Fatty Liver – T2D 25

posted in: Diabetes, Health and Nutrition | 57

Dr. Alfred Frohlich from the University of Vienna first began to unravel the neuro-hormonal basis of obesity in 1890. He described a young boy with the sudden onset of obesity who was eventually diagnosed with a lesion in the hypothalamus area of the brain. It would be later confirmed that hypothalamic damage resulted in intractable weight gain in humans, establishing this region as a key regulator of energy balance.

In rats and other animals, hypothalamic injury could experimentally produce insatiable appetites and induce obesity. But, researchers quickly noticed something else, too. All these obese animals shared characteristic liver damage, which was occasionally severe enough progress to complete destruction. Looking back at hereditarily obese strains of mice, they noted the same liver changes. Strange, they thought. What does the liver have to do with obesity?

Dr. Samuel Zelman first made the connection between liver disease and obesity in 1952. He observed fatty liver disease in a hospital aide who drank in excess of twenty bottles of Coca-Cola daily. This was already a well-known complication of alcoholism, but this patient did not drink alcohol. That obesity could cause similar liver damage by itself was completely unknown at that time. Zelman, aware of the animal data, spent the next few years tracking down twenty other obese, non-alcoholic patients with evidence of liver disease. One oddity he noted was that they unanimously preferred carbohydrate rich diets.

It would be almost thirty years later, in 1980, that Dr. Ludwig and colleagues at the Mayo Clinic described their own experience. Twenty patients had developed fatty liver disease, similar to what is found in alcoholics but they did not drink alcohol. This ‘hitherto unnamed disease’ was termed Non-Alcoholic Steatohepatitis (NASH), by which it is still known today. Once again, the patients were all clinically linked by the presence of obesity and obesity-associated diseases such as diabetes. Other than enlarged livers, there was also varying evidence of liver damage. When fatty infiltration is obvious, but without evidence of liver damage, the term Non-Alcoholic Fatty Liver Disease (NAFLD) is used.

This discovery, at the very minimum, saved patients from their doctor’s repeated accusations that they were lying about their alcohol intake. Dr. Ludwig wrote that it spared doctors “the embarrassment (or worse) that may result from the ensuing verbal exchanges.” Some things in life never change. Today, when patients have difficulty losing weight on an ‘Eat Less, Move More’ diet, doctors accuse patients about cheating, rather than accept the bitter fact that this diet simply does not work. This age-old game is called “Blame the Victim”.

With the new recognition of NAFLD, research confirmed the extraordinarily close association between obesity, insulin resistance and fatty liver. Obese individuals have five to fifteen times the rate of fatty liver. Up to 85% of type 2 diabetics have fatty liver. Even without the diabetes, those with insulin resistance alone have higher levels of liver fat. These three diseases clearly clustered together. Where you found one, you almost invariable found the others.

Hepatic steatosis – the deposition of fat in the liver where it should not be, is consistently one of the most important markers of insulin resistance. The degree of insulin resistance is directly related to the amount of fat in the liver. Rising alanine transaminase levels, a blood marker of liver damage, in obese children are directly linked to insulin resistance and the development of type 2 diabetes. Even independent of obesity, severity of fatty liver correlates to pre-diabetes, insulin resistance and impairment of beta cell function.

The incidence of NAFLD in both children and adults has been rising at an alarming rate. It is the commonest causes of abnormal liver enzymes and chronic liver disease in the Western world. NAFLD is estimated to affect at least 2/3 of those with obesity. The news is even worse for NASH. It is estimated that NASH will become the leading cause of cirrhosis in the Western world. It has already become a leading indication for liver transplant and will likely become the undisputed leader within a decade. In North America, the prevalence of NASH is estimated at 23%.

This is a truly frightening epidemic. In the space of a single generation, this disease went from being completely unknown, with even a name, to the commonest cause of liver disease in the North America. From virtual unknown to world heavyweight champion of the world, this is the Rocky Balbao of liver diseases.

Fatty Liver – the core issue

The liver lies at the nexus of food energy storage and production. After absorption through the intestines, nutrients are delivered directly through the portal circulation to the liver. Since body fat is essentially a method of food energy storage, it is little wonder that diseases of fat storage involve the liver intimately.

Insulin pushes glucose into the liver cell, gradually filling it up. The liver turns on DNL to convert this excess glucose to fat, the storage form of food energy. Too much glucose, and too much insulin, over too long a period of time leads eventually to fatty liver.

Insulin resistance is an overflow phenomenon, where glucose is unable to enter the cell that is already overfilled. Fatty liver, a manifestation of these overfilled cells, creates insulin resistance. The cycle proceeds as follows:

  • Hyperinsulinemia causes fatty liver.
  • Fatty liver causes insulin resistance.
  • Insulin resistance leads to compensatory hyperinsulinemia.

Hyperinsulinemia causes insulin resistance, and is the initial trigger for this vicious cycle.

Fatty Liver leads to Type 2 Diabetes

Fatty liver is clearly associated at all stages from mere insulin resistance to pre-diabetes to full blown diabetes, even independent of overall obesity. This relationship holds in all ethnicities, whether Asian, Caucasian or African-American.

The crucial piece necessary for development of insulin resistance is not overall obesity, but fat contained within the liver, where there should not be any. This is the reason that there are underweight patients, as defined by the Body Mass Index, who still suffer from type 2 diabetes. These patients are often termed “skinny diabetics” or TOFI (Thin on the Outside, Fat on the Inside). Overall weight matters less than the fat carried around the midsection and the liver. This central obesity, rather than generalized obesity is characteristic of the metabolic syndrome and type 2 diabetes.

Fat carried under the skin, called subcutaneous fat, contributes to overall weight and BMI but seems to have minimal health consequences. It is cosmetically undesirable, but seems to be otherwise metabolically innocuous. This is easily demonstrated by metabolic studies of liposuction, the most common surgical procedure done under anesthesia in the United States. Over 400,000 procedures are performed annually.

The surgical removal of large amounts of subcutaneous fat reduces body weight, BMI, waist circumference and the hormone leptin decreases. However, metabolic parameters are not improved even with the removal of ten kilograms (22 pounds) of subcutaneous fat. There are no measurable benefits in blood glucose, insulin resistance, inflammatory markers or lipid profiles. This lack of benefit occurs despite similar levels of fat loss compared to most dietary weight loss programs.

By contrast, weight loss through dietary intervention often result in marked improvement in all metabolic parameters. Conventional weight loss methods reduce subcutaneous fat, visceral fat, and intra hepatic fat whereas liposuction only removes subcutaneous fat.

Visceral fat is a far superior predictor of diabetes, dyslipidemia and heart disease compared to overall obesity. But a difference still exists between fat within the organ and fat around the organs (omental fat). Direct surgical removal of omental fat also carries no metabolic benefits.

The development of fatty liver is a crucial stepping-stone to elevated insulin resistance, the essential problem of type 2 diabetes. With sufficient glucose available as substrate, insulin drives new fat production and ultimately fatty liver. Insulin tries vainly to move more glucose into the overflowing liver cell without much success, much like the overflowing subway train. This is insulin resistance in the liver.

Fat contained within the organs is other than the liver also plays a leading role in disease. Little fat is normally contained directly within organs, and this abnormality causes most of the complications of obesity (18). This includes the fat contained within the liver, but as we shall see later, also the fat contained with the skeletal muscles and pancreas.

Fatty liver precedes the diabetes diagnosis often by ten years or more. The emergence of the metabolic syndrome follows a consistent sequence. Weight gain, even as little as 2 kilograms (4.4 pounds) is the first detectable abnormality, followed by low HDL cholesterol levels. High blood pressure, fatty liver, and high triglycerides emerge next, at roughly the same time. The very last symptom to appear was the high blood sugars. This is a late finding in metabolic syndrome.

The West of Scotland study confirmed that fatty liver and elevated triglycerides precedes the diagnosis of type 2 diabetes by at least 18 months. The triglyceride level increased more than 6 months before the diagnosis. This is strong evidence that accumulation of liver fat is crucial to the development of insulin resistance, but also may act as a trigger for the development of type 2 diabetes.

While virtually all patients with insulin resistance have fatty liver, the opposite is not true. Only a minority of patients with fatty liver have full-blown metabolic syndrome. This suggests that fatty liver is the precursor to insulin resistance, consistent with the overflow paradigm. Over decades, chronic excess insulin leads to accumulation of more and more liver fat, which now resists further glucose influx. The overfilled, fatty liver creates insulin resistance.

In type 2 diabetic patients, there is a close correlation between the amount of liver fat and the insulin dose required reflecting greater insulin resistance. In short, the fattier the liver, the higher the insulin resistance.

By contrast, in type 1 diabetes, insulin levels are extremely low, and liver fat is lower than normal. This is strong evidence that insulin levels are a key causal factor in developing fatty liver. Insulin drives fat production in the liver and low levels of insulin lead to less fat in the liver.

57 Responses

  1. Dear Dr jason could you please send me an IDM by arabic ?

  2. And fasting breaks this vicious cycle. Thanks for your work, Dr. Fung…and thanks for your videos, books and blogs. I have learned so much: life changing lessons. You are reaping massive amounts of good karma 😊

  3. Anne Matuscak

    To reverse this fatty liver and insulin resistance and T2 diabetes, I am assuming from this article that one must lose weight by dieting. I am obese with T2 diabetes going on 10 years. I need more information on reversing this horrible disease with diet. Am adopting a LCHF diet and trying to be more active. Never had a weight problem until the last 20 years and now weigh in the 290s for 5’7″. Age 68. I am looking to heal myself. Weight kept creeping up as I used more insulin. Any diet advice would be welcomed. Thank you.

    • Anne… LCHF diet is the way to go, and the folks at dietdoctor.com have built a tremendous support system for that. Well worth the subscription.

      Two things to do immediately:

      1) Good news – don’t worry about being more active. That is not the problem.
      2) From this moment forward, eliminate wheat and high fructose corn syrup from your life. There are other things you will eventually need to do – like eat more high protein, high fat meats like ribeye and salmon – but wheat and HFCS are toxic and destroying your health. Eliminating them will give you a good start on getting your life back.

      • Steve, HFCS is toxic, but so is regular table sugar. Why not mention that, too? Wheat is bad, but so are other grains and starches for T2DM.

        Anne, you are making the right choice going with LCHF. You might want to check out dietdoctor.com for recommendations.

        • Chris, without arguing levels of toxicity, I single out wheat and HFCS for two reasons:
          1) Modern Wheat contains proteins (gliadin,etc.) that stimulate appetite and wreak havoc on the intestinal system. Corn/rice/etc. have similar problems, but not to the level of wheat. They should all go, but knowing that people need to transition, it sometimes is necessary to do these things in stages.
          2) HFCS goes straight to the liver and wreaks havoc metabolically. Table sugar does not.

          That’s why eliminate those two immediately.

          • From what I understand, it is specifically the fructose component that is the bad guy for the liver. HFCS is 55% fructose and 45% glucose. Table sugar on the other hand is a 50/50 mixture. Based on that, I would say that table sugar is only a small bit less harmful than the HFCS. I try to minimize both in my diet.

    • Sue and Tony

      Anne ~ you can reverse this disease. Please read all the free advice that Dr. Fung has given us on this blog. Please go to dietdoctor.com for help with recipes and how to eat a LCHF diet. Everything you need to know is in this blog. This is completely reversible.

    • Stuart Woodside

      For me the key to weight loss and kicking T2D was Intermittent Fasting. There’s plenty of guidance in Dr Fung’s blogs for that. I enrolled in their long-distance (I’m in New Zealand) program and felt it was well worth it.

    • Roger Bird

      Anne, good for you. It takes courage to decide to take responsibility for your own health.
      I am doing the following that I have personal experience helps: ketogenic diet; intermittent fasting, baker’s and nutritional yeast (combine them; no reason not to. I take about a tablespoon per day of this combo in my smoothie. Tastes bad. Your needs may vary.); spirulina; absolute avoidance of all sugar and flour (they increase hunger); flax and chia seeds cracked and liquefied with your own blender just before you eat it in your smoothie; 2 raw eggs in my smoothie; EWOT or Exercise with Oxygen Training; light on the fruit and heavy on the veggies.
      I hope that this helps.
      (:->)

    • Sandy Bahr

      Hope it’s okay to post this comment. Join the “Reversing Diabetes” group on facebook. Some of our members are in Dr Fung’s distance program. We use the LCHF diet to reverse high blood sugar and we agree with Dr. Fung and use his videos and the info from Dr Eric Westman and Dr Sarah Hallberg who are also well known in this area.

    • Just go long term fast. Lchf just takes too long. I achieve major improvements in reversing my metabolic syndrome in just 3 5 days fast. I was on lchf for maths and d results was excruciatingly slow. What I discover is long term fast gives me the motivation that I am on the right track. Intermittent fast is now for me just a lifestyle.

      For those who prefer lchf, there is always the possibility that you will get high cholesterol at the end. As dr fung puts it, in lchf, where does all the fats goes if it is not burnt off either thru intensive exercise or fasting. Lchf works for body builders and sportsman bcos of their intensive workouts. But for the common layman, it is just simple, honest to goodness fasting. One or two 5 days fast and you will see the results and that will give you the motivation to strive on not just on diabetics but many others diseases.

      For me within a few months, I came off all my diabetic, high b;old pressure, cholesterol and blood thinners medications. Fatty liver reverse, snoring stops, weak knee joints probpen solved. Back aches becomes almost normal. Heartbeat drops dramatically.

      You have to either enroll in the program or just do it by reading all of dr fung post.it is worth it . Giving back 6.8 maths of yr life back to your health is just a small price to pay. If you do it properly, after6.8 wks, the results will be so amazing, you will want to adopt it as a lifestyle.

    • https://campus.recap.ncl.ac.uk/Panopto/Pages/Embed.aspx?id=c3bef819-e5f4-4a55-876f-0a23436988ed

      This is the must watch presentation by Dr Roy Taylor. I did this, not with Optifast or Slimfast but by using MyFitnessPal and trying to drop 2-3 lbs/week. Also, get Dr Michael Mosley’s book 8 week blood sugar diet. Whether you do it in 8 weeks or 52 weeks, you have to want to do it and stick with it. First obstacle…will power or lack thereof.

      • I also enjoyed Dr Mosley’s 8 week blood sugar diet, and am presently doing that eating OMAD late afternoon.
        Thanks for the presentation link, will watch this afternoon.
        Huge fan of Dr Jason Fung who tirelessly gives such good and free information. Dr Fung considered the 8 Week Blood Sugar Diet one of the ‘best books of the year’.

  4. I sure missed your blog posts the past few weeks. I so enjoy and look forward to reading more every week and hope you continue your work for many years yet. Fast and Feast then rinse and repeat.

  5. Dr. Fung, thank you for this great article. I’ve read your books and have lost 20 lbs in the last 4 months by following your LCHF and fasting protocols. I have a tremendous amount of respect for what you do and how freely you share your knowledge. I was a TOFI when I was diagnosed with metabolic syndrome 32 years ago and although I gained some weight over the years, I was never obese. My BMI is now back to 23.6 but I still struggle with blood glucose levels and fatty liver…my waist-height ratio is not ideal. Do you have recommendations on the best way to lose that visceral fat? I plan to continue LCHF and fasting, however I’ve read conflicting information about whether it’s best to lose weight quickly or slowly to get rid of fatty liver. Any experiences you could share from your practice would be appreciated.

  6. Is there a commonly available test for fatty liver? Something we could ask our physician to order. Thanks.

    • thebigpicture

      If you are genuinely concerned ask for the combination of liver function tests (blood tests) and ultrasound of the liver, which should be sensitive enough to diagnose.
      Having said that, the management will be the same. Dietary changes and weight loss.

    • Phillip Actor

      Have them check ASAT, ALAT and gamma GT, should all be very low, if elevated, and thats anything above value 20 here in Europe, you have trouble on the way. LCHF takes care of this quite effectively but it takes time. Maybe someone here knows the US metrics

      • Phillip,

        What units are used to report those lab tests in Europe ?
        I can calculate the equivalent in US units.
        I am wondering if the cutoff a are different here.

      • AST/SGPT units/L normal range 21-52
        ALT/SGOT units/L normal range 17-59

        Assuming those are the same tests you refer to Phillip.

        • AST/SGPT units/L normal range 21-73 (not 53).

        • As the above disagrees with what I find via google I do see the range is relative to the protocol used. On my test results it give the normal range as I did above, ymmv.

        • While those are the “normal” ranges, realize that many “normal” Americans have some degree of fatty liver. I personally like to see them “below halfway to the top of the range” to be fully reassured.

  7. Two things I have found in my extensive review of the journal literature that answer two question. Why don’t those on a high crab, low sugar diet get fat? As Dr. Fung has pointed that peoples such as the Japanese who eat a high carb (glucose) diet don’t get fat; their sugar averages 14 grams a day. On the western diet with its sugar, they get fat. The USDA figures that the average American eats 100 lbs of sugar per year, which means half of them eat more. It takes more than DNL (de novo lipogenesis) otherwise the traditional diet of the Japanese (70%) carbs) would cause an obesity epidemic, especially the poor ones such as following WWII who would be eating the most rice and noodles. It is the fructose in the sugar not the glucose that is causing the pandemic of obesity and diabetes.

    The damage to the liver is covered by the journal articles of Dr. Lustig and his book Fat Chance. Fructose he writes is more reactive than glucose. Over 95% of it is metabolized in the liver; therefore, it accumulates in the liver. With a high-glucose meal, fructose’s metabolism in the liver is slowed because of the metabolism of glucose in the liver mitochondria. Fructose through the process of glycation (attaching to proteins) starts the process leading to a fatty liver. In excess the glycation overwhelms the repair system. The damage hepatocytes slowly clear the glucose, and this slowness leads to insulin resistance. Dr. Lustig places the amount of fructose at 40 grams, though I would put a wide range depending on lifestyle, drugs, and health (including age). Thus I place glycation as the primary cause, not insulin resistance, which developed from ROS (reactive oxygen species) from glycation as the starting point. Fructose and galactose (from milk) are the most reactive of our sugars. For other observation, such as why some don’t get fat, go to my website at http://healthfully.org/rh/id8.html The website has an internal google search engine.

  8. Sue Skrzelinski

    Hi Dr Fung,
    I’ve read your books, they are wonderful. I can’t believe how much they’ve improved my health. After embracing a LCHF diet and fasting with great success after a diabetes diagnosis in April 2016, I’ve lost 12kg, even though I was not considered very overweight at 60kg.
    I’ve avoided going on any medications, now have great triglyceride/HDL levels but am wondering if there’s any way to check if my liver still has fat in it. This interests me particularly because I’ve had IBS for about 10 years and although I think it’s improved on the LCHF diet, it still makes an appearance sometimes.
    Thanks for the blog, I always look forward to reading it,

    Sue

  9. This is so reasonable and easy to understand. Thank you.

  10. sten bjorsell

    Dear Dr. Fung, thanks for more clarifications and here is a question for you
    I wonder why fatty liver often is indicated first(?) on the outside by larger belly.
    And is fatty liver = enlarged liver ?
    The liver is attached under the rib cage, high up in the abdominal cavity.
    Is it that an enlarged liver necessarily is pushing the rest of the organs down, this way causing the larger belly ?
    How much larger/heavier can a DB-2 liver on a very obese 65 year old man taking insulin daily be ? Compare to “normal” size.

  11. I have bought 2 copies of your books, one to loan to a friend. I have watched all your lectures. You have the best grasp of the diabetes (obesity & diabetes) pandemic and how to return from it to health.

    I ate a western diet with the typical love for sugar. I have always been at normal weight ((took of weight gain promptly before my adipose tissue hormone rest to the new weight). When I gained 5 to 7 pounds, I took it off. I started in 1969 doing the logical things of not eating late at night, skipping breakfast, not pigging out, and eating less empty calories. I was in graduate school philosophy. There is a big difference between the long-term overweight and those who respond to the weight gain within the first 2 years. The obese, of course, have a long-term weight problem; their system with insulin and the hormones made in the adipose tissue have rest their normal weight to current levels. Based on your lectures I have been recommending short-term fasting. So I had to try it though I am at my youthful weight. I like it so much that 6 mornings per week I fast. I feel better physically and mentally without breakfast. All I have is green tea with lemon juice.

  12. Hi Dr Fung

    ‘Fatty liver precedes the diabetes diagnosis often by ten years or more.’

    I’m wondering if there is a way to detect fatty liver? If so, it can be used as a preventative screening just like smear testing for cervical cancers.

    Infant, it could even be used to monitor the progress of treatment. Treatment is progressing well as fat reduces around the liver.

    • sten bjorsell

      Ultrasound, liver panel tests including GGT. But simplest is waste circumference larger than half body length….
      Eye whites becoming whiter is a side effect of higher fat intake I noticed! More dietary fats means more bile with more toxins flushed out early from the liver….

  13. Rajesh Pankaj

    Hi Dr. Fung

    Thank you for such a wonderful article once again. I seriously think that you must be recognised and awarded with NOBLE PRIZE for starting a new way of eradicating the most horrific and pandemic disease: T2D. Your work is same as any other scientists work who invent drugs to eradicate disease causing bacteria or viruses. Same way you’re devising new ways to end this Pandemic with your “medicine”, even better “Medicine: without any drugs”. Hoping and waiting for your article on Underweight and normal weight lean T2D patients.

    Regards:
    Rajesh Pankaj

    • I think so

    • Debra Griffith

      I agree wholeheartedly! How do we nominate him?!

      • Rajesh Pankaj

        I wish they open their eyes to new ways of treatment rather than bookish and “Pouring the chemicals into your body” methodologies. Until then, I think they are deaf.

  14. Excellent post–well written and easy to understand! So in the movie was Rocky really calling for Andreas (our beloved DietDoctor) and not Adrian?? 😉

    I’ll be sure to ask about my liver function numbers at next Dr visit. Is there an ideal range to look for (US measurements)?

  15. thebigpicture

    For what it’s worth, I’ll add my personal experience here. I’m a 36 year old male, started to get fatter around age 32. Currently bmi about 26, with some abdominal obesity. No diabetes. I also need to get in better shape, and thankfully it’s not too late yet, but I really do feel like it’s now or never.
    With regards to fasting, have twice tried water fasting, aiming for length (7 days or longer) and twice failed at around 48 hours. I’d like to try again, but I don’t know if it’s psychological or not. Although a useful thing, I didn’t like the feeling that you can’t sleep but you can’t concentrate either, and both of these were immediately relieved by a meal.
    On the other hand, I’ve found it quite easy to fast 24 hours, going multiple days on end with 1 meal at dinner, and have thus far lost about 10 lbs over 2 months. I’ve given up excessive sweets, but not entirely, and only eat them sparingly during meals.

    So my experience has been that low carb + intermittent fasting is very doable and works. Long term fasting is hard and not for the faint of heart.

    • In my , experience and a few of my friends, it is very difficult to go on long term fast and not suffer many consequences like, giddiness, light meanness, hot body, ache and pains.

      However, if we cut carbo down to the bare minimum of less than 5% , for a few weeks either by skipping one meal or just 3 meals without carbo for a few weeks, than long term fast are actually very easy. I guess the body gets use to having no carbo and have shifted to burning fats so the craving and hunger pangs will no longer be there once you start long term fast.

      For me, a 5 day fast is actually a breeze. No hunger pangs or cravings at all and I do feel a lot more alert. Normal for me to lose 5% of my weight in 5 days of water fast. The first time was more difficult bcos of the psychological effects. I.e. I have not truly believe my body will not get hungry. It is just a mental thing. Once , i hv the expereince , the. Mind just believe and stop interfering and fasting becomes a breeze I would go so far as to say it is addictive for me.i just love to fast.

    • sten bjorsell

      I agree 100% with what Terry teh describes. The metabolic difference eating LCHF and fasting with a few fat kilos to spare is very very small. Mainly same fuel, no hunger. Fat from food or from body fat makes mainly means no prep time for the latter! Adding the hidden benefits cleaning out dysfunctional and inflamed body proteins allover through the naturally following autophagy makes 5 days fasting also close to 5 free days in a super body shop, both inside and outside! I now aim to fast 5 days in a row 3- 5 times a year.

      Fasting from a higher carb start point is a trauma as dropping blood sugar will not easily be compensated with lipolysis and liver glucogenesis until insulin levels drop off significantly, which can take up to 3 days of suffering.

      • I third Terry and Sten. It took me a year to get really comfortable, as I as winding down consumption of carbs. But then fasting became easy. Patience grasshoppers, I now have the fasting insulin of a caveman and ideal BMI but it took time.

  16. Deb Griffith

    I have been working in a pharmacy as a technician, my first experience in the field, and the manufacturers bottles of most drugs are about the size of a bottle of aspirin that you buy at the store; the bottles of diabetes medications are TEN TIMES that size, because every sixth or seventh prescription is for diabetes related meds. It makes me sick, and sad, and a bit angry, when I hand these people their medications, and see them buying soda, or see the McDonald’s bags in their car at the drive thru, and wonder if their Dr is so clueless about how to reverse their disease, or if they just don’t want to put in the effort. Even one of the ladies I work with who has to be pushing 300 says she has always been heavy, so she has learned to accept it! So frustrating to see so many people suffering when they don’t have to, and so many millions of dollars spent when they don’t have to be.

    • Deb, a lot of doctors know they are doing diabetics no good, but their hands are tied because they feel like they can’t go against the Diabetes Association recommendations. DAA recs are heavily influenced by the pharma and processed food industries. It’s a perfect storm that makes and keeps people sick. I share your frustration.

  17. So I’m stuck being a ticking time bomb? An ultrasound revealed that I have mild fatty liver disease after my liver enzymes were elevated for no apparent reason ( I went to the doctor for persistent nausea). I’m wondering what I can do about it. I’m a 5’4″ 155lb non-diabetic who has tried intermittent fasting and the LCHF diet for weight control and energy boosts. Any suggestions are welcome.

    • thebigpicture

      Doesn’t sound like you are in terrible shape. Probably need around 20 lb weight loss to get bmi down to 23, and also measure your waist as well.
      Of course low carb diet, smaller meals and strict fasts will help. You can get a little nausea with this, but persistent is not normal. Any other symptoms? If it persists insist that your doctor does more workup, you don’t want to miss something.

      • Thank you thebigpicture, my ultrasound was about a year ago. My liver enzymes jumped up again this summer when I was taking Tylenol regularly for a ligament injury. I’m wondering if I just have a “lazy” liver? I lost 10lb last winter following Dr Fung’s suggestions but fell off the wagon and gained it back. I’m back in ketosis and plan to stay that way! I’ve never experienced the energy bursts that people describe on the LCHF diet but I really enjoy not being hungry. When I eat “normally” I experience extreme nausea and dizziness when I skip meals but my blood sugars are fine. BTW I’m a 37 year old female.

        • One possibility is that the body the liver produces more cholesterol after the initial stage of improvement. This is one of the side effects of lchf diet. As dr fung mention , the prob with lchf is the fats ingested, where do they go if you do not burn it off either with vigorous exercises or fasting. So imo, lchf can only work with at least IF.

          The other scenario is as the body heals, d liver will pump out more fats that it has not initially pump out, resulting in elevated liver enzymes . There is no research studies to prove this point, but dr fung suggest this is a real possibility as even patients whilst fasting can experience higher cholesterol levels.

          In my experiences, you have to be very strict on low carb to enable the body to switch to fat burning. Cheating will only mean your body is still burning carbo and d effort is usually wasted. if you are impatient , just go on a 5 day fast. My friends and me regularly lose 3-5 %. Of our weight during this 5 days and than maintain a very strict no carbo diet to reset the body set weight for about a month. To go back to carbo diet immediately after the fast usually result in very fast weight regain.

          For me, losing weight is a breeze and only a fringe benefit. The health effects are far more important.i suggest you get your body used to no carbo for a few weeks than go on a 5 day fast. The effects is usually astounding and losing 10 lbs in a month will be a breeze. For me it is better to suffer 5 days . Lchf and IF is just too slow .

  18. Continue with fasting IF and LCHF, it might take longer than you would like, but you should get there if you persist. Maybe you need longer IF, or more often, or you just need to persist. Read more on the blog, and carry on.

  19. I am just wondering how long it would take to bring the liver levels down.I have a fatty Liver and have had it for years and apparently the Dr.dosen’t worry about it.I have Diabetes and have struggled for years .I want to try the fasting but only want to skip breakfast ,have a light lunch and dinner at night as I find this is enough as I eat dinner at 6pm at night usually waiting until the next day to eat lunch at 12pm the next day .That totals to 18 hours without food.
    Anyway I will try and see what happens ,my diet is very low carb,hopefully this plan will work.
    I just want to thank Dr J Fung,he is wonderful to share all his knowledge with us.

    Here in Australia the diabetes Association don’t believe and oneday in the future surely they will understand their method of teaching is so wrong.I am a strong believer in what Dr Fung has discovered.He should be awarded for this.

    • It took about a month for me to lose 10 lbs and my recently diagnosed fatty liver went away. My doc said that the first weight you lose comes mostly from the liver so it only takes as long as it takes to lose the first 10 or 20 lbs to see a difference in your liver enzymes.

  20. Good article! I would suggest that fatty liver precedes diabetes for the same reasons hyperinsulinemia does, and this suggests that while there is certainly an interplay between the two, for instance fatty liver does increase hepatic insulin resistance, which can in itself raise hepatic glucose output, livers don’t get fat by themselves, and the combination of excesses of insulin and carbohydrate over a period of many years is what is doing our livers in.

    Of course the primary target of all of this is the alpha cells of the pancreas, and people can have very fat livers but have normal blood glucose levels, but you can’t have normal levels after the massive amounts of excess glucagon start flowing out of the alpha cells. Glucagon and adrenal hormones are the liver’s boss, the liver does what they tell them to do, but being too fat does make this all worse.

    When we see reductions in organ fat, the liver and pancreas both, this is probably more like the canary in the coal mine recovering, and again there is an interplay here, the organ fat does contribute to the problem, but big daddy insulin going easier on them now is likely the biggest player.

    So this means, of course, that we need to normalize hormones, especially since diabetes is a hormonal disorder. When we do so, meaning normal levels of insulin, glucagon, cortisol, leptin, etc, we have fixed the problem because this is where it all lies. Organ fat will normalize as well, one’s weight will, all metabolic markers will, because now we’re addressing what is behind all this stuff.

  21. Is it possible some people are genetically predisposed to this condition….3 out my 4 grandparents had fatty liver and I am fairly certain I have this now or put myself on the road for it unintentionally. Cutting my consumption of fruits and drinking more high quality black coffee to try and address this.

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