The Obesity Code

Why do most diets fail despite strict calorie counting? In The Obesity Code, Dr. Jason Fung argues that the conventional “eat less, move more” message misunderstands obesity’s true cause. Weight gain isn’t simply about excess calories—it’s primarily a hormonal disorder, driven by chronically elevated insulin and the metabolic adaptation that follows. Fung calls this the “calorie deception,” and he builds a unified framework that merges physiology, endocrinology and social environment to explain why the epidemic persists and how to escape its grip.

Calories: The Proximate But Not Ultimate Cause

You’ve been told that calories in minus calories out determines fat gain. Fung redefines this equation by separating proximate causes (what happens immediately) from ultimate causes (what drives the system). Reducing calorie intake lowers both food energy and basal metabolism; your body responds by slowing down to defend its weight set point. Experiments like Ancel Keys’ 1944 Minnesota Starvation Study showed that semi-starved men burned 40% fewer calories and developed obsessive food thoughts—proof that biology defends weight like a thermostat. Mere restriction without hormonal correction triggers predictable countermeasures: lower metabolism, increased hunger and faster regain.

Insulin: The Master Regulator

Fung positions insulin as the core conductor of energy storage. When insulin levels rise—typically in response to refined carbohydrates and frequent eating—your body locks energy inside fat cells and prevents access to stored fuel. Clinical evidence solidifies this link: diabetic patients who receive high-dose insulin gain weight even when eating fewer calories. Medications that raise insulin, like sulfonylureas, produce weight gain; drugs that lower insulin, like SGLT2 inhibitors, cause fat loss. The message is unmistakable: to lose fat, you must lower insulin exposure.

Insulin Resistance: The Self-Reinforcing Trap

Chronically elevated insulin eventually desensitizes its own receptors, forcing the pancreas to produce even more insulin—a vicious cycle that builds a higher “set point” of fatness. Over time, weight loss becomes harder because homeostatic defense mechanisms adjust energy expenditure. The longer you stay in a high-insulin state, the deeper resistance sets in. Liver, muscle and brain respond differently: the hypothalamus may remain sensitive, so rising insulin keeps signaling hunger and fat storage. Breaking that cycle is the real challenge of obesity reversal.

Fructose and Dietary Change

Historical dietary shifts amplified the problem. In 1977, McGovern’s Dietary Goals pushed Americans toward high-carbohydrate, low-fat diets. Food manufacturers replaced fat with sugar and refined starches, unleashing high-fructose corn syrup (HFCS) into nearly every food. Fructose has a uniquely harmful metabolism—it targets the liver, drives fatty-liver disease and promotes insulin resistance. The modern obesity wave emerged in parallel with rising refined carbohydrate consumption, not higher fat intake.

Timing and Frequency Matter

Beyond what you eat, Fung emphasizes when you eat. In the 1960s, most people ate three meals daily, allowing long fasting periods that kept insulin low. Today’s habit of near-constant snacking maintains elevated insulin 12–18 hours a day, fulfilling both criteria for insulin resistance: high concentration and persistence. Childhood obesity programs that reduced calories and fat failed, but those that cut sugary drinks and snacks—like Australia’s Romp & Chomp and Britain’s Ditch the Fizz—succeeded by effectively lowering insulin exposure.

Policy and Poverty

The epidemic isn’t only biochemical; it’s economic and political. Government subsidies favor corn and wheat, turning them into cheap refined ingredients while fruits and vegetables remain costly. Big Food’s research funding biased science toward favorable conclusions—a 700% higher chance of pro-industry findings, according to David Ludwig’s analysis. As a result, low-income populations consume the most insulin-raising foods because they’re the most affordable, perpetuating metabolic illness across generations.

Putting It All Together

In this integrated model, obesity is the outward symptom of internal hormonal imbalance, amplified by processed food, sugar and social structures. Fung’s prescription is not moral willpower but metabolic rehabilitation: lower insulin naturally through meal timing, real food and fasting. The rest of the book moves through specific mechanisms—insulin’s activity, fructose toxicity, fiber’s protection, and fasting’s restorative power—to show that sustainable weight control means managing hormones, not calories.

Core message

You don’t get fat because you eat too much—you eat too much because your hormonal signals push you to store fat and conserve energy. Fix your physiology, not just your plate.

Fung dismantles the century-old calorie dogma by showing how biological feedback maintains weight regardless of short-term restriction. The “calories in/calories out” model treats humans like simple combustion engines, ignoring adaptive responses such as reduced metabolism and increased hunger. You might burn less as you eat less, creating a plateau most diets can’t escape.

Five Wrong Assumptions

• Calories in and out are not independent; cutting intake lowers expenditure.
• Basal metabolic rate is not stable; it can drop up to 40% under semi‑starvation.
• Food intake isn’t under full conscious control; hormones regulate hunger.
• Fat storage is regulated hormonally—you can’t simply order fat cells to shrink.
• A calorie isn’t equal across foods—sugar and fat trigger distinct responses.

Historical trials confirm these truths. The Minnesota Starvation Experiment and the Women’s Health Initiative both showed temporary losses and long-term rebound. These failures illustrate a key insight: calorie restriction attacks the symptom, not the system. Without correcting insulin and hormonal adaptation, the body restores lost weight automatically.

Fung reframes dieting as a negotiation with biology, not a battle of will. Your body’s defenses protect weight like it protects temperature—through homeostasis.

At the center of Fung’s model lies insulin, the hormone that governs whether your body stores or burns energy. When insulin is high, glucose converts to glycogen and then to fat; when insulin is low, stored fat becomes accessible. Chronic insulin elevation locks fat stores and prevents weight loss—even if you reduce calories.

Clinical Proof

Diabetic treatment studies demonstrate cause and effect. The DCCT trial (1993) showed that intensive insulin therapy improved glucose control but added nearly 10 pounds of fat. The UKPDS found similar results. Patients on high-dose insulin gained weight despite eating fewer calories, proving insulin’s dominance over caloric equations. Drugs like sulfonylureas (increase insulin) promote gain, while metformin and SGLT2 inhibitors (lower insulin) induce weight loss.

Mechanistic Understanding

Frequent carbohydrate eating, sugary drinks and snacks keep insulin elevated all day. Even non‑caloric sweeteners can mimic sweetness and raise insulin through cephalic responses. This is why diet sodas can fail or even worsen metabolic risk. If insulin is the “fat storage hormone,” then effective strategies must reduce insulin exposure—through lower carbohydrates, reduced meal frequency, or fasting.

(Note: Dr. Robert Lustig’s work on fructose toxicity complements Fung’s, showing how sugar raises insulin indirectly by causing fatty liver and insulin resistance.)

Fung describes insulin resistance as a slow-moving biological loop that keeps getting worse. When high insulin exposure desensitizes cells, the pancreas compensates with more insulin—raising levels further. Over months and years, this escalates the body’s defended fat set point.

The Thermostat Analogy

Think of your body as a thermostat. Insulin acts as the dial. When it rises, your fat “set point” adjusts upward. Lose weight temporarily, and your body cools metabolism by a few hundred calories daily to restore the previous weight. The longer the system runs hot, the harder it is to reset. This explains why recent weight gain reverses easily, while long‑term obesity resists change even with strict diets.

Breaking the Loop

To disrupt resistance, you must combine dietary change (carb and sugar reduction), spacing meals, stress and sleep repair, and sometimes medication. Each reduces insulin exposure time. Over months, this lowers the set point, allowing sustainable fat loss instead of transient calorie-driven results.

Insulin resistance is time-dependent. Patience and consistent low-insulin states—not short-term diet plans—restore sensitivity.

Here Fung shifts focus to fructose—the most metabolically dangerous simple sugar. Unlike glucose, fructose bypasses insulin signaling and goes straight to the liver. There it converts to fat, raising intrahepatic triglyceride stores and driving fatty-liver disease, a precursor to insulin resistance.

Scientific Evidence

Early studies from 1980 showed that adding 1,000 daily fructose calories worsened insulin sensitivity by 25% within a week. Later trials confirmed that high-fructose beverages promote fatty liver and pre‑diabetes even when total calories remain constant. Dr. George Bray’s data linked rising HFCS intake to the obesity curve of the early 2000s. Fung’s takeaway: fructose toxicity unfolds silently, hidden behind its low glycemic index.

Where Fructose Hides

HFCS appears in sauces, breads, soups and dressings. Even “natural” sweeteners like agave and honey are rich in fructose. To protect your metabolism, you must reduce all added sugars—not just HFCS. Whole fruits are different: their fiber and water slow absorption.

(Note: Fung’s hepatic lens echoes Dr. Ben Bikman’s work, which also places fatty liver at the heart of systemic insulin resistance.)

Processing turns safe foods into metabolic hazards. When fiber, protein and natural fats are stripped away, sugars and starches absorb quickly, spiking insulin and blunting satiety. The book points out it’s easier to drink five oranges than eat five—the removal of fiber collapses natural intake control. Modern processed staples—refined flour, HFCS, seed oils—create hyper-palatable combinations that drive frequent eating.

Economic Forces

Policies subsidize cheap ingredients and encourage mass production. Corn and wheat—raw materials for sugar and starch—receive over 40% of U.S. agricultural subsidies, while vegetables get less than 5%. This economic distortion keeps the most insulinogenic foods easiest to afford. Fung argues obesity is policy-driven as much as biology-driven.

The metabolic solution is local and personal: prioritize whole, minimally processed foods, reintroduce natural fats, and ignore front-label marketing claims. The content, not the calorie count, determines hormonal impact.

Not all calories are threats—some nutrients act as biological defenses. Fiber slows carbohydrate absorption and lowers glucose and insulin peaks. Soluble fibers form gels that delay gastric emptying, while fermentable fibers nourish gut microbes that generate short-chain fatty acids to stabilize metabolism. Epidemiologic studies show high cereal-fiber intake dramatically reduces diabetes risk.

Rehabilitating Fat

The book dismantles “fat phobia.” Saturated fat was wrongly blamed because industrial trans fats and processed omega‑6 oils contaminated the data. Once separated, saturated fat shows little consistent harm. Healthy fats—olive oil, nuts, avocado, butter—improve satiety and support metabolic flexibility. The Mediterranean diet’s success (PREDIMED) proves fat quality matters more than quantity.

Combine fiber and fat and you have metabolic armor: fiber blunts insulin spikes; fat extends satiety, reducing snacking frequency. This combination forms the guiding principle of traditional diets worldwide.

Fung concludes with practical application: intermittent fasting. If constant insulin promotes storage, then planned absence of insulin promotes release. When you stop eating, insulin falls, growth hormone rises and fat oxidation increases. Contrary to myth, fasting preserves lean mass and may even raise metabolism slightly through adrenaline and hormonal adaptation.

Phases of Fasting

Within 24 hours, glycogen depletes and fat metabolism begins. By 48 hours, ketones fuel the brain, reducing hunger naturally. People often feel better on the second fasting day than the first. Long supervised fasts (like Dr. Duncan’s 382‑day case) confirmed safety and efficacy.

Protocols That Work

Common plans include alternate-day fasting, 16:8 time‑restricted eating or 5:2 diets. Fung’s clinic typically uses 24–36-hour fasts twice weekly combined with real-food meals. Fasting, unlike chronic restriction, is temporary and restores insulin sensitivity. In trials comparing fasting to daily calorie reduction, both groups lost weight—but fasting produced lower insulin and better metabolic improvements.

Intermittent fasting is not deprivation—it’s a reset button that allows the body to re‑access stored energy and break hormonal captivity.