A New Paradigm of Insulin Resistance

Analysis of Type 2 Diabetes, Fatty Liver, Insulin Resistance, and Internal Starvation

Dr. Jason Fung

Discover how Dr. Jason Fung reframes insulin resistance, fatty liver, and type 2 diabetes as a reversible “energy overload” problem—and what that means for using food and fasting instead of more medication to restore metabolic health.

Dr. Jason Fung explains why type 2 diabetes, fatty liver, and obesity are not caused by “starving” cells that cannot receive glucose, but by organs that are already overloaded with sugar and fat. He shows how chronic high insulin, excess refined carbohydrates, and especially fructose drive fatty liver, which then causes insulin resistance, high blood sugar, and the complications we label as metabolic disease. Using relatable analogies like an overfilled suitcase or packed subway car, he argues that standard treatment with more insulin forces even more sugar into already full tissues, temporarily lowering blood glucose but worsening long‑term damage. He then presents evidence that type 2 diabetes is remarkably reversible with strategies that lower incoming sugar (low‑carb eating) and burn off stored sugar (intermittent fasting and similar approaches), and reviews human data from bariatric surgery, fasting protocols, and glucose‑wasting drugs that all work by reducing total body sugar load rather than just changing lab numbers.

Summary

Type 2 diabetes unfolds over many years as insulin resistance and compensatory high insulin quietly rise, long before fasting glucose becomes abnormal.
The conventional “lock and key” model assumes cells are starving for glucose, but real‑world patients with type 2 diabetes have abundant fat in the liver and body, not a state of internal starvation.
Fatty liver emerges as the central driver of insulin resistance: a chronically “overstuffed” liver stops accepting more fuel and instead spills glucose and triglycerides back into the blood.
Excess refined carbohydrate and especially fructose are key culprits, because only the liver can metabolize fructose and it rapidly converts it into fat, promoting non‑alcoholic fatty liver disease.
Standard treatment that adds more insulin or insulin‑stimulating drugs may normalize blood sugar but pushes more energy into already overloaded tissues, which explains why intensive glucose‑lowering with drugs has repeatedly failed to reduce mortality.
Clinical evidence from bariatric surgery, very‑low‑calorie diets, and fasting shows that when liver and pancreatic fat are reduced, beta‑cell function and insulin sensitivity can recover and diabetes can go into remission.
The core therapeutic strategy is simple in principle: stop putting sugar and refined starch in (low‑carb / low‑sugar diets) and create regular periods to burn stored sugar off (intermittent fasting or other fasting‑mimicking patterns).
Dr. Fung emphasizes that type 2 diabetes is a dietary disease, not an inevitable chronic decline, and calls on patients and clinicians to adopt nutrition‑centered interventions instead of relying solely on medications.

Video description from YouTube

Dr. Jason Fung completed medical school and internal medicine at the University of Toronto before finishing his nephrology fellowship at the University of California, Los Angeles at the Cedars-Sinai hospital.

He now has a practice in Ontario, Canada where he uses his Intensive Dietary Management program to help all sorts of patients, but especially those suffering from the two big epidemics of modern times: obesity and Type 2 diabetes.

Dr. Fung uses innovative solutions to these problems, realising that conventional treatments are not that effective in helping people.

A .PDF version of the slides used in this presentation is available here; http://denversdietdoctor.com/wp-content/uploads/2017/05/Jason-Fung-A-New-Paradigm-of-Insulin-Resistance.pdf

Transcript Summary

The two‑phase development of type 2 diabetes

Fung begins by outlining how type 2 diabetes usually develops in two phases: a long, silent period of rising insulin resistance with compensatory high insulin, followed by a later phase when the pancreas can no longer keep up and blood glucose finally rises into the diabetic range. During that first phase, blood sugar appears “normal” because insulin output ramps up, a state he calls compensatory hyperinsulinemia. Once beta‑cell output falls or resistance becomes too strong, glucose rises and diabetes is diagnosed, but the underlying process has already been in motion for a decade or more.

Why the “internal starvation” model fails

He then critiques the popular “lock and key” model in which insulin is the key, receptors are locks, and insulin resistance is portrayed as a broken lock that prevents glucose from entering cells, supposedly leaving them in a state of internal starvation. That model predicts weight loss and inability to make fat, analogous to uncontrolled type 1 diabetes, but this is the opposite of what we see in most people with type 2 diabetes, who are overweight and have fatty liver. He points out that if liver cells genuinely could not take up glucose, they would not be able to synthesize fat, yet type 2 diabetes is strongly associated with increased liver fat and triglyceride production. This mismatch suggests that the conventional internal starvation narrative is wrong and that something else must explain insulin resistance.

Fatty liver and the “overloaded cell” paradigm

Fung introduces an alternative “overload” paradigm: the problem is not that cells cannot get fuel, but that they are already overfilled with energy, particularly in the liver. Using analogies such as an overstuffed suitcase and a jam‑packed subway car, he explains that once the liver is full of glycogen and fat, it becomes progressively harder to push additional glucose and fat inside. Under chronically high insulin and high‑carbohydrate intake, the liver becomes fatty and enlarged, and attempts to off‑load excess energy by exporting triglycerides into the bloodstream, which we see as elevated triglycerides and non‑alcoholic fatty liver disease. This fatty, “overloaded” liver responds poorly to insulin’s glucose‑lowering effect, generating the appearance of insulin resistance even though the primary issue is storage capacity, not a broken receptor.

How fructose and refined carb drive fatty liver

He highlights fructose as a major driver of fatty liver because only the liver can metabolize it, whereas glucose can be used by nearly all tissues. When someone consumes sugar (sucrose), half is glucose distributed across a roughly 170‑pound body while the fructose half must be handled by a roughly 5‑pound liver, which is quickly overwhelmed and forced to convert fructose into fat. This explains why sugar and high‑fructose foods are so strongly linked to fatty liver and why simply “counting calories” misses the organ‑specific toxicity of fructose. He contrasts this with dietary fat, which generally bypasses the liver via chylomicrons and lymphatics, meaning eating fat does not automatically cause fatty liver in the same way that excess fructose and refined starch do.

Chronic high insulin, fatty liver, and insulin resistance

From there, Fung ties the pieces together into a feedback loop: eating a lot of refined carbohydrate raises insulin, which promotes de novo lipogenesis (new fat creation) in the liver, which leads to fatty liver and insulin resistance, which then drives even higher insulin levels. Over time, this cycle produces the classic picture of metabolic syndrome: central obesity, elevated triglycerides, fatty liver, and type 2 diabetes. He emphasizes that fatty liver often appears years before diabetes is diagnosed; studies such as the Whitehall cohort show gradual increases in liver enzymes long before fasting glucose is abnormal, a “silent scream” from the liver that something is wrong.

Why simply adding more insulin backfires

Fung then evaluates standard treatment strategies that focus on reducing blood sugar with medications, especially insulin or drugs that increase insulin secretion. If the problem is an overloaded “sugar bowl” (the body’s stores of glucose and fat), then giving more insulin just forces more sugar from the bloodstream into already stuffed tissues, similar to hiding household garbage under the sink instead of taking it out. Large trials like ACCORD, ADVANCE, VADT, and TECOS showed that intensive drug‑induced glucose lowering can reduce A1c but does not improve—and can even worsen—overall mortality, which is exactly what we would expect if we are just redistributing sugar rather than eliminating it. He argues that these outcomes are predictable once you accept that the fundamental problem is too much stored energy in the body, not a deficiency of insulin.

Evidence that type 2 diabetes is reversible

To show that beta cells are not “burned out,” Fung reviews evidence from bariatric surgery and very‑low‑calorie diet studies. After gastric bypass, many patients with decades of diabetes who are on multiple medications see their blood sugar normalize within days to weeks, long before significant fat loss occurs, indicating a rapid metabolic reset as liver and pancreatic fat start to fall. Similar improvements occur with strict calorie restriction or medically supervised fasting: as ectopic fat in the liver and pancreas decreases, insulin secretion and sensitivity rebound and diabetes can go into remission. He notes that these interventions demonstrate that type 2 diabetes is not an inevitably progressive, irreversible disease but a metabolic state that can be reversed by removing excess fat and sugar from key organs.

Therapeutic tools: low‑carb diets and fasting

Fung distills treatment down to two core steps: stop putting sugar into the system and burn off the excess already stored. Practically, this looks like low‑carbohydrate or low‑sugar diets, which reduce the inflow of glucose and fructose, and intermittent fasting or extended fasting, which create windows where insulin falls and the body has to tap into stored glycogen and fat for energy. He points to Acarbose, a drug that blocks carbohydrate absorption, and SGLT2 inhibitors, which cause glucose loss in the urine, as proof‑of‑concept that interventions which prevent sugar entry or promote sugar exit from the body improve cardiovascular outcomes even when A1c changes are modest. For most people, he suggests, dietary approaches can accomplish similar goals without surgery or expensive medications, provided they are implemented consistently and safely.

A call to reframe responsibility and treatment

In closing, Fung challenges the narrative that patients are to blame for their diabetes because they “ate too much and exercised too little.” He argues that the real failure lies in a medical model that misunderstood the disease, focused on blood sugar rather than total body sugar load, and promoted treatments that made long‑term outcomes worse despite short‑term improvements in lab numbers. He envisions a world where type 2 diabetes, its renal complications, amputations, blindness, heart attacks, and strokes become rare by treating it as a dietary disease and applying nutrition‑based therapies at scale. He urges both patients and clinicians to step through this “doorway” into a different paradigm and to share this understanding widely so that fewer people are trapped in an avoidable chronic condition.

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