnormality which means that these poor unfortunates have almost no fat cells. How many of them have type II diabetes? Well, all of them actually.

I then looked for the population with the highest rate of diabetes in the world. This happens to be the Pima Indians of North Mexico/Southern US. I have seen figures reporting that over 80% of adult males Pima Indians have type II diabetes. It may even be more. And yes, they are very obese.

However, there are two other very interesting facts about the Pima Indians. First, they have a very low rate of heart disease. Or they did last time I looked. Perhaps most importantly, in their youth, when they are not obese, they produce far more insulin in response to food than ‘normal’ populations. Or, to put this another way, they are hyper-insulinaemic before they are obese, and long before they become diabetic. So their excess insulin production is not a result of becoming fatter. The causal chain is the other way around.

I have found that if you speak to most doctors about these facts, a look of complete incomprehension passes over their faces. ‘That cannot be right.’ Of course if you believe in the ‘blowing up a balloon’ model of diabetes, then the Pima Indians, Sumo Wrestlers and those with Beradinalli-Siep lipodystrophy do not make any sense. However, in science, when observations do not fit your hypothesis, it is the hypothesis that needs to change, not the facts.

Just to summarize these ‘paradoxical’ facts:

  • You do not need any fat cells to develop diabetes/if you have no fat cells there is a 100% probability that you will be diabetic
  • You can be very , very, obese and not have diabetes
  • You can have increased insulin production long before you become obese (and/or insulin resistant). You become obese later

Just to remind you of the current model.

  • You eat too much
  • You get fat
  • As you get fat you become more insulin resistant
  • In order to overcome this resistance you produce more insulin
  • Eventually you cannot produce enough insulin, the system ‘burns out’ and you develop type II diabetes

Where and how can the paradoxical facts be fitted? The answer is that they cannot. Ergo, the model is wrong. However, luckily, there is another model that fits all the facts. One that I prepared earlier:

  • You produce too much insulin
  • This forces your body to store fat
  • You become obese
  • At a certain point insulin resistance develops to block further weight gain
  • This resistance becomes more and more severe until…
  • You become diabetic

This model explains the Pima Indians. Can Sumo wrestlers be fitted into this model? Yes, with a couple of addendums. Sumo Wrestlers eat to become fat, because added mass provides a competitive advantage if you are trying to shove someone else out of a small ring, before they do it to you.

To achieve super-obesity, they wake up, train for two hours, then eat as much as they can of a high carbohydrate, low fat, broth. They then lie about for a few hours allowing the high insulin levels created by the high carbohydrate diet to convert excess sugars to fat, storing this in adipose tissue. Later on they train very hard again, then eat, then sleep. Rpt.

The reason why they do not become diabetic is on this regime is simply because they exercise very, very, hard. They burn up all the sugar/glycogen stores in the liver and muscle whilst exercising, which means that when they eat, the sugar(s) can – at least at first – be easily stored in muscle and liver (so there is no insulin resistance to overcome). However, once these guys stop training, things do not look so good. Diabetes lurks..

Those with Beradinelli-Siep lipodystrophy have the reverse problem to Sumo Wrestlers. Because they have no fat cells there is nowhere to store excess energy to go. If they eat carbohydrate/sugar, the first 1,500 calories can be stored as glycogen – after that there is nowhere left. If the liver converts sugar to fat, there is nowhere for that to go either. So, you get ‘back-pressure’ through the system. It doesn’t matter how high the insulin level gets, if you have nowhere to store energy you have nowhere to store energy. End of.

Whilst those with lipodystrophy cannot tell us much about diabetes and obesity in ‘normal’ people. This condition does make it very clear that diabetes – insulin resistance, high insulin and high sugar levels – is primarily an issue with energy storage and how the body goes about this storage, and the role that insulin plays. If there is somewhere for excess energy to go easily, insulin levels will not go up, and nor will blood sugar levels.

But what of ‘normal’ people. Can normal people be fitted into the updated model of type II diabetes? Well, of course, they can. But you need another step in the new model, the first step. Which means we have a new causal chain, and it looks something like this ‘You eat too much carbohydrate.’ Adding in this step gives us the new model:

  • You eat too much carbohydrate/sugar
  • You produce too much insulin
  • This forces your body to store fat
  • You become obese
  • At a certain point insulin resistance develops to block further weight gain
  • This resistance becomes more and more severe until…
  • You become diabetic

The best thing about this model is that it works. It is not contradicted by Sumo Wrestlers, Pima Indians of those with lipodystrophy. It explains the association between obesity and diabetes, and how insulin resistance develops. It may not be perfect, but it is a bloody site better than the simplistic model we have got. The one that says, if you eat fat, you will get fatter, then diabetic…. Bong! If you are diabetic you should eat carbohydrate and sugar, not fat…Bong!

How long before mainstream medicine rejects this mainstream model? Another fitty years or so, I would guess

214 thoughts on “What happens to the carbs – part II

  1. John Brindley

    I like your explanation, but you should review your balloon analogy. Balloons are hard to start inflating, but get easier as they expand.

  2. Adam Goldwter

    Great article showing once again that just because something is the “generally accepted view”, doesn’t mean that it is correct.

    The more I read about evolution, nutrition and diet, the more I keep coming back to the fact that anything that causes your insulin levels to repeatedly spike (grains, sugars, carbs, etc), can cause severe health problems over time, so this article is particularly interesting.

  3. Janet Beach

    Thank you, Dr. Kendrick, for yet another excellent, thought-provoking and informative post.
    As I’m sure you know, the advice for diabetics was not always as it is these days. Back in 1958 At the age of 15, I was diagnosed with what was then called ‘mild diabetes’ rather than ‘type 2’, as was my brother at the same age but 7 years before. Both of us were very thin (my brother had TB at the time). The diabetes was discovered because my mother from time to time would test everyone’s urine for glucose – my Grandmother was insulin-dependant.
    At the diabetes clinic I was given a booklet listing foodstuffs ‘freely allowed, weighed and ABSOLUTELY FORBIDDEN’ and a prescription for Rastinon. Imagine the horror for a 15 year old being told – no cakes, pies, puddings, biscuits, thickened soups, thickened sauces, no nuts (oddly), dates, sweets, chocolate Etc. etc. etc. Argh! On the other hand meat, fish, eggs, cheese, butter, cream, some vegetables, some fruits were all freely allowed. The rest – bread, potatoes, other starchy vegetables, most fruits had to be weighed. It amounted to 120 grs. carbohydrate a day……actually that seems like a lot to me now but I was a growing girl with ‘hollow legs.’ To this day, I weigh bread and have only 2/3 of an ounce with my (two) breakfast eggs. Now i have 40 to 50 grs plus gliclacide and metformin.
    Now then,what I would like to know this this. How would someone (not necessarily me) thin as a rake, very active, as children were back then, develop type two diabetes? Even to this day, this particular someone has never had at BMI over 23 – it’s 18.5 right now and a waist measurement of 25 inches which is not bad for a tennis playing 73 year old.
    What amazes me is the stupid dietary advice issued to newly diagnosed diabetics. You know the sort of thing -plenty of whole grains, rice, pasta and low fat or nasty fat. Ugh.
    Back to me, me, me. I had been told by a couple of diabetic consultants that my brother and I were “mody” which is very different from the obesity-fuelled juvenile diabetes today. Does that diagnosis still exist? My diabetic nurse, when I mentioned it to her just said, no, no no. You’re insulin resistant. Can this be so? When I’m so lean (and well, apart from pretty consistent 6 – 7 m/mol fasting blood glucose and a bit of a postprandial spike.
    There must be lots of people like me who need proper guidance but constantly frustrated by wrong advice – “your diabetic because you’re fat or your fat because you’re diabetic.” But I’m NOT FAT, NOT FAT, NOT FAT.
    Sorry to rabbit on. I do find your blog and your books immensely useful as must be apparent from this long rant.
    Oh, yes, another thing before I go. Why, if a person is insulin resistant, is gliclacide prescribed to boost insulin production when that insulin cannot be utilised properly because of insulin resistance?
    Thanks for reading.

    1. johnnyv

      Janet Beach
      If you want a possible explanation of how a non obese could develop T2DM, there is a logical explanation here: http://high-fat-nutrition.blogspot.co.nz/2011/10/adipocyte-insulin-resistance.html
      Related to mitochondrial dysfunction allowing FFA leakage from an adipocyte even under elevated insulin. With properly functioning mitochondria the adipocyte needs to be distended from hypertrophy to leak significant FFA against the action of insulin.

      I really like that explanation as it can plausibly explain how apparently lean people can develop T2DM.

      1. Cindy C

        Studies report a link between diabetes and our microbiome(which can also be inherited) Reports of diabetes after statins, after antibiotics, and after chemical exposure. Those affect our mitochondria, which produces energy. Our micobiome affects our mitochondria as well. Feeding microbes with some starch and fiber is one thing, but a diet of too much sugar and grains and not enough fatty acids(which work against some bacteria) can over produce certain strains of bacteria.






        Also in mothers milk


    2. Jake Speed

      If one believes the folks at the Broda Barnes Foundation (and I do) (http://www.brodabarnes.org/) throwing yet another monkey wrench into the equation, is the silent epidemic of hypothyroidism. Maybe 50% of the population may have silent hypothyroidism, and not know it. Since one’s thyroid controls one’s metabolism, it’s not hard to understand why people with hypothyroidism find it almost impossible to lose weight, no matter how hard they exercise. A sluggish thyroid can lead to metabolic syndrome, metabolic syndrome can lead to diabetes, and diabetes can lead to heart disease.

    3. Brian (BSC)

      Kay is correct, some forms of Monogenic Diabetes cause higher blood sugars and are characterized by excretion of glucose. I have explored MODY and have written about it on TuDiabetes.org and my blog at (http://brian-the-bsc.blogspot.com/ ). I recently got tested for MODY and although it came back negative I learned a lot. I also am not overweight. Type 2 diabetes is not a single thing, it is highly complex, polygenic and involves multiple defects beyond simply insulin resistance in muscles and loss of insulin production. Type 2 in practice seems to just be a diagnosis of exclusion and really just means “Diabetes of Unknown Cause.”

    1. rockingbass

      Yes… but that is the other side of the coin Jane .Dr Wolfgang Lutz in his biography My life without Bread -Dr Lutz at 90 by Valerie Bracken explains why this is and why over consumption of carbohydrates are the problem.The University Clinic in Vienna before the second world war stabilised type 2 diabetics successfully by limiting carbohydrate consumption to 72 grams per day..Hope this helps.

      1. Jeff Wilson

        This seems a logical explanation to me. Yes, that is a profoundly interesting book Rockingbass. I don’t know that I have “lipodistrophy” but I am definitely on the lite side by being more thin than fat :-). (I overcame years of Crohn’s colitis and blood sugar problems 3 – 4 years ago, feel great compared to how I used to feel. However I still hope to gain healthy weight like Dr. Wolfgang Lutz did (went from an “over-thin” 65 kilo to 79 kilo within 4 years accompanied with much superior health all by radically reducing carbs). Would love to contact his neice/author Valerie Bracken but don’t know how. Can you help?? I live in Australia and understand she is somewhere around the UK

      2. Jeff Wilson

        Yes My Life Without Bread is a profoundly interesting book. If anything I am over-thin rather than fat. (Overcame Crohn’s colitis 3-4 years ago, feel great to how I used to feel however, I’d still like to gain more weight. At age 44 with declining healh Dr wolfgang Lutz went from an “over-thin” 65 kilo to 79 kilo within four years….) Love to get in touch with Valerie Bracken author but don’t know how. Can you help??

  4. jo

    When I was a child, diabetes was called “sugar diabetes”. It was caused by sugar (and obviously carbs, which turn to sugar when they hit the blood stream I believe)

  5. Turan

    Good post!
    I am not sure about the term “Insulin resistance”. If fat cells of a type II diabetc individual do resist against the insulin how is it then possible that they remain still obese? Fat cells can remain “fatty” only when they respond to the insulin and take the sugar off the plasma. If fat cells get insulin resistance they should get soon leaner and leaner! Or Insulin resistance refer only to muscle, liver, etc.?
    Thanks for your response!

    1. Dr. Malcolm Kendrick Post author

      Insulin resistance refers almost exclusively to resistance of the effects of insulin in the liver and skeletal muscle. Subcutaneous fat cells do not really become insulin resistant at an point. Which is why you can become almost ridiculously fat

      1. johnnyv

        They become insulin resistant as they increase in size, the way to become “ridiculously” fat(not just fat) is via hyperplasia, you need to increase the number of cells to restore insulin sensitivity and proceed with further hypertrophy. Hyperplasia can explain insulin sensitive obese, but it also means if they lose fat mass they will have much lower circulating leptin.

        I saw a nice paper on mice(I know). Normal low fat chow, chow + 10% butter and two chow + 10% polyunsaturated blends. SFA apparently promotes hypertrophy and PUFA hyperplasia.

      2. NY

        Hi Malcolm,

        What about non obese daibetics then? Their fat cells are not expanding. Saying that if fat cells are insulin resistant, it must also ALWAYS translate into release of FFA (as mentioned by Turan above) is not correct in my opinion because by this logic no one would get fat. My guess is that fat cells can be highly insulin sensitive when it comes to storing fat and insulin resistant when it comes to releasing fat or vice versa. LPL and HSL have a key role in storing and releasing fat in response to insulin, the higher the LPL activity,the more fat is stored, the higher the HSL activity the more fat is released.

  6. Turan

    Another question: Is not it true that protein causes also insulin production? Probably not in the same level as carbs but amino acids should be broken down to be stored within the cells. What are your thoughts about protein in general and it’s role on diabetic?

  7. Jennifer

    So, in a nutshell…the quantity of food bears little relationship to obesity? ,therefore dismiss counting calories, as that is a red herring we have been encouraged to follow for years.
    So, is it the composition/ ratio of macronutrients?
    Dr Lustig concentrates on sugar and fructose being the main problem, and that is the point at which I successfully entered the debate a couple of years ago. But I think Dr Kendrick seems to be saying it is the quantity of carbs, from any source, that must be taken into consideration, and I have come to that conclusion too. Even consumption of ‘healthy’, ‘natural’, unadulterated carb sources must be watched carefully. As to whether certain proteins also increase insulin production, rather than increasing blood glucose levels, my feeling is that it is far more difficult to over-indulge in that type of food, when compared to any form of carbs.
    Once the public is educated to understand what healthy fat is, what good protein is, and how any carbohydrates are superflous to life, we may be winning the war. But we don’t have to be absolute purists to follow a decent, pleasant dietary intake…..just keep away from the junk, steer clear of anything produced artificially, and be very moderate in eating things we have had pushed at us from factory food outlets…just be aware, that the food industry has been intoxicating us with added sugars and toxic preservatives as though they we doing us a favour, rather than lining their own pockets.

    1. SJ

      As I think I MAY have mentioned on a few occasions, I’m a great believer in the adage, ascribed to Hippocrates, that “disease begins in the gut”; that doesn’t mean every illness begins in your intestines, it means that what you eat determines your overall state of health, and my frustration has long been that the NHS is pushing a diet that’s the very opposite of healthy. What Dr. K says is perfectly true, nutrition isn’t taught hardly at all at med school, I’ve had junior docs look at me as though I had 3 heads when I told them that all carbs are converted to sugar (none had even HEARD of the Krebs’ Cycle!). The same is probably true for ALL docs, and the nation’s health isn’t going to improve until the teaching of nutrition improves – and correct nutrition at that. The diet we’re being told is healthy is completely alien, so I’m not in the least surprised the NHS has budget problems! If correct nutrition was taught as the foundation stone of medical practice, then the NHS would be in better shape financially, and staff wouldn’t be stretched to breaking-point – and beyond! There’s one phrase that’s 100% GUARANTEED to make me scream ‘low in saturated fat’ (‘low in salt’ is another, but low-fat is far more ubiquitous). It’s all led to me becoming increasingly cynical in that, perhaps, NICE (most ironic acronym on Earth!) doesn’t WANT people to know the truth, it wants to keep the nation ‘not sick’ which is a zillion miles from ‘healthy’.

      I see it with my own parents; Dad’s on statins, of course, but they’re both TERRIFIED of everything the NHS tells them they need to be terrified of; they won’t eat red meat, they use Lo-Salt, Flora Pro Activ, and are eating an increasingly vegetarian diet (though they still eat some fish and chicken). I see Dad suffering from the obvious serious adverse health events caused by statins, but he refuses to believe they are (I’ve mentioned what he thinks of Dr. K before; until his own GP starts saying the same things, he won’t believe them).

      The crux of the matter is, to my mind, is that we’re being told to eat things that didn’t really form any part of our diet until around 10,000 years or so ago and, in the scale of human evolution, that’s a blink. To start telling people foods which have been a part of the human diet almost since modern humans have existed (and prior) are going to kill ’em is irresponsible to say the least. My mother refuses to eat red meat now because she’s terrified it’ll give her breast cancer, because the NHS says it will.

      Every species has its own dietary blueprint, which it’s evolved to eat, humans didn’t evolve to eat a diet based around grains and starches, so is it any wonder we’re not exactly in the best shape…? Personally, I believe the optimal ratios are around 75% fat, 20% protein, 5% carb – and certainly don’t count calories! That’s the nub right there – the message I get from the NHS Choices weight loss pages is that the only criterion for determining how healthy a food is, is calories! Certainly, looking at its 12-week ‘lose a stone for summer’ progress chart, it only has 3 columns: calories consumed, calories expended, calories net. If that worked, well the UK wouldn’t be the world’s second most obese nation, would it…?

      Okay, rant over, except to say that Dr. K I love you to bits, but reading your blog has me fighting my inner pedant – writing is the only thing I’m remotely good at (writing, I don’t often make too much sense, though, because nobody understands much – if any – of what I write. I’m high-functioning autistic, and I’ve got no edit function, I can only write as it ‘sounds’ in my head). I think a lot, I’m probably far too introspective for my own good – it’s frustrating because I have Ideas, I just can’t do anything about implementing ’em!

      1. Sean Coyne

        Be careful when we ascribe all humans to a 10,000 year old change in diet that’s rooned us all. Humans groups vary enormously, migration confuses the picture , evolution can move fast in stressed populations (think disease in early cities) and local diets are based on what is easy (and yummy) to catch, dig up or pick (speaking of hunter gatherers). A diet that’s “good” for a stone age culture will thus depend on their ancestry, where they lived and what stresses they were under. Australian aborigines do poorly on modern western diets, as do many other recently hunter gatherer groups, but they may well do worse on the diets of hunter gatherers from different environments (unlikely maybe but I don’t think I’d last long eating blubber all day). And that’s before you factor in change in exercise norms, alcohol, tobacco, societal stress etc. Paleo diets and such are thus approximations at best and don’t take into account one’s precise ancestry, let alone that we don’t know enough to actually say what people really did eat location to location from thousands of years ago…although we are learning.

        What we do know is that the average supermarket in the West is 90% processed crap and 10% real food and that’s before you get to the booze aisle to cope with the stress… Sigh.

      2. Richard Gibbs

        Sj, although agriculture started ~10K years ago, cooking wild grains started at least 100K years ago. I believe the biggest fallacy about diet and disease is the assumption that the same dietary conditions apply to everyone. There is published evidence that the microbiome, and hence the ability to digest different foods, is strongly affected by one’s ABO blood type. There is evidence that type A is better adapted to eating grains, but handles a high fat diet poorly. From the evolutionary point of view, types O and B evolved from A, which subsequently may have disappeared, suggesting it was a disadvantage. Subsequently type A reappeared as a result of interaction between types O & B. Because A has an advantage over O and B for surviving on a grain based diet, it survived after man starting consuming cooked grains.

      3. Stephen

        SJ, that’s a great e-mail. My niece is training to be a nurse and is being taught that carbohydrates are essential. “We need them for energy, uncle Steve.” I swim a mile’s front crawl four mornings a week and eat a low carb diet, so where’s the energy coming from?

        It is rather depressing that intelligent and curious minds in the NHS are still being taught this guff.

  8. SimpleLivingOver50

    What I got out this is that by simply reducing the amount of carbohydrates in you diet each day and developing a good exercise regime works in favor of not developing T2D. I already have it and am maintaining good glucose levels by taking these steps. Although I have found that certain things like getting sick can throw things off. This is what I am going through right now, but have been there before and once my immune system wipes out those foreign invaders I will return to seeing my morning glucose return to normal numbers. This was a very insightful article and I hope you don’t mind if I repost it on my blog. 🙂

  9. Jonathan Christie

    Brilliant analysis and totally consistent with my experiece of insulin-dependance: no carbs, no problem. HbA1c 5%, BMI 24, coronary artery calcium zero after 16 years on Dr Bernstein’s diet

    1. Dr. Malcolm Kendrick Post author

      On a certain level this is just common sense. You have problems controlling blood sugar levels. Well STOP eating so much sugar. By sugar I mean all carbohydrates. How hard can this be to understand, exactly.

      1. D. Smith

        I think labeling on foods is a big problem. Personally, I try to eat foods that don’t come with a label; meats, eggs, fresh veggies, etc. If carbs and sugar as basically the same thing, why are there two separate categories listed on labels? I think this is why most people simply don’t understand “carbs” . . . I know I don’t. Even after all the reading I’ve done the actual meaning of what is a carb still eludes me. So bananas are good but bananas are bad? How does this work?

      2. Janet Beach

        It isn’t hard to understand but one size doesn’t fit all, necessarily. Here am I, type 2 for 57 years, thin and fit and only consuming 50 grs. Carb per day. But still my fasting, early morning BG hovers for the most part at 6-7, except on those glorious occasions when it’s only 4.5 (for no apparent reason) and I always get post prandial spikes even after consuming five grams low GI carb.
        The more I read the more I come to the conclusion that scientific world still has a lot of learning to do and it really doesn’t help when so called ‘experts’ keep on giving us all really stupid dietary advise and prove themselves to be so inflexible in their thinking. As you correctly say – if the facts and the hypothesis don’t fit, change the hypothesis not the facts.
        Carry on carrying on, Dr. Kendrick. You seem to be a voice in the nutrition wilderness and it must be very lonely sometimes.
        P.s. I love the way my iPad spell checker always changes “post prandial” to “post prawn dial”…….I don’t even like prawns.

      3. terpsichore4691

        (I hope I’m not misremembering this …)

        I remember in grade school science class (more than once) we would get these iodine strips, I think they were. And we were told by Teacher that they would turn purple in the presence of sugars. We’d stick one in our little mouths and it would come out the same color (because it was before lunch and no one was allowed to chew gum, etc.).

        Then Teacher would feed us a cracker. Then we stuck another strip in our little mouths.

        Talk about major purpleness!

        The point of the experiment was to show how our saliva changed the chemical composition of the cracker. It turned the cracker into pretty much … all sugar.

        This is why it seems sensible to me, for weight loss, to reduce carbohydrates. That’s part of what I’m doing while trying to lose twenty-five pounds in twenty weeks.

  10. Jennifer

    It isn’t difficult to understand, just a bit difficult to follow if the NHS guidelines keep telling us otherwise.
    It is not easy to countermand the GP AND the Diabetic Nurse Specialist, ……so my motto is ” avoid the carbs and avoid the surgery”.
    Not simple….but necessary.

    1. Nigella Pressland

      I agree with Jennifer’s point. It is not just the NHS, GP’s & diabetic nurses espousing the consumption of vast amounts of carbs (although they do like to say complex carbs now!), the whole nutritional advice of the last 40 years has been to eat low fat & high carb.

      There are plenty of businesses who have made a fortune out of this advice (because wheat is so cheap) and who endlessly reinforce in our minds that the best way to eat is a low fat diet. Think of all those disgusting, highly-processed low fat foods on the supermarket shelves. There are hundreds (if not thousands) of them & all of them are marketed aggressively by the companies that make money from them. They are going to fight as hard as they possibly can against any move to suggest that high carb is not the way to go.

      I have friends & colleagues (as well as a sibling who is a GP) who rabidly follow the low fat mantra – they are literally terrified of fat. I’ve been a low carb advocate for the last 20 years and I have heard it all! How, I’m going to have a heart attack, ruin my kidneys, become nutrient deficient, get high blood pressure, high cholesterol and so on. They are absolutely scared stiff of fat.

      So running in the face of all that opposition requires a considerable degree of ‘spine’ for want of a better description!

      1. Jennifer

        Nigella. I am a relatively new-comer to consciously eating fat, and must admit that giving up carbs was not the easiest of tasks. As Dr K said, what’s not to understand about the concept, especially if we look at the explanations logically. It is a no-brainer really, but the indoctrination of the last 40 years will take some shifting.
        I have this urge to fling all the rubbish carbs and low fat products out of supermarket baskets whilst I stand in the queues! But it would just confirm to my critics that I am indeed off my trolley.
        I am alive and kicking, which is a far cry from a couple of years ago, when my GP etc could only offer me more of the very things that were causing my demise. I no longer tell folks how I have achieved my current state of good health because I got sick of experiencing their strange looks, and watching my pontifications slip over them like a tub of margarine on a hot summer’s day. Very few even try to understand the logic of low carb, high fat, eating pure, natural food, because it is the antithesis of their lifelong experiences, and after all, why change? They are managing OK, aren’t they? Or are they?

    2. Flyinthesky

      I used to have a GP as a customer, he asked me one day how I kept so well, easy I said, avoid you!

  11. Gary

    There is also a crucial difference between a diet rich in cellular carbohydrates (fruits, vegetables, and tubers) versus a diet rich in dense, acellular carbohydrates (flour, sugar) in metabolic health.

    1. Stephen

      The speed with which they’re converted into glucose differs but the eventual hit is the same. Most fruits are high in sugar (berries are lowest), but most vegetables aren’t high. It’s a mistake to put fruit and veg in the same list.

  12. paganheretic

    I am less interested in the question “how long” will it take to accept the the facts about diabetes, but more in the question “why” is it so that the mainstream medical “science” keeps rejecting the facts? Another interesting question is “who” is supporting or causing that myth-believing behavior among the academics and why are they not yet getting fired?
    Stan (Heretic)

      1. paganheretic

        I think, the medical system may have reached the stage that we will probably need good lawyers as much if not more than doctors. 8-:)
        Best regards,
        Stan (Heretic)

  13. rockingbass

    Has worked for me over the last 16 years..or so..Thank you for a great post.My wife Valerie Bracken has written a book for teenagers and adults explaining the whys and wherefores in a conversation with her Uncle Wolfi .Would you like me to send you a copy? please e mail info@justperhaps.co.uk

  14. Jan Vyjidak

    And perhaps this is one of the most eloquent description of why Dr Russell Wilder at Mayo Clinic had such an amazing success when he treated Type 2 diabetics with very low carbohydrate diets back in 1910 (see his Primer for Diabetics, 1927). And several other doctors after him, to this day.

  15. Flyinthesky

    •You eat too much carbohydrate/sugar
    •You produce too much insulin
    •This forces your body to store fat
    •You become obese
    •At a certain point insulin resistance develops to block further weight gain
    •This resistance becomes more and more severe until…
    •You become diabetic
    The missing element, from my perspective, is an insertion at bullet point 4. When you eat too much carb/sugar the resulting spike in insulin reduces the blood sugar level very quickly leading the body to think it’s short of fuel, hunger. It’s cyclical, the only relief from the feeling, varying from general malaise to abject anger is to eat more carbs and sugar. It’s a self perpetuating nightmare.

      1. Flyinthesky

        While listening to a well known lunchtime radio show featuring a well known radio doctor this phenomenon wasn’t mentioned at all, she, oops, proposed that people should refrain from eating free sugars and get the required energy from carbohydrates, slower release maybe but the net result is the same, too much sugar and the cycle continues.
        The inference, as it would be taken by many, is you shouldn’t have a can of cola but it’s ok to have a meat and potato pie in a barmcake, so long as it’s a wholemeal barmcake and the pie is low salt and fat.
        Me being the cynical B I am tend to think that it’s not about resolution of problem it’s about retaining an authoritative place in the game while and by portraying hand wringing concern. After all if you solve a problem you no longer need the relative expert.

  16. David Bailey


    Your previous post was left up for so long, I started to worry that someone had made you an offer you could not refuse (for one reason or another) 🙂

    Do you have evidence for this step in your argument:

    “At a certain point insulin resistance develops to block further weight gain”

    i.e. is there a feedback mechanism of this sort, or is this just your inference?

  17. Art Davidson

    Dr. Kendrick,
    Does this not mean that even at step one “You eat too much carbohydrate/sugar” something in the metabolism is already broken or missing? Anecdotally, few people even with diabetes can over-eat rib-eye steaks, but many people do overeat carbs.

    If it is possible to over-eat some type of food, you are already sick, I think.

    1. Catherine Reynolds

      Art – take a look at Zoe Harcombe’s blog – she has some excellent observations about why you might “crave” certain foods, in particular sugary, carbohydrate-loaded ones. Dr K – this is brilliant – I get SO fed up with having my blood sugar tested every time I go to my GP. I’m not what you would call “slim” but I’m definitely not unhealthy, and there’s always this look of almost amazement when my blood sugar is shown to be “normal”, as if to say, “but you’re fat, why aren’t you diabetic?”. I know several people who have Type 2 who have most certainly never been fat/overweight, and have often wondered, therefore, why, other than yourself, the medical profession don’t seem to have picked up on this apparent phenomenon.

  18. merrilie2015

    I am really grateful for your very interesting and informative Blogs. Do keep them coming. I Have just read a review of a book that will be out at the end of this month, and which might be of interest to some of your followers called “The Real Meal Revolution.” Amazon’s blurb states: “This book will radically transform your life by showing you clearly, and easily, how to take control of not just your weight, but your overall health, too – through what you eat. And you can eat meat, seafood, eggs, cheese, butter, nuts . . . often the first things to be prohibited or severely restricted on most diets. This is Banting, or Low-Carb, High-Fat (LCHF) eating, for a new generation, solidly underpinned by years of scientific research and by now incontrovertible evidence.”
    I have been trying to avoid carbs for a while now and slowly the weight is going down! It is not always easy when you are cooking for friends and family or out for a meal. My weakness is fruit, which I’m sure contains a lot of fructose. I will persevere and continue to follow your very informative blogs. Thank you!

      1. John U

        There is a good post by Dr. Georgia Ede on Fructose – a 4 part series, but only 3 parts have been completed – http://www.diagnosisdiet.com/blog/
        I don’t believe that Fructose is a villain at all in normal doses, and fruit is only seasonal in the colder climates. In the tropical climates, fruit is ubiquitous most of the time.

  19. Dr. Göran Sjöberg

    Malcolm – A great post again!

    My severely diabetic (T2) wife totally reversed her strong peripheral neuropathy, regained her night vision and her glaucoma diagnose was no longer there after a year on strict LCHF. Her IBS syndrome disappeared amazingly in a few days. By coincidence me and my wife lost 20 kg and 12 kg, respectively, without any intentions to acquire any ‘greek bodies’.

    As I mentioned in your previous blog I was, as a strong LCHF advocate, invited to review a book full of ‘hatred’ agains LCHF – or shortly ‘low carbing’ for health. The book is appropriately named “The Low Carb Myth” (by Ari Whitten and Wade Smith) and I have now forced myself half way through the book (a bought paper copy by the way). For sure the book is an interesting reading about all the LCHF counter arguments – some seemingly very convincing – but the vicious arguing style which permeates the book is as far as I can imagine from what I myself consider to be any scientific attitude in a book worth reading and this style is unfortunately blocking my clear thinking and also my normally inquiring research mind. I think this is a pity and wonder if this is the actual purpose with the obvious aggressive style.This is why I have to force myself to continue reading the book. To deliver a proper review, and not as now just my strong feelings about it, I guess I must at least read the full book an digest it and put it in a proper perspective.

    As you indicate in your post this whole book seems also to be all about ballooning along the following ‘established’ nutrition lines.

    “You just eat too much of whatever – you poor stupid – and you get fat, sick and diabetic – period.”

    Or put in another more vicious , but though heavily ironic, phrasing, which in my mind summarises the whole official calorie counting paradigm. The ‘strong’ language in the phrase is by the way pretty much the same as I find between the lines in the book.

    “You just don’t have the willpower of abstaining from one single gram of food from any of your plates. It doesn’t take a ‘rocket engineer’ to figure out that those five extra grams per day will add up to at least one kilogram of extra body fat during the course of a year. Guess what will happen in 40 years?

    It was just ONE GRAM per plate you had to abstain from to avoid getting as fat as you have got!”

    1. David Bailey

      I am one of those people – born not too long after the war – who virtually always eats every bit of what is on my plate!

      I have a suspicion that this has helped to keep me slim. It means, for example, that I would never agree to eat a meal (leaving part of it) if I wasn’t suitably hungry. Whenever I visit to a cafe or restaurant, I avoid meals that are likely to be too big, and while I eat everything put in front of me, I see many others – typically a lot fatter than me – leaving a good portion of their food.

      My gut feeling (sorry about the pun) is that part of the obesity crisis is the result of a gradual erosion of traditional eating discipline. This may have been helped by the number of carbohydrate foods that don’t fill you up for long, and encourage people to think that eating and drinking at any time is reasonable.

    1. Bil

      It doesn’t; with the exception of beer, champagne and mixed drinks e.g. some cocktails. Red wine 2 to 3g carbohydrate per 100g. On LCHF you can drink wine and spirits, no problem. I’ve been doing it for 20 years.

      1. Sonysunshine

        I was under the impression champagne is very low carb. I have certainly been putting that impression into practice.

        1. Dr. Malcolm Kendrick Post author

          I think that we should probably see alcohol as a type of carbohydrate – from a metabolic perspective. As with many things, how you define something has a significant impact on how you decide to think about that thing.

      1. Ash Simmonds

        I don’t know why this is going over folks heads here…

        Beer CONTAINS alcohol, it is NOT alcohol itself.

        As with my earlier burger analogy, is a Big Mac meat because it contains it, therefore we should consider meat carby?

      2. Ash Simmonds

        “C2H6O – Ethanol, Formula a carbohydrate”

        Love getting schooled on the science of booze. Back to school for you bro, you get a big fat F.

        Lauric acid (ie, much of coconut oil): C12H24O2 therefore a carbohydrate?

        Omega 3: C60H92O6 therefore a carbohydrate?

        Glucose (a carbohydrate): C6H12O6

        Fructose (a carbohydrate): C6H12O6

        Galactose (a carbohydrate): C6H12O6

        Might be starting to see a pattern here, best to investigate the meaning of the terms CARBO and HYDRATE to understand why the composition matters, it’s not just a random word…

      3. Ash Simmonds

        Sorry, the above came off as smarmy/snarky – excuse the terseness, I’ve just been dealing with the “alcohol is carbs brah!” daftness for too long, and as a lover of science and booze it just melts my head sometimes the things people say to me.

        Point being, carbs 101:

        Carbo-Hydrate: *generally speaking* is one carbon to one water. Water being H20, you’ll typically see carbohydrate right on or very near the 1:2:1 ratio of CHO, for those not up with the molecular stuff sugar is C6H12O6 which can be simplified down to CH2O <– presto, carbohydrato! 🙂

        Just because stuff is made up of carbon/hydrogen/oxygen (basically everything) doesn't mean it's a carbohydrate. Hope that clarifies and makes up for my grumpo.

      4. mikecawdery

        Alcohol contains C H and O. a carbohydrate. I was well aware that it was metabolized differently to what is usually termed as “carb”. I was merely commenting on your assertion.

      5. mikecawdery

        Alcohol contains C H and O. a carbohydrate. I was well aware that it was metabolized differently to what is usually termed as “carb”. I was merely commenting on your assertion. It is still la source of energy!
        ‘Ethanol as a source of Energy’
        1 gram of Ethanol=7 Calories

      6. Ash Simmonds

        Just because it’s made up of C H and O doesn’t mean it’s a carbohydrate.

        I don’t know how many times I can stipulate this.

        I was being polite, but this is just becoming really stupid, and I wish folk who own a keyboard could do some research before responding to me, it really wastes my braincells the amount of facepalm I have to do.

      7. mikecawdery

        What I was referring to was that alcohol, like a carbohydrate, is made up of C, H and O, but with a higher energy content. The use of “carbohydrate” rather than C, H and O was an unfortunate mistake. As I have spent some 4 decades in research in close contact with nutritionists I am very aware of what is and what is not particularly in the area of digestibility and metabolism.

        Unfortunately while I tick the boxes for notification nothing happens so I have to go searching

      8. Ash Simmonds

        | “What I was referring to was that alcohol, like a carbohydrate, is made up of C, H and O, but with a higher energy content.”

        Look man, I get what you’re talking about, but that was nothing to do with the discussion – calories are an even more dumb topic.

        | “The use of “carbohydrate” rather than C, H and O was an unfortunate mistake.”


        I just get a lot of people trying to tell me what a carbohydrate is and does based on whatever headlines/articles they’ve read today, and I have only so much patience to steer a ship of fools.

        The takeaway is I hope some lurking readers have learnt some stuff about alcohol vs carbs vs metabolism vs health etc. And if not, I’m happy to point out the science as we know it.

    2. Stephen

      I love beer but since I went low carb I now react badly too it. Apparently it’s the sugar and wheat that I’m no longer used to. I’ve moved onto wine. Sometimes we have to make sacrifices.

  20. Martin marsh

    Yes this may all be so but what is the link between heart disease and diabetes ? I have had a heart attack but have never been diagnosed as diabetic (annual blood tests). So why are you more likely to have a heart disease if you are diabetic ? Surely there has to be a common factor ? I do not see it. Apologies if I am being thick, the rest of your fans seem much more knowledgeable than me.

  21. Alicia

    Hi. I’d like to ask you what do you think about vegans, fruitarists and the people eating the so-called high carb low fat raw vegan diet? they can eat up to 3000-5000 kcal/day of mainly CHO (80-90%E comes from carbs and rest from protein and fat) and generally they are very lean. do you think they’ll develop IR later or is it also about genetics? I mean, some people handle larger amt of CHO (when fat intake is relatively low) w/o getting obese OR developing IR…

      1. David Bailey

        Since carbohydrates can be converted by the body into fats (see your previous post!), how does this work? Is it the specific fatty acid that is important?

    1. Dr. Göran Sjöberg


      Me and my wife have now spent six years on strict LCHF and I have during the time tried my best to understand medicine, and specifically nutrition and health, though with my metallurgical research background eyes. And I have definitely arrived at the same position as Dr. Kendrick. Physiology is an incredibly complex subject, at least as compared with the ‘simple’ ‘rocket engineering science’ of metallurgy which I am very familiar with.

      In this endeavour to understand nutrition I started with reading the well referenced ‘thick’ book, “Good Calories & Bad Calories” (GCBC for short), by the much rewarded science journalist Gary Taubes. That GCBC book is generally considered to be ‘difficult to read’, an opinion which I personally don’t understand, and Taubes was evidently forced to produce a ‘light’ version of the same book which I generally can not recommend since it lacks the rigours. For me GCBC was an excellent, true ‘tour de force’, though not intended for any quick reading, with an, at the same time, profound humble inquiring mind (typical for any scientist worth the name). Along the line, he was advocating the hypothesis that it is the insulin driven by the high amount carbohydrates which may be regarded as a main culprit, talking diabetes and other ‘ailments’ in the ‘metabolic’ syndrome.

      The book I am now trying to read, “The Low Carb Myth”, is of a completely different grain. As mentioned I have serious problem with the ‘language’ in the book with it’s so strongly categoric attitudes (no humble scientific position here!) and the main target of attack is evidently Gary Taubes and his GCBC book. Irrespective of my own difficulties with the arguing attitude in the book I still find very interesting facts and thus facts which I think needs to be scrutinised.

      One of those facts mentioned in the book relates to the vegan ‘high carb’ diet and diabetes as you brought up. Evidently, and there is no reason for me to mistrust this information without digging deep into it, a strict vegan diet seems to be very beneficial for diabetics and the insulin resistance. On the opposite side I can ‘guarantee’ that a strict LCHF can be very ‘healing’ for a severely injured T2 diabetic.

      So my present attitude to carbs is, with Malcolm, that the physiology involved seems to be incredibly complex and where categoric attitudes does not fit in at all.

      1. Alicia

        thanks both! I think so too but am not sure of course. And I’m pretty sure also amount of fibre in the diet may influence the outcome, eg compare eating plain white rice or potatoes, or combining them with fiber-rich vegetables, beans etc. Or then just stick to oats which high in fibre and betaglucan. I’ve also heard berries and cinnamon with high carb meals are beneficial due to antioxidants and whatever was in cinnamon that reduces inflammation or something 🙂 But yeah, fascinating yet sooo complex issues!

      2. John U

        I believe that what is missing perhaps in the book is the total calories consumed. There should not be any problem remaining thin if the energy consumed is roughly what the person requires, that is isocaloric eating at a weight maintenance level. The problem with the SAD is that carbs and fats are consumed in prodigious quantities which mostly exceed the energy needs of the individual, thus excess calories are stored. The rest of the story is the same as we all know it regarding insulin resistance and the effect of high levels of insulin for too long.
        Many vegetarians just don’t eat “too much” and don’t eat the fast carbs which spike insulin. This has to make a difference.

  22. JPA

    I used the following analogy to explain insulin resistance to one of my patients.

    Imagine a company which is funded by a philanthropist. The philanthropist hears that the workers do not have the resources they need to do their job (muscle cells not getting enough energy leads to hunger). The philanthropist hears the workers and sends a check to the company (the person eats food). The top managers cash the check and put the money in their bank accounts and the workers don’t get what they need (insulin resistance, the muscle cells can’t get the energy and it gets stored as fat). The workers complain that they still don’t have resources (more hunger). The philanthropist writes another check (person eats again), and the top managers take the money (fat cells get fatter). And the cycle repeats.

    The tragedy for fat people who are insulin resistant is that they really are hungry. The cells doing the work need energy. But eating doesn’t give those cells energy because they are insulin resistant. Heavy exercise reduces insulin resistance, but that is a very difficult way to reduce it, and if someone who is out of shape starts to exercise they are almost certain to overtrain and their brain stops them from exercising to prevent injury. So fat people are fat, not because they are eating comfort food or are lazy, but because they are insulin resistant and do not have the resources to reduce that.

  23. lyn

    As you know, people with Parkinsonism (me) and who are treated with levo-dopa/carbi-dopa end up tying themselves in knots (and becoming vegans) because pretty much any protein they eat interferes with the absorption of the medication – and most proteins come with some kind of fat that slows down the gut. Current treatments advise taking a lower dose of l/c-dopa more often to avoid dyskinesias. Many of us now take the medication every couple of hours – it is hard to plan to eat protein at least a half hour after the med is taken, then wait at least an hour before the next pill is due, when you are on an almost continuous intake of the pills. In fact, the geniuses called Movement Disorder Specialists/Neurologists are developing a pump that shunts a gel formulation of the drug and pumps it through the abdominal wall into the small intestine (still doesn’t work when protein present). Then they wonder why most of us get fat, and why there is a link between PD and diabetes. Same with thyroid chaos. Whacko….how did this happen?
    I enjoy your articles and always pass them on,

  24. Ari

    Spot on! I have found two other sources, who have come to same conclusions. Seems like a strong evidence to me.
    First is this study: http://press.endocrine.org/doi/full/10.1210/jcem.86.8.7763
    It says practically this: if you manage to keep your blood sugar under 4.5 mmol/L (80mg/dl) under any circumstances (also during glucose tolerance tests), you are free of diseases like heart disease, cancer, hypertension, cerebrovascular disease and type 2 diabetes.
    The study was finished in 2001, but took terribly long before it was published in 2013 – makes one wonder, if it was delayed on purpose? Think of the consequences, if all the people would manage to lower their blood sugar that much! Devastating (to big pharma)!

    Then there’s Dr Joseph Kraft. He, too, mentions “obesity must be considered hyperinsulin, type 2 diabetes until proven otherwise” (chapter 20), but also recognizes, that not all t2 diabetics are obese. He names the condition as “Pathology of Hyperinsulinemia”: first you get hyperinsulinemic (get insulin resistance) –> endothelial dysfunction –> vascular dissemination –> atherosclerosis –> coronary artery disease –> cerebral vascular disease –> nephropathy –> peripheral vascular disease –> full blown type 2 diabetes. This phase-model is described in his book: Diabetes epidemic & You. And in table 1 on page 6 there is drastic reduction in hidden diabetics (who are not discovered via fasting blood sugar, but via combined glucose tolerance and insulin tests) with blood sugars – you guessed it – under 4.5!

    And now Dr. Kendrick writes the same story from a different angle. I’m convinced.

      1. Stephen

        Is it true that they became fat after being forced onto reservations and made almost entirely reliant on grains?

  25. Bruce Miller

    As a T2 (actually t1.5 after exposure to Agent Orange in Viet Nam) I appreciate your commentary on the “conventional wisdom.”

    Unfortunately a friend of mine from under grad school (and now a PhD.) had a heart attack and is/has blamed dietary fat as the culprit (never carbs which he ingested by the wheel barrow full) and now has excluded virtually all fats from his diet.

    Neanderthals’ DNA legacy linked to modern ailments
    This was interesting.. Have not raced the original paper yet.

  26. Soul

    I can remember all those years ago, 25 years by this point, seeing doctors about an IBD condition. The specialists had run out of ideas. There wasn’t any medication that could help. All of them were saying I’d have to live with it. But as I’d point out, this wasn’t living! So I did what I could, and began reading, educating myself about dietary ideas that might help.

    What surprised me going forward was when I’d see the doctors for checks up, and bring up dietary articles I had read, all were fairly uninterrested, in a few cases hostile, and sometimes didn’t seem to know what I was talking about. It was only later that I learned how little schooling physician’s receive on nutrition. Their reaction made some sense then, nutrition was a foreign topic. It was disappointing from my stand point, but it was an area left up to patients to read and experiment with on their own.

    With diabetes, I personally doubt officially new dietary recommendation will be made soon. Well, as you post, new dietary recommendations are in the works, but not directly pointed out with diabetes. Hopefully though some with the condition and inquisitive minds will try eating lower carb to control their diabetes. I’ve seen a small study on Dr. Briffa’s sight with mention of lower carb eating helping significantly around 75% of diabetics. And with that I’d guess improve outcomes with other disease associated with diabetes, such as heart disease and some cancers.

    Dr. Davis’s simpler avoid wheat for weight loss and glucose control seems intriguing. Seems that idea has taken hold with many. I remember seeing even the Prime Minister of the UK, David Cameron, saying he was looking to loose weight, to be “patriotic” and was going to let the bread maker gather dust. Hopefully it helped.

    it seems all the western world leaders look much older once they leave office. Often it’s said to be the stress of the job that ages them quicker. I’ve wondered if instead it wasn’t the rich diet often served.

    “Cameron’s breadmaker gathers dust as PM gives up carbs in the ‘great patriotic struggle’ with his weight”


  27. Jan

    My daughter is 14, VERY thin, and highly insulin resistant. She has the signs and symptoms that you would expect to see in a very obese teen who eats junk food all day: high insulin and testosterone levels, severe acne, acanthosis nigricans, amenorrhea. We try to feed her mostly whole, real foods, easy on the carbs, and she does not overeat. I had the same symptoms at her age and I was very thin, too.

    We have an inherited form of PCOS (my mother, too). After monkeying with my hormones trying to conceive the weight piled on, and of course I’m pre-diabetic. I am tired of doctors assuring me that if I “would only lose weight, my PCOS and pre-diabetes would be gone.” They are baffled that my daughter so clearly has insulin resistance and she is so thin. The weight did not cause this, but the insulin resistance most assuredly caused my weight gain. We prove your hypothesis, too.

    A low carb diet has helped me a lot. I’ve lost and kept off 75 lbs for years. My daughter was conceived when I was first trying low carb and metformin.

  28. Aila

    Excellent post. Sorry for being such a hairsplitter, though. Type 2 diabetes should be written type 2 diabetes and not type II diabetes. The first one is pronounced “type two diabetes” and the second “type second diabetes”.

  29. Anne

    I have never been obese, nor even fat, am on the thin side but not like those people with no adipose tissue, and I am not insulin resistant, but, according to the NHS I am a Type 2 diabetic. That’s becasue the NHS likes to categorise diabetes into Type 1 and Type 2. My endocrinilogist, however, says I am a “monogenic” type diabetic which is neither Type 1 nor Type 2. There are several rarer sub groups of diabetes, expensive to do the genetic testing for so I don’t know which monogenic type I am. Regardless, the best treatment is an extremely low carb diet 🙂 🙂

    1. Dr. Malcolm Kendrick Post author

      there used to be a thing called LADA. Latent Autoimmune Diabetes in Adults. It was a big issue, then it seemed to disappear – now it is coming back again? Basically, you have a form of type I diabetes, but it takes years and years to develop. Rather than hitting you when you are a child.

  30. T Hart

    What puzzles me is, that three years ago when I was 7 kilograms heavier, my bloodsugar was 82. Now after two years of low carbing and a nice weight of 52 kilograms, my bloodsugar is up to 94 and the year before 93. Shouldn’t it be lower than the 82?
    Triglycerides went from 143 to 91

    1. DBM

      T Hart

      When you restrict carbs for a long period of time you develop a form ‘physiological’ insulin resistance. The brain still needs glucose to function so a way ensuring that it gets enough to do so is to render the muscles resistant to taking up glucose leaving whats left for the brain.

      Also for the liver to function properly it needs an adequate store of glycogen. If you don’t eat many/any carbs your body has to get glucose from somewhere. It does this by glygoneogenesis by raising cortisol levels to break down protein to get the raw materials to make glucose. If you don’t eat enough protein your own muscle mass is at risk of decreasing.

      I think it’s the rise in cortisol that drives this physiological insulin resistance. I also suspect that this consequence of low carbing, the rise in cortisol, would explain a lot of the anti-inflammatory effects of low carb diets ie improved asthma , inflammatory bowel disease, arthritis etc

      1. Jan Vyjidak

        What often gets missed is that the brain does not only use glucose. When insulin levels drop to low levels and stay there, the brain (and other tissues, mainly skeletal muscles) gradually switches from glucose to betahydroxybutyrate. We can see that on PET/CT scans in fasting people and in people on ketogenic diets (very similar metabolic effects, as noted by Dr Russell Wilder in 1921). For more details, see the work of Dr Hoffer. On top of that, whilst glucose in the brain requires astrocytes, betahydroxybutyrate does not – neurons can process BHB directly, sparing the energy-conversion capability of astrocytes altogether.

        1. Dr. Malcolm Kendrick Post author

          Yes, this use of other energy sources in the brain is very interesting. Yet, if blood glucose drops too low, we enter a coma and die. I find the entire ‘brain energy use’ area very confusing.

      2. Ash Simmonds

        I think the basic way to look at it is that our “primal” (basic function) areas of the brain require the glucose (original fuel) exclusively, but some of our “higher functioning” areas operate optimally on ketones (evolved fuel).

        Oversimplified, but yeah, the whole hindbrain/forebrain stuff is pretty fascinating.

      3. Jennifer

        After removing porridge from my diet in order to go ‘low carb’, I can now say I am in a good place nutritionally, and have re-introduced the product, because I believe it has benefits.
        However, I use what I consider a much superior oatmeal……Pinhead Scotch Oatmeal. It requires a few hours steeping before cooking, and is a million miles from the ready-brek stuff foisted onto the uninitiated trying to do their best for the kids.
        In the NHS of ’60s, we always steeped oatmeal overnight for the patients’ breakfast, and one of my jobs in the ward kitchen ( now that’s a thing relegated to history! ), was to keep an eye on the porringer whilst it gently cooking its contents. Steeped, oatmeal porridge is more properly digested in the gut, and pinhead is as unprocessed as we are likely to achieve in a useable form. Rolled oats are not quite the same stuff, but better than ready brek mush.
        By the ’90s, I was putting in a complaint to the dieticians that it was neither good nutrition, nor good aesthetically, to feed the elderly with ready brek and reconstituted dried milk powder, sloppily mixed in the actual bowl served to the patient. It landed on deaf ears. Back then, the ‘ nutritionists’ had lost the plot regarding any understanding of correct food production, and were being brainwashed by the efficiency experts in their far off offices.
        So, there are good carbs and bad carbs…..and more’s the point….good methods of food production, and bad methods which may make the food taste the same, but which do not work the same in the gut.
        We need a darned good food revolution across the globe, before we are all permanently mal-nourished.

  31. Anna Watson

    My husband is T2D and we control his blood sugar by eating a Primal / Paleo diet. No grains, no sugar and no starchy vegetables and nothing low fat. He is not on medication. At his last diabetic assessment he had put on a little weight (a bit of overindulgence at Xmas and New Year) and the nurse gave him a diet sheet. It was full of high carb, low fat rubbish. I put it straight in the bin. He has lost the weight again.

  32. Ken Strain


    Though mostly in the context of T1DM, Sonsken and Sonsken [Brit. J. Anaesthesia 85, 2000] show evidence that adipocytes accept glucose through other than the insulin controlled GLUT 4 transporters, when the glucose gradient is high (as in DM). (There are many other relevant comments in the same paper.)

    In that context, the claims of Unger and Cherington [JCI 122, 2012] ” that glu-
    cose-responsive β cells normally regulate juxtaposed α cells and that without intraislet insulin, unregulated α cells hypersecrete glucagon, which directly causes the symptoms of diabetes” suggest that hepatic glucose production is the equal or leading cause of high blood glucose. Again this is mainly for T1DM.

    However, this can be brought into the context of T2DM:
    “Our findings suggest that the pathophysiology of the exaggerated glucagon response differs between the types of diabetes. Intra-islet insulin deficiency and alpha cell insulin resistance may be the primary contributors to this condition in type 1 and type 2 diabetes, respectively.” [Tsuchiyama et al, Diabetes Care 2007 ]

    The presence of many adipoytes that are not overloaded allows the overproduction to be partially absorbed; when this mechanism is inadequate glycosuria ensues. So it appears to me that insulin resistance of the pancreatic alpha cells is the main player in T2DM. This may also be consistent with the rapid recovery in the diets of Roy Talyor and Jason Fung (among others).

    In lipodystrophy, it explains the lack of protection (I’m guessing that in that case there is no IR, and even normal glucagon levels saturate the system with glucose). In the Sumo, new adipoytes are added to take up the gluose burden (interesting balance of stem cells producing both muscle and fat at the same “time”, right?).

    I wonder if the Pima have very strong mitochondria. Or perhaps the UCP2/3 polymorphisms that reduce their BMR don’t also lead to CVD. [Walder et al Hum Mol Genet. 1998 Sep;7(9):1431-5]


    1. Dr. Göran Sjöberg


      As you I found Professor Unger’s view on the interrelation between the alfa and beta cells shaking my present view on diabetes, the established one, both types. The most interesting part of Unger’s research was to me that in T2 the glucagon production in the alfa cells do not shut down following an insulin spike from the beta cells which takes place in a healthy person.

      And then there was the poisoning of the beta cells, specifically the mitochondria, by ‘disturbing’ fat deposits.

      1. sankoo388

        May I request your help in deciphering the complexities of metabolism? It is such a complex creature, something which even after about 2 yrs of reading, I just can’t seem to put a finger on a simple unified theory that explains it all. Too many feedback loops and such. Seeing that you have a scientific background, albeit in a different field, and have attempted to study this mystical creature through rigorous independent study, will you please help me decipher the mysteries of this creature?

      2. Dr. Göran Sjöberg


        “May I request your help in deciphering the complexities of metabolism? It is such a complex creature, something which even after about 2 yrs of reading, I just can’t seem to put a finger on a simple unified theory that explains it all.”

        I am a research metallurgist but have now spent about six years now to understand some ‘basics’ in our physiology and metabolism but have to admit, as you, that the complexity is overwhelming. We have about 20 000 different proteins in our bodies which are interacting with one another in very little understood manners – that is poorly understood physiology to be frank.

        Realising this physiological complexity I am today almost allergic to any categoric statement about how we ‘work’.

        Still I ‘believe’, by personal experience and physiological logic, that too much carbs is not good for your health when you have entered the pathological state called the metabolic syndrome. And if you have reached so far into this metabolic state to become a diabetic it doesn’t make sense to me to eat stuff that increases you blood sugar. But to my astonishment this is what actually is recommended officially and only to the benefit of the market for insulin.

        And with Malcolm, and with my favourite philosopher Xenophanes, 400 BC, I think it is possible to to get more knowledgeable but all the same that we never will reach the “truth” and if with by coincidence will reach that truth we will never understand that we actually have the ‘truth’ in our hands.

  33. John McCholesterol

    Reaven says now that visceral fat is not so important after all.

    The world is not upside down, rather it is being shaked 24/7, in almost every issue.

    I believe science needs some serious philosophical reformation. At least, in the area of communicating to the public. And scientists in all fields should be very wary of politicians and salesmen and the hybrid types. They are just too naïve!
    Or maybe not so naïive and they are actually implicated in the con.

  34. Indian@large

    Ok, I have been reading your blog for about a couple of months – don’t exactly remember how I ended up here in the first place though. To put it short, as can be guessed from my handle, I am Indian, and of the Asian type. So over the last couple of years, my love of reading led me to start learning about fats,carbs,proteins and the like – like what really causes heart disease and the like – like everyone else, I have been fed a steady drip of ‘scientific hypothesis’ regarding the causes of heart disease – it is fat only, and that too saturated fat, and then the only way out is to lower your own cholesterol levels by using statins – now, being of an inquisitive bent of mind, and not afraid of taking the less used path, I decided to get into the great wide web world – and boy – I was kind of blown away – when you discover that all the so called hypothesis actually never had any scientific basis to them, it was merely by wont of being regurgitated ad-hoc by ‘figures of authority’ , that such stuff came to be accepted as dogma – and the people of the world have indeed been worse off for it – guess the natural greed for money is the primary cause behind all this – it truly and well corrupts even the well intentioned at times – ok – since Indians have a predilection for heart attacks, it has always been assumed that the primary reason is genetic – but on closer examination, the real reason to me is that the normal Indian diet is loaded with carbs – lots of rice and wheat based bread are used as staples – plus, a lot of us Indians have a big sweet tooth and tend to gorge on a lot of sweets , and then, fried snacks are rather popular with us – the worst thing about eating such fried snacks outside your home is that they are fried in vanaspati(basically like margarine and full of transfats), and even then, that oil gets re-used – even within homes, for reasons of economy, the oil tends to be re-used – that causes a lot of radicals to be generated – and we generally use a lot of seed based oils – sunflower oil, ground nut oil and the like – no Indian curry can be made without the use of cooking oil – ghee being a higher derivative of butter is of course a much superior alternative, but it is rather expensive to procure for a lot of Indians , and hence is used only by a very small miniority – I guess I have rambled long enough as to why I think Indians in general tend to be prone to heart attacks – Ok, I really need some help from you all folks here – I have plugged away hard at to the whys and hows of we get fat, why heart attacks happen and all that – I am in no way a scientist of any sort, nor do I claim to be an expert on biology and medicine in general, but I crave knowledge – so I have basically plugged away at a great sort of blogs, books and the like – and I do have an idea about what really matters – healthy mitochondria , the krebs cycle, NADH, glycolysis, gluconeogenesis, warburgs theory of cancer(anaerobic respiration), transfats, seed oils(where antioxidants are destroyed through use of solvents), conversion of glucose into fat, inhibition of fat breakup in fatty adipose cells in the presence of insulin, low grade inflammation damage due to excess radicals within the body and all that – the problem is that I simply cannot grasp all of that information into one coherent general theory that is not too deep in scientifc detail either – would really help me when I try to attempt to explain to the others as to why we are really eating a wrong diet and stuff. Ok, thanks for the help in advance and I do hope to post more often on here.

    1. Sue Richardson

      Indian@large. Send for Dr Kendrick’s book ‘The Great Cholesterol Con’. It’s easy to read and will definitely help you get a grasp on things.

  35. Grex

    Dr Kendrick, by “at a certain point insulin resistence develops to block further weight gain”, you are referring to adipocyte insulin resistence when they can’t take anymore, not general insulin resistence? It seems to me the notion of obesity “causing” type 2 diabetes is underpinned by the idea of diabetes being temporal punishment of moral sin of gluttony and sloth, but if omega6/ refined carb “cafeteria diet” leads to disruption of ability to maintain appropriate energy balance/energy stores for the perceived environment, or autumnal “make hay while the sun shines” fattening for a fatburning metabolic winter that never comes, the process of becoming obese in those genetically capable of it temporarily PREVENTS positive energy balance causing the high blood glucose and cells that don’t want it that would get you a diabetes diagnosis, “Which is why you CAN become almost ridiculously fat” is of course not true for most people. The young Chinese adopting Western diet with pre-diabetic blood sugars are shaping up for an epidemic of diabetes which will NOT be preceded by an epidemic of obesity as in the West, what will the moralisers’ interpretation of that looming tragedy be?

  36. BobM

    Dr. Kendrick, I think you’re totally correct on this.

    If you want (or anyone else wants) another doctor’s perspective on why insulin causes obesity (and other maladies), see the following by Dr. Fung:


    I particularly recommend viewing the lectures on the aetiology of obesity:


    Dr. Fung treats people for Type 2 diabetes by putting them on intermittent fasting. He’s ostensibly able to cure their diabetes. Fasting reduces insulin resistance, and he believes Type 2 diabetes is caused by insulin resistance (not by high blood sugar levels, which instead are a marker for insulin resistance).

    One thing I find troubling about all of this is that the “powers that be” always choose one option instead of leaving their options open. In this case, they’ve chosen the “obesity leads to insulin resistance” instead of saying, “we don’t know what causes insulin resistance; until we do, we’re not going to make any definitive statements on this topic.” The same could be said for diet: I don’t think anyone knows what the proper diet is for every single human, yet (in the US) they selected a low fat, high carbohydrate diet and told everyone to go on it. At the time, there was just as much evidence sugar (and not fat) was bad for you, but the “powers that be” had to make a choice. In my opinion, they choice they made was wrong. That’s 50 years of being wrong.

    1. Mark Sanders

      If someone is restricting their carbs to have normal or close to normal blood sugar readings, I assume they are still “insulin resistant.” According to this doctor’s theory are they still in a bad way even though their sugars are down?

    2. Stephen

      Bob, I think the McGovern commission in the 1970s also listed sugar as a problem, but somehow all the focus went onto fat. As we know, when they took the fat out of products they tasted awful and sugar was added. Low fat/high sugar was born and we can see the consequences.

  37. Jonathan Christie

    Two studies which elucidate a benefit of low-carb diets are almost unknown, yet they greatly advance our understanding. They show that low-carb diets deplete glycogen stores in the liver, which lessens glycogenolysis even when insulin is low and glucagon is high since (anthropomorphism alert) the liver insists on keeping a reserve of glycogen around for emergencies. As a consequence, the elevated fasting blood sugar characteristic of diabetes disappears – all one needs to know really if one is diabetic or insulin-resistant.

    “A low-carbohydrate/high-fat diet improves glucoregulation in type 2 diabetes mellitus by reducing postabsorptive glycogenolysis” Allick 2004, and “The effects of carbohydrate variation in isocaloric diets on glycogenolysis and gluconeogenesis in healthy men” Bisschop 2000.

    Solid gold – these studies say: the ADA diet will kill you …

  38. John U

    A great post as always. In the post you say,
    “However, mild to moderate insulin resistance, even if blood sugar levels are not consistently raised, is not benign. It is associated with a whole series of other metabolic abnormalities such as: central obesity, raised VLDL/triglycerides, low HDL, high blood pressure, high levels of blood clotting factors…..”

    I have been looking for information regarding blood clotting factors which may be being caused by diet and I have found very little on the web related to high carb eating. Could you elborate a little on this issue or provide some references which may lead to more info? I have a friend who is fit and thin, but suffers from blood clotting and is medicated with warfarin or equivalents.

  39. DBM

    Excellent as always. However there is a different way to view this whole situation. It is a given that if you are insulin resistant one of the easiest ways to manage your glucose levels is to avoid the stuff all together. What interests me is what makes you insulin resistant in the first place.

    There is an assumption here that sugar causes insulin resistance, but I don’t think this is true even though it feels intuitively true. After all diabetes is a condition of raised blood glucose that can be managed by reducing ones glucose intake. Therefore eating too much glucose causes diabetes and reducing your intake of glucose can prevent diabetes. Easy, problem solved, ban sugar regulate it or tax it to death and all our health problems are solved. But I don’t think this is true.

    There is not a great deal of robust evidence that states that Carbs actually cause insulin resistance. Stephan Guyenet, a fairly high profile blogger and obesity researcher at whole health source, wrote an interesting blog series on insulin resistance. He ended up by listing the main causes

    1.Increased cellular energy
    2.Physical inactivity
    4.Very low carb diets(<10%)
    6.Insulin resistance in the brain
    7.Low birth weight /size
    8.Inappropriate micronutrient status
    10.High heat cooking
    11.Excessive physical or psychological stress

    Note none of these include carbs as a cause though low carbing is. I think the main problem is to do with excessive intracellular energy. Is this due to too much glucose, fatty acids or both? I think that increased intracellular fatty acids are the culprit.

    A healthy cell can seamlessly switch between burning fatty acids and glucose but the diabetic cell lacks this metabolic dexterity and really struggles with oxidising glucose. Normally glucose is broken down to pyruvate and then to acetyl-coA which then gets oxidised. This last step is controlled by the enzyme PDH (pyruvate dehydrogenase). If the level if intracellular fatty acid gets too high PDH gets switched off and there is a backlog of pyruvate and glucose. The pyruvate is converted to lactate which is fairly toxic and puts further breaks on PDH amplifying the problem. The increased glucose spills out of the cell causing hyperglycaemia hyperinsulinaemia etc etc.

    In this model it the presence of excess fatty acids that kicks off the process of insulin resistance.

    Could this explain what is going on in the three examples? The Summo wrestlers don't get diabetes because of their low fat diet. They get fat not because of the magical fattening properties of carbs but because they eat an unreasonable amount of Calories. The excess carbs are converted to palmitic acid are then dumped into the adipose tissue. It is interesting that despite the high amount a fatty acids floating around that insulin resistance does not ensue. Saturated fat must be protective against the development of diabetes.

    The poor chaps with Beradineli-seip lipodystophy are probably screwed what ever they eat. However, I'd wager they do better with a low fat diet as they can not store any excess fat and should avoid anything that would interfere with the efficient oxidation of glucose.

    It is interesting the the Pima do not develop cardiovascular disease despite their insulin resistance. I think their insulin resistance is a little easier to explain. The Pima of Mexico have a far lower incidence of diabetes than their American cousins because their diet is closer to the traditional diet of squash, corn,beans meat and fish (70% carbs14% fat). The Pima in New Mexico eat a typically SAD of 44%carbs 44%fat) the incidence if diabetes nicely correlates with the increase of fat (mainly PUFAs) in their diet.

    So, the low fat diet of the Sumo wrestlers protects them from diabetes, the presence of fat may make the insulin resistance of lipodystophy worse and the increase of fat in the diet of the Pima correlates with the increased incidence of diabetes.

    Just some food for thought…

    1. Jennifer

      DBM. I think this is most interesting, and I certainly like the 11 points you attribute to Stephen Guyenet. There is obviously a starting point, (or perhaps the plural points,) in the process that leads to type 2, and it is so easy to latch on to the long established belief that it is solely excess glucose. Maybe we have just taken the line of least resistance, and so missed other causes.

    2. Dr Robin Willcourt

      Very informative. Dr Tom Aoki, from the Joslin Clinic, studied the release of insulin in the animal model then slowly acquired human data to show that insulin is released in 4 to 6 minute pulses after a certain threshold of glucose has been reached in the portal vein. Using pulsed insulin infusions iv mimicking the natural pattern of insulin delivery, (PIVIT) he found that by doing serial; measurements of the respiratory quotient, the diabetics changed from poor glucose burners to normal, after 3 to 6 hours of the iv treatment (RQ changed from 0.7 to 1.0 typically).

    3. David

      “Stephan Guyenet, a fairly high profile blogger and obesity researcher at whole health source”.
      Says all you need to know.

      1. DBM

        I don’t get your point. Who should you trust? Where should you get your information from? One of the major themes of Dr Kendricks blog is the problem around the acquisition and dissemination of knowledge, especially medical knowledge. If you are happy to leave the responsibility for knowledge about your health with the powers that be then you are in for a rough time, because the advice they give is often misguided ,biased or just plain wrong.

        So if you want to find out what to do you have to do the work yourself.

        The problem is that there is so much (dis)information out here on the net that its difficult to know where to start and what to believe so you have to apply certain filters to make sense of it all. Obviously, a lot of people here have a ‘Post Taubesian insulino-centric’ view of health which helps to explain a lot, but you have to be aware of confirmation bias and not just discard information that does not fit your model of looking at the world.

        I’m not particularly a Stephan Guyenet fan but he has a PHD in neurobiology and has done a lot of reading and research in the area of obesity. I see him as a useful filter to help piece together a lot of the information out there. So when he’s written a comprehensive series on insulin resistance and has not found carb/starch/fructose intake to be a cause of insulin resistance I find that interesting challenge to the sugar-causes-diabetes-meme.

      2. John U

        Personally, I found his blogs lacking in scientific rigour. I am not a fan of his writings nor his research. I am not sure how to interpret your comment.

  40. Richard Gibbs

    I think there are three things that should also be included in a theory of diabetes.

    You need to mention Adiponectin when talking about insulin resistance. A lack of this hormone is associated with insulin resistance. It’s produced in adipose tissue, hence none is produced if you have Beradinelli-Siep. Adiponectin production declines with increasing adipose tissue.

    High blood sugar is the result of the failure to regulate glucagon, which is the hormone that causes adipose tissue to produce sugar. So diabetes can be a failure of of the pancreas to produce sufficient insulin to inhibit glucagon production in the pancreas. Injections of insulin do not produce a sufficiently high concentration of insulin in the pancreas to effectively inhibit glucagon production.

    The Pima Indians come from an area where historically their blood type was almost exclusively type O. Dr. Kendrick, I’ve been encouraging you to look at the evidence that ABO blood type is a major factor in the suitability of a diet. Grains, including corn (maize), are particularly bad for type Os. You can tell when Native Americans started to consume corn from the appearance of arthritis in the remains studied in the Indiana burial mounds. So it may be that a high grain diet is more likely to cause diabetes in type Os, thus there would be a higher incidence in populations with a higher occurrence of type O blood.

  41. Gordon Rouse

    I am sure you will find populations on very high-carb diets that do not get diabetes (at least on their traditional non-western high-carb diet).
    I think Stephen Guyanet did a great job debunking a similar model being put forward by Taubes.

    If you want to understand diabetes and obesity, you have to throw away the whole idea that obesity is caused by over-eating, or even eating specifically too much item x. Simply put, people do not in general over eat unless something is seriously wrong in the first place. Most “overweight” people do not over-eat either, they eat how much their body wants them to eat:

    It seems like a chicken and egg problem, however that is because we are forgetting something really crucial: the whole thing began in the womb. The determinants for both obesity and diabetes are determined by genetics and how those genes are switched on in the womb environment.
    Obesity does not cause diabetes, and diabetes does not cause obesity. The pre-natal body responds to environmental conditions in the womb. Obesity should be seen as a protective mechanism against an uncertain environment, it gives the body more room to shunt away excess sugars, and provides a buffer when food is scarce. Remember, obesity is not predictive of an early death, only morbid-obesity carries a statistically significant greater change of early death, and still not as dangerous as being under-weight.
    Once the first few years of life are passed the weight for age profile of the person is already determined.

    To see evidence of the the epigenetic pre-determination of obesity, I suggest you look up Jed Friedman’s moneys:

    Please note, that the researcher told me the mothers of the most effected offspring had higher omeg 6 / 3 ratios in their blood – (this he interpreted as a surrogate marker for saturated fat intake, for the interpretation I certainly disagree with).

    1. DBM


      I think you are right on track with this. People who are overweight don’t just steadily get fatter gradually over time, they tend to gain weight in fits and starts with short periods of weight gain, often during times of stress (so likely driven by cortisol) followed by long periods of no weight gain at all. Some obese people stay the same weight for years regardless of what they eat.

      I think that the omega 6/3 ratio is probably one of the most useful and insightful markers of health around. The higher the ratio to more ‘unhealthy’ you are and it reflects the amount of omega 6 fat you have consumed over time. Interestingly , the omega 6/3 ratio in breast milk has increased in the last few years as well which can not be a healthy thing

    2. Flyinthesky

      I can accept that certain predispositions can be genetically inherited however what has to be considered is lifestyles are also inherited. Parents who eat too much will usually feed their children in the same manner. It isn’t clear cut by any means.

      1. Gordon Rouse

        The problem is that no one has discovered a diet that maintains weight loss long term. I am prepared to believe that low-carb diets may have health benefits for a significant proportion of the population. I do not doubt that low-carb diets can cause short term weight loss, as too can vegan diets and many other diets. But the law of rebounding weight seems to apply no matter what the diet is.

        If lifestyle controls weight, then I would assume that lifestyle can be changed and therefore weight can be permanently changed – yet all evidence says that apart from ridiculous levels of self-control that few people can maintain, there is no way to change your weight long term.

        The conclusion to draw from this is either that there is some serious psychological stuff going on (which is a popular theory amongst the more patronizing health professionals ) or that weight is pre-determined by a combination genetics and early stage epigenetics (ie womb environment).

        Most health scientists are aware of evidence like the ‘Dutch Famine’, and some may have even read about Friedman’s monkeys, yet they tend to think of genetics and epigenetics as minor pieces of the jigsaw. Genetics has often been ruled out, because it cannot explain how obesity rates can increase within a generation, yet epigenetics provides the solution to this, and actually provides a mechanism by which diet and lifestyle does affect weight despite the contradiction that it cannot change an adults weight long term.

        By process of elimination, genetics and womb environment explain it all far better than any other theory out there. This theory leads to the question – what are the dietary and lifestyle factors which switch on inevitable diabetes and/or obesity in a foetus? I am sure some smart people here can come up with some good hypothesises.

      2. Flyinthesky

        Gordon, Epigenetics, I don’t know about the functioning of the placenta in sugar regulation, perhaps someone could enlighten me, but it would appear to me in a simplistic way that the infant in the womb could possibly be on the insulin rollercoaster before they are born. So it could be more environmental than genetic.

  42. MaikeC

    I’ve read all the posts to here and since a lot of people have wondered how a skinny person can be diabetic (though not officially by the current standards) I thought I’d repost part of a comment I made about a month ago:

    “…….most studies are based on overweight people with “metabolic syndrome” and visceral fat around the middle. I don’t fit that model .

    I have been slender all my life. Still very active. No physical problems. Eyes ok. Blood pressure around 60/100 w/o meds. However (for at least 20 years or so that I know of) my Fasting BS is never under 100 . BS will rise to 160-180 or sometimes over 200 depending on the amount of carbs I consume at the time, but settle down to around 120 usually two to three hours after a meal. A1C 6-6.2 %. No family history of diabetes. (I’m now 72).

    And remember the fasting cutoff number for diabetes used to be 140 then 126 and now 100. I realize lower/normal blood sugar is better for everyone.”

    [It’s also noteworthy that as soon as my blood sugar approaches 120 and lower I get very hungry. And for those who might wonder, I am 4ft11 and weigh 90 lbs.]

    And here is Dr. Kendrick’s reply:
    The whole blood sugar thing is yet another area of concern to me. As you may be unsurprised to know. As with most areas of ‘preventative’ medicine. Just because a high level of something is associated with an increased risk of, say, CVD. This does not mean the high level is causal, nor that lowering it will do any good – and may do more harm than good. The model of medicine in these areas has gone horribly, catastrophically, wrong.

    I am glad Dr. Kendrick is addressing this subject now in more detail as we clearly need a change of direction in looking at diabetes, also.

    1. ROB

      Yes there’s a reason fasting blood sugar levels for diabetes was lowered….hmmmmm…now let me see what that was… Ummmm…oh that’s it..if we lower it down to 100 then we can expand the amount of patients we can get drs to prescribe drugs too and the drs can get more kickbacks in return …ahhh a win win.

      The metabolic syndrome applies to both obese and skinny people alike but in different proportions. 80% of obese people exhibit metabolic syndrome and 40% of skinny people present with metabolic syndrome issues. Noone dies of obesity per se its from the complications that arise from metabolic issues. So that’s now…60% of American and rising since the late 70s. Only 30 to 40 years.
      Lack of mobility…ie introduction of computers….lack of sat fat and cholesterol to transport sugars and processed carbs out of the body and an totally incompetent ruling by dietary authority who were hell bent on blaming sat fat and cholesterol rather than excess sugars and processed carbs.

  43. David Bailey


    You aren’t by any chance taking statins, are you? These are documented to raise blood sugar, and indeed when I was taking statins I did get into the “raised blood sugar” category.

  44. mikecawdery

    A most interesting and thought provoking essay and another excellent Dr Kendrick. Once again thank you!

    I was distressed at the following comment:
    “For most doctors nutrition takes up about an hour of the medical degree course.”
    Given the adage “You are what you eat” this lack of attention to nutrition is a disastrous flaw in medical education. The comment by “SJ” is pertinent “…….., it means that what you eat determines your overall state of health, and my frustration has long been that the NHS is pushing a diet that’s the very opposite of healthy……..etc”.
    It also reflects the “step function attitude” of medicines to deficiency diseases. For example, rickets is a vitamin D deficiency while no rickets is taken as Vit D sufficiency and is reflected in the RDI. In fact Vit D deficiency to optimal Vit D levels is a distribution. Many other examples of this.

    Janet Beach pointed out that back in 1958 to quote:
    At the diabetes clinic I was given a booklet listing foodstuffs ‘freely allowed, weighed and ABSOLUTELY FORBIDDEN’ and a prescription for Rastinon. Imagine the horror for a 15 year old being told – no cakes, pies, puddings, biscuits, thickened soups, thickened sauces, no nuts (oddly), dates, sweets, chocolate Etc. etc. etc. Argh! On the other hand meat, fish, eggs, cheese, butter, cream, some vegetables, some fruits were all freely allowed. The rest – bread, potatoes, other starchy vegetables, most fruits had to be weighed. It amounted to 120 grs. carbohydrate a day……actually that seems like a lot to me now but I was a growing girl with ‘hollow legs.’ To this day, I weigh bread and have only 2/3 of an ounce with my (two) breakfast eggs.

    Where did this basically sound nutritional advice go in the last 60 years? It has been replaced by obese creating food advice.

    On the subject of obesity, I came across the following report (The obesity paradox in chronic disease – facts and numbers) in the J Cachexia Sarcopenia Muscle (2012) 3:1–4, DOI 10.1007/s13539-012-0059-5 (can be downloaded and Yes a largely unknown journal probably because no mainstream medical journal would touch it – contradicts the Gospel of the allopathic medical establishment). A telling quote: For patients with established chronic disease, there is sufficient evidence to support the benefits of large body size, i.e., the obesity paradox.

    Another interesting report (Am J Public Health. Published online ahead of print July 16, 2015: e1–e6. doi:10.2105/AJPH.2015.302773 – downloadable) relates to the failure of conventional programmes to control/reduce obesity. The following quote says it all: Conclusions. The probability of attaining normal weight or maintaining weight loss is low. Obesity treatment frameworks grounded in community-based weight management programs may be ineffective.
    Why not try locarb/hifat?

    I would also like to draw attention to:
    SACN Carbohydrates and Health Report
    and Zoe Harcombe’s comments there on, a pertinent quote from Chapter 12.8 is
    Total dietary carbohydrate

    12.8 “Overall, the evidence from both prospective cohort studies and randomised controlled trials indicates that total carbohydrate intake appears to be neither detrimental nor beneficial to cardio-metabolic health and colo-rectal health.”

    i.e. we spent seven years looking at evidence on carbohydrates and we can’t say that it’s harmful or helpful. That’s quite funny – unless you’re the poor sod who funded all of this. Hang on a sec – that’s me, as a UK taxpayer!

    Really the “official” advice on food and its consequences on health are depressing to say the least

  45. Lew Stalwarter

    To quote from the NHS Website
    “Type 2 diabetes occurs when the body doesn’t produce enough insulin to function properly, or the body’s cells don’t react to insulin. This is known as insulin resistance.”

    This being the case then we really have two (at least two) conditions but with the same symptom (Hyperglycaemia).
    As I understand it.
    With insulin resistance the insulin levels increase creating more IR until the pancreas can’t keep up.
    In obese people accumulation of fat around the pancreas results in lack of insulin. This would explain why significant weight loss would reverse T2DM.

    So, what in people with T2DM is causing the Heart Disease? Is it excess glucose or excess insulin?
    Are the obese, with non IR insulin deficiency protected against heart disease?

    Re the Pima Indians. Could the obesity result in fat around the pancreas resulting in lower insulin levels and thus protecting against heart disease?

    Just an idea.

    1. Dr. Malcolm Kendrick Post author

      Perhaps. But the Pima produce excess insulin from an early age. They are hyperinsulinaemic before becoming diabetic. Possibly due to a thrifty gene that causes them to store fat as quickly as possible, saving up for times of famine I would suppose.

      By the way, I would just like to say a big thank you to everyone for contributing such fascinating insights, and doing it with an open and honest desire to either educate, or learn. My hope was always that this blog could become an open scientific discussion forum where people were free to disagree, without being disagreeable. And where we could all learn from each other.

  46. timsteppingout

    I recently stumbled on the fact that different people have a different number of copies of the gene that controls salivary amylase secretion.

    Do you have thoughts or know of any studies that demonstrate how large a role this might play in carbohydrate metabolism, and role in development of metabolic syndrome and diabetes?

    1. David Bailey

      Maybe I am just way too cynical by now, but I remember joking some time back that one way for medical science to finesse the fact that 50 years of dietary advice has been completely wrong, was to confuse the story by discussing each individual fatty acid!

      There’s more and more evidence emerging that shows that not all fats are bad for us,

      I’d like to know if any naturally occurring fatty acid is actually bad for us!

        1. Dr. Malcolm Kendrick Post author

          I think you will find that every single fatty acid will be dissected and discussed to the point where even I will lose the will to live, before looking at each one in detail. As a wise man said (sic) ‘If you are winning the argument, tighten it. If you losing, broaden it.’ In the case of ‘fats’ throw everything into the air, keep spinning and blowing it about, and no-one will ever be able to argue with you ever again, because you can just change the subject whenever it suits.

      1. David Bailey

        The bad news is that apparently some of the fatty acids in foods are branched chain! This means that the total number of such acids must be thousands – so the debate can rage for centuries!

  47. katherine

    Hello Dr Kendrick

    I think you’ve missed something out in your model, which is that type II diabetes has a strong genetic component – some ethnic groups develop it more and at a lower BMI than others. And interestingly enough, people who have familial hypercholesterolaemia have a lower chance of developing type II diabetes.

    Well that is people who are diagnosed as supposedly having familial hypercholesterolaemia. Because genetic testing is rare and diagnosis is usually done on cholesterol levels alone this group actually includes anyone who has a “high” cholesterol level.

    I think the answer lies in the functioning of the mevalonate pathway. We know statins can produce type II diabetes – this is because they suppress the functioning of this pathway and hence the production of COQ10.. And people who naturally have suppression of the mevalonate pathway because of their genetic make up are more likely to develop type II diabetes.

    Us lucky types with high cholesterol on the other hand have mevalonate pathways that work well and plenty of COQ10. So COQ10 production is the missing factor here. The Sumo wrestlers will have plenty, as you say, because they exercise.

  48. mikecawdery

    I have recently come across work on MCT (medium chain triglyceride: Neurobiology of Aging xxx (2012) 1e10 – A ketone ester diet exhibits anxiolytic and cognition-sparing properties). There are many others

    MCTs are very easily absorbed into the blood stream. In the basic lipid profile would they be measured as triglycerides? Can triglycerides in the profile be sub-divided in to “good” and “bad” triglycerides? MCTs from olive oil and coconut oil are recognized (by some at least) as good.

    1. Dr. Malcolm Kendrick Post author

      I dont think it matters, but no doubt a million people wil ltell me otherwise. Clearly VLDL/triglycerides can contain different fatty acids, but I cannot believe that this can have any effect on what they do?

      I am also not a fan of calling molecules ‘good’ and/or ‘bad’. It is not terribly scientific.

      1. mikecawdery

        That is why bad and good were in inverted commas. My reason for asking was that recent “views” suggest that the triglyceride/HDL is a better “marker” of CVD risk than the current NHS ratios TC/LDL.

        I emphasize “marker” as there is a squadron of “black swan” reports showing that high TC and LDL are good predictors of survival.

      2. Ash Simmonds

        Doc K – I’m just amazed you’re even bothering with this any more. I’ve only cared about the fat/cholesterol/diet/health/etc crap for ~5 years and I think I’ve learnt all I need for life, even back in 2011 (not long after) I’ve got lucid posts/emails/etc about not stressing about this stuff, so intend to just ignore the entire industry and social commentary at some stage very soon and pursue other intersests.

        I just find the diet/health thing is all consuming/overwhelming, everyone has a bellybutton and are an expert in their own bellybutton – oh and same goes for nutrition and health.

  49. Nigella Pressland

    Did anyone see Trust Me, I’m a Doctor on BBC2 last night? They had a huge section on reducing cholesterol, having interviewed Professor Naveed Sattar, who was described as one of world’s leading authorities on heart disease. He said that lowering cholesterol was a key factor in reducing the risk of heart disease. The programme ran some dietary experiments on groups and also on Michael Mosley and concluded that to reduce cholesterol people should reduce saturated fat, eat oats, foods containing plant sterols, soy & almonds. Professor Sattar also said that statins were safer than asprin.

    So, there we have a programme that will have been watched by millions, still pushing the low fat, high carb (albeit not cakes & sweets) diet. Had I not done my own research, followed Dr Kendrick etc, I would have come away with the impression that this was gospel truth & the evidence they chose to release with it seemed convincing! It’s all up on the BBC2 website, should anyone care to have a look.

    1. David Bailey

      There seems to be a thought out and very sinister approach to maintaining scientific orthodoxy regardless of its validity. The technique is to simply avoid debating with anyone presenting another point of view – to pretend there is no dispute about the ‘science’ and above all, to present a consistent message (regardless of its truth). The more I see of this, the less I understand why it is going on, and why the bulk of scientists tolerate it.

    2. Flyinthesky

      Truth is a near insignificance. Opinions are formed by the perceived gravitas of the person uttering them and compounded by the size or the audience. It doesn’t matter how right you are if you’re not the “right” person and compounded again by your limited audience.
      Science has become an entity of nepotism and sponsored cronyism, if you don’t have the “right”, in many cases wrong, opinion you’re not getting the stage.

    3. clare

      Naveed Sattar also said that the worst food was processed meat because of the saturated fat! I looked up his research funding lots of the biggies BHF, diabetes UK etc – and where do they get their funding from.? He also said he was responsible for international guidelines ….is there no hope in the mainstream!?!

  50. Stephen

    DBN, if you don’t agree with Gary Taubes’ explanation for the ten fold rise in obesity in the last thirty years, what’s yours? And I’d be interested in your explanation for the nine fold rise in diabetes during the same period.

    1. DBM


      ‘Good calories , Bad calories’ is a real tour de force and presents an impressive argument for the carbohydrate hypothesis of obesity but unfortunately it is also an excellent demonstration of confirmation bias on a grand scale. Throughout the book, Taubes presented data that was aligned with his hypothesis and completely ignored any data that contradicted this or did conform to his view. Having said this his destruction of the diet heart hypothesis was epic in scope but this silly concept had previously been eviscerated by Dr Kendrick, Dr Uffe Ravnskov and Dr JamesLe Fanu back in the mid 90s in his excellent book The Rise and Fall of Modern Medicine.

      Carbohydrates alone are not inherently fattening. Fact. Cultures throughout history have eaten high carb diets and have remained perfectly healthy without obesity or diabetes or cancer. Almost all remaining hunter gatherer societies eat a large proportion of their diet as carbohydrates and are to all intents and purposes healthy and not obese. While they may not all be the picture of health, there aren’t many fat vegans and even fewer chubby fruitarians. There is not one metabolic ward study that has compared iso-caloric high-fat and high-carb diets that has proved that either diet is more fattening than the other.

      There are plenty of reasons for the rise in diabetes and obesity in the last 30 years. The environment has become increasingly obesogenic with altered epigenetics, increased sedentary lifestyles, increased generalised stress and decreased sleep by which I mean decreased quality and quantity of sleep. The main hormonal driver of the last two is cortisol not insulin.

      If one where to blame anything in the diet , of course the obvious culprit is the increased consumption of processed foods. When folk talk of the evil fattening carbs they tend to refer to biscuits, cakes, bread, pizza, crisps, fries and the like forgetting to notice that all of these foods contain about half their calories as fat. Most of this fat is in the form of omega 6 oils because they are cheap to produce and process and are seen to be less bad for us than the irrationally demonised saturated fats.

      Yes, the guidelines in the late 70s advised a low fat diet, but no one actually paid any attention to this. According to the USDA Economic Research Service, the 2007 calorie consumption as flour and cereal products increased 3% from 1970, while added sugar calories decreased 1%. Calories from meats, eggs, and nuts decreased 4%, from dairy foods decreased 3%, and calories from added fats increased 7%. The percentage of calories from fruits and vegetables stayed the same. The average person consumed 603 calories per day more in 2007 than in 1970.

      So given this, the rise in diabetes and obesity correlates with increased caloric consumption which has probably been driven by the increased food reward of the addition fat (mainly in processed food) in the western diet.

      Over a 100 years ago the only readily available source of omega 6 fats were in nuts, seeds and some meats and it was virtually impossible to over indulge in them. Now it is virtually impossible to avoid them unless you refuse eat anything packaged in plastic or cardboard.

      Well of course this is only correlation. Can omega 6 oils cause obesity and diabetes? Yes. PUFAs can reduce the metabolic rate ( that why squirrels eat nuts in the autumn before they hibernate). Its quite hard to stay slim if your metabolism is sluggish.They can also prevent the efficient intracellular oxidation of glucose that can directly lead to glucose intolerance/ decreased insulin sensitivity and frank diabetes. ( if you interested for a more detailed explanation of this please read, http://www.andrewkimblog.com/2013/03/diabetes-dangerous-fat-and-protective.html)

      1. Dr. Malcolm Kendrick Post author

        It is, of course, quite a deal more complex.( BTW I do have personal experience of knowing a vegan who was fat.) If you don’t eat more than your body is going to use, for energy and other activities, you cannot get fat. So, if you watch your diet, you can eat anything without getting fat. The questions comes, if you eat too much, which type of food is more likely to make you fat? Genetics plays a part, exercise plays a part, cortisol plays a part, thyroid hormone(s) plays a part. However, if you want to keep things simple – which I always do – if you alter the food balance from fats to carbs/sugars, and you eat too too much, and you don’t exercise, you will most likely put on fat. If you do the opposite, you will most likely lose fat.

        1. Rob Crisdale

          isnt one of the answers to all this is that our gut and microbiomes have been damaged as part of a continual onslaught of bad dietary changes since the early 1900’s .
          take for example thyroid issues – commonly we treat the the thyroid 1st and yet 60-70% of thyroid conversion happens in the gut where a signal is then sent to the thyroid to increase or decrease as the case maybe depending on intake.

          before the 1960’s also, the population only knew basically to use either lard, dripping or butter to cook in. With a shortage of these on supply, American and Japanese scientists developed seed oils and vegetable oils as cheaper alternatives but at the time misunderstood the consequences on human gut health and how important this area really is to overall health.

          Modern medicine practices thru antibiotics and drugs destroy both bad and good gut bacteria and have another knock on effect.

          diabetes, alzheimers, parkinson etc…the list goes on can all be traced back to an unhealthy gut system which is sending abnormal signals to the rest of the body and the brain.

          Since processing began in the early 1900’s we have seen a steady increase in diseases which werent even on the radar.

          The message here is – get back to eating real whole foods and drink proper fluids not carbonated or sugar and go back to consuming more healthy fats (at least 50% ) incl 30% protein and 20% unprocessed carbs will not only improve wons lifestyle but have huge benefits for govt health budgets all around the world ….

          1. Jennifer

            Rob, your analysis is spot on as far as I am concerned. I commend all the scientific explanations of physiological, cellular activity and hormonal involvement that contributors are sharing on this blog, in order to demonstrate the ‘why’ of the explosion in obesity and type 2 diabetes.
            But in terms of practical, day to day understanding for the average shopper perusing the supermarket aisle, it is a well constructed, thought provoking response, and we would all benefit by accepting your nice explanation. Especially those who haven’t the time, or inclination, to dig deep into the academic theory.
            There is room on Dr K’s excellent blog for each end of the discussion.

      2. Jennifer

        DBM. Thank you for the link. I have excersised my brain cells by reading and trying to understand the detailed paper, and it seems good stuff.
        I do worry that I become a slave to the last book/paper I have just read!

      3. mikecawdery

        DBM many thanks for the URL. Most interesting. And like your good-self I suspect that the omega-6/omega-3 ratio in food is an important factor. However, in my own case the “official advice” on a high carb/low fat diet was a disaster but then with the high omega-6, hitrans fats involved…………….. Who knows.

      4. DBM

        This chap is not doing bad for a 100 year old. Fred Kummerow is still working as a professor in the University of Illanois ; he found the link between trans fats and ischaemic heart disease back in the 1950s, and it only took the FDA 60 years to take notice and decide to ban them from processed foods…and that was only after he sued them!

        He practices what he preaches and tries to avoid all trans fats and vegetable oils and looks pretty good for it:

        http://www.washingtonpost.com/news/to-your-health/wp/2015/06/16/the-100-year-old-scientist-who-pushed-the-fda-to-ban-artificial-trans-fat/Fred Kummerow,

        A little more controversially his research has lead him to believe that omega 3 fats are also potentially damaging and is appalled that people consider them as a health supplement.

      5. David Bailey


        I know there are things called whole body calorimeters, and I wonder if any work has been done looking at the exact energy balance for normal and obese people.

        Is the experiment impossibly hard?

        I wonder a bit about the idea that stress is greater now. The Cuban Missile Crisis and the whole Cold War was pretty damn stressful back then!

        As I mentioned above, I do notice a very different (and regrettable) attitude to food nowadays. People order food when they are not really hungry, and then only eat part of it. This suggests to me that either they might have done that in the past if food had been sufficiently cheap, or something has changed psychologically.

        By dividing the weight gain over a number of years by the number of days, you do indeed get a ridiculously small number. However, if one of the psychological feedback mechanisms is disturbed a bit – such as the normal tendency to only eat when hungry – couldn’t that imbalance simply accumulate.

        They do say that “If Your Only Tool Is a Hammer Then Every Problem Looks Like a Nail”, and I wonder if in this case the hammer is the exact chemical composition of our food! Isn’t it more likely that a feedback mechanism gets disturbed, because clearly there are very effective feedback mechanisms that generally keep us the same weight regardless.

  51. Dr. Göran Sjöberg

    Gary Taubes great (not easy to read?) book “Good Calories & Bad Calories” was an eyeopener, at least to me, and he advocates the hypothesis, and his is very specific about that he is proposing a hypothesis, that insulin contributes to storing fat in your body,

    Taubes view is however viciously and to my dismay categorically (on this point I am just allergic) attacked by Guyenet and his followers but I wonder if these guys have actually read Taubes book with any open eyes. The attitude of the Inquisition to Galileo comes to my mind.

    The bottom line of this dispute is to me that, on the average, you get fat very slowly. That is to say that you just gain a few grams per day but in thirty years you have gained those extra 30 kg of fat. To me it is not unreasonable, and with Taubes, to assume this fat accumulation is not due to any ‘overeating’ by a few grams per day (this is obvious nonsense to me since a couple of grams are actually ‘nothing’ compared with the amount of food you usually consume each day) but rather due to some hormonal effects where insulin seems to be a reasonable candidate culprit if now being overweight can be looked at as an undesirable state but this seems more to be a cultural idea.

    No reasonable person, though, denies that it is quite possible to gain weight if this is your intention – the Sumo wrestler and the Ethiopian feminine nobility may serve as prominent examples as Taubes points out. And if you add a lot of carbs to the diet it seems like it is easier to accomplish this feat. But to explain the slow but undesirable weight gain by age through the official overeating,’ underexercising’ hypothesis is to me less credible.

    By the way I am now, with an almost inhuman effort on my behalf, almost through with “The Low Carb Myth” (written in the spirit of Guyenet) and I must say that I have seldom read something more “categoric” when it comes to nutrition and I cannot just figure out why the book has to be so categoric? Is there something wrong with the actual arguments, where some are quite interesting, so you have to raise your voice? And why has the main author to display his muscular torso in his presentation in the book? Is this to threaten any opponent?

      1. Dr. Göran Sjöberg

        Malcolm, I don’t know how to interpret your comment but still I think you are right.

        Gary Taubes book actually not only made me start questioning the cholesterol/fat/heart/statin anathema but along the line all other categorical statements from the medical establishment , e.g. about heart attacks, diabetes, mental illness or cancer and related ‘adequate’ treatments and all this seems to be very disputable to say the least.

        I have I friend who now called me today from the intense care heart ward unit where he has been ‘locked in’ (as he put it) now on the second week after a dubious ‘heart event’. They convinced him against his will to make an arteriography on him and based on that they are now very keen to make a by-pass although he seems to be in a much better shape than myself 16 years ago. The by-pass was scheduled for next week but he has decided to escape as I did myself. And I guess that there are no means by which they can do any operation by ‘force’.

        The sad thing is that all this makes me more angry with time and angrier the more I learn about the ethics involved in the medicine industry.

        1. Dr. Malcolm Kendrick Post author

          Aristotle discussed anger. There are several different type. Becoming angry about such things as injustice – good. Becoming angry with someone for disagreeing with you – bad. So, when I say that the angrier someone gets, the more likely they are to be wrong. This is a comment on those who use anger to cover up their weakness and try to bully you into silence. When I see this type of anger being used I consider this a very powerful ‘weather vane’ which tells me very clearly that the angry person is wrong, and must revert to instilling fear in their opponent. This knowledge has served me well. A friend once described it thus. ‘You know you are over the target when the flak is at is greatest.’

  52. Chris Harvey

    Dear Dr Kendrick,
    Have I understood carbs 101 correctly? Say I get up in the morning, stuff myself with the 1250 calories of carbs that can be stored as glycogen/glucose, get on my bike and ride for two and a half hours, which is about 1250 calories, and then eat a plate of chips, get on my bike etc ad infinitum without stocking excess carbs as adipose fat. Sometimes I do a charity ride where my bike computer shows 5000 calories for 9 hours cycling, where do these come from since there is no corresponding weight loss, quite the contrary.

    1. Dr. Malcolm Kendrick Post author

      Most of your energy will always come from fat, not carbs. It takes a hell of a lot of exercise to clear out your carb stores completely. The ‘wall’ in a marathon appears to represent the point where your glyocgen stores are running out and your body switches to convert protein to glucose. Your obdy doesn’t like this and says ‘stop.’

      Sprinters use virtually all carbs, anything at lower intensity will be mainly free fatty acids.

      I did read, can’t remember for sure, that power lifters can blow one thousand calories in one lift. This seems unbelievable. Perhaps someone can confirm, or tell me I am talking bollocks.

    2. Flyinthesky

      The variable you have to factor in is with increased exercise you increase muscle mass and muscle is heavier than fat. An illustration of this phenomenon is often expressed by the ladies. I’ve tortured myself at the gym but I haven’t lost an ounce and declared off camera my bum is still as big as it was before. You can’t exercise mass away without reducing calorific intake.
      What I find with a few friends and a daughter is they will undertake violent and strenuous exercise to justify the double steak pudding, chips and peas they think they have burned off.
      The cycle computer can only be used as a comparative, it’s calorific accuracy will be in the ball park of +/- 50% at best.

  53. sankoo388

    What of the impact of Vitamin D on diabetes? I have read of some anecdotal reports where high doses of Vit D have significantly contributed towards keeping blood sugar of diabetics within limits. If I remember correctly, NIH is still conducting a live study of the impact of Vitamin D on diabetes or something to that sort.

  54. Stephen

    The current NHS explanation for obesity is that thirty years ago a large section of the population suddenly got lazier and greedier. I’ve read enough history to be sceptical that humanity suddenly became greedy and lazy around 1980. It’s just not plausible. Several contributors have mentioned lack of exercise as a factor. I’ve exercised all my life and used to believe lack of exercise was a big factor. I now think it’s insignificant.

    I’ve read that if I eat a Mars bar I need to swim a mile to use up the calories. That’s a lot of exercise for one snack. Most people could never exercise enough to compensate for eating a sugary diet. The only time in my life when I’ve put on some significant weight is when I drank a lot of ‘healthy’ fruit juice, which of course is packed with sugar. I stopped drinking fruit juice and the weight disappeared fairly quickly.

    Taubes’ hypothesis that a sugar and carb rich diet triggers an insulin response makes more sense to me than anything else I’ve seen. The fluctuating blood sugar level tells we’re hungry and the cycle continues. This is a much more plausible explanation for the astonishing rise of obesity than we suddenly became greedy. Lots of things don’t help.

    People who go low carb overwhelmingly do well. Without any effort I lost weight and felt better both physically and mentally. I need the low carb sceptics to explain that? We seem to be doing something right.

  55. dwayne

    I wish MORE in the medical profession would look at this disease logically…
    More carbs=more glucose=more complications risks.
    Diabetics have a carb problem.
    Similar to those with a nut allergy. Yet no one tells them to eat carbs, but the status quo for us is to eat carbs!

    Bravo for “getting it!”

  56. John U

    I find it peculiar that DBM cannot see the absolute clarity of the Taubes hypothesis.The fact that Taubes picked references which supported his arguments is quite normal. We all do this. That is what we are supposed to do. If you have counter arguements, you should provide references which support yours. GT actually blogged on this very matter. DBM did not provide and arguements which could be considered as plausibly good science. Only correlations. The insulin/carb hypothesis is good science. The effect of insulin may not be the only factor at work, but it is probably the most dominant one. We all know that T1 diabetics could not store fat without exogenous insulin, i.e before Banting and Best, not matter what they ate, even fat which does not require insulin for metabolism. They all eventually died usually from ketoacidosis. This in itself should make it obvious that insulin is necessary to store fat in our fat cells. No insulin, no fat storage. Now we know that insuliin levels above baseline will deter the moblisation of the fat cells, so if you are insulin resistant even to a small degree, your blood insulin levels will likely be higher for longer and your fat cells will not provide any nourishment to your body during the time that insulin level is too high. This is science. It is not disputed. Is it not reasonable to believe that this process may be at work in our (insulin resistant) bodies, and over time we gain weight? Should we not do a study to check out this hypothesis? It would be easy and fast. Why is this issue still being debated when getting an answer would be easy? I think we all know the answer to this question and it is related to politics and money. Let’s not look for causes of obesity and T2D that might be correlated with cortisol, etc. until this hypothesis is checked. Indeed it has already been done, but ignored, just like so many other inconvenient results.

  57. MaikeC

    @David Bailey: No I have never taken any statins having read many times over the years that older women in particular do better with higher cholesterol. For those 20 years or more , my cholesterol was somewhere between 220 and 270 but always with a high HDL (70+) and very low Trigs (around 50). That gave me enough confidence that I should not worry.

    1. John U

      Kudos to you. You must be very brave and very confident in your ability to distinguish bad science from good.

  58. Dr Liz Stansbridge

    Please allow me a little boast. I have done it. Sorted my Type 2 Diabetes and lifelong weight problem.
    I was diagnosed with T2DM about 15 years ago. I had just had a hysterectomy for Endometrial cancer, caused by PCOS, a condition bound up with insulin resistance. It was all very obvious I would develop T2.
    The advice I was given was…..’just avoid sugar, no need to go mad’. That suited me, I didn’t have a sweet tooth but I loved pasta, tatties, wholemeal bread, fruit, rice. I carried on, the T2 got worse, I lost weight the T2 got better, I regained the weight, the T2 got worse.
    I have been overweight for 40 years. Lost many, many stones on diets, put it all back on and more. Eventually I decided it was doing more harm than good and stopped dieting.
    A year and a half ago, crunch time came. I was staring at the computer screen at pictures of my retinas. Peripheral haemorrhages. Early diabetic retinopathy. I had started to go blind through my T2.
    The time had come, the consequences of T2 were staring me in the face. Something had to be done. A core of strength stirred within me. ‘I will sort this, I will not let this happen’.

    I went onto the net. Diabetes UK told me a ‘healthy diet’ of complex carbs and more exercise would do it. But I also found ‘Blood sugar101’. That was an eye opener. I bought a glucose meter and tested, tested, tested. How very upsetting and dispiriting it all was. Brown rice, kidney beans acted like pure sugar, so did fruit! Don’t even contemplate bread or pasta! How could all the medical advice I had been given be wrong? No comfort food whatsoever!
    That core of strength stirred again. ‘So if that’s what it takes, that’s what I will do’.
    So I settled down to consuming about 3g carb at breakfast (most diabetics find their carb intolerance is worst in the morning) and 5g at all other meals. At these levels even onions, tomatoes and carrots are restricted. You can eat all the meat, fish, eggs, cheese and leafy veg you like. Nuts, very dark chocolate and berries are OK in limited portions.

    My HbA1c came down from very high to non-diabetic levels in a few months, but an extraordinary side effect: weight was falling off me! Of course, I was on Atkins, or to put it another way, low carb/high fat diet.
    I got to liking the weight loss, liked it a lot. So when the rate of loss slowed, I cut back on fat too. The weight plummeted. It showed how in control of my diet I was. Hunger had gone. Controlling the blood sugars had stopped cravings.
    I never weighed myself at the start, never even thought about it. Controlling my diabetes was my sole aim but my GP has my initial weight at 21.5 stone. 14 months later, I am at my target of 12.5 stone with a BMI of 25.5. I deliberately stopped there to keep myself slightly overweight, the healthiest weight group. I am playing at maintenance now. A little more carb: my insulin resistance has improved so I can eat 10-15g carb per meal. Hurray! Unlimited tomatoes, onions, some fruit, crispbread, even a portion of battered cod occasionally.
    Am I afraid the weight will go back on again like it always had before? Not really. It seems that controlling your diabetes controls your weight to a large extent. The complete opposite of the establishment’s view. Was I a greedy slob who became diabetic because of laziness and lack of will power? No! Diabetes causes uncontrolled hunger. Dare I say exercise has nothing to do with it either!

    The other benefits of a low carb diet: within a week I felt I had woken up from a drugged sleep. I was and remain alert, excellent mood, sleep well, awake refreshed. Waterworks better, ankle swelling gone, intra-ocular pressures reduced (I had borderline glaucoma), visual acuity improved, various skin fungal infections gone. Haven’t even had a cold for over a year.

    I feel I have done miraculous things for my health by one simple lifestyle change. Low carbing, ‘eating to my meter’. I have not done one step of extra exercise, not taken a load of pills, although I continue my Metformin, it seems to make about 5g difference to my carb sensitivity and frankly I want that 5g!
    Has the medical establishment helped me control my diabetes? Well no, GP’s muttering about extra medication, insulin. Dietary advice was completely counter-productive. I had to find out how to do this on my own.
    Even now I have a tussle to get strips for my glucose meter from the surgery, doled out grudgingly. My strips will have cost about £150 over the last year. What price health? They would be happy to put me on gliclazide, insulin, statins, pay for lazering of retinopathy, hospital stays for limb amputation. Not joking. I have an acquaintance who has had all these things without anyone addressing his diet.
    Here I am at maintenance. I tried adding the fat back in. Oh my god! Bloating, windy, uncomfortable! Weight up 2lb in one day! Back on the mod. carb, low fat. It seems clear that diabetics can’t cope with carbs and fat together. Zoe Harcombe says you can’t eat carbs and fat together, I am sure that’s true. All the surveys of people who live longest in this world show that food restriction helps you live longer.
    So, back on my Lenten way. It has it’s compensations. Sorry that I moan occasionally. Low carb takes much of the pleasure out of food. But, boy do I look and feel good!
    Not a fat, middle aged woman anymore, a svelte gorgeous woman in control!
    But if I was just overweight,not diabetic, I would succumb to an offer of cake. The prospect of going blind supersedes everything. So thank you diabetes, I will never be overweight again.

    1. Jennifer

      Dr Liz, you have taken my breath away this morning!
      Your story should be broadcast across the nation, especially as you put it so eloquently.
      A number of bloggers here have successfully bucked the NHS mantra of silly dietary advice and endless prescriptions for drugs, but your personal story is an indication of just how damaging the care being offered by NHS surely is. We need a radical overhaul of diabetic management in the NHS, it is a disaster.
      In my case, I was never overweight….in fact, as you state, a BMI tipping over 25 is classed as being more healthy than under 25. I have fluctuated between 23 and 27 all my life, but when I made a commitment to conquer the diabetes two and a half years ago, I kick started the offensive by stopping all meds, eliminating carbs and introducing excercise. My BMI quickly dropped to 23, and I was 2 stones lighter within a few months.
      That was my base line on which I have built a very healthy body, free of all medications, devoid of unnatural exercises, other than the normal excercises of daily living….housework, leisure walking, running for the bus occasionally.
      I have gradually increased carbs, the so-called carb-creep as Dr Atkins called it, except that I now know which carbs to add to my diet.
      My weight has gone back up to a BMI of 25, but my figure is a far different shape to when I was previously the same weight……..5 inches lost off my waistline have never returned.
      I am repeating here my personal info which bares repetition in the context of your concern for your eyesight…..I have had the wonderful news that my eye health is at optimum levels…..not a hint of diabetic damage, no age-related deterioration whatsoever, and an optical prescription giving me 20:20 vision (I have needed specs since age 5 following measles). I hope this gives you hope that diabetic eye conditions are seemingly successfully managed, using good food for blood glucose management, rather than drugs.

      1. ROB

        Well done malcolm….
        The thing that the bmi doesnt take into account of is muscle and that’s why many see there weight go up but not waist line…many a weight lifter who have bmi of over 25 or 30 and yet lean body fat.

        1. thelastfurlong

          Thanks – nice link – going to watch the video. I watched the program on low carb eating that people were put on in the Canadian (or was it Alaska?) village on our TV some years ago. Why is it the authorities in UK are still offering the advice that diabetics must base their meals on carbohydrates? Logically, to me, there must be some huge profit to keep people ill. The BMA and MHRA here have board members who are directors of Drug Companies. This should ABSOLUTELY not be allowed. I look at it as a criminal action to advise diabetics so poorly. https://thelastfurlong.wordpress.com/2015/07/26/i-kid-you-not-eating-advice-from-the-nhs/

        2. Kay

          Rob, thanks for posting that Jay Wortman video. I’ve known about him and his program for years, but don’t think I’d ever watched the video. That nay-saying dietician was something else. I hope she didn’t live in the community and stay behind after the experiment, or all will be lost for sure.

    2. Pat

      Congratulations and thank you very much indeed for sharing your experience with us. This is very interesting.

      I have had more help from Dr K’s work, from people like you and other fellow bloggers on this web site than the surgery. Your earlier moan reached me because I often feel like that too.

      I think Dr Bernstein’s book is a very useful source of information for T2s since it contains lots of things in one place I found out piecemeal over the years and much more. Jenny Ruhl has given me a decent explanation of why I can occasionally go low.

      Thank you all for sharing ideas, comments and especially Dr K for the two carb blogs.

  59. thelastfurlong

    The internet is full of “anecdotes” about type II diabetes and diet and people demonstrating practically, that they can manage it themselves. I am another one. My moment of illumination was not going blind, nor being overweight which I’m not, but observing the route my husband was railroaded to by the NHS. One pill has led, over the years, to the whole menu! To me, it seems that the medication – Avandia for a while – and then, injecting something mimicing lizard poison (can’t remember the name) both taken off the market now, not to mention all the other drugs, are bringing on conditions he never had before! He is not cured – just made ill!

    I would have loved him to have refused all medication and restricted his eating instead. But I think, in the beginning, he was under the illusion that medications would fix the blood sugar and so he would be able to eat anything. Some people HAVE to eat. Hunger rules it all. Hunger is my husbands constant companion.

    Since those days, when we (both) confidently expected medication to deal with the sugar problem, we have discovered many of his pills actually make him hungrier!

    I discovered fat. I am on a high fat, high protein, low carb diet. The fat removes the hunger. I eat carefully and very little. Fortunately, I love fat and rich food. But my husband does not. Since 2002, my cholesterol has remained the same even though I have been a high fat primal eater for several years now.

    Dr Liz’s story is remarkable – it takes real courage to override the power that the medical profession have over the minds of people. My husband is a believer. I am not. This is a difficult situation. Everyone deserves confidence in the path they follow.

    It might be too late for him. Even so, at some times when enthusiasm rules, and he eats less – much less – he has been able to halve his insulin. But such discipline is very, very difficult for some people, especially if they might secretly suspect their wife is possibly a raving looney advocating something the doctor never told him!

    Love your blog!

    1. Kay

      Alas, people are led to believe that medication will fix the diabetes problem — will, in essence, make it go away. So medication is seen as a “more efficient” way of dealing with diabetes than fiddling endlessly with diet.

  60. Lee Pettersson

    Dr Liz you have given me hope. I am not diabetic but struggle continuously with high cholesterol. I to measure my protein levels every day as I am worried about diabetes as it runs in my family and non are over weight with the exception of my self which at 90kg is a struggle. My GP states it is due to the medication but I fail to believe her diagnosis but this does not help shift the weight. I take 50mg Topamax twice daily for migraines, 75mg lyrica twice daily for nerve pain from my back along with HRT troches. I have tried Ketogenic & Paleo but find I lose weight to start with and then I gain twice as much within 4-6 weeks. I find now I just eat very little but shakes I make myself this has helped stabilize my weight and my cholesterol. I will now try again with a different idea and looking at what you have done and see what results I get. Thank you for the inspiration. What goes into ones mouth is not always the cause of weight …..I can not eat but fast for a week on lemon and water for a week and gain more than if I ate for a week.

  61. good4yougoodies

    I’ve been meaning to reply here for at least a week – when the comments only numbered 73. 🙂 This will probably be a long post, but I do hope people will read it, since I’ve been doing both Theory and Praxis on these subjects for the last eight years, to great success for me, and for others.

    “Gordon Rouse wrote: The problem is that no one has discovered a diet that maintains weight loss long term. If lifestyle controls weight, then I would assume that lifestyle can be changed and therefore weight can be permanently changed – yet all evidence says that apart from ridiculous levels of self-control that few people can maintain, there is no way to change your weight long term.”

    I have found that way and it’s one that can work for everyone reading this. First, about me. I’m nearly 70, weigh 132, wear junior size 7 skinny jeans, have biceps off which you can bounce a quarter. My body fat (measured) is 22.9%. My triglycerides are 42, my HDL is 100, my A1c is 5.1, my fasting insulin is <2 and I'm not hypothyroid. My leptin level is 5.5. My heart is normal, my blood pressure is 115/60 and my resting pulse 68. I eat about 3000+ calories a day. The only medication I take is metformin, and given the lower risk it gives me for cancer and heart disease, they'd have to pry it out of my cold, dead hands. Every year I get a little slimmer, and a little healthier – and no 'self-control' is required. I eat like a dockworker.

    Eight years ago I weighed 245, wore a size 24 tent, er, dress, had 52.5% body fat, fasting insulin 15, leptin 60. My blood pressure was 195/110 when diagnosed; I was put on three medications. Everything else measurable was horrible (I was so hypothyroid it's surprising I could get out of bed in the morning), and I ate a 'healthy' diet of only 10% fat, 15% protein and the rest carbs, all the way up to the 1100 calories a day I ate back then. I have now lost an entire whole person – and have not gained back an ounce or an inch for the last six years.

    In fact, not only was I severely insulin and thyroid hormone resistant – I had what I now call Metabolic Syndrome XX, a term I coined. Read about it at:

    That's my blog and Doc – you and "The Great Cholesterol Con" are featured on the home page. 🙂

    Gary Taubes saved my life. Reading his piece in the NY Times Sunday Magazine ("What If It's All Been A Big, Fat, Lie"), which predated GCBC by a few years, opened my eyes to the science of nutrition. It took me years of medical and science research to fix myself – first the insulin resistance, then the leptin, then the hypothyroidism. It took me two years to lose the bulk of the weight (down to 163), but another two years to get truly slim and genuinely insulin sensitive again. Aside from not eating added sugars (no part of any food group) except for a bit of maple syrup now and then — I eat anything that doesn't eat me first. Because just as a calorie is NOT a calorie, a carb is NOT a carb. Not created equal at all.

    Lots and lots of fat of course, modest protein, and all complex carbs out there. If I want bagels, I make them myself ( 80 g rye sourdough each – all my breads are sourdough, even my brioche), pizza, same thing. I eat all fruit in season, one or two a day, with lots of fat. Dark chocolate, no problem. I do Body By Science workouts, which is roughly 15 minutes twice a week.

    But – and it is a big one – intermittent fasting is definitely part of my Protocol. Everyone on Protocol starts with Metabolic Blood tests (also listed on the blog) that doctors almost never do, and should always do. Everybody's metabolism is broken in a unique way and at different levels. Telling everyone to eat same (or not eat the same foods) to fix it makes no sense, so everyone's Protocol is individually designed for them based on their results. It's why Atkins, Paleo, Primal all work if you are already metabolically healthy — but why none of them will fix you if you're broken. Not for the long term, which in my mind is forever.

    And for the woman from the UK that said her doctor said she was 'fine' from doing a simple fasting blood sugar – you're not fine. Not if you have excess adipose fat, either externally (obesity) or internally (TOFI – thin outside, fat inside), which is even more dangerous than obesity. And the only way to get diagnosed is by taking all the 'sister' tests together: fasting glucose, fasting insulin, leptin and thyroid hormones. And by paying no attention whatsoever to 'ranges' but instead learn what true normal is from sites like BloodSugar101.

    Everyone starts out eating one meal per day, between 11 and 1. Everyone takes their fasting and Postprandial blood sugars (one and two-hour) so they can actually see how the food they're eating affects their bodies. Intake mimics the 'lean times, good times' cycle of hunter gathering. Two weeks of lean, to get into lipolysis and finally open up the locked adipose fat cells. Four weeks of good to get the brain to accept the new lower fat and weight set points, then back to lean again and so forth. This works like a charm, every time, every person. During the good times, new foods that previously caused spikes are slowly added back, until by the time Lifetime Maintenance is ready to start, Participants are eating everything, and I do mean everything – and a lot of it. Except added sugars and processed food, of course.

    The goal is true normal fasting, and especially true normal PP's. All fat and weight loss (and 'goals' are measured with a tape measure, not a scale!) is a by-product of getting healthy again, and usually DT2 is gone within six months. True insulin sensitivity takes a year or two more. A year or so after that, hypothyroidism is gone as well. By this time, everyone is doing Body By Science HIT training and eating twice a day. A small breakfast, and a BIG meal no later than 3 p.m. No one regains anything. It's a one way ticket to Slim-ville. 🙂 Proof? Data (and not someone's word for it) is critical in Science. So I only agree to take someone on if they agree to post a journal on the blog daily. Weight, food, blood sugars, comments – and measurements every Monday. I now have four years of accumulated data on the blog, and it's free and accessible to anyone who wants to read it.

    Long post, I know. Hope I haven't bored anyone. 🙂


  62. George

    Question on carbohydrate ingestion. What about the corner case of someone eating carbohydrates in excess of their glycogen storage capacity but still eating at or below weight maintenance? Would the excess carbohydrates be converted to and stored as fat, but be utilized for energy sometime during the day since the person is remaining weight stable? Would this person develop hyperinsulinemia, but not insulin resistance (since they’re not gaining weight)? Thanks! Was always curious about this.


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