Fatty Pancreas – T2D34

posted in: Diabetes, Health and Nutrition | 45

Fatty Pancreas

The English friar and philosopher William of Ockham (1287-1347) is credited with developing the fundamental problem solving principle known as lex parsimoniae or Occam’s Razor. This principle holds that the hypothesis with the fewest assumptions is most often right. The simplest explanation is usually the most correct. Albert Einstein is quoted as saying, “Everything should be made as simple as possible, but not simpler.”

With that in mind, let’s remember that type 2 diabetes reflects two fundamental problems:

  1. Insulin resistance
  2. Beta cell dysfunction

Insulin resistance, an overflow phenomenon, is caused by fatty infiltration of the liver and muscle. Without dietary intervention, defect #2 virtually always follows #1, albeit by many years. Also, #2 is almost never found without #1. Yet somehow, we are asked to believe that the mechanism behind insulin resistance and beta cell dysfunction are completely and utterly unrelated? Occam’s razor suggests that both defects must be caused by the same underlying mechanism.

Hyperinsulinemia stimulates de novo lipogenesis transforming excess dietary carbohydrates into new fat. The liver packages and exports this new fat as VLDL making it widely available for other organs. The new fat deposits in skeletal muscles takes up much of this fat, as do the fat cells in and around the abdominal organs leading to the central obesity that is an important component of metabolic syndrome.

As fat begins to deposit within the organs, specifically the liver and muscles, insulin resistance develops, gradually leading to rising blood glucose. In response, the body secretes even more insulin to bring the renegade blood glucose back down. The extra insulin ‘overcomes’ the rising insulin resistance, but sets up a vicious cycle.

To relieve fatty congestion in the liver, it is exported out. Some ends up in the muscle and some around the organs to create central obesity. Recent research has revealed that the pancreas also becomes heavily infiltrated with fat and this plays a pivotal role in the development of type 2 diabetes.

The relationship between pancreatic weight and total body weight was first noted in 1920. In 1933, researchers first discovered that pancreases from obese cadavers contained almost double the fat of lean cadavers. By the 1960s, advances in computed tomography (CT) and magnetic resonance imaging (MRI) allowed non-invasive measurement of pancreatic fat and firmly established the connection between fatty pancreas, obesity, high triglycerides and insulin resistance. Virtually all patients with fatty pancreas also had fatty liver.

Most importantly, fatty pancreas is clearly associated with increasing degrees of diabetes. Type 2 diabetic patients have more pancreatic fat than non-diabetics. The more fat found in the pancreas, the less insulin is secreted. Pancreatic and hepatic fat content is much higher in diabetics even if they are of equal age and weight. Simply put, the presence of fatty pancreas and fatty liver is the difference between an obese diabetic patient and an obese non-diabetic one.

Bariatric surgery can normalize pancreatic fat content accompanied by restoration of normal insulin secreting ability. Despite weighing an average of 100 kg, patients successfully reversed type 2 diabetes within weeks of surgery. By comparison, obese non-diabetic patients had pancreatic fat was normal to start and unchanged despite similar levels of weight loss. The excess pancreatic fat is only found in type 2 diabetics and is not related to the weight loss of surgery.

The insulin secreting beta cells of the pancreas were clearly not ‘burnt out’. They were merely clogged with fat! They merely needed a good cleaning out. What is shocking is that it only took the removal of 0.6 grams of pancreatic fat to reverse type 2 diabetes.

In addition to fatty pancreas, type 2 diabetic patients differs from non diabetics by the presence of fatty liver. Eight weeks after bariatric surgery, this liver fat had decreased to normal levels accompanied by normalization of insulin resistance.

The COUNTERPOINT study established these same benefits using a very low calorie (600 calories/day) diet. Over the eight-week study period, pancreatic fat content slowly decreased associated with restoration of insulin secretory ability.

The difference between having type 2 diabetes or not is not simply the total weight of a person. Instead, fatty liver drives insulin resistance, and fatty pancreas drives the beta cell dysfunction. These are the twin cycles of type 2 diabetes.

  1. Insulin resistance caused by fatty liver, fatty skeletal muscle
  2. Beta cell dysfunction caused by fatty pancreas

The two fundamental defects of type 2 diabetes were not caused by two completely different mechanisms. They are once and the same. Both are problems related to fat deposits within organs, ultimately relating back to hyperinsulinemia.

The Twin Cycles

The natural history of type 2 diabetes mirrors the development of the twin cycles. Insulin resistance develops long before the high blood sugar clinches the diagnosis. The Whitehall II study plotted the trajectory of blood glucose in the years prior to the clinical diagnosis of type 2 diabetes.

Insulin resistance emerges almost fourteen years prior to type 2 diabetes. The mounting insulin resistance produces the long slow rise in blood glucose. The compensatory hyperinsulinemia prevents the rapid rise in blood glucose. For over a decade, blood glucose stays relatively normal.

Underneath the surface of normality, the body is trapped in a vicious cycle, the first of the twin cycles – the hepatic cycle. Excessive carbohydrates intake provokes excessive insulin secretion, leading to de novo lipogenesis.

The vicious cycle has begun. High insulin generates fatty liver, which increases insulin resistance. In turn, this increases insulin, which only perpetuates the cycle. This dance goes on for more than a decade gradually worsening each time we go around.

The Pancreatic Cycle

Approximately three years before the diagnosis of type 2 diabetes, blood glucose takes a sudden sharp upswing. This heralds the beginning of the second of the twin cycles – the pancreatic cycle.

The liver decompresses its growing fat stores by exporting it as VLDL transferring this newly created fat to other organs including the pancreas. As the pancreas becomes clogged with fat, it is unable to secrete insulin normally. Insulin levels, previously high to offset the high blood glucose, begin to fall.

The loss of this compensation results in a rapid rise in blood glucose and ultimately, the diagnosis of type 2 diabetes. Glucose spills over into the urine causing the symptoms of frequent urination and thirst. Even though insulin drops, it stays maximally stimulated by the high blood sugars.

The hepatic (insulin resistance) cycle and the pancreatic (beta cell dysfunction) cycle together form the twin vicious cycles responsible for the development of type 2 diabetes. But they have the same underlying mechanism. Excessive insulin drives fatty organ infiltration. The underlying cause of the entire cascade of type 2 diabetes is hyperinsulinemia. Simply put, type 2 diabetes is a disease caused by too much insulin.

45 Responses

  1. Dr Shivanand Nelogal

    Tipping point is fatty pancreas.If you go that for you will develop T2DM. Sir, what about amount of fat in normal insulin sensitive lean individuals.Do they have some fat or they don’t have any fat in pancreas? .Any data?
    One more thing I assume that skeletal muscle fat also comes down with carbohydrate restriction/bariatric surgery.
    Thank you sir.

  2. Missing Link

    The timeline described here pretty much describes my situation to a T. I was diagnosed as pre-diabetic back in 1999, when I was extremely overweight. Under the guidance of a dietitian I went on a low-fat diet high in wholegrains and lost about 20kg, at which point I was told I was no longer pre-diabetic. However, I couldn’t sustain the LFHC diet and gradually put the weight back on (and lost then gained weight several times thereafter), ending in a diagnosis of DM Type 2 in 2012. Of course, I blamed myself for not having the willpower to sustain my diet and felt guilty and ashamed that I had allowed myself to lapse into diabetes, despite having been given a “warning” 13 years earlier.

    However, if I have read Dr Fung’s post correctly, I never really addressed my insulin resistance at all, and these twin cycles were motoring on in the background. Even though for most of that 13 year period my blood sugar levels were not yet within diabetic ranges my liver and pancreas eventually got to a tipping point where they could no longer cope.

    I’m sure I’m not the only person to say “I wish I’d known back then what I know now”.

    • Fortunately though the beta cell dysfunction and the fatty liver (and T2DM) are reversible with proper diet. Real unprocessed foods in LCHF fashion (less than 25g carbs daily in above ground veggies), moderate protein (0.6g per kg of body weight) and eating healthy fats until you feel satisfied is the path!

    • Stephen T

      Missing link, like many people you were given terrible advice from low-fat ‘wholegrain’ dietitians. I’m glad you’ve found you way to advice that will work.

      • Missing Link

        Indeed. I now look forward to a long and fulfilling relationship with my feet, fingers, kidneys, eyesight etc.

  3. Mediterranean ape

    Only thing that makes sense to me ,is that as T2D , I should lose’ my body fat and fat from both liver and pancreas as a result ,managing my diabetes or reversing it.by max nutrition and calorie reduction of carbs ,sugar.

    • sten bjorsell

      Mediterranean ape!
      Yes, but it would be rather stressful to follow a 600 calorie diet for 8 weeks to achieve similar results as in the COUNTERPOINT study referred to in the main article above. Suggest combining a normal calorie diet as you describe with Intermittent Fasting (IF) instead, aiming to achieve even better results in much shorter time, which I did. I was diagnosed with severe angina in 2005 and the cardiologist wanted to put in at least one stent after an angiogram. I refused as it did nothing to address the root cause. After 7 years suffering on a standard diet with as much exercise I could do between attacks, I started LCHF in December 2011. Within a month I could walk freely again, without the need to stop after a few minutes to allow chest pain to disappear. It was a wonderful recovery, with zero medication! After a few years, I noticed that I started to get pains in both wrists after walking hard a few minutes. It was consistent, also that it went away after 2 minutes rest. I say it was “connected” to my old angina. At this stage, I also noticed that my fasting blood glucose (FBG) was often over 6 (110) instead of around 5 (90), indicating the last stage of prediabetes as per the diagram from the Whitemill study above! It confirmed for me the strong link claimed by many including Kummerow and Kraft between Heart Disease and Diabetes type 2. With Dr Fung’s book and this blog in my mind, I fasted one or two days a few times last spring and then I went for a 3 day fast. At the 3rd day, I felt that I had more energy than since in my forties and therefore continued to 5 days fasting. After that, I fasted from Sunday night to Friday night for a 2 more weeks in a row. I lost 9 kgs and felt great. And in the weekend before the last 5 day fast, I took my standard walk, and noticed that the wrist pain at the 3-minute mark I had from 100’s of walks before never showed again! It was gone completely and it is this far permanently gone. That was April 2016. I fasted again for 3 days last week and my blood glucose dropped to 3.3 on the 2nd day and 2.8 the 3rd day. Since I was full of energy it indicated that I was burning fat very well! I broke this last fast with a meal, entrecote and butter fried broccoli, last night. No breakfast and my midday BG was 3.3.
      From what I understand I cleared the fat in and around the liver and regained a lot better BG control through these fasts.
      Since I did not start out as a full blown T2D, more 5 day fasts are required the more deranged one is from start.
      Again calorie restriction even on LCHF is not hunger free like fasting, and the time to target is less than half than with calorie restriction. It seems also that combining fasting with (moderate) exercise gives better results. Naturally as more energy then required. And muscles apparently build very well according to the recent heavyweight champion guest on this blog.

  4. After my first pregnancy at the age of 21, I started on the road of metabolic syndrome. First weight gain, then high blood pressure, poor lipid profile, high triglycerides, stable angina, with fatty liver and T2D diagnosed 15 years ago at the age of 56. All I was ever offered by the medical profession were drugs, which I refused to take as they made me feel so ill that life was no longer worth battling for. I had been dieting regularly in all this period, losing and regaining large amounts of weight as soon as I went back on the high carb diet which was considered the right thing at the time. So 15 years ago I took matters into my own hands, did a lot of research online, and slowly came to the knowledge that I am highly carb intolerant. I have since brought my weight down from my 96 kg maximum to my present 70 kg, although not without some yo-yo-ing. I think it has taken this long for my body weight set point to be slowly brought down.

    By choice and not from necessity I no longer see any doctors or have any blood tests, but I can test my own blood glucose levels. They are not perfect, as I seem to have a high ‘set’ level of fasting blood glucose (my body seems to want to be at around 100), but the spikes after meals are minimal. I am happily assuming that all the other metabolic syndrome issues are also being slowly resolved. If not, tough luck – I prefer to die from my diseases rather than from medications.

    Discovering Dr. Fung has been my most recent eye opener. I had been scared off longer term fasting by tales of muscle loss and lowered metabolic rates, but I have now included fasting in my tool kit. HFLC keep my weight stable and my appetite and carb cravings beautifully controlled, and fasting is taking off the few extra kilos of fat they I still have on my lower abdomen. During fasting my blood glucose levels are what is regarded as normal, and I hope that as my insulin resistance is reduced, I will have more normal fasting levels at all times. Dr. Mercola has been a big help on this long journey, and now I also have Dr. Fung to help me. My heartfelt thanks, Dr. Fung.

    • My morning blood sugar is also right around 100. To get it less, I have to fast, and even then my blood sugar becomes less only after a few days of fasting. This week’s values (fasting from Sunday night to Thursday at “lunch”): Monday, 105; Tuesday, 98; Wednesday 99; Thursday 72. Since I’m eating today (Thursday), my morning blood sugar will be above 100 tomorrow.

      Also, my ketones are all over the map. If I eat ANY carbs (such as some olives and pepperoncini in a salad, maybe yoghurt, sauces that my wife makes to accompany meat), I can get kicked out of ketosis. I have to shoot for zero carbs to continue ketosis. Even then, if I enter a fast with a high (for me) value of BOHB 1.0, this value sometimes goes DOWN even while fasting. Other times, it does not. If I get out of ketosis, even with a minor amount of carbs, I have to fast several days before I can get back into ketosis. If I eat food, even keeping the carbs as low as I can, I find it very difficult to get back into ketosis. About the only thing I’ve seen as a trend is that I get higher values of ketones if I eat more fat.

      • Bob, I’ve been trying to figure that out, more fat is better. I would encourage people to try keto calculator, https://keto-calculator.ankerl.com/. This is a great playground to test carb/protein/fat proportions and see graphically how it effects weight and bmi. Here’s my problem. If you don’t significantly reduce carbs, the body will produce glucose from it. Ditto with protein as it can fairly easily be converted to a carb. So if the only food source is fat the body will burn it producing ketones and fatty acids. But the goal is to get your body to burn stored fat not dietary fat. It seems to me if your daily caloric requirements were satisfied by meals there would be no purpose in going after stored fat as there would be no deficit. The idea is you body has a very limited reserve of glucose/glycogen/glocagon but, in some, an almost unlimited reserve of fat. This theory of mine is supported by the keto calculator. That, of course, presupposes the keto calculator is at all accurate. The model is, you set your invariant carb and protein leaving fat as the only variable the user can throttle.

        If you play with that, mapping it’s projections, against your experience, I’d love to hear your conclusions.

        • Great clarification in your response here — it is the “Refrigerator/ Freezer” analogy Dr. Fung uses. Fasting and veggies only is the best way to kick start the glucogenesis reboot, yes?

      • Hi Bob, it seems that we are both good at gluconeogenesis. My morning fasting levels are often in the range of 110 – 120, but they settle down to around 95 -100 for the rest of the day, after the meal spikes have gone. Since Dr. Fung’s article on the Dawn Phenomenon, I am obsessing less about the blood glucose levels, and thinking more about improving insulin tolerance. I do not want to go extremely low carb, as I eat my own organic fermented vegetables and my home-made natto every day, for their wonderful health benefits. I don’t measure my ketones, but can tell that I move into ketosis a few days into my fast. Much to my regret, I have had to abandon my homegrown organic fruit, as fruit causes unacceptable spikes. I understand your frustrations, when you think you are doing everything right.

  5. This all looks to be the case with me, I have always had low body weight because i have been a fitness nut all my life.
    Hgb A1c is 6.0 (moving steadily up over the years).
    Can someone who has low body weight (172 Lbs – 5′ 10″) suffer from fatty liver/ pancreas?

    • Yes. TOFI Syndrome, or “skinny fat.” You may not see your visceral fat, but it seems to be there. Good luck.

    • Stephen T

      JHall, you might be interested in the work of Professor Tim Noakes, who has a large number of talks posted on YouTube. He was a marathon runner and increasingly diabetic until he changed to a low carb diet when his condition improved dramatically.

      Tim Noakes, a top scientist and South African, became one of the world’s leading advocates of a low-carb diet. Third-rate dietitians then felt threatened by advice that actually resulted in improved health and weight loss, so they tried to silence him by making a ridiculous complaint but lost. He had to spend three years of his life fighting this nonsense.


    • Yes, TOFI, go to Dr Michael Mosley’s website for 8 week blood sugar diet. He posted his own MRI of his liver and pancreas to demonstrate that you can be normal weight but still be diabetic w/ intra organ fat.


    • yes

    • Ignatius

      5’10″/172# = BMI of 24.7, which is at the high end of the normal range (normal range tops out at 24.9)

  6. Can you say something about high cholesterol without high blood sugar? I seem to have all all the symptoms insulin resistance combined with very low energy and difficult-to-control obesity. It has been like that for over 10 years, but my blood sugar is always normal, even low at times.

    • I would encourage you to research the work of Dr Joseph Kraft who did landmark research into how the routine FBG test only detects diabetes after you’ve got it whereas a glucose tolerance test can detect it more than 10 yrs in advance of it showing up as high fasting blood glucose. And some people just have high cholesterol.

  7. Roger Bird

    Thank you, Jason. You have become the Newton of diabetes, with much better social skills than Newton. (:->) And an excellent sense of humor.

  8. Great article and explanation of what is going on (silently) before a person is diagnosed with insulin resistance.

    I was diagnosed with insulin resistance last year, and had high ALT results as well. It probably didn’t help that my doctor had prescribed a course of hydrocortisone pills because my cortisol production was severely under the lower range by a significant margin. He thought that the very low level of cortisol was negatively impacting my thyroid hormone production, an issue that I have had for decades following a diagnosis of subacute granulomatous thryroiditis, which severely impair the gland.

    I have since stopped this medication and feel myself again. After taking it for a couple of months my fasting blood glucose was 107mg/dL and just 3 months later my fasting glucose was 112 mg/dL!
    My ALT enzyme was 40; the lab’s range is 0 to 32. My baseline A1C was 5.9 and after one year of closely watching my diet, only eating ketogenic foods, I managed to bring it down to 5.7. It is still a bit high, so I’m not out of the woods yet.

    I had a much improved blood test in March of this year, where my fasting glucose is closer to 100 mg/dL and my ALT is in range, although as of yet towards the high end of the range.

    I will follow up with another blood test in 3 months and I really hope to see significant improvement as I have been fastidious about my diet, LCHF, by which I limit glucose producing foods to 20 grams per day AND in the last 5 weeks I have undertaken a fasting routine.

    I fast following the advice from Dr. Fung’s book, fasting three times a week, each time for 36 hours. I feel really good and with lots of energy. I sleep well and am able to live my normal life AND exercise. I do high intensity interval exercise twice a week and resistance training three times a week. This combination of LCHF, fasting and exercising is working out for me and my lifestyle/family life. I have lost 2 inches from my abdomen/waist, 3 inches from by bust line, and 2 inches from my hips. So, I have lost 7 inches in total from my entire torso so far. This is very encouraging and I am looking forward to seeing more good results.

  9. Hi All

    I am fasting since last three years & lost 40 LBs. My A1C is 5.5 but Fasting Blood Sugar is always above 7 & below 8.5. I am unable to get Fasting BS under 6. Any Suggestion ?

  10. Josh Miller

    Phenomenal post Dr. Fung. Probably a dumb question – does the pancreas ever actually completely stop working/break down? Or, does it become so covered in fat that the insulin it produces can’t get through to control blood sugar, hence Type 2? Put another way, is Type 2 diabetes always and forever reversible if only the patient goes on an LCHF/Ketogenic/Intermittent Fasting protocol to reduce pancreatic fat, making it possible for insulin to once again get through to control blood sugar? Is there a pancreatic Point of No Return, in other words? Or, is it always still functional, just engulfed by fat and thereby can’t do its job?

  11. Excellent post! We know exactly what happens here, All this extra fat poisons the alpha cells in our pancreas. This causes it to be less sensitive to insulin and glucose, perceiving our blood sugar to be lower than it is. This elevates glucagon levels, which the liver uses to perceive whether or not we need extra glucose secreted. So the elevated glucagon causes it to secrete more, as this will in itself lower the insulin to glucagon ratio, and then excess fat has also caused the liver to be less insulin sensitive, which further confuses it in thinking we are low when we’re high.

    The net result is inappropriate and excessive endogenous glucose secretion, which is supposed to keep us from going too low but now, instead, it’s keeping us from going down to normal.

    So the culprit is visceral fat which is caused by both elevated insulin and cortisol. Insulin does take most of the rap here as it should, but we can’t forget other hormones, the most notable of which are adrenal hormones out of balance.

    • Hi Ken, your explanation assumes that neither the fatty pancreas nor the fatty liver are capable of accurately measuring glucose levels in the blood, leading to elevated glucagon levels. You may well be right, but I prefer a simpler explanation (Occam’s Razor). It could be that insulin resistance is preventing the rapid clearance of the glucose delivered by the dawn phenomenon, in the same way that it prevents rapid clearance of the glucose delivered by a meal. Two days into a fast and my blood glucose levels (even the morning one) are in the low normal range. The pancreas and the liver do not provide more glucose than I need to function correctly. When I eat again, I am back to high normal blood glucose levels, with a dawn phenomenon level above normal. I don’t think my pancreas and liver are moving in and out of ‘fattiness’. Having been insulin resistant for several decades, I suspect it will take a lot of time to become fully insulin sensitive again, if ever.

  12. BernardP

    *** How does one get rid of the fatty liver and fatty pancreas? ***

    The vital question is : How does one get rid of the fatty liver and fatty pancreas? After prolonged intermittent fasting, total body weignt is comfortably in the normal range. Yet, the slightest provocation will send blood sugar at too-high levels, for example at 11 two hours after eating a moderate portion of spaghetti or pizza.

    In this case, it seems T2D is not “cured” but managed with diet and fasting. The conclusion seems to be that the liver and pancreas are still full of fat, despite the normalized body weight.

    It appears that the liver and pancreas are the first to get full of fat and the last to get rid of that fat. So, the only way I see to get rid of liver and pancreas fat is to increase fasting so as to lower weight even more, in the hope that eventually, the fat will get out of the liver and pancreas.


    • That may well be your situation. I, again, refer to my above post regarding, https://thebloodsugardiet.com/michaels-story/
      Another point you raised is ‘managed’ vs ‘cured’ or ‘reversed’. This is the very question I’ve asked several times. The landmark study proving T2DM is not chronic and progressive was done by Dr Roy Taylor of Newcastle University. The Counterpoint Study Fung references was, in fact, authored by Dr Taylor. I think it’s a huge mistake to assume diabetes or metabolic syndrome is tied to obesity, though it often is but the weight is likely a proximal cause not the essential cause.
      The following presentation by Dr Taylor you need to see.


      His studies and clinical trials focus on a tightly controlled (hospitalized) group of subjects fed about 700-800cal/day for 2 full months. No keto, no low carb, just 3 Optifasts (Slimfast) meals/day plus a small dinner salad. There are fanboys about any dieting thing, be it juicing or keto or atkins. Dr Taylor’s research has been replicated and peer reviewed. I will report back when Dr Taylor responds to my request for clarification on the term ‘reverse’ vs ‘cure’.

      • BernardP

        Thanks. I was already aware of these two resources. I have watched Dr. Taylor’s presentation some months ago. As for Dr. Michael Mosley, he is generally less into pure fasting than Dr Fung.

        I’m hoping that Dr. Fung will specifically address getting rid of liver and pancreas fat in an upcoming post. The current post and the preceding one seem to be leading to that.

    • Stephen T

      Bernard, I don’t know if visceral fat, which surrounds your organs, includes fat inside the liver and pancreas, but logically I think it probably does.

      I do know that when you improve your diet, and stop feeding the insulin cycle, that visceral fat is the first to go. Your body wants to get rid of it the first chance it gets when you can stop making new fat and start using that surrounding your organs. It makes sense that this includes fat inside the liver and pancreas or the symptoms of type 2 diabetes wouldn’t disappear so quickly with a low-carb diet and, for some, fasting. This was a two stage process for me. First, a low carb diet give me control of my appetite and modest fasting of 16 – 18 hours followed quite easily.

  13. Ok, so we have these 2 cycles and we are now considered type 2 diabetic or prediabetic; what i want to hear is how to get rid of this excess organ fat accumulation. Any advice?

    • George, I think everyone agrees on this one, reduce/eliminate refined and processed carbs (pasta, bread, cereal), sugar, anything with HFCS (high fructose corn syrup). Dr Michael Mosley suggests eating a Mediterranean diet for 5 days and on the remaining 2 days eat only 25% of your normal daily food consumption. Depending on how severely you perceive your intra organ fat situation to be, simply water fast for those 2 days. They don’t need to be consecutive. The idea behind that is you want to empty out those organs. There are more ‘severe’ approaches you can take like IDF where you eat conservatively every other day and only have 1 meal on the intervening days 3-1-3-1. Or 3-0-3-0

    • sten bjorsell

      George and Walt. High insulin keeps glucose (glycogen) inside the liver while low enough insulin releases excess stores. Same as seen in the dawn syndrome. During a fast longer than a night insulin continues to slowly drop. Yet for many, high BG during first and sometimes also during the second day of fasting the BG is not falling below normal (without meds), indicating there is still plenty of glycogen in the liver. As long as BG is not falling below normal, the release of liver fat into the bloodstream for energy has not started, as I understand it. The progress from not fasting to the stage of “reaching the liver fat”, takes time! Exercise can reduce the time by burning the excess BG from the liver faster. Consequently, I understand that until a clear drop in BG is seen (without taking meds!) there is no real liver fat burning/reduction, meaning that fasting of only one day at a time can often be wasted.
      Yet it can be checked via BG which is now easy and cheap to measure. I also think that we all see satisfaction when BG finally drops below 3 and one is full of energy at the same time, clearly indicating that all sorts of fat burning are well underway.
      The fasting up to this point is often only emptying glucose from the liver, never reaching into liver fat stores.

      • Hi Sten, that is exactly what I was thinking. The liver seems to be happy delivering a fairly high dawn spike when it still has glycogen stores. When these are used up as in a fast, the liver becomes more parsimonious in its dawn spike, probably because it is more reluctant to dip into the stored body fat, or because it takes more effort, or both. Two days into my fast, I had no dawn spike this morning. I was at 101 at 2.30 a.m. (happened to wake up) and at 93 at 7.30 am. I am aiming to fast again for 5 days, and am curious to see what happens to BG.

      • Thanks Sten! Hey, would you drop me an email at the following walt at cornova dot org? There is a conversation I’d like to have with you that is likely, at least initially, too involved to exchange on here? Thanks!

        I get confused when on here and people in different parts of the world measure things differently. For instance, in US, BG is, I believe, mg/dl and normal is 70-100. Yet HgA1C is normal below 6.0 or 6.1. My last 3 or 4 have been mid 5’s, last 5.5. I am due for another one in Aug and I am going to try to get the Dr to order NMR LipoPanel with IR. When I’ve been fasting in the past I’ve seen my FBG be as low as 59 and as hgh as 138. Vry Confusing

  14. Discussing this with my Vegan son: ” the surplus consumption of saturated fat (palm oil) caused a markedly greater increase in the amount of fat in the liver and abdomen (especially the fat surrounding the internal organs, visceral fat) in comparison with the surplus consumption of polyunsaturated fat (sunflower seed oil) …”


    • 2017 study (Sweden) adds: https://www.sciencedaily.com/releases/2017/05/170508112325.htm
      ” … the epigenetic changes in the study participants’ fat tissue, through biopsies taken before and after the project. … the epigenetic pattern in more than 3,000 genes … had changed differentially, depending on whether the participants had eaten saturated fat or polyunsaturated fat … contribute to the difference in fat storage, in which saturated fat has a more negative impact …”

    • sten bjorsell

      Poha! A high carb diet (muffins) with large calorie surplus like in the study always means excess stored as fats. Maybe our bodies prefer the saturated fat before the polyunsaturated as it “knows” that it lasts longer without getting rancid, also in our bodies? After all, fat storage in the liver is a survival mechanism left from the times when abundance was rare, yet happened a few times a year and fat storage in the liver together with building stores whenever possible were then main priorities promoting survival.
      But note also that old studies (2014?) often lumped saturated fats with trans fats, which still is not banned in Sweden, where the study was carried out. Bakery goods are the worst trans fats offenders. In Denmark, trans fats were banned in 2003, and their heart disease rates have now dropped faster than in any other country, and no other known significant change has taken place in Denmark. http://www.euractiv.com/section/health-consumers/news/denmark-sees-70-fall-in-cardiovascular-disease-deaths/

  15. Thank you, Sten, for the great info and link. True: calorie surplus with carbs yields an overflow visceral fat (not glycogen) lodged in liver (and pancreas), blocking normal function with it’s ickiness. The 2014 study showed that if the calorie surplus was in the form of saturated fats, the body fat lodged more in organs and one’s middle; poly unsaturated fat was lodging (I would assume) more all over and subcutaneous? As I try to stay keto, but have a social life, occasionally: when I partake in some carbs I notice that all calories then count by a 1.3 multiple for weight effect, for several days (due to spiked insulin?), since I am still eating healthy fats (not sunflower seed oil) to satiety. As Dr Fung says: enjoy family life, feast when there is feasting, then get back on track. My son (Vegan) and I were discussing this with the animal saturated fats (me) outlook, and the vegan unsaturated (and saturated) fats (him) for satiety. All fats are both, actually, to an extent.

    • Stephen T

      Poha, when you look at the food available for social occasions, it’s a reminder of how insulin and fat generating the ‘standard’ diet is. Bread, pasta, potatoes and sugar mixed up in various ways with small amounts of real food here and there. Your son might well look at the food in a very different way.

      There’s a very long way to go.

  16. Srinath

    Thanks for the very informative post.
    Could you please explain the role of Free fatty acids in causing Insulin resistance and if there is a way to reduce the IR via reduction of FFA.
    Because I lost 90 lb recently but still have 10-15lb fat left, but I may still be insulin resistant. I have low insulin but my IR may still be high.

    • why do you think you’re insulin resistant? That is checkable via a blood test

      • Srinath

        I have many of the symptoms that Dr Berg says are signs of insulin resistance. I still tend to put on weight easily and that is another indication. What test is there for insulin resistance specifically ?

  17. Hi everyone. I’m from Japan. The Mongoloid people might often progress to T2D before developing obvious obesity. Reading the Dr. Fung’s story of the fatty pancreas, It came to my mind that the volume ( the space for fat deposit) of the pancreas of Mongolian people might be relatively smaller than that of Western people and therefore our threshold of developing T2D could be low. Could it make sense? Usually, the reasoning for it is often attributed to the difference of insulin secreting capacity among those people. I’m happy if you could share your thought on the above issue.

  18. Hi everyone I have been searching for answers as to why my fasting insulin level was so low @ 1.9. My A1C went from 5.4 in April to 5.9 in July. Fasting insulin usually in mid to high 90s. I started LCHF diet in June including daily intermittent fasting (approx 18 hrs fasting daily). I was concerned with such low insulin level I was becoming LADA (type 1.5 diabetic). But found this article of Dr Fung’s re fatty pancreas and wondering if this may be my issue. Any guidance on any blood tests or diagnostic testing that would tell me for sure? My own doctors just want to put me on metformin as the answer which I know is not a remedy.

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