Making Human Foie Gras – T2D 20

posted in: Health and Nutrition | 38

Fatty liver is a duck or goose is known as Foie Gras. But humans get it too. Here it’s known as fatty liver disease or non alcoholic steatohepatitis (NASH). How do we get NASH? It all comes down to what we eat.fattyliver2

Foods are broken down in the stomach and small intestine for easier absorption. Proteins are broken into amino acids. Fats are broken into fatty acids. Carbohydrates, composed of chains of sugars, are broken into smaller sugars. Carbohydrates raise blood glucose where proteins and fats do not. Some carbohydrates, particularly sugars and refined grains raise blood glucose effectively, which stimulates insulin release.

Dietary protein also raises insulin levels but not blood glucose by simultaneously raises other hormones such as glucagon and incretins. Dietary fats raise both blood glucose and insulin levels minimally. Absorption of fatty acids differs markedly from both amino acids and sugars. Amino acids and sugars are delivered through the intestinal bloodstream, known as the portal circulation, to the liver for processing. The liver requires insulin signaling for proper management of these incoming nutrients.

Fatty acids, on the other hand, are absorbed directly into lymphatic circulation subsequently emptying into the systemic circulation. These can then be used for energy or stored as body fat. Since liver processing is not required, insulin signaling is not necessary. Dietary fat therefore has minimal effect on insulin levels.

Insulin promotes energy storage and fat accumulation. At mealtimes, we eat a mix of macronutrients – fat, protein, and carbohydrates and insulin rises so that some of this food energy can be stored for later use. As we stop eating (fasting), insulin falls. Food energy must be taken out of storage to be made available for body functions. As long as feeding (insulin high) is balanced with fasting (insulin low), no overall fat is gained.

Insulin plays several key roles to deal with the incoming food energy. First, insulin facilitates the uptake of glucose into cells for energy, by opening a channel to allow it inside. Insulin works like a key, fitting snugly into the lock to open a gateway. All cells in the body are able to use glucose for energy. However, without insulin, glucose circulating in the blood cannot enter the cell.

In type 1 diabetes, insulin levels are abnormally low due to destruction of the insulin secreting cells in the pancreas. Unable to pass through the cell wall, glucose builds up in the bloodstream even as the cell faces internal starvation. Patients cannot gain weight no matter how much they eat, since they are unable to use the food energy. Untreated, this is often fatal.

Second, after immediate energy needs are met, insulin stores food energy for later use. Amino acids are required for protein production, but the excess is converted to glucose, since amino acids cannot be stored. Excess dietary carbohydrates also provide glucose to the liver where they are strung together in long chains to form glycogen in a process called glycogenesis. Genesis means “the creation of”, so this term literally means the creation of glycogen. Insulin is the main stimulus of glycogenesis. Glycogen is stored exclusively in the liver and can be inter-converted to and from glucose easily.

But the liver can only store a limited amount of glycogen. Once full, excess glucose must be turned into fat by a process called de novo lipogenesis (DNL). De novo means “from new”, and lipogenesis means “making new fat” so this term mean literally, “to make new fat”. Insulin creates new fat to store incoming food energy. This is a normal, not a pathologic process, since this energy will be required when the person stops eating (fasting).

Third, insulin stops the breakdown of glycogen and fat. Before the meal, the body relies on stored energy breaking down glycogen and fat. High insulin levels signal the body to stop burning sugar and fat and start storing it instead.

Several hours after a meal, blood glucose drops and insulin levels begin falling. In order to provide energy, the liver breaks down glycogen into component glucose molecules and releases it into general circulation. This is merely the glycogen-storage process in reverse. This happens most nights, assuming you don’t eat at night.

Glycogen is easily available but in limited supply. During a short-term fast (up to 36 hours), enough glycogen is stored to provide all the glucose necessary. During a prolonged fast, your liver will manufacture new glucose from body fat stores. This process is called gluconeogenesis, meaning literally, the “making of new sugar”. In essence, fat is burned to release energy. This is merely the fat-storage process in reverse.

This energy storage and release process happens every day. Normally, this well-designed, balanced system keeps itself in check. We eat, insulin goes up, and we store energy as glycogen and fat. We don’t eat (fast), insulin goes down and we use our stored glycogen and fat. As long as our feeding and fasting periods are balanced, this system also remains balanced.

The new fat made via DNL should not be stored in the liver. This storage form of fat, composed of molecules called triglycerides, is packaged together with specialized proteins call lipoproteins and exported out of the liver as very low-density lipoprotein (VLDL). This newly synthesized fat can be moved off-site to be stored in fat cells, known as adipocytes. Insulin activates the hormone lipoprotein lipase (LPL), allowing adipocytes to remove the triglycerides from the blood for long-term storage.

Excessive insulin drives fat accumulation and obesity. If our feeding and fasting periods fall out of balance, then disproportionate insulin dominance leads to fat accumulation.

I can make you fat

Here’s a startling fact. I can make you fat. Actually, I can make anybody fat. How? It’s really quite simple. I prescribe you insulin. Insulin is a natural hormone but excessive insulin causes obesity.

Insulin is prescribed to lower blood glucose in both type 1 and type 2 diabetes. Virtually every patient taking insulin and every prescribing physician knows very well that weight gain is the main side effect. This is strong evidence that hyperinsulinemia directly causes weight gain. But there is other corroborating evidence as well.

Insulinomas are rare tumors that secrete persistent very high levels of insulin. This causes low blood sugars and persistent weight gain, underscoring once again insulin’s influence. Surgical removal of these tumors results in weight loss.

Sulphonylureas are drugs that stimulate the body to produce more of its own insulin. Once again, weight gain is the main side effect. The thiazolidinedione (TZD) drug class does not increase insulin levels. Rather it increases insulin’s effect resulting lower blood glucose but also weight gain.

But weight gain is not an inevitable consequence of treating diabetes. Currently, metformin is the most widely prescribed medication worldwide for type 2 diabetes. Rather than increasing insulin, it blocks the liver’s production of glucose (gluconeogenesis) and therefore reduces blood glucose. It successfully treats type 2 diabetes without increasing insulin and, therefore does not lead to weight gain.

Where excessively high insulin levels leads to weight gain, excessively low insulin levels leads to weight loss. Untreated type 1 diabetes is an example of pathologically low insulin levels. Patients lose weight no matter what you try to feed them. Aretaeus of Cappadocia, a renowned ancient Greek physician, wrote the classic description: “Diabetes is . . . a melting down of flesh and limbs into urine.” No matter how many calories the patient ingests, he or she cannot gain any weight. Until the discovery of insulin, this disease was almost universally fatal. With the replacement of insulin, these patients gain weight once again. The drug acarbose blocks intestinal carbohydrate absorption, reducing both blood glucose and insulin. As insulin falls, weight is lost.

Increasing insulin causes weight gain. Reducing insulin causes weight loss. These are not merely correlations but direct causal factors. Our hormones, mostly insulin, ultimately sets our body weight and level of body fat.

Obesity is a hormonal, not a caloric imbalance.

High levels of insulin, called hyperinsulinemia, cause obesity. But this alone does not cause insulin resistance and type 2 diabetes. The conundrum is why fat becomes stored in the organs such as the liver rather in adipocytes.

How to get fatty liver

Here’s a startling fact. I can give you fatty liver. I can give anybody fatty liver. What’s the scariest part? It only takes three weeks!

Excessive insulin drives new fat production. If this occurs faster than the liver can export it out to the adipocytes, then fat backs up and accumulates in the liver. This can be achieved simply with overfeeding of sugary snacks. Glucose and insulin levels quickly rise and the liver handles this glut of glucose by creating new fat through de novo lipogenesis. Hey presto, fatty liver disease.

Overweight volunteers were fed an extra one thousand calories of sugary snacks daily in addition to their regular food consumption. This sure sounds like a lot, but actually only consisted of eating an extra two small bags of candy, a glass of juice and two cans of Coca Cola per day.fattyliver1

After only three weeks on this regimen, body weight increased by a relatively insignificant two percent. However, liver fat increased disproportionately by a whopping twenty-seven percent! The rate of DNL increased by an identical twenty-seven percent. This accumulation of liver fat was far from benign. Markers of liver damage also increased by thirty percent.

But all is not lost. When volunteers returned to their usual diets, their weight, liver fat, and markers of liver damage completely reversed. A mere four percent decrease in body weight reduced liver fat by twenty five percent.

Fatty liver is a completely reversible process. Emptying the liver of its surplus glucose, and allowing insulin levels to drift back to normal, returns the liver to normal. Hyperinsulinemia drives DNL, which is the primary determinant of fatty liver disease, making dietary carbohydrates far more sinister than dietary fat. High carbohydrate intake can increase de novo lipogenesis 10 fold, whereas high fat consumption, with correspondingly low carbohydrate intake, does not change hepatic fat production noticeably.

Patients with fatty liver derive more than three times more of that fat from DNL compared to those without. Specifically, the sugar fructose, rather than glucose is the main culprit. By contrast, in type 1 diabetes, insulin levels are extremely low, causing decreased liver fat.

Encouraging fatty liver in animals has been long known. The delicacy now known as foie gras is the fatty liver of a duck or goose. Geese naturally develop large fatty livers to store energy in preparation for the long migration ahead. Over four thousand years ago, the ancient Egyptians developed the technique known as gavage. Originally done by hand, modern, more efficient methods of provoking fatty liver involve only ten to fourteen days of over-feeding.dm20-1

A large amount of high starch corn mash is fed to the geese or ducks directly into the animal’s digestive system through a tube called an embuc. The basic process remains the same. Deliberate overfeeding of carbohydrates provokes high levels of insulin and provides the substrate to develop fatty liver.

In 1977, the Dietary Guidelines for Americans, strongly advised people to eat less fat. The ensuing food pyramid reinforced this notion that we should be eating more carbohydrates such as bread and pasta, dramatically increasing insulin. Little did we know that we were, in essence, making human foie gras.


38 Responses

  1. How is fatty liver diagnosed? How do regular joes like us know if we have it or not?

    • The easiest way to diagnose fatty liver is via ultrasound. The liver tissue will appear much brighter than the tissues of the kidney and spleen. It can also be seen on CT.

    • Also high, even normal high liver enzymes, high fasting blood sugars, high cholesterol, and, I am guessing this one, the right ribs sticking out more than the left ribs.

  2. Phillip Kostroun

    Good post. I use the same discussion in my diabetes classes when we talk about carb intake and how excessive carb intake lead to fatty liver, insulin resistance and weight gain. Thanks for your perspective. Fed vs fasting state has been especially enlightening concept.

  3. Aptly said: “Making Human Foie Gras”

  4. “Dietary protein also raises insulin levels but not blood glucose by simultaneously raises other hormones such as glucagon and incretins.” This is not true. Even in so-called “prediabetics” on a low-carb diet dietary protein WILL spike blood glucose. I have proved this hundreds of times through personal experimentation and have seen tens of others experience the same phenomenon. Gluconeogenesis is real and significant. I once did seven months of zero-carb (i.e., only meat) eating and my blood sugars were often over 100 mg/dl, including my waking sugars. Now that I have reduced my meat intake and have upped my fat intake, (as well as skipping meals frequently), my sugars almost never exceed 100 mg/dl. If I were to maintain my calories, but reduce the extra fat (butter and olive oil) my blood sugars would soar.
    This is a major point and must be understood by anyone who wants to reduce or eliminate their dependence on exogenous insulin (or other blood-sugar-lowering medications).


      I’ve wondered this, I’ve noticed when I eat just meat, like steak, or just eggs, I am so hungry 2 hrs later, I feel like i hvnt eating all day. I hv to have some kind of carb with my meat or I’m starving 2 hrs later. What’s that about?

      • @Diana. Our bodies get used to what we eat, both psychologically and physically. Perhaps you are used to having carbs with your meals and just don’t feel satisfied without that extra something? If so, this is a habit that can be changed or substituted if desired. For my friends I’ve advised them to eat something high fat if they are feeling hungry to help adapt and not feel like they aren’t eating enough.

        Physically, if your body is used to getting a steady influx of carbs, it will need to adapt and rev up your fat metabolism so it’s not dependant on regular carb intake for energy. I know of people who got headaches and shakes if they didn’t regularly ingest carbs. For them I’ve recommended starting slow with intermittent fasting. For most people gradually pushing breakfast to later is the day seems easiest since we have already been fasting all night. Eventually, after a few weeks of “pushing it” the headaches went away.

        Since I have been intermittent fasting and fasting, I’ve found that grumbling from the stomach isn’t really hunger but a temporary discomfort perhaps caused by they body trying to maintain eating patterns…

        I don’t think what you’re experiencing is related to what Mike described. Our bodies don’t keep a protein store, so excess protein above what is needed is converted to blood glucose for energy and stimulates an insulin response. Not really what we want when trying to lose fat weight. Protein needs vary greatly from person to person.

        Good luck!

      • @Diana what Rob C said is so true–our mind and body routines are so ingrained that if broken we can end up feeling that we have to have more. I was one of those people who–if I skipped a meal I would get shakey and sweaty and have to get food right away. When I started LCHF I figured the IF part would not be doable for me. I could not be more wrong. When I went grain-free and added sugar/sweeteners I was sick for 4 days. Nonstop migraine, irritable, lethargic, trouble with daily activities. Once the 4 days were over–I found I could easily miss a meal without trouble. My second day of fasting I fasted 20 hours with no ill affects.
        All I needed to do was re-train my body. The physical stuff stopped after 4 days (so did cravings), the “habit hunger” is still hanging around some days.


    • I think the protein thing varies per person. Some people can eat protein to excess and the hormonal effect will at least be neutral or even positive. For others I think protein should be viewed as essentially carbs light. I think I’m unfortunately in the proteins are carb-light camp.

    • Hi Mike- could you let us know what your basic diet is then? Would appreciate it! Thanks

  5. Thanks for another great post, Dr. Fung.

    On, there are two new videos featuring Jacqueline Eberstein, RN. One is her lecture from the recent Low Carb Cruise (or maybe it was the San Diego conference) and the other is an interview with Andreas Enfeldt. She is talking about women, hormones, weight and menopause. A few of the tips that she offers to women over 50 include to eat regularly, maintain total (NOT net) carbs at a max of 20g per day, and to avoid dairy and nuts (which I assume would include butter and very high fat nuts, like pecan…maybe not.) I’m 55 and currently having good luck doing daily fasting (anywhere from 16:8 to 20:4 hours) with a low carb, high fat dinner in the evening. I can maintain weight on a low carb, high fat diet, but without the fasting, I cannot loose weight. Luckily, I don’t find the fasting to be hard at all.

    A while back, you did a post on women and fasting. It would be wonderful if you might consider doing a post on women, menopause and fasting. I would love to hear about your views and/or clinical experience on this topic.

    • I meant to add that Jacqueline Eberstein also said that for some women, “diet is a stressor”. She mentioned that point in the context of talking about the effects of cortisol on weight gain in women. But in combination with her other recommendation to “eat regularly”, it raised the question for me about whether fasting could act as a stressor (which has not been my experience). She made no mention of IF. But again, if you were to consider creating a post on this topic, that would be wonderful and much appreciated.

    • Hi Karen-
      Thank you for raising the Big M question in all of this! I was interested in the ‘hints’ by J.Eberstein, RN, which include “A few of the tips that she offers to women over 50 include to eat regularly, maintain total (NOT net) carbs at a max of 20g per day, and to avoid dairy and nuts “. My question is then, eat what? If we need to keep our protein low, avoid dairy & nuts…. what do you eat? Thank you! corrie

      • I’m still working on a complete answer to that question but currently my go-to foods are some sort of meat with either salad, BBQ veggies, or stirfry, all with a couple tbs of either olive oil or coconut oil. Since I don’t count the carbs, I think I sometimes overdo the veggies, but I try to keep the protein in check. Avocados are a good snack item too, as is seaweed (except for the canola oil it’s made with).

        • Thank you LyndaF for your reply. I’ve been doing ‘lowish’ carbs for a while, but my weight never goes down by more than 3lbs then slowly up again. I know I rely too heavily on dairy (full fat greek yogurt, kefir, hard cheese) but I just haven’t found a good combo of foods that are satisfying and helpful with the weight loss.

          • Reluctantexan

            I’m considered elderly and have been using IF since February 2015 in conjunction with LCHF eating. Recently, I gave up all dairy and experienced immediate weight loss after a year of no weight loss. Of course, all bodies are different, but, hard as it was, giving up dairy was obviously good for me.

      • Corrie: I eat a lot of fat. I make a “bread” from ground pecans and ground flaxseed. I top that with butter, ghee, or very high fat cheese, like Boursin or brie. I eat big bowls of homemade bone broth soup with all the fat and marrow, plus shirataki noodles, which have fibre but no digestible carbs, plus an avocado sliced up with a big handful of spinach; pour the hot broth over the noodles. Pecans are very high in fat, as are macadamia nuts. I eat caulflower, broccoli, all leafy greens. Oily fish like salmon, but in small portions with a lot of olive oil or butter. Whole olives are high in fat and those are my go-to snack. The cookbook “The Fat Fast” has a lot of great recipe ideas.

        If I eat 80-90% of my calories from fat AND do intermittent fasting at least four days a week, I loose weight. With a more moderate fat intake of about 70-75% calories from fat plus two days of IF, I can maintain weight, or loose weight, but very, very slowly.

        • gingerperth

          Karen, i am finding the same as you — a strict LCHF diet is not enough to get rid of my belly fat. and your high fat meals sound similar to mine. instead of salmon (can no longer trust pacific wild-caught to be free of Fukushima radiation) i eat sardines and anchovies. i’ve recently added a tsp of resistant starch (potato and tapioca) to feed the good microbes in my colon with butyrate, without adding any digestable carbs.

          i am currently on an every-day 24 hour fast (one average size LCHF meal per day) and it is working very well for me. in 2 months i have painlessly lost 20kg. but i’ve found that even a single lapse (cheesecake for a birthday party) has made me gain back 3kg and takes over a week to recover. i still have too much belly so will continue until that dangerous fat deposit is gone.

        • Thank you so much Karen! I appreciate your time~ and will def. check out this book.

  6. Dr. Fung, thank you for this. It’s a great exposition of the metabolic processes going on in our bodies. At some point I’d like to see you address the difference in the body’s processing of long-chain and medium-chain fatty acids. I had understood that MCFA’s are delivered directly to the liver, unlike other fatty acids. I would love some clarification here. Thanks!

  7. Thanks for this post; very educational. I have a question about how the body deals with toxins and medications that are released from the liver and fat stores when in a fasted fat burning state. How can a person avoid being overwhelmed with the chemicals, poisons and hormones(ie testosterone in hormonally unbalanced peri-menopausal women) etc that are ‘packed away’ in fat cells but then are released in a toxic flood into the blood when fat is released? I hope someone will be able to give some advice on how to deal with this.

    • gingerperth

      Abi, i am also very concerned about the effects of detoxing while fasting. i found this article because i was searching for an answer to this question. i’ve read that belly fat is mainly caused by the body trying to store excess toxins to protect the organs. so when i fast and my belly starts to shrink, where are those toxins going? am i reabsorbing them in other fat cells? is one stool a day enough to eliminate all the newly-released toxins? should i be taking chelating agents while fasting? i wish Dr Fung would write a long article about this.

      • My acupuncturist suggested detoxing foods: 3 oz of raw grated beet a day, or the juice from that. There are various homeopathic remedies that are also very good (in Canada, Chelidonium Plex by Unda is a very good one that has helped me.) When I first started LCHF with intermittent fasting, I started to get eczema in a “classic” mirror image pattern, such as around both sides of the nose and upper lip, and between the eyebrows, as well on each inner elbow. After about two weeks in ketosis, it started to go away. Apparently, burning fat can also release stored estrogen; if a woman has low progesterone, that can mean increased night sweats (almost like a kind of detox in itself.) But that subsided for me after a while.

  8. without insulin, glucose circulating in the blood cannot enter the cell

    “in the face of hyperglycaemia, tissue glucose uptake is usually increased above normal even when insulin deficiency is severe. This cannot be reconciled with the concept that insulin is required for glucose uptake by insulin‐sensitive tissues. Indeed it proves beyond question that insulin is not required.” (source

    • Vicente, your source paper from the British Journal of Anaesthesia dates from July 2000. This is fascinating paper to read. It supports Dr. Fung’s overall tenets. What I find most interesting is the following statement from 16 years ago.

      “All type 2 diabetics, even those who require insulin for good control, produce endogenous insulin, and their metabolic state improves with fasting. Indeed studies have shown that prolonged starvation for up to 3 weeks normalizes glucose metabolism in type 2 patients.”

      Fasting has been known to help type 2 diabetes for a long time. Dieticians and GPs are still very much opposed.

      • Hi Mike,
        I am not agains fasting.

        It is in the idea of how insulin acts where I see something weird. From the same article:

        “The consequence of this error was the (fallacious) concept of insulin being ‘required’ for glucose entry into cells rather than just accelerating glucose uptake”.

        “fasting hyperglycaemia of diabetes results from hepatic over‐production of glucose alone, since peripheral glucose utilization is increased despite the lack of insulin. Insulin treatment reduces glucose concentration through inhibiting hepatic glucose production“. Under these conditions glucose utilization decreases, thus insulin administration reduces glucose utilization. This indicates that the plasma glucose concentration, rather than plasma insulin, is the prime determinant of glucose uptake. There are clearly sufficient glucose transporters present, even in the newly diagnosed diabetic state, to ensure adequate glucose metabolism. Thus insulin regulates glucose production more than glucose utilization.

    • If that was true then type 1 diabetics would not need insulin to survive …. but they all do .

      • ¿How so? Type 1 produce little to no insulin. Thus, if insulin indeed inhibits liver glucose production and lipolysis while activating lipogenesis, not producing enough insulin would cause:
        1.- No glucose being turned into fat (so no glucose withdrawal by lipogenesis)
        2.- Fat being turned into glucose (so glucose keeps on being added to blood)
        3.- Liver maintaining glucose production (so glucose keeps on being added to blood)

        All this on top of exogenous (=feeding) glucose.

        So, even if insulin indeed is not required for glucose transport (the paper states it accelerates somewhat an already quite fast process, that is, insulin has an effect, but is not the main driver), insufficient insulin production would cause glucose to soar over the limit where kidneys start to filter it out. In other words, food would just “go through” (this is what diabetes means, ethimologically) the patient without sticking, causing the “scarecrow look” of untreated type 1 diabetics.

  9. […] IDT: Making Human Foie Gras – T2D 20 […]

  10. […] Jason Fung kirjoittaa: ”Insuliini edistää energian varastointia ja kerryttää rasvavarastoja. Ruokaillessa syömme sekoituksen makroravinteita – rasvaa, proteiineja ja hiilihydraatteja ja insuliini kohoaa siten, että osa ruoasta varastoidaan myöhempää käyttöä varten. Kun lakkaamme syömästä (paastoamme), insuliini laskee. Ruoan energia pitää ottaa ulos varastosta, että se saadaan käytettäväksi elimistön toimintoihin. Niin kauan, kun syöminen (insuliini ylhäällä) on tasapainossa paastoamisen (insuliini alhaalla) kanssa, ylimääräistä rasvaa ei kerry”. […]

  11. so,,,how do we lose the weight?

  12. It would be wonderful If there was a pill that would lower insulin, LOL. Have our cake and eat it too!

  13. Ha! Human Foie Gras. Now that’s funny.

  14. @ab @gingerperth @karen. Re: detoxing, my personal experience on LCHF plus reading tells me that the process of LCHF and IF result in significant detox-ing. No need to add in other aids to detox at all. Heard of the ‘keto flu’? …that is detox. Also remember that your bowel is not the only elimination organ, kidneys plus skin also perform this job.

  15. Question:……..The whole time I was reading this very interesting article, which I fully agree with and accept, I was asking myself a question. If we know so much about the bodies fat storage activities and people agree that this is correct, then why can’t our government and doctors tell us what we should be eating?????? I do not understand why this is so difficult to change. I love your blog because I feel it is the the only place that I can find a reasonable answer to all of our questions of, “what the hell should I be eating or not eating.”

  16. john koroloff

    Huh? “Carbohydrates raise blood glucose where proteins and fats do not..” You have mentioned in other posts that proteins are very insulinogenic…that whey protein is more insulinogenic than white bread. You also point out that excess protein cannot be stored and is then converted, via the ornithine cycle in the liver, to glucose. Ergo, is not the 18oz Porterhouse Steak is really just an expensive form of sugar.? And does’nt the de-aminated amino acid, that is now in the form of glucose, trigger insulin as much as glucose from polysaccharides??

  17. If the following is true – “Glycogen is easily available but in limited supply. During a short-term fast (up to 36 hours), enough glycogen is stored to provide all the glucose necessary. During a prolonged fast, your liver will manufacture new glucose from body fat stores. This process is called gluconeogenesis, meaning literally, the “making of new sugar”. In essence, fat is burned to release energy. This is merely the fat-storage process in reverse” – then I don’t understand how a 16:8 or 24 hour fast allows the body to burn stored fat and lose weight? can someone explain please? Thanks

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