The Obesity Code: Jason Fung's Hormonal Theory of Obesity

Table of Contents

1. The Book and How It Came About
2. The Calories-In, Calories-Out Model He Rejects
3. Insulin as the Cause of Obesity
4. The Body Set Weight Thermostat
5. The Insulin-Dose Evidence He Cites
6. Sulphonylureas, Metformin and Body Weight
7. Why Eating Less Fails, in His Account
8. Meals, Fasting and the Low-Fat Era
9. The Carbohydrate–Insulin Model in the Academic Literature
10. Later Trials on the Same Question
11. From The Obesity Code to The Hunger Code
12. Key Research Papers
13. Connections
14. Featured Videos

1. The Book and How It Came About

The Obesity Code: Unlocking the Secrets of Weight Loss was published in 2016 by Greystone Books in North America and by Scribe in the United Kingdom and Australia. It was the first of a series of “Code” books: The Diabetes Code followed in 2018, The Cancer Code in 2020 and The Hunger Code in 2026, with an Obesity Code Cookbook in 2019.

By his own account in a 2018 profile, Fung spent his first seven years of practice following conventional advice — low-fat diets and strict blood-sugar control for his kidney patients, many of whom had type 2 diabetes. He names three 2008 trials as turning points. One was a trial in the New England Journal of Medicine that compared a low-carbohydrate diet, a Mediterranean diet and a low-fat diet, in which the low-carbohydrate group lost the most weight (Shai and colleagues, 2008). The other two were the ACCORD and ADVANCE trials of intensive blood-glucose lowering in type 2 diabetes, whose results he read as showing that pushing blood sugar down with more medication did not deliver the expected benefit.

After these results, the profile reports, he rejected the energy-balance (calorie) theory of obesity, began lecturing colleagues and patients around 2011–2012, and started treating patients with low-carbohydrate eating and intermittent fasting. About 2014 a publisher approached him after one of his lectures, and that meeting led to The Obesity Code. Much of the book’s argument first appeared as a numbered series of blog posts titled “Hormonal Obesity”, from which the quotations on this page are taken.

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2. The Calories-In, Calories-Out Model He Rejects

The standard explanation of weight gain is energy balance: if a person eats more calories than the body burns, the surplus is stored as fat, so the remedy is to eat less and move more. Fung’s central move is to reverse the direction of cause and effect. In the fifth post of his Hormonal Obesity series he writes:

“Eating more and moving less is the result of obesity not the cause of obesity”

He then quotes the science writer Gary Taubes to make the same point: “We do not get fat because we overeat / We overeat because we get fat.” The line is Taubes’s; Fung adopts it as a summary of his own view.

Fung argues that body weight is regulated automatically, the way other body functions are. In the same post he writes: “We don’t control our body weight any more than we control our heart rates.” If weight is regulated, then a conscious decision to eat fewer calories is, in his account, fighting the regulator rather than resetting it. His conclusion is phrased as a slogan that recurs through the book’s argument: “The key is NOT balancing calories – it is to balance hormones.”

He defines the condition itself in hormonal terms: “Obesity is a hormonal dysregulation of fat accumulation.” In a 2025 video he restated the idea in almost the same words, describing obesity as not a caloric imbalance but a hormonal imbalance.

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3. Insulin as the Cause of Obesity

Of all the hormones involved in appetite and fat storage, Fung singles out insulin. Insulin is the hormone the pancreas releases after a meal; it moves glucose into cells and signals the body to store energy, including as fat. A persistently raised insulin level is called hyperinsulinemia. In the fourth post of his series, “Insulin Causes Weight Gain”, he writes:

“It appears that insulin is not merely associated with obesity but causes obesity.”

The fifth post names the framework: “According to Hormonal Obesity Theory (HOT), we postulate that high insulin levels causes obesity.” He reduces the theory to two sentences:

“Raising insulin levels causes weight gain. Lowering insulin levels causes weight loss.”

From this he draws the practical question he believes medicine has been asking wrongly: “The question is NOT how to balance calories, the question is how to balance our hormones.” In his 2025 restatement he describes insulin as a fat-storage hormone that also blocks lipolysis — the release of stored fat for use as fuel — so that while insulin stays high, he argues, the body cannot easily reach its own fat stores.

Fung’s view connects to a wider debate in diabetes research about whether hyperinsulinemia comes first and insulin resistance follows, or the other way round. Two papers set out the “insulin first” possibility: a 2008 review by Shanik and colleagues titled “Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse?”, and Barbara Corkey’s 2011 Banting lecture, “Hyperinsulinemia: cause or consequence?”, in which she proposed that excess insulin secretion may be an early driver of metabolic disease rather than only a response to it.

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4. The Body Set Weight Thermostat

The second pillar of the theory is the idea of a set point. Fung argues that the body has a target weight it defends, much as a thermostat defends a room temperature: if weight falls below the target, hunger rises and energy use falls until the weight returns. He calls this target the Body Set Weight and names insulin as the hormone that turns it up:

“Insulin is the hormonal signal to the body to increase weight – the Body Set Weight (BSW).”

In this picture, cutting calories without changing insulin is like opening a window in a heated room: the furnace simply works harder. Weight may fall for a while, he argues, but the set weight stays where it was, so hunger and a slower metabolism eventually pull the weight back up. Lowering insulin, by contrast, is in his account the way to lower the thermostat itself, so that the body no longer fights the loss.

The set-point idea itself predates Fung and has been studied directly. A 1995 study by Leibel, Rosenbaum and Hirsch measured energy use in people held 10 to 20 percent below, or 10 percent above, their usual weight. Holding weight 10 percent or more below the starting weight lowered total daily energy use by about 6 to 8 kilocalories per kilogram of lean body mass, and holding it 10 percent above raised energy use; the authors concluded that these compensatory changes oppose any weight different from a person’s usual one. Fung’s contribution is to name insulin as the setting on that thermostat.

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5. The Insulin-Dose Evidence He Cites

Fung’s main line of evidence comes from his own field of medicine: people with diabetes who are given insulin as a drug. If insulin causes weight gain, he reasons, then people injecting more insulin should gain more weight, even when calories are controlled. He writes plainly: “The more insulin you take, the more weight you gain.”

He describes a trial of intensive insulin treatment in type 2 diabetes in which patients ate less yet still gained weight, and concludes: “That means that it was not the calories that was driving the weight gain.” The study pattern he describes matches a 1993 six-month outpatient trial by Henry and colleagues in Diabetes Care. In that trial, fourteen people with type 2 diabetes were treated with intensive insulin. Blood sugar came under control within a month, but the insulin dose needed was large — about 100 units a day by six months — and average body weight rose from 93.5 to 102.2 kilograms. Weight gain was directly correlated with both the average day-long insulin level and the total insulin dose. The authors wrote that the metabolic improvement required large doses of insulin and “results in greater hyperinsulinemia with progressive weight gain.”

For Fung, this is the clearest experiment available: an outside dose of a single hormone, given to adults under observation, produces weight gain that tracks the dose. He uses it to argue that insulin is not a bystander to obesity but a driver of it.

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6. Sulphonylureas, Metformin and Body Weight

Fung extends the argument to the oral drugs used in type 2 diabetes, which differ in how they affect insulin. Sulphonylureas work by making the pancreas release more insulin; metformin lowers blood sugar mainly by other routes and does not raise insulin. In his account the weight effects line up with the insulin effects. He writes that sulphonylureas also increased weight “but not as much as insulin”, and that “The metformin group was weight neutral.”

The comparison he is describing comes from the United Kingdom Prospective Diabetes Study (UKPDS), a large randomised trial of 3,867 people newly diagnosed with type 2 diabetes. UKPDS 33, published in the Lancet in 1998, compared intensive treatment with a sulphonylurea (chlorpropamide, glibenclamide or glipizide) or insulin against conventional treatment with diet. Over 10 years, weight gain was greater in the intensive group (an average of 2.9 kilograms) than in the conventional group, and people assigned insulin gained more (4.0 kilograms) than those assigned chlorpropamide (2.6 kilograms) or glibenclamide (1.7 kilograms). Hypoglycaemic episodes were also more frequent with intensive treatment, highest on insulin. The trial’s own conclusion was that intensive glucose control reduced microvascular complications but not large-vessel disease.

Fung reads these figures as a ranking: the more a treatment raises insulin, the more weight follows. His statements about what this means for diabetes treatment are reported on the The Diabetes Code page; this site gives no medication advice.

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7. Why Eating Less Fails, in His Account

A theme throughout Fung’s writing is that cutting calories day after day leads the body to cut its own spending. In his 2025 video he describes the sequence: eating less lowers metabolism, and the lowered metabolism leads to regain. In his framework this is the Body Set Weight defending itself, because daily calorie restriction leaves insulin, and therefore the set weight, unchanged.

He frequently cites a 2016 follow-up of contestants from a televised weight-loss competition, published in the journal Obesity under the title “Persistent metabolic adaptation 6 years after ‘The Biggest Loser’ competition”. Fourteen of the original sixteen competitors were measured. At the end of the 30-week competition they had lost an average of 58.3 kilograms and their resting metabolic rate had fallen by 610 kilocalories a day. Six years later they had regained an average of 41.0 kilograms, yet their resting metabolic rate was still 704 kilocalories a day below where it had started. Those who had kept off more weight showed more metabolic slowing. The authors concluded that metabolic adaptation persists over time and is a proportional but incomplete response to efforts to reduce body weight.

A second study in the same vein examined appetite hormones. In 2011 Sumithran and colleagues put 50 people with overweight or obesity on a 10-week very-low-energy diet; they lost an average of 13.5 kilograms. One year later, the hormones that encourage eating had not returned to their starting levels: leptin and peptide YY remained lower, and reported hunger remained higher. Insulin was among the hormones that fell with the weight loss. The authors concluded that the circulating signals that encourage regain after diet-induced weight loss do not revert to their pre-diet levels.

Fung presents findings like these as the body behaving exactly as his thermostat model predicts. The study authors themselves frame them as metabolic adaptation and hormonal adaptation to weight loss.

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8. Meals, Fasting and the Low-Fat Era

If insulin is the setting on the thermostat, then the practical question becomes how to lower it. Fung’s answer has two parts: what people eat and how often they eat. Insulin rises after each meal, so in his account frequent eating keeps insulin elevated for most of the day, and a diet high in refined carbohydrates raises it further. He describes fasting as the most direct tool: “Fasting is the most efficient and consistent strategy to decrease insulin levels.” His account of fasting physiology, safety statements and the trials on intermittent fasting are on the Therapeutic Fasting page.

He opposes the low-fat dietary advice that dominated his early training. On a 2026 masterclass page of the fasting program he co-founded, he places the start of the obesity and diabetes epidemics at the 1977 dietary guidelines that advised Americans to eat more carbohydrates and less fat. In his account the shift toward carbohydrate-heavy eating, eaten more often through the day, raised the population’s insulin levels and with them its body weight.

These are Fung’s own statements about diet and history, reported here as his. The trials that have since compared low-carbohydrate and other diets are described in section 10.

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9. The Carbohydrate–Insulin Model in the Academic Literature

Fung’s Hormonal Obesity Theory sits beside an academic hypothesis with a similar core, the carbohydrate–insulin model of obesity, developed chiefly by the endocrinologist David Ludwig and the nutrition researcher Cara Ebbeling at Boston Children’s Hospital and Harvard Medical School.

In a 2018 paper in JAMA Internal Medicine subtitled “Beyond ‘Calories In, Calories Out’”, Ludwig and Ebbeling wrote that, according to the model, recent increases in processed, high-glycemic-load carbohydrates produce hormonal changes that promote calorie deposition in fat tissue, worsen hunger and lower energy expenditure. They also noted that conventional calorie-restricted diets continue to lack long-term efficacy.

A 2021 restatement in the American Journal of Clinical Nutrition, signed by seventeen authors including Gary Taubes, framed the model as a reversal of causal direction: increasing fat deposition, driven by the hormonal responses to a high-glycemic-load diet, drives the positive energy balance, rather than the other way round. The authors called for rigorous research to compare this model with the energy-balance model, since the two have substantially different implications for obesity management.

The academic model and Fung’s version share the claim that insulin directs fat storage and that obesity is more than a matter of calorie arithmetic. Fung’s version places more weight on the timing and frequency of meals and on fasting as a way to lower insulin.

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10. Later Trials on the Same Question

The insulin-centred view of obesity has been tested in several carefully controlled studies since 2016. Their findings are summarised here as reported by their authors.

• Isocaloric ketogenic diet on a metabolic ward (2016). Kevin Hall and colleagues housed seventeen men with overweight or obesity on metabolic wards: four weeks on a high-carbohydrate diet, then four weeks on a ketogenic diet with the same calories and protein. Energy expenditure rose slightly on the ketogenic diet (for example, by 57 kilocalories a day in the metabolic chamber), but body-fat loss slowed rather than sped up. The authors concluded that the diet was not accompanied by increased body-fat loss and that the increase in energy expenditure was small, near the limits of detection.
• Hall’s review of the model (2017). In a review in the European Journal of Clinical Nutrition, Hall wrote that two carefully controlled inpatient feeding studies had failed to support key predictions of the carbohydrate–insulin model and that, in his view, important aspects of it had been experimentally falsified.
• Energy expenditure during weight-loss maintenance (2018). Ebbeling, Ludwig and colleagues randomised 164 adults, after they had lost about 12 percent of their weight, to high-, moderate- or low-carbohydrate diets for 20 weeks. Total energy expenditure was 209 kilocalories a day higher on the low-carbohydrate diet than on the high-carbohydrate diet, and the difference was larger (308 kilocalories a day) in people with the highest insulin secretion at the start. Ghrelin was lower on the low-carbohydrate diet. The authors described the results as consistent with the carbohydrate–insulin model.
• The DIETFITS trial (2018). Christopher Gardner and colleagues randomised 609 adults to a healthy low-fat or a healthy low-carbohydrate diet for 12 months and tested whether baseline insulin secretion predicted which diet worked better. Average weight change was −5.3 kilograms on the low-fat diet and −6.0 kilograms on the low-carbohydrate diet, a difference that was not statistically significant, and baseline insulin secretion was not associated with the diet effect.
• Ultra-processed food (2019). In an inpatient randomised crossover trial, Hall and colleagues gave twenty adults either ultra-processed or unprocessed meals, matched for presented calories, sugar, fat, fibre and other nutrients, for two weeks each, and let them eat as much as they wished. People ate about 508 kilocalories a day more on the ultra-processed diet and gained weight, and lost about 0.9 kilograms on the unprocessed diet.

Researchers on both sides of the debate continue to cite these trials. Fung’s later writing, described in the next section, turns to ultra-processed food as part of his account of what raises the body’s set weight.

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11. From The Obesity Code to The Hunger Code

Ten years after The Obesity Code, Fung published The Hunger Code: Resetting Your Body’s Fat Thermostat in the Age of Ultra-Processed Food (Greystone Books and Scribe, 2026). The subtitle carries forward the thermostat image from the first book — the Body Set Weight — and links it to ultra-processed food, the subject of the 2019 inpatient trial described above.

Across both books the core claim is unchanged: in Fung’s account, body weight is set by hormones, insulin above all, and lasting weight loss depends on lowering that setting rather than on counting calories. His related books, his fasting program and the rest of his published work are listed on the Books, Clinic and Legacy page, and his application of the same insulin theory to type 2 diabetes and to cancer is reported on The Diabetes Code and The Cancer Code pages.

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Key Research Papers

1. Henry RR, Gumbiner B, Ditzler T, Wallace P, Lyon R, Glauber HS. Intensive conventional insulin therapy for type II diabetes. Metabolic effects during a 6-mo outpatient trial. Diabetes Care. 1993;16(1):21-31. — PubMed PMID: 8422777
2. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet. 1998;352(9131):837-53. — PubMed PMID: 9742976
3. Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, Witkow S, Greenberg I, et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med. 2008;359(3):229-41. — PubMed PMID: 18635428
4. Shanik MH, Xu Y, Skrha J, Dankner R, Zick Y, Roth J. Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse? Diabetes Care. 2008;31 Suppl 2:S262-8. — PubMed PMID: 18227495
5. Corkey BE. Banting lecture 2011: hyperinsulinemia: cause or consequence? Diabetes. 2012;61(1):4-13. — PubMed PMID: 22187369
6. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. 1995;332(10):621-8. — PubMed PMID: 7632212
7. Sumithran P, Prendergast LA, Delbridge E, Purcell K, Shulkes A, Kriketos A, et al. Long-term persistence of hormonal adaptations to weight loss. N Engl J Med. 2011;365(17):1597-604. — PubMed PMID: 22029981
8. Fothergill E, Guo J, Howard L, Kerns JC, Knuth ND, Brychta R, et al. Persistent metabolic adaptation 6 years after “The Biggest Loser” competition. Obesity (Silver Spring). 2016;24(8):1612-9. — PubMed PMID: 27136388
9. Ludwig DS, Ebbeling CB. The Carbohydrate-Insulin Model of Obesity: Beyond “Calories In, Calories Out”. JAMA Intern Med. 2018;178(8):1098-1103. — PubMed PMID: 29971406
10. Ludwig DS, Aronne LJ, Astrup A, de Cabo R, Cantley LC, Friedman MI, et al. The carbohydrate-insulin model: a physiological perspective on the obesity pandemic. Am J Clin Nutr. 2021;114(6):1873-1885. — PubMed PMID: 34515299
11. Hall KD, Chen KY, Guo J, Lam YY, Leibel RL, Mayer LE, et al. Energy expenditure and body composition changes after an isocaloric ketogenic diet in overweight and obese men. Am J Clin Nutr. 2016;104(2):324-33. — PubMed PMID: 27385608
12. Hall KD. A review of the carbohydrate-insulin model of obesity. Eur J Clin Nutr. 2017;71(3):323-326. — PubMed PMID: 28074888
13. Ebbeling CB, Feldman HA, Klein GL, Wong JMW, Bielak L, Steltz SK, et al. Effects of a low carbohydrate diet on energy expenditure during weight loss maintenance: randomized trial. BMJ. 2018;363:k4583. — PubMed PMID: 30429127
14. Gardner CD, Trepanowski JF, Del Gobbo LC, Hauser ME, Rigdon J, Ioannidis JPA, et al. Effect of Low-Fat vs Low-Carbohydrate Diet on 12-Month Weight Loss in Overweight Adults and the Association With Genotype Pattern or Insulin Secretion: The DIETFITS Randomized Clinical Trial. JAMA. 2018;319(7):667-679. — PubMed PMID: 29466592
15. Hall KD, Ayuketah A, Brychta R, Cai H, Cassimatis T, Chen KY, et al. Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake. Cell Metab. 2019;30(1):67-77.e3. — PubMed PMID: 31105044

PubMed Topic Searches

1. Carbohydrate–insulin model of obesity
2. Hyperinsulinemia as a cause of obesity
3. Insulin therapy and weight gain in type 2 diabetes
4. Metabolic adaptation after weight loss
5. Body-weight set point

Further Reading

• Fung J. Insulin Causes Weight Gain – Hormonal Obesity intravenous (2 December 2013). thefastingmethod.com
• Fung J. I Can Make You Thin…Insulin – Hormonal Obesity V. thefastingmethod.com
• Why Do We Get Fat? Part 2 – Insulin Is the Key (video page, 2 December 2025). thefastingmethod.com
• Dr. Jason Fung: Dismantling diet dogma, one puzzle piece at a time (profile, 2018). dietdoctor.com
• Fung J. The Obesity Code: Unlocking the Secrets of Weight Loss. Greystone Books; 2016. Open Library record
• Fung J. The Hunger Code: Resetting Your Body’s Fat Thermostat in the Age of Ultra-Processed Food. Greystone Books / Scribe; 2026. Book listing

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Connections

• Dr. Jason Fung: Fasting, Insulin and The Obesity Code
• Jason Fung: Life and Career
• Jason Fung on Intermittent and Therapeutic Fasting
• The Diabetes Code: Jason Fung on Type 2 Diabetes
• The Cancer Code: Jason Fung’s Evolutionary Theory of Cancer
• Jason Fung: Books, Clinic and Legacy
• Contemporary Practitioners
• Obesity
• Insulin Resistance
• Fasting Insulin Test
• Intermittent Fasting for Weight Loss
• Metformin

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