Fatty Liver Disease or How Not to Make ‘Foie Gras’ at Home

Liver faceted

Fatty liver in a duck or goose is known as Foie Gras. But humans get it too, all the time. Here it’s known as fatty liver disease or non-alcoholic steatohepatitis (NASH) and it’s extremely common.

How do we get NASH? It all comes down to what we eat.

Foods are broken down in the stomach and small intestine for easier absorption. Proteins are broken down into amino acids. Fats are broken down into fatty acids. Carbohydrates, composed of chains of sugars, are broken down into smaller sugars. Carbohydrates raise blood glucose where proteins and fats do not. untitled-4Some 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 raising 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.

Insulin makes fat

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 literally means, “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.

fattyliver1After 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.

dm20-1-1024x683Encouraging 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.

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.

Jason Fung


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  1. Vicente
    "without insulin, glucose circulating in the blood cannot enter the cell"

    Insulin: understanding its action in health and disease

    “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."

    Reply: #5
  2. Apicius
    Not sure I'm following your logic here. What happens to a child born with type 1 diabetes? Without insulin treatment, why do they become skinny and die? What role does the insulin treatment play in their case, and how does that relate to Dr Fung's statement?
    Replies: #3, #4
  3. Vicente
    Hi Apicius,

    it's not "my" logic, the quote is from an article published in the British Journal of Anaesthesia.

    Fung says "without insulin, glucose cannot enter the cell"

    The article says: "the concept of insulin being required for glucose entry into cells is fallacious"

    I see a problem here: someone is wrong and I would like to have an explanation.

    Regarding to your question, the article says: "the fasting hyperglycaemia of diabetes results from hepatic over‐production of glucose alone, since peripheral glucose utilization is increased despite the lack of insulin". And they also explain the role of insulin: "Insulin treatment reduces glucose concentration through inhibiting hepatic glucose production"

    I don't know why untreated T1D become skinny.
    I don't know either why they die. Diabetic ketoacidosis?

  4. Vicente
    From the wikipedia:

    Lack of insulin -->
    ketone bodies are generated -->
    ketone bodies inhibit glucose uptake (from the article)-->
    blood sugars rise even more

    You have acidic blood (because of the ketone bodies), you are losing water (because of the high blood glucose), you are depleting your body fat reserves (because of the lack of insulin).

    May be it is not directly the lack of insulin what blocks the entry of blood glucose into cells, but the presence of ketone bodies (caused by the lack of insulin).

  5. Tim
    Heh, the article you point out concludes...

    The further management of all diabetic patients should be dictated by frequent assessment of glycaemic control and the patient’s ability to resume a normal diet (see reference 4). Hyperglycaemia in any diabetic patient unable to take a normal diet should probably be treated with an intravenous infusion of insulin from an infusion pump, the rate being guided by a sliding scale.

    Duh, whatever the cause, if you don't take in sugars, your body doesn't need to deal with it. The article is basically an exercise in confusion. Why take a, so-called, 'normal' diet if it causes high blood sugar with a resultant need for insulin, which causes fat storage?

    Reply: #6
  6. Vicente
    Hi Tim,

    I don't conclude that the physiological facts they explain are wrong just because they are wrong about what is the best diet for diabetes.

    "Estimation and kinetic analysis of insulin-independent glucose uptake in human subjects"
    These results indicate that in postabsorptive human subjects 75-85% of glucose uptake is noninsulin-mediated and provide additional support for the concept that insulin may increase glucose uptake merely by providing additional transport sites

    "The Contribution of Insulin-Dependent and Insulin-Independent Glucose Uptake to Intravenous Glucose Tolerance in Healthy Human Subjects"
    We conclude that insulin-independent glucose uptake is a major determinant of intravenous glucose tolerance

    Insulin-independent glucose uptake?

  7. Tim
    I would think it obvious they don't know the physiological facts if they don't know the cause.
    Reply: #8
  8. Vicente
    Fung should say if he sticks to his statement or, otherwise, acknowledges he is wrong about the role of insulin. Silence is a bad option.
    Reply: #10
  9. Vicente
    From another article: "Metabolic Effects of the Very-Low-Carbohydrate Diets: Misunderstood "Villains" of Human Metabolism

    Contrary to popular belief supported by the leading physiology and biochemistry textbooks, there is sufficient population of glucose transporters in all cell membranes at all times to ensure enough glucose uptake to satisfy the cell's respiration, even in the absence of insulin [21]. Insulin can and does increase the number of these transporters in some cells but glucose uptake is never truly insulin dependent. Even under conditions of extreme ketoacidosis there is no significant membrane barrier to glucose uptake – the block occurs "lower down" in the metabolic pathway where the excess of ketones competitively blocks the metabolites of glucose entering the citric acid cycle. Thus, insulin is not needed for glucose uptake and utilization in man [21]. In fact, the process appears to be general for all polar (water-soluble) substrates, as transporters are the mechanism by which they are transported across the highly non-polar (lipid) cell membranes. When insulin is administered to people with diabetes who are fasting, blood glucose concentrations falls. It is generally assumed that this is because insulin increases glucose uptake into tissues. However, this is not the case and is just another metabolic legend arising from in vitro rat data. It has been shown that insulin at concentrations that are within the normal physiological range lowers blood glucose through inhibiting hepatic glucose production [21].
    Reply: #11
  10. Tim
    You see, Dr Fung's reputation doesn't rest on replying to you in some comment blog, it rests on results...which he gets.

    What real world results have these people, whom you quote, gotten? Words are just wind until they turn into real world results. These people don't even know what causes the problem...

  11. Apicius
    Vicente, this is very interesting stuff you have here. Did a lot of reading on insulin, and its lipophobic (polar) characteristic, and came across some interesting info on GLUT 1 to GLUT 6 glucose transporters, that basically usher glucose through lipid membranes -
    simple explanation from wiki here: https://en.wikipedia.org/wiki/Glucose_transporter

    The GLUT 4 transporter is an insulin-regulated glucose transporter. If I understand the literature correctly, the lower the insulin, the lower working efficiency of GLUT 4. Furthermore, GLUT 4 is found in adipose tissue (fat) and striated muscle (skeletal and heart muscle). So again, if I understand this correctly, the less fat you have on your body, the less GLUT 4 is present...because it virtually has no place to reside.

    What I find particularly interesting is that exercising muscle encourages GLUT 4 effectiveness in transporting glucose into the muscle. This makes sense...the mechanism encourages glucose availability to keep the body adequately fueled.

    Now, given all this, I'm still not convinced that Dr Fung is incorrect. The lower levels of insulin do indeed discourage glucose uptake. and, if a person fasts, and loses weight, less GLUT 4 is present. It's a good chain reaction...less insulin >> less GLUT 4 >> less adipose (fat) >> less GLUT 4 >> less glucose uptake...etc etc etc.

    Now, pay attention to the following diagram https://en.wikipedia.org/wiki/GLUT4#/media/File:Signal_Transduction_D...
    "The insulin signal transduction pathway begins when insulin binds to the insulin receptor proteins. Once the transduction pathway is completed, the GLUT-4 storage vesicles becomes one with the cellular membrane. As a result the GLUT-4 protein channels become embedded into the membrane, allowing allowing glucose to be transported into the cell."

    Notice that insulin is still a player in the whole scheme.

    How do we reduce these biological activities to take place?...by reducing the secretion of insulin. And how do we reduce insulin secretion?...by reducing insulinogenic foods or fasting. Sugar, carbs and protein is much for insulinogenic than fat. If you increase fat, you reduce insulinogenic response. Fasting also reduces insulinogenic response.

    Ok...those are my two cents. Even though I don't really agree with all you wrote, Vicente, and I still think Dr Fung is correct...I still appreciate all the literature you brought to my attention. I got to explore and learn a lot more. And I'm grateful for that. I like that in this forum we can have this sort of intelligent and thoughtful exchange.

  12. Marcin
    To Vicente and Apicius - Try using Wikipedia as a reference source in a thesis and see what the response is? You may be surprised
    Reply: #14
  13. Vicente
    Hi Apicius,
    "The lower levels of insulin do indeed discourage glucose uptake. "
    "insulin is still a player in the whole scheme"
    "How do we reduce these biological activities to take place?...by reducing the secretion of insulin. And how do we reduce insulin secretion?...by reducing insulinogenic foods or fasting. "

    I don't disagree with you.
    Thank you for your reply. I am also learning here.

  14. Apicius
    Marcin - I agree what you said about Wikipedia. I only used it for the post so that others can join in the conversation and not alienate them. In fact, in my post it says "in a simple explanation"...

    I'm not a medical professional, but I am an engineer. I also notice that there are A LOT of engineers in the low carb world looking at the medical research and making more sense of it than the medical professionals. sorry....don't mean to kick the doctors out there...but...that is my observation quite frankly. I think we are better suited in root cause analysis and looking at failures and seeing where cascading issues went wrong that led up to errors/defects/crashes.

    also, I think the medical industry are experts in using flowery language...hiding behind big words...making it more difficult to understand what is really going wrong. Typical engineers break down the problem into little bites, and expose each bite for what it is. No need for flowery language. and, there is also a normal process of getting together as a group of engineers, looking at the problem together, and challenging each other...that's how you get to the root cause.

    Let me put it this way...there is no risk of Big Airplane or Big Bridge to sell the public a phony and defective design. It takes one airplane crash for example, and Boeing, or Airbus or whoever goes out of business real fast! So, engineers have built up a really good practice of root cause analysis.

    So...want to ridicule me for using wiki to get others engaged on the discussion? Go ahead. But, let me see your flowery big words to refute or support the concepts I am bringing forth. I'm "bilingual"...doesn't bother me.

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