Insulin Resistance is Good? – T2D 7

posted in: Diabetes, Health and Nutrition | 73
FettkeInverson
Dr Gary Fettke – looking devilishly handsome! (Tasmania, devil, get it?)

Everybody says that insulin resistance is bad. Very bad. It’s the root cause of type 2 diabetes (T2D), and metabolic syndrome, isn’t it? So, if it is so bad, why do we all develop it in the first place? What’s the root cause? My friend Dr. Gary Fettke from Tasmania wrote an illuminating book called ‘Inversion’ where he describes how you can learn a lot from looking at things from another perspective. Invert (turn upside down) your perspective, and see how your horizons are immensely broadened. So let’s look at why we develop insulin resistance. Why is it good?

Root Cause Analysis

What is the root cause of insulin resistance? Some people say inflammation or oxidative stress or free radicals causes insulin resistance. Those are total cop-out answers. Inflammation is the body’s non-specific response to injury. But what causes the injury in the first place? That’s the real problem. The inflammation is only the body’s response to whatever is causing the injury.

Think about it this way. Suppose we are battlefield surgeons. After decades on the job, we decide that blood is bad. After all, every time we see blood, bad things are happening. When we don’t see blood, bad things are not happening. It must be the blood that is dangerous. So, deciding that blood is what is killing people, we invent a machine to suction all the blood of people. Genius! The problem, of course, is what’s causing the bleeding, rather than the blood itself. Look for the root cause. Bleeding’s only the response, not the cause. Bleeding is a marker for disease. So is inflammation.

Something causes bleeding, the body’s non specific response. Something causes inflammation, the body’s non specific response. Gunshots cause bleeding, knife wounds cause bleeding, and shrapnel causes bleeding. Those are root causes. You got shot. You bleed. But the problem is the gunshot, not the bleeding. The same applies to inflammation.

Whatever is causing the injury (the root cause) is also stimulating inflammation (the nonspecific response to injury). Inflammation is simply the marker for disease. So people say that cardiovascular disease, diabetes, neurodegenerative disorders, obesity and cancers all involve chronic inflammation. But the inflammation is not causing the disease, it is only a marker of it.

If inflammation was actually a root cause of heart disease, for example, then anti-inflammatory medications (prednisone, ibuprofen, NSAIDs) would be effective in reducing heart disease, or obesity, or cancer. But they are not. Whenever people talk about inflammation being the cause of disease, they just bandying around the latest buzzword.

This is not to say that inflammation (or bleeding) is not useful as a marker of disease. If the bleeding stops, then the treatment (tourniquet) is highly likely to be effective. But it’s not effective because bleeding stopped. It was effective and bleeding stopped (it’s a marker for effectiveness). Similarly in inflammation and T2D, as I previously wrote, insulin therapy does not decrease inflammation, which marks this likely an in-effective treatment overall.

The same goes for oxidative stress (or free radicals). Tell me what is causing the oxidative stress. That’s why antioxidant therapy is so startlingly ineffective. So Vitamin C, or E or N-acetylcysteine or other antioxidant therapies never work whenever they are tested rigorously. Because the oxidative stress is only the response (like inflammation) to whatever the underlying disease process actually is. If somebody goes on and on about oxidative stress (or free radicals or inflammation, or bad gut microbiomes) as the cause of XXX disease, run, don’t walk the other way. “Insulin resistance is caused by inflammation” is like “gunshot wounds are caused by bleeding”.

Insulin Resistance

So, back to insulin resistance. Why does the body develop it so frequently (up to 50% of the American population)? This simply cannot be mal-adaptive. Our bodies are not designed to fail, since we lasted for several millennia before the modern diabesity epidemic. Insulin resistance must serve a protective function, being so common. Maybe this IR is actually protective. Regulation of insulin sensitivity is part of the normal physiologic response – it can go up or down depending on lots of things, including other hormones (eg. pregnancy) or availability of nutrients. So how can IR be protective?Hoarder

Consider this. Excessive glucose in the blood is bad for us (high blood sugars). If this high glucose level is toxic in the blood, why wouldn’t it also be toxic in the body, too? Shouldn’t we get rid of the toxic levels of glucose instead of merely shoving it from the blood into the tissues of the body? After all, insulin doesn’t actually get rid of the glucose. It shoves the excess glucose out of the blood and forces it into the body. Somewhere. Anywhere. Eyes. Kidneys. Nerves. Heart.

Imagine you have too much garbage in your house. But you like to keep your chair nice and neat by moving everything elsewhere. Instead of actually throwing the garbage out of the house, you merely shift it around in the same house. Not a great idea. For glucose, instead of reducing the total amount of whole-body glucose, we merely shove it from the blood into the body.

So,if this high glucose is toxic, then the natural response of the tissue (body) is to protect itself against this excessive glucose load. Suppose you live on a street of houses in DiabetesVille (each house is a cell of the body). Everybody is friendly and normally leaves their door open (just as a cell is open to glucose in the insulin sensitive state). A truck full of toxic waste (glucose) comes down the street. And the garbageman (Insulin) really wants to get rid of this slime. So, every time he sees a door open, he shovels in some toxic waste (glucose).

'Toxic Waste Disposal, satisfaction guaranteed or double your waste back.'

After a few days of this, what would you do? You’d bar your f***ing door, is what you’d do! You’d say,”I don’t want this toxic slime!” That’s insulin resistance, baby! You make it really difficult to shove that toxic stuff into your house. It’s not a bad thing, it’s a good thing. The insulin resistance is trying to protect the cell from the toxic levels of glucose that the insulin is trying to shove in the door.

What is Insulin Resistance protecting us from? It’s very name gives the answer away. Insulin Resistance. It’s a reaction against excessive insulin. It’s protecting us from the excessive insulin. In other words, as we’ve written before, Insulin causes Insulin Resistance. But the root cause here is the Insulin, not the Insulin Resistance. The tissues (heart, nerves, kidney, eyes) are all busy increasing their resistance to protect themselves from Insulin which is trying to shove some toxic glucose into their house.

So we call the specialist Dr. Endocrine. Dr. Endo decides that the slime is indeed toxic, and we must get it off the streets immediately. There are some options – like reducing the production of toxic glucose (Low Carb diets) or burning off the toxic glucose (Fasting). But instead, he decides that he will hire more garbage men (insulin) to shove this toxic glucose into the houses. At least then, Dr. Endo won’t be able to see it anymore. Now Dr. Endo can pretend he is doing a great job. Look! The streets are nice and clean. But all the toxic glucose goes into the houses (tissues).

And what happens over time? Well, all the tissues of the body just start to rot. We are inadvertently ‘overcoming’ the tissue-protective insulin resistance developing. Instead of targeting the insulin, and reducing the total amount of glucose that we have to deal with, we are increasing how to get rid of it. So, by prescribing lots of insulin for patients, we are not making things better, we are making them worse.IR is Good

Warning – Technical talk ahead – feel free to skip ahead. Normally, there is an inverse relationship between blood glucose and free fatty acid (FFA). In the fasted state, glucose is low and FFA is high. The body is burning fat for energy. As you eat, insulin goes up, glucose goes up and lipolysis is inhibited and FFA levels fall.

But in T2D, insulin levels are high. Glucose is high. But because of excessive IR, FFA is also high. So, the tissues of the body are now at risk of receiving both excessive glucose and fat, which is now causes the oxidative stress and the inflammatory response. But the inciting factor here, is the excessive glucose and insulin. (See pretty picture above for graphical explanation). Excess glucose to the mitochondrion overloads the electron transport chain and results in excessive ATP production as well as Reactive Oxygen Species – all causing oxidative stress.

Glucose metabolized through the anaplerosis pathways that produce AcCoA and MalCoA which becomes substrate for cholesterol and fatty acid synthesis. MalCoA inhibits FACoA resulting in steatosis, or the production and abnormal deposition of this fat.How to Get Fatty Liver

OK, technical speak over. Welcome back. So, in the liver, excessive insulin produces fatty liver. We can easily demonstrate this in humans. In this study, 16 test subjects were overfed an extra 1000 calories of sugary snacks per day. This consisted of 1 can of Pepsi, 30 ml of fruit juice and a bag of candy. Over 3 weeks, there was only a 2% increase in total body weight. However, there was a disproportionate 27% increase in liver fat due to DeNovo Lipogenesis.

In other words, insulin is driving much of this excess glucose into the liver and it’s being turned into fat. Some of this fat can be exported out of the liver to other tissues such as muscle and pancreas giving you ‘fatty pancreas’.

In the muscle cells, we get fat deposits between the strands of muscle. You could call this ‘fatty muscle’. Technically, this is called intramyocyte lipid accumulation. Many think this causes insulin resistance, but it is more likely the result of   excessive glucose and insulin. The accumulation of fat between muscle fibres (where there should not be any), in cattle, is called delicious.

Cattlemen, of course, know exactly how to develop marbling in cows. The most important determinant is the type of feed. Cows are ruminants, which means that they normally eat grass. However, by feeding a high energy, grain heavy diet, ranchers can increase the growth rate of cows as well as increase marbling.

See if you can spot the difference between well marbled beef and lean beef.CornFedvsGrassFedBeef-steaksonly The grass fed beef develops no marbling, which gives steak much of its flavour. For this reason, many grass fed cows are ‘finished’ with feeding corn in order to develop the fat marbling. Insulin and glucose. No secret. It works in humans as well.

You can see the same sort of fat deposits in the muscle cells of the heart and this may contribute to congestive heart failure. ‘Fatty Heart’.

A New Paradigm

So inversion forces us to see T2D from a new perspective. The toxic agent here is the excessive glucose, and its co-conspirator, insulin. Moving the toxic glucose out of the blood and forcing it into the body has no net benefit, as has been amply demonstrated by multiple long term randomized studies – ACCORD, ADVANCE, VADT, and ORIGIN.

Instead insulin resistance develops precisely because it is a protecting the tissues against the blood trying to shove all its toxic load into the cells. This is why the development of the insulin resistance is universal. It’s a good thing, not a bad one. Giving exogenous insulin to overcome this IR is actually detrimental. So the problem is not the IR at all. Instead, look for the root cause – the excess glucose and excess insulin. Take that away, and the T2D goes away.IR is Good2

So there are good treatments for T2D, and there are bad ones. The bad ones overcome the tissue insulin resistance which is there precisely to protect the tissues. These are insulin and sulfonylureas. The good treatments get rid of the glucose out of the body. You can do this by preventing it from coming into the body in the first place (LCHF diets, Acarbose), or burning it off (Fasting) or urinating it out (SGLT-2 Inhibitors). This explains the power of this new class of medication in terms of cardiac protection.

Insulin resistance is bad? No, not at all. It is good. Insulin resistance is not the root cause. It’s the natural, protective reaction to the root cause – high insulin levels. It’s the insulin, stupid!

Update – Dec 4

What’s the practical implication? Think about it this way. If your house is full of garbage, you can do 2 things. Stop putting garbage in (LCHF). Or you can start throwing garbage out (Fasting). It would be faster throwing garbage out AND fasting (LCHF + IF).

73 Responses

  1. PCOS–my mother had it, I have it, and my teen daughter (BMI of 18% incidentally!) has it too. Genetics is definitely an underlying factor in our family. I get that genetics loads the gun and diet pulls the trigger, so I am NOT saying that PCOS is the only reason we are IR. I ate poorly most of my life and I take responsibility for that.

    However, we’ve been fairly careful with my daughter’s diet all her life, and she STILL has severe insulin resistance and all the metabolic issues related to insulin resistance (acanthosis nigricans, severe acne, amenorrhea, high testosterone levels, fasting BG’s that seem too high to me). Her diet is not very low carb, but since she was born the family has eaten a fairly “clean” paleo-ish diet (with full-fat dairy and a limited amount of grains).

    I am pretty strictly LCHF for the past 5 years and beginning to do IF according to your recommendations. We are both on Metformin.

    So this post is making me think. Is the Metformin–in its role as an insulin sensitizer–actually letting MORE glucose into our cells??? Is it working against us?

    Daughter’s testosterone level has come down a lot with Metformin, but it has not helped her other IR related issues.

    As for me, I’ve always thought that Metformin was standing between me and a conventional diagnosis of diabetes, because even with Metformin and LCHF my fasting BG’s are pre-diabetic levels. I’m hoping your IF protocols will help me turn that around. Should I consider getting off the Metformin? My doctor really doesn’t think I need it because “I’m not diabetic yet” (sigh. . . ).

    • It seems your warning is correct: “There are three ISAs currently on the market, and at this writing I prescribe all three of them—metformin (Glucophage), rosiglitazone (Avandia), and pioglitazone (Actos). ”
      (ISA: Insuline-sensitizing agents). I guess Dr Jason will remove the ISA’s from the figure above, in time….

      Case in point: If one is cutting insulin from 27 to 20 units with metformin, an example from the article below, It could well mean 25% more sugar into the cells (by night). Thanks for your vigilance! http://www.diabetes-book.com/insulin-sensitizers-mimetics/ I guess ISAs were also part of “aggressive” treatment studies like ACCORD and other listed above that increased all cause deaths instead of health therefore prematurely (thankfully) discontinued.

    • I’m insulin resistant on lchf mostly paleo as well. Recently I was tested for sleep apnoea. The doctor said sleep resets hormone levels including estrogen, lowers testosteone raises insulin, ghrelin and leptin and leaves me hungry all the time. He said everyone with PCOS should be tested for sleep apnoea. It is hereditary due to the shape of your soft palate. It’s a simple oximeter worn on your finger overnight, then fedexed back to the lab. Measures both oxygen in the fingertip (blue for apnoeas, pink when breathubg) and heart rate. He showed me how my heart rate spiked at the same time as the apnoeas. He said it’s like being strangled 100 times a night on your adrenal stress response, raises risk of hear disease and stroke. I had no symptoms, never snored, but got tested because my mother had it badly. I now have a cpap machine and my abdominal obesity (sign of insulin resistance) is shrinking as I find it much easier to control hunger.

  2. Metformin has some advantages, search on Pubmed for many studies. No doubt Pharma is looking for ways to incorporate it in a pill for a new expensive wonder drug. http://www.ibtimes.com.au/us-fda-gives-ok-human-trial-metformin-anti-ageing-drug-prolong-life-until-120-years-1488127

  3. wow! such clarity, thank you Dr Fung.. I will print this out & had it over to my 70 yr old dad’s doctor who keeps increasing insulin dosage.

  4. RE – ” Insulin resistance is bad? No, not at all. It is good. Insulin resistance is not the root cause. It’s the natural, protective reaction to the root cause – high insulin levels. It’s the insulin, stupid!”
    Following your logic in this post, the problem is not insulin —-> insulin is the body’s way of trying to deal with the energy overload – ie high glucose or high FFAs in the blood. The cells are saying they don’t want the energy molecules either, so they exhibit IR. So the real root cause is caloric overload, and energy overloaded environment in the blood. ?Yes?

    Dr. Jason Fung: Good question, but not quite. There are many things that increase and decrease insulin levels, of which excess energy is only one. Pure fat, for example has calories (energy) but has minimal effect on insulin.

  5. Hi Dr Fung, You finish the article by saying that the glucose can be burned off by “fasting;” doesn’t exercise also burn off excess glucose, and wouldn’t high intensity exercise be the most effective because the harder one exercises the greater the proportion of glucose, as opposed to fat, the body burns because glucose is the body’s quick access form of energy?

    Dr. Jason Fung: Only to a point. Exercise suffers from compensation effects. You can review the ‘Exercise’ series from a while ago.

    • Dr. Fung, I believe Martin is referring to high intensity exercise (e.g. brief, intense, infrequent strength training). Your exercise series was about low intensity exercise (e.g. running) and so does not speak to his question. Exercising at maximum intensity a few minutes a week is completely different, physiologically, than exercising at low intensity hours a week. And, I think, it is precisely the hormonal consequences of high intensity exercise that make it far more beneficial than “aerobics.” Not as important as diet for weight loss, no doubt about that. Not Batman. Buy probably not Robin, either. Myokines appear to be one of the reasons for the apparently major physiological benefits of strength training, which go way beyond helping to facilitate good body composition. Doug McGuff has written about this recently.

    • Thanks for your comments Dr Fung and Bill, they give me a couple of other leads to follow up on to investigate the effects of exercise (particularly high intensity as Bill mentions) on insulin resistance and the progression (or hopefully lack of it) of type 2 diabetes.

  6. Re – ” Insulin resistance is not the root cause. It’s the natural, protective reaction to the root cause – high insulin levels. It’s the insulin, stupid!”
    If you follow the logic of this post, then insulin is just a middleman, not the root cause. Insulin increase occurs in response to energy overload, too much glucose and FFAs. Insulin is just directing the traffic. My interpretation of the information that you present is that the primary culprit , the root cause, is the glucose and the FFAs floating around in the blood, and these molecules arrived in the circulation by ingesting them.

    • Would it not be better to break down the “energy” by its effect on insulin then?
      Carbs (1) proteins (.5) and fat 0.05.
      The type of energy by its insulinogenic effect can then become a good bit more precise, not just glucose and free fatty acids.

      And you are right, of course insulin is a middleman, the gate keeper, very important.

      And the main message of the article is that not letting more glucose and FFA’s in is the right response, not a defect, which I think you agree with.

  7. Another excellent post. Thank you Dr. Fung.

  8. Newbie I did a 21 day fast and my fasting blood glucose was steadily going down from 110 to low 80s and then it hung in the low 70s. On day 14 of my 21 day fast I started preparing to go to a conference and needed to finish paperwork and stayed up late. Suddenly I was feeling stressed. Nothing changed remember, because I was fasting! Nevertheless my fasting blood sugar shot up to mid 90’s. Once I got to my conference, I was able to relax and get some sleep guess what? Yup blood glucose went right back down to low 80s and 70s. I was fasting remember so no caloric overload. Insulin is a hormone that a critical player in an intricate dance played in the body by the interaction of other hormones and their environmental and physiological triggers!

    • Those are interesting responses to stress. I’ve only had one fasting blood sugar test taken while fasting (on my fifth day), and it was in the low 60s. It’s interesting to see how fasting affects others differently. A 21 day fast is quite impressive.

    • Hi Rebecca, Can you please share with us your plan of fasting for 21-day? I would really appreciate it and see if I can follow it.

    • Aliatino

      Your body treats all stress via the sympathetic nervous system by going into the primitive response of fight or flight. Both responses require a physical action. To give you energy your body drops liver glycogen into the blood stream along with the production of adrenaline and cortisol. Adrenaline and cortisol both go through pathways to be converted to sugar for sustained energy. Nowadays our stress are non physical so the sugar remains in the blood waiting for insulin to remove it

  9. George Henderson

    Great post Jason.
    To the question about metformin, although it’s known as an insulin sensitiser it reduces absorption and production of glucose – so this is dealing with something closer to a root cause.
    Also, there are cells you do want to be sensitive to insulin; alpha cells, which secrete glucagon, and the hepatocytes that make glucose. The receptors that inhibit gluconeogenesis are different insulin receptors from the ones that store fat.

  10. Guido Vogel

    Fantastic post. Reminded me of Richard J. Johnson’s book “The Fat Switch” where he described IR as a benign state in some cases. Some animals use it to get fat before hybernation. Grizzly bears eat 100.000 berries a day in the fall to convert fructose into fat. No wonder they will, literally, do anything to get hold of honey!

    Johnson claims that we have a similar mechanism to stock up for the winter where food sources where more scarce. Most of our time as humans we spent in colder climates. It also might explain differences between people from different climates. Polynesian, Hispanic, AfroAmericans all seem to be more prone to become obese/diabetic. Maybe the never adapted to colder climates. And once exposed to sugar and white flour, they become obese/diabetic quite easily.

    What do you think?

  11. “But in T2D, insulin levels are high. Glucose is high. But because of excessive IR, FFA is also high.”

    I don’t understand. I thought Insulin is a hormone that inhibits lipolysis? Why FFA can be so high in T2D? Is it only if the adipose tissues have developed IR too? Sorry for my bad english

    Dr. Jason Fung: Good question. Due to insulin resistance, glucose is stuck outside the cell. Inside, the cell has no fuel so signals to increase Free Fatty Acids for fuel. So the abnormal situation exists where blood levels of glucose AND FFAs are high.

  12. “But because of excessive IR, FFA is also high.” OK, so to me, that sentence means that high insulin levels with high blood sugar allows the liver to produce FFA faster than the high insulin levels can push the FFA’s into fat cells and keep them there. Or I guess, that the liver produced FFA’s are captured by the cell as the FFA’s are going from the liver to the adipose tissue.

    Also, “MalCoA inhibits FACoA resulting in steatosis.” To me, that means that the cell has no mechanism to stop sucking in FFA, even though it is accumulating lipid droplets inside itself. So, what is the mechanism that allows FFA to enter a cell?

    • Opps, I forgot to say thanks for the post!

    • Also, thanks for thinking while doing a head stand!

    • FFAs come from white adipose tissue, not from the liver. WAT insulin resistance is key in both obesity and diabetes. It seems that until you are able to recruit new, insulin sensitive fat cells (called hyperplasia), these protect you from developing diabetes. That’s why we see 250 kg (550 pounds) people who are not diabetic and only show mild symptoms of the metabolic syndrome. On the other end of the spectrum are the lean diabetic, who have very limited capacity of adding more fat cells and the few ballooned up (hyperplasia) adipocytes they have become inflamed and severely insulin resistant early.
      Severe hypertrophy, inflammation and subsequent insulin resistance of WAT results in uncontrolled lipolysis, and that is what we call type 2 diabetes. NB, type 1 diabetes is also a problem of uncontrolled lipolysis, but in that case the root cause of course is lack of insulin, not severe insulin resistance.
      This is a great study of WAT in children in which we are able to see the progress. Unfortunately the researchers excluded diabetics from the study, so we cannot see the whole progression in one paper.
      “Evidence of early alterations in adipose tissue biology and function and its
      association with obesity-related inflammation and insulin resistance in
      children”
      http://diabetes.diabetesjournals.org/content/early/2014/11/05/db14-0744

  13. Look! The streets are nice and clean. But all the toxic glucose goes into the houses (tissues).

    Is this how diabetes supposedly becomes “progressive”–the garbage trucks keep coming more and more often, bringing bigger and bigger loads?

    Dr. Jason Fung: Exactly right. The standard treatment of T2D is to eat low-fat diets and take insulin. So we are put more toxic slime into the houses. Eventually, the houses get full, and the garbagemen (insulin) can’t stuff anymore into them. So what do we do? Get more garbagemen (increase the dose of insulin). And the cycle keeps repeating.

    Because this leads to worsening diabetes over time, the ‘authorities’ say that T2D is a chronic and progressive disease, which is a lie.

    • “the ‘authorities’ say that T2D is a chronic and progressive disease, which is a lie”

      There’s no question there’s a ton of misinformation and even worse when it comes to the so-called authorities, but on the progression front, even for many who are medication and insulin free, I thought the progression we sometimes see was due to beta cell death, everything else held constant, so to speak. What are your thoughts on beta cell death, regeneration (or is that really a myth), and the BG levels which make regeneration possible vs. not?

      Fantastic blog, protocol, and presentations, by the way. Please continue the really outstanding work.

      Dr. Jason Fung: I will discuss this in the future. I think beta cell death is only seen in the very end stage of T2D and is reversible for the majority of people (ie. 98%)

      • Thanks Dr. Fung, looking forward to that discussion/post and have already put in a pre-order for your book! I wish I had more direct access to your protocol/team (long waiting list and of course, geographic separation).

  14. Dr Fung,

    Is there any easy way to measure insulin resistance?

    • John Anthony

      No easy way that I know, but you can get an approximation by measuring your blood glucose levels every hour after a high carb meal and plot the curve. In an insulin sensitive person, the glucose levels should drop to baseline after 2 hours, 3 h max. The area under the curve (AUC) is a good indicator of your IR. Of course you would need to compare your area with that of someone who is still insuling sensitive.

    • Eric Leppert

      You could get your fasting insulin when you get your fasting blood glucose and plug those numbers into a HOMA calculator to determine your insulin resistance.

  15. Thank you for this post, Dr. Fung. It is so brilliantly simply put! I am curious about statements on increasing insulin sensitivity through fasting. Some like Dr. Peter Attia said they reversed IR through LCHF and IF. I believe you mentioned in your earlier posts that, as it took decades of getting to the point of IR and diabetes so it might take as long to reverse it… If lowering intake of foods that provoke high glucose production followed by that of insulin can bring stable good BG level, must one strive for that long to achieve insulin sensitivity?

    Dr. Jason Fung: Think about it this way. If your house is full of garbage, you can do 2 things. Stop putting garbage in (LCHF). Or you can start throwing garbage out (Fasting). It would be faster throwing garbage out AND fasting (LCHF + IF).

    • Irene,
      I am afraid Dr. Fung is correct. I was not diabetic but I was overweight. So I went low carb and lost 25 lbs. But I still wanted to lose 10 lbs so i did alternate day fasting and LC and it worked exceedingly well. Never-the-less i still had that extra belly fat. That was disappointing. So I started weight training. And that is good but little belly fat is still there. So I did an oral glucose tolerance test. And despite being a very disciplined LCHF adherent, with good FBG and A1c my result indicated Impaired Glucose Tolerance. Wow! I was hoping I could eat more carbs after 5 years. But, I guess not. I may have dodged the Diabetes bullet.

  16. […] Continue to T2D part 7 “Insulin Resistance is Good?” […]

  17. Michael McEvoy

    Dr. Fung – You wrote ,
    So, back to insulin resistance. Why does the body develop it so frequently (up to 50% of the American population)? This simply cannot be mal-adaptive. Our bodies are not designed to fail, since we lasted for several millennia before the modern diabesity epidemic.
    Simply cannot be ? I am not so fast to conclude that when I think from an evolutionary perspective . It is probably adaptive, or has been for many millennia . But has to be ? OK, this is a nit picky point , but I want more folks to grasp the concept of evolution, especially here in the US where there is so much ER (Evolution Resistance)
    So I would state that IR did work in the environment our ancestors dealt with for a long time. I believe you agree.
    Thanks for your dedication to a very educational website . This latest blog contains some great imagery to teach with. I am an FP so I will steal your garbage truck analogy if that is OK .

  18. Excellent deductive post Dr Fung. I had a double bypass in August and am now suffering high blood sugars that I’m advised to treat with higher insulin doses. I follow LCHF and IF but think my excess sugars are being dumped into my blood by my cells. I was diagnoses T2D in 1992. Any thoughts

  19. No medically related question or point but simply to say great post and that the sentence: “The accumulation of fat between muscle fibres (where there should not be any), in cattle, is called delicious” made me laugh, which is rare for nutrition articles (and great because it can be a pretty dry subject). Keep up the fantastic work Dr. Fung.

  20. i am 26 having diabetics(type 2) from my 18 and my father too having for past 20 yrs. can u please help me to cure this pls. i am from India

    • Martin Williams

      Suba: This is none of my business. But if you read Jason Fung’s posts, you’ll have his solution, right or wrong. It may take you a couple of days, but that’s all.

      The essence of it is this. Do everything you can to reduce the production of insulin. If you do this for lengthy periods, e.g., by fasting, you will also reduce insulin resistance (which is the same as increasing insulin sensitivity).

      The other simple way to do the same thing is to eat a LCHF diet, i.e., a diet low in carbohydrates. This is variyingly defined as a diet that contains between 25 and 50g of net carbohydrates.

      Fung is pretty clear on one point: It can be done in more than one way, and fasting is the simplest one to understand.

      Although I truly think that Fung covers everything in this site (it is a huge database of information), may I suggest that you look up a YouTube channel called SteveTheTruckDriver. if you’re sensitive to bad language, then give it a miss. If you’re an adult, you’ll find very, very good advice there from a man who has tried many different fasting protocols alongside various low-carb and high-carb regimens.

      It’s an intelligent resource, and should not be ignored for its cursing and burping. I think he’s a wonderful chap.

  21. Dr.S. Vijayaraghavan

    Dear Suba
    I am a primary care physician based at Chennai, (who is an ardent follower of Dr Jason Fung), helping Diabetics reverse. My email id is dr.s.vijayaraghavan@ gmail.com.
    Please feel free to correspond. Shall definitely do the needfu.

  22. Excellent post Dr. Jason Fung! The analogy of garbage truck really helps in understanding the article very easily. I loved the sentence “The accumulation of fat between muscle fibres (where there should not be any), in cattle, is called delicious”. Sentences like this make reading your articles so interesting. Keep up the great work!

  23. […] Dr.Jason Fung odlično o tem, da je inzulinska rezistenca dobra. Slabo je povišanje inzulina! https://intensivedietarymanagement.com/insulin-resistance-good-t2d-7/ […]

  24. […] when insulin starts to fall? You have a huge fatty liver that wants desperately to deflate itself (see last post). As soon insulin falls, sugar comes rushing out of the liver and into the blood. This results in […]

  25. Not all IR is created equal……
    First let me say that insulin resistance, in regard to T2 diabetes, and leptin resistance go hand in hand. You cant have one without the other, This is why T2s are generally overweight. When you are overweight, if you have excess insulin, you also have excess leptin. Without leptin working correctly, you will not loose weight.
    Diabetes (in my former case of) should be looked at as a problem of the immune system. I was I/LR (insulin/leptin resistant) for a long time, with high, but not to high, levels of insulin. Pre-pre or pre diabetic level. Having suffered for years from sinus problems, I tried an OTC product, cromolyn sodium. It is a mast cell stabilizer. Before I tried it I started researching if it would raise my BS. I ran across some interesting studies done on obese, diabetic rats. (search: cromolyn sodium diabetes)
    I could never loose weight, I am highly active very physical job, and always ate a good diet, not SAD. Come from a very skinny family, through 5 generations known to me. Body fat at 30%. If I tried cutting carbs, I got sick. Body would not run on fat or protein. Only steady carbs. But no fast weight gain either. Only slow steady weight gain, regardless of how much I ate. My weight was always stable within 2 lb range. After 4 days using cromolyn sodium (nasal inhaler), I lost 4 pounds, and lost my appetite. I knew something was going on. What I really lost was my I/L resistance, although I didn’t know it at the time. With leptin resistance gone, the weight was coming off and curbing my appetite.
    However…with still eating normal (no calorie cutting) and no exercise (I wasn’t working for a few weeks) I lost 18 lbs in 3 weeks. Then I decided to start testing my postprandial glucose levels at the 1, 2, and 3 hour marks. A lot of testing. I was still IR as shown by my glucose meter. One example….1 hr @ 185, 2 hr @ 145. This was typical. However when I added the cromolyn sodium PP @ 1 hr after a 185, it drove my 2 hr mark down to 102. This was repeated over and over and over. Once my 2 hr mark was 187. Ouch. I used the cromolyn sodium at that 2 hr mark. At 3 hrs I was at 84. This was also repeated several times. This tells me that the cromolyn sodium reverses my IR possibly instantly and totally, but only for its several hour duration in my system. The over 100 point drop was due to higher insulin levels at the 2 hr mark, which I know to be accurate from an oral glucose tolerance test I took with insulin draws also.
    My insulin and leptin resistance started to disappear at about 20% body fat, as per my PP glucose testing. Currently @ 15% body fat and absolutely NO sign of diabetes, insulin, or leptin resistance. My first and second phase insulin response are excellent.

    I hope this helps someone else with I/L resistance. I hate to think it was only good for myself and a bunch of obese, diabetic rats.

    David
    [email protected]

    Further reading
    http://www.ncbi.nlm.nih.gov/pubmed/22069285

    http://www.sciencecodex.com/zaditor_and_cromolyn_common_allergy_drug_reduces_obesity_and_diabetes_in_mice

  26. DR Jason,
    In people that have not diabetes type 1, when is a situation arising that blood glucose is high AND cell glucose too low ? This would be a situation when insulin would be useful, if it exists.

  27. I juts finished a 52 hour fast and my morning BS went from 6.2 to to 5 the 2nd day. I resumed eating same evening, last night. I noted then that my Tinnitus had reduced but this morning it is gone completely in one ear and reduced to less than half in the other ear! I googled and found several references to correlation between high BS and Tinnitus, also a 2 year study where significant Tinnitus reduction was achieved through a blood sugar lowering diet. See link below. (They did not try correlating results with fasting blood sugar, for instance, only with “adherance”). Two things I find amazing with this my first longer than 24 hour fast: 1/ Reducing Tinnitus on only 52 hours similarly to what has achieved on two year long diets, thanks to you! 2/ The fast recovery of morning blood sugars. Before I usually awake 5-7 although just before 8 is my time to rise. Now I slept through to just 8, better rested than usual! (I am 69.) I guess the hormonal responses by adrenalin, cortisol etc. weakened through the fast, leaving me a better morning blood sugar. (Less visceral fats immediately?) Great results, thank you Dr Jason! From now on Tinnitus will for me also remain a great warning signal, a “built in” high blood sugar warning, thanks to the fasting. Here is the link:
    http://www.tinnitusformula.com/library/sugar-metabolism-affects-tinnitus/#.VnEzrEqLRhE

  28. Why are the vegan docs (Fuhrman, Gregor, Ornish, McDougall) having what they call “reversal of diabetes” with no fat diets?
    McDougall uses mostly starch based, but the others are more fruits and veggies. Absolutely no oils and no animal products of any kind. They bring up Walter Kempner, who in 1939, reversed diabetes with a fruit and rice diet. Well, yeah, very little calories there, so all of them lost weight. They claim the diabetes was gone forever, unless they added back animals and fat.

    Considering that animal protein does raise insulin, some of it may make sense, but they claim that fat causes insulin resistance, not sugar or carbs. Also, we do need micronutrients (much more important than macros), so I would think that vegetables would carry that the most. Of course, I would always add plenty of veggies to a HFLC meal. Lots of fiber and the carbs are negligent. What say we to these guys who are claiming “getting rid of diabetes as well as heart disease for good”? Are they liars? Does fat really make us IR?

    • As you hinted, the effect is probably only a result of extremely low calorie intake.
      If fat or anything is added back that doesn’t increase calories results should be same. Long term effects on liver and health would be poor when fat is needed to absorb vitamins and antioxidants from fruit and vegs and promote bile flow.

      • When I see this, I get truly baffled and wonder which camp is right.
        Does fat cause IR? Do we have to go one way or the other and be extreme about it?
        I’m talking T2D and IR. I’m not overweight, been weight lifting for over 30 yrs. and yet, I’m IR.

        http://www.forksoverknives.com/fat-insulin-resistance-blood-sugar/

        • I think that both work as they moderate/minimize insulin. It really depends on what you can sustain long term because if you go back to what you were doing same issues will reemerge.

  29. Brilliant article! After understanding the physiology of insulin and glucose it makes so much sense.. I like the cattlemen analogy it gives you a visual from a different species.. I would also comment that the french figured this out also with their famous dish foie gras, the fattened duck liver which they achieve by force feeding the ducks with corn.. after understanding this concept of insulin and glucose it boggles my mind how the recommended diet is High Carb low Fat is the same diet as the livestock to fatten them up, its no wonder we have an obesity T2D epidemic!

  30. You have done it again, Dr. Fung wonderful and brilliant as usual!

  31. Mary Baechler

    Omg, this is so brilliant. Thank you Dr. Fung. I am a licensed nutritionist, and I am thinking, “why didn’t someone explain this in my Master’s classes?”. Wow.

  32. irshad Alam

    Ist does not explain why it develops gradually, because Insulin-resistance is not from birth, it develops over time. Eg I could eat sugar/carb in my youth and my bs would not go up. But now that Im older, it does. Why?

  33. Through 3 days of fasting and my blood glucose is much higher than normal. I take no drugs but an Type 2. With very low carb eating I can keep my glucose in a range of 80 – 120. If I eat junk like sugar and high carbs I can go as high as 250. For three days fasting I have zoomed up to scary 300 and now and at 225. It has not gone below 200. WTF as Dr Fung would say. help

    Dr. Jason Fung: This is simply the Dawn Phenomenon. Think about this. If you are not eating, where is this sugar coming from? It must come from your own body stores! You are liberating sugar so that you can burn it off. It’s just coming a little faster than you would like.

    • Dr Fung – so is it ok to have high fasting blood glucose due to Dawn phenomenon, while fasting? Eventually it will get to normal?

  34. George. E. M.

    I claim to have cured my T2DM by practicing a diet developed for own use based on a one line advice of my maternal uncle, an Ayurveda physician. T2DM was diagnosed by my cardiologist in 2006. FBS, PPBS, HbA1c, OGTT & Serum Insulin tests indicated that I was not diabetic any more by Sep 2009. Then switched back to usual diet.
    My latest results are FBS 73.0 mg/dl & PPBS 81.0 mg/dl.
    Learning about inflammation, IR & my former colleague’s Serum insulin reading of 200 it appears to me that the diet regimen might have reset the IR & inflammation in me.
    Some followers of my diet have reported weight loss & feeling of being energetic.

  35. George. E. M.

    Hi Dr Jason Fung,
    Thank you very much for this post which explains the genesis of IR that leads toT2DM which culminates in failure of vital lifesustaining organs in due course.
    I am not a medical man. Thank you once again for explaining IR related processes in most unambiguous terms . This has made facts crystal clear even to a layman like me & answered the unanswered questions that were stalling my efforts to explain things.
    Thank you once more. May God Almighty empower you further to bring up more works like this.
    GEORGE. E. M.

  36. Mary Anne Sautner

    Dr Fung,
    I have pre diabetes and am trying fasting to nip it in the bud and hopefully solve this problem. I have been doing the 20:4. Only a four hour food window between 1-5pm. I have been doing it for a full week and my morning blood sugar is still staying between 100-115. (where it has been,no change) It’s driving me crazy!!! How long does it take for this fasting to work?

  37. How do you create and maintain a healthy gut microbiome on a high fat diet? My understanding is that one needs to have a lot of healthy complex carbohydrates (all kinds of vegetables) along with some fermented foods like sauerkraut, kimchi, etc.

  38. Thank you Dr fung,you are doing great job .please continue the good work .You are giving new life and hope to so many lives and families , by sharing your brilliant knowledge .All the best for your endeavors and may you get all the success .Thanks

  39. […] when insulin starts to fall? You have a huge fatty liver that wants desperately to deflate itself (see last post). As soon insulin falls, sugar comes rushing out of the liver and into the blood. This results in […]

  40. […] The cells are already over-filled with glucose (see previous post – A New Paradigm, and Insulin Resistance is Good?). Like trying to blow air into an over-inflated balloon, it simply takes more force. The […]

  41. […] me’. So the glucose piles up outside in the blood. The insulin resistance is not a bad thing, it’s a protective mechanism. What’s it protecting us from? The very name tells you. Insulin resistance develops to resist […]

  42. […] So the glucose piles up outside in the blood. The insulin resistance is not a bad thing, it’s a protective mechanism. What’s it protecting us from? The very name tells you. Insulin resistance develops to resist […]

  43. […] So the glucose piles up outside in the blood. The insulin resistance is not a bad thing, it’s a protective mechanism. What’s it protecting us from? The very name tells you. Insulin resistance develops to resist […]

  44. Dr Fung!
    Thanks a lot for DP clarity.
    Doubt:
    I am already under weight by 10 kgs T2D for 16 years. If I fast , my weight may be reduced further. Is it not a harm for me?. How should I improve my weight?.
    I think the liver again become fatty at the time of weight improvement and the same problem repeats.

    Fasting is good for those people who are over weight but what about under weight people.
    Please clarify my doubts.,
    —-Balu

  45. Hi Dr. Fung, I am a fan or your work, purchased your book. I follow a LCHF diet, practice 24 hr fasting and participate in moderate exercise 5 times a week. Even so, I have been having difficult losing weight (lost 70 lbs LCHF). I started tracking my FBS and post prandial BS – these numbers are very stable in the mid 90’s to very low 100s most of the time. I’ve considered that perhaps my inability to lose weight is related to my BS not going any lower. Research led me a couple of websites that seem to implicate a high fat diet as a reason for IR – which I found shocking. Their premise being that FFA clog up the insulin receptors of the cells. I was wonder if you could comment on this theory. If I am still experiencing some form of IR, should I look at reducing fat intake as well (low carb, moderate protein, moderate fat)?
    A couple articles:
    “Curr Opin Clin Nutr Metab Care. 2007 Mar;10(2):142-8. “Free fatty acids and insulin resistance” Delarue J1, Magnan C.
    http://www.ncbi.nlm.nih.gov/pubmed/17285001
    “How high fat foods impact diabetes and metabolic syndrome” Date:May 22, 2012 Source:University of Michigan Health System Summary:The Bcl10 protein helps the free fatty acids found in high fat foods impair insulin action and raise blood sugar, new research shows.
    https://www.sciencedaily.com/releases/2012/05/120522114536.htm

  46. Yea how do you explain IR decide to visit us when into our 20+ /30plusses age
    You eat how ever much sugar/ carb during your younger years no IR problem

  47. […] Verensokerin laskemisesta insuliinilla ei ole T2-diabeetikoille mitään hyötyä. Sen osoittaa tämä artikkeli tutkimusviitteineen. Jason Fung osaa kuvata mestarillisesti, mitä tapahtuu elimistössä, kun insuliinilla alennetaan verensokeria (T2-diabeetikolla): […]

  48. Dear jason fung, I ravi aged 49years from india. I was recently observed weight loss. When i checked i reduced from 86kgs to 75kgs in two months. When i checked my fasting blood sugar is 317 and plbs is 406. The reduction in weight loss is due to diabetes. Without much excercise i reduced. This is due to supply of glucose to organs by the liver by burning fat and muscle of the body as the pancreas in unable to produce require insulin. If my organs are overloaded why they further require glucose from liver. How much further weight i will loose if i am not willing to take medicine. Is this type of reduction in weight is bad for my body?. Do i develop more keotones? Do my organs affect due to further weight reduction ? Pl advise.

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