The Diabetes Code: Jason Fung on Type 2 Diabetes

Table of Contents

1. The Book and Its Argument
2. Type 2 Diabetes as a Disease of Too Much Insulin
3. The Overflow Paradigm
4. The Twin Cycles: Fatty Liver and Fatty Pancreas
5. Insulin Resistance as Protection
6. A Reversible Condition
7. The Glucose-Lowering Trials He Names as Turning Points
8. Fasting in His Own Case Reports
9. Medication Safety in the Fasting and Diet Studies
10. Later Research on Diet and Remission
11. Key Research Papers
12. Connections
13. Featured Videos

1. The Book and Its Argument

The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally was published by Greystone Books in 2018, with a foreword by the journalist Nina Teicholz. It followed The Obesity Code (2016), in which Fung argued that obesity is driven by insulin rather than by calorie balance, and it was followed in 2021 by The Diabetes Code Cookbook, written with Alison Maclean.

The book drew on a numbered series of blog posts on type 2 diabetes (“T2D”) that Fung wrote between 2015 and 2017. Across the series and the book, his argument runs in a single line: type 2 diabetes is a disease of too much insulin; the high blood sugar that doctors measure is a symptom of that excess rather than its cause; the excess sugar and fat are stored where they do not belong, above all in the liver and the pancreas; and because the disease is built by that overload, he argues, it can be taken apart by removing it.

Fung presents the book as a challenge to the usual way of describing type 2 diabetes as chronic and progressive. The sections below follow his argument in the order he builds it, with each claim attributed to him, and then turn to the trials and studies on the same questions.

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2. Type 2 Diabetes as a Disease of Too Much Insulin

Fung describes type 2 diabetes as “a disease of too much insulin (hyperinsulinemia)”. In the conventional account, the body’s cells stop responding to insulin (insulin resistance), the pancreas pours out more insulin to compensate, and diabetes appears when the pancreas can no longer keep up. Fung turns the order around: in his account the high insulin comes first, from a diet and eating pattern that keep insulin raised for most of the day, and the insulin resistance follows from it.

He is not the only writer to ask which comes first. A 2008 review in Diabetes Care by Shanik and colleagues, titled “Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse?”, gathered situations in which insulin itself appears to drive insulin resistance. It describes mice given extra copies of the insulin gene, whose insulin levels were two to four times higher than normal and which developed insulin resistance and high blood sugar while staying at normal weight; rats and humans given escalating doses of insulin, who showed both high insulin and insulin resistance; and many patients with an insulin-producing tumor (insulinoma), whose response to injected insulin was reduced. The review concludes that hyperinsulinemia “is often both a result and a driver of insulin resistance.”

Barbara Corkey of Boston University took up the same question in her 2011 Banting Lecture to the American Diabetes Association, the association’s highest scientific award, under the title “Hyperinsulinemia: Cause or Consequence?”. Fung, with A. Berger, wrote his own 2016 review on the subject, “Hyperinsulinemia and Insulin Resistance: Scope of the Problem”, in the Journal of Metabolic Health.

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3. The Overflow Paradigm

Fung contrasts two pictures of what is going wrong inside the cells. The first, which he calls the “Lock and Key” model, treats insulin as a key that opens the cell to glucose: in insulin resistance the lock is jammed, glucose cannot get in, and the cell is starved while sugar builds up in the blood. Fung rejects this picture of “internal starvation”.

In its place he puts what he calls the “Overflow Paradigm”. In his account the cells are not starving at all; they are already “jam-packed with glucose”. He compares the cell to an overstuffed suitcase: once it is full, pushing in more clothes takes more and more force, and whatever does not fit spills out. Insulin is the force; the sugar that spills back into the blood is the high blood glucose of diabetes. On this view, more insulin can push more glucose into an already full system, but it does not empty the system.

The way out, as Fung describes it, is to stop filling the suitcase and to let the body use up what is stored. In his words, low-carbohydrate diets and intermittent fasting “empty the cells”: with less incoming sugar and long periods without food, insulin falls, the body draws on its stores of glycogen and fat, and the overflow recedes.

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4. The Twin Cycles: Fatty Liver and Fatty Pancreas

Type 2 diabetes involves two defects: the body responds poorly to insulin (insulin resistance), and the beta cells of the pancreas, which make insulin, stop working properly (beta-cell dysfunction). In his 2017 post “Fatty Pancreas – T2D34”, Fung argues that the two share a single cause. High insulin drives the liver to turn excess sugar into new fat (de novo lipogenesis). Fat deposited in the liver and in muscle produces insulin resistance; fat deposited in the pancreas produces beta-cell dysfunction. Invoking Occam’s razor — the simplest explanation that covers the facts — he argues that both defects come from one mechanism: fat stored in organs that are not built to hold it.

Fung builds here on the work of Roy Taylor, a diabetes researcher at Newcastle University in England, who named this the “twin cycle” hypothesis. Taylor’s 2008 review in Diabetologia traced the sequence from the results of bariatric surgery. After surgery, he wrote, liver fat falls within days, normal insulin sensitivity of the liver returns, and blood glucose moves back toward normal, while muscle insulin resistance stays abnormal for weeks to months. Taylor concluded that the effect of the surgery is explained by energy restriction alone. In his model, insulin resistance in muscle, from inherited and environmental factors, eases the build-up of liver fat when people take in more energy than they use; the extra insulin then needed adds still more liver fat; and fatty acids reaching the beta cells suppress insulin secretion — a change that is reversible at first but becomes permanent over time.

In “Losing a single gram of fat can reverse diabetes? – T2D 9” (2015), Fung discusses Taylor’s finding that the loss of a very small amount of pancreatic fat went with the return of insulin secretion; in “Towards a Cure” (2017) he puts his conclusion in one line: “the pancreas is simply clogged with fat.”

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5. Insulin Resistance as Protection

A central and unusual claim in Fung’s writing is that insulin resistance is not simply a fault. In “Towards a Cure – T2D35” (2017) he writes: “Insulin resistance protects the liver from too much insulin.” In his reading, a liver already full of fat and sugar resists insulin because it cannot take any more in; the resistance is the body’s defence against further overload, in the same way that a full suitcase resists more clothes.

A similar idea appears in a 1995 surgical paper that Fung uses as evidence that type 2 diabetes can be reversed. Pories and colleagues at East Carolina University followed 608 people with severe obesity over 14 years after gastric bypass surgery. Among those with adequate follow-up, 121 of 146 patients (82.9%) with non-insulin-dependent diabetes and 150 of 152 (98.7%) with impaired glucose tolerance kept normal levels of blood glucose, glycated hemoglobin (hemoglobin A1c, HbA1c) and insulin. The authors wrote that these effects appear to be due primarily to a reduction in calorie intake, “suggesting that insulin resistance is a secondary protective effect rather than the initial lesion.” The operation carried a perioperative mortality of 1.5% and a complication rate of 8.5%.

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6. A Reversible Condition

From the overflow picture and the twin cycles, Fung draws his main conclusion. In “Towards a Cure” he writes that “both defects of insulin resistance and the beta cell dysfunction are entirely reversible by removal of the excess fat clogging the organs”, and on his clinic’s website he puts it more simply: “Type 2 Diabetes is a fully reversible condition.” If the disease is the result of too much insulin and too much stored fuel, then, in his account, lowering insulin and burning the stored fuel undoes it. Fasting and low-carbohydrate eating are the tools he describes for doing so; his account of fasting itself is on the Therapeutic Fasting page.

Taylor’s own group tested the reversal idea directly, using a very low-calorie diet rather than fasting. In a 2011 study, eleven people with type 2 diabetes followed a 600-calorie-a-day diet for eight weeks. After one week their fasting blood glucose had returned to normal, from 9.2 to 5.9 mmol/L. Over eight weeks liver fat fell from 12.8% to 2.9%, pancreatic fat fell from 8.0% to 6.2%, and the first-phase insulin response of the pancreas rose from 0.19 to 0.46 (in the paper’s units), approaching that of people without diabetes. The authors concluded that “the abnormalities underlying type 2 diabetes are reversible by reducing dietary energy intake.”

A 2016 follow-up asked whether the change would last. Thirty people who had had diabetes for between half a year and 23 years followed a very low-calorie diet for eight weeks and then a weight-maintenance program. Their weight fell from 98.0 to 83.8 kg and stayed near that level for six months. Twelve of the thirty reached a fasting glucose below 7 mmol/L on returning to normal eating, and thirteen at six months. Those who responded had had diabetes for a shorter time and had higher fasting insulin at the start; their hemoglobin A1c fell from 7.1% to 5.8% and stayed at 5.9% at six months. Taylor set out the wider argument in a 2013 review in Diabetes Care, “Type 2 diabetes: etiology and reversibility”.

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7. The Glucose-Lowering Trials He Names as Turning Points

Fung has described his first seven years of practice as conventional: low-fat diets and strict control of blood sugar. He names two large trials published together in the New England Journal of Medicine in June 2008 as turning points in his thinking about type 2 diabetes. Both asked whether pushing blood sugar down toward normal levels would prevent heart attacks, strokes and deaths. Their published findings are set out here as the papers state them.

• ACCORD (Action to Control Cardiovascular Risk in Diabetes) randomly assigned 10,251 people with type 2 diabetes and heart disease or added heart risk to intensive therapy, aiming for a hemoglobin A1c below 6.0%, or standard therapy, aiming for 7.0–7.9%. After one year the groups had median hemoglobin A1c levels of 6.4% and 7.5%. Heart attacks, strokes and heart-related deaths together did not fall significantly (352 events against 371). Deaths from any cause were higher in the intensive group — 257 against 203 — and the intensive therapy was stopped after a mean of 3.5 years. Low blood sugar needing another person’s help, and weight gain of more than 10 kg, were more frequent with intensive therapy.
• ADVANCE randomly assigned 11,140 people to standard or intensive glucose control based on the drug gliclazide plus others as needed. After a median of five years, mean hemoglobin A1c was 6.5% against 7.3%. Combined major events fell from 20.0% to 18.1%, mainly through less kidney disease (nephropathy, 4.1% against 5.2%); there was no significant effect on heart attacks and strokes, on heart-related deaths or on deaths from any cause. Severe low blood sugar was more common with intensive control (2.7% against 1.5%).

An older trial is often discussed beside these two. The United Kingdom Prospective Diabetes Study (UKPDS 33, 1998) assigned 3,867 newly diagnosed patients to intensive treatment with a sulphonylurea or insulin, or to conventional treatment with diet. Over ten years, intensive treatment lowered the risk of any diabetes-related endpoint by 12%, mostly through a 25% fall in small-vessel (microvascular) complications such as retinal damage needing laser treatment; it did not significantly change diabetes-related deaths or deaths from any cause. Weight gain was higher with intensive treatment — a mean of 2.9 kg — and highest in those given insulin (4.0 kg, against 2.6 and 1.7 kg with the two sulphonylureas chlorpropamide and glibenclamide). Major low-blood-sugar episodes per year were 0.7% with conventional treatment, 1.0% with chlorpropamide, 1.4% with glibenclamide and 1.8% with insulin. Fung cites this pattern of weight gain on insulin in his writing on obesity; that argument is on The Obesity Code page.

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8. Fasting in His Own Case Reports

From 2012 Fung and Megan Ramos ran a Toronto fasting clinic and dietary-management program, and several case reports from it appeared in journals with Fung as co-author. They are individual cases, not trials; they show what happened to particular patients, not what would happen in a group.

• Three patients on insulin (BMJ Case Reports, 2018). Furmli, Elmasry, Ramos and Fung describe three people referred to the clinic with insulin-treated type 2 diabetes. According to the paper, therapeutic fasting reversed their insulin resistance and they stopped insulin therapy while keeping their blood sugar under control; they also lost substantial body weight, reduced their waist circumference and lowered their hemoglobin A1c.
• A normal-weight woman (BMJ Case Reports, 2020). Lichtash, Fung, Ostoich and Ramos describe a 57-year-old woman of normal weight whose type 2 diabetes had not been controlled on metformin and a strict standard diabetic diet; her hemoglobin A1c was 9.3%. She moved to a ketogenic diet combined with intermittent fasting. The fasts began at 24 hours three times a week, then 42 hours three times a week, then 42 hours twice a week plus 16 hours once a week. Within four months her hemoglobin A1c was 6.4% without diabetes medicine. At eight months a maintenance phase began, with a 16-hour fast each day and a 24-hour fast three times a month, and metformin was restarted. At 14 months her hemoglobin A1c was 5.8%, and her body mass index had changed very little.
• A four-month case study (Journal of Metabolic Health, 2017). Ku, Ramos and Fung reported a further case under the title “Therapeutic fasting as a potential effective treatment for type 2 diabetes: a 4-month case study”.

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9. Medication Safety in the Fasting and Diet Studies

The studies on this page share one practical fact: cutting food or carbohydrate lowers blood sugar quickly, and medicines that lower blood sugar keep working when the food is gone. Insulin and sulphonylureas can therefore push blood sugar dangerously low (hypoglycemia) during a fast or a sudden change in diet. The papers state how they handled this.

• In a 2018 Australian trial of intermittent energy restriction in type 2 diabetes, medicines likely to cause hypoglycemia were reduced at the start under a medication-management protocol. Even so, low- or high-blood-sugar events in the first two weeks affected 35% of participants (16 of 46) who were using sulphonylureas and/or insulin.
• A 2018 study of a carbohydrate-restricted, remotely supervised care model states in its introduction that carbohydrate restriction “markedly improves glycemic control” in type 2 diabetes “but necessitates prompt medication changes”; in that study insulin was reduced or stopped in 94% of users and sulphonylureas were withdrawn entirely.
• In the 2016 Newcastle very low-calorie diet study, all diabetes tablets and insulins were stopped at the start; the DiRECT trial withdrew diabetes and blood-pressure medicines at the start and enrolled only people not using insulin.
• In ACCORD, ADVANCE and UKPDS, hypoglycemia was more frequent with intensive lowering of blood sugar, and in UKPDS major episodes were most frequent with insulin.

Fung’s own writing on fasting also draws a line: in his post on refeeding syndrome he states that patients who are severely underweight or malnourished “should not fast”, because refeeding syndrome — a dangerous shift in body salts when food is restarted after starvation — arises mainly in starvation and wasting.

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10. Later Research on Diet and Remission

Since The Diabetes Code appeared, several larger studies have looked at whether diet and weight loss can put type 2 diabetes into remission or match standard care. Their findings are reported here as the papers state them.

• DiRECT, one year (2018). In 49 primary-care practices in Scotland and Tyneside, England, 306 people diagnosed with type 2 diabetes within six years, and not on insulin, were assigned by practice to a weight-management program or to best-practice care. The program stopped diabetes and blood-pressure medicines, replaced food with an 825–853 calorie-a-day formula diet for three to five months, then reintroduced food in steps with long-term support. At 12 months, 68 of 149 participants (46%) in the program were in remission — hemoglobin A1c below 6.5% after at least two months off all diabetes medicines — against 6 (4%) in the comparison group. Remission tracked weight loss: none of 76 who gained weight, 7% of those who lost up to 5 kg, 34% of those who lost 5–10 kg, 57% of those who lost 10–15 kg, and 86% of the 36 who lost 15 kg or more.
• DiRECT, two years (2019). At 24 months, 53 program participants (36%) and 5 in the comparison group (3%) were in remission. Of participants who kept off at least 10 kg, 64% were in remission. The authors concluded that sustained remission was linked to the extent of sustained weight loss.
• Intermittent versus continuous energy restriction (2018). In a 12-month Australian trial, 137 adults with type 2 diabetes were randomly assigned to eat 500–600 calories on two non-consecutive days a week and their usual diet on the other five, or to eat 1,200–1,500 calories every day. Hemoglobin A1c fell by a similar amount in both groups (0.3% and 0.5%), and the authors judged the two approaches comparable; weight loss averaged 6.8 kg and 5.0 kg.
• Carbohydrate restriction with remote care (2018). A one-year, non-randomized study of 262 adults following nutritional ketosis with continuous remote medical supervision, compared with 87 in usual care, reported hemoglobin A1c falling from 7.6% to 6.3% and weight from a mean of 116.5 kg by 13.8 kg; diabetes prescriptions other than metformin fell from 56.9% to 29.7% of participants. The usual-care group showed no significant change.

Together these studies show remission of type 2 diabetes in a substantial share of people who lost weight, through calorie-restricted formula diets, part-week fasting or carbohydrate restriction. In the DiRECT trials and the Newcastle studies, remission was most likely in people who lost the most weight and had had diabetes for a shorter time. None of these studies tested Fung’s own fasting schedules directly; his clinic’s results remain in the case reports described above.

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Key Research Papers

1. Furmli S, Elmasry R, Ramos M, Fung J. Therapeutic use of intermittent fasting for people with type 2 diabetes as an alternative to insulin. BMJ Case Rep. 2018;2018:bcr2017221854. — PubMed PMID: 30301822
2. Lichtash C, Fung J, Ostoich KC, Ramos M. Therapeutic use of intermittent fasting and ketogenic diet as an alternative treatment for type 2 diabetes in a normal weight woman: a 14-month case study. BMJ Case Rep. 2020;13(7):e234223. — PubMed PMID: 32641437
3. Ku M, Ramos M, Fung J. Therapeutic fasting as a potential effective treatment for type 2 diabetes: A 4-month case study. Journal of Metabolic Health. 2017. — DOI: 10.4102/jir.v2i1.31
4. Fung J, Berger A. Hyperinsulinemia and Insulin Resistance: Scope of the Problem. Journal of Metabolic Health. 2016;1(1). — DOI: 10.4102/jir.v1i1.18
5. 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
6. Corkey BE. Banting lecture 2011: hyperinsulinemia: cause or consequence? Diabetes. 2012;61(1):4-13. — PubMed PMID: 22187369
7. Taylor R. Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause. Diabetologia. 2008;51(10):1781-9. — PubMed PMID: 18726585
8. Taylor R. Type 2 diabetes: etiology and reversibility. Diabetes Care. 2013;36(4):1047-55. — PubMed PMID: 23520370
9. Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia. 2011;54(10):2506-14. — PubMed PMID: 21656330
10. Steven S, Hollingsworth KG, Al-Mrabeh A, Avery L, Aribisala B, Caslake M, et al. Very Low-Calorie Diet and 6 Months of Weight Stability in Type 2 Diabetes: Pathophysiological Changes in Responders and Nonresponders. Diabetes Care. 2016;39(5):808-15. — PubMed PMID: 27002059
11. Pories WJ, Swanson MS, MacDonald KG, Long SB, Morris PG, Brown BM, et al. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg. 1995;222(3):339-50; discussion 350-2. — PubMed PMID: 7677463
12. Action to Control Cardiovascular Risk in Diabetes Study Group, Gerstein HC, Miller ME, Byington RP, Goff DC Jr, Bigger JT, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med. 2008;358(24):2545-59. — PubMed PMID: 18539917
13. ADVANCE Collaborative Group, Patel A, MacMahon S, Chalmers J, Neal B, Billot L, et al. Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med. 2008;358(24):2560-72. — PubMed PMID: 18539916
14. 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
15. Lean ME, Leslie WS, Barnes AC, Brosnahan N, Thom G, McCombie L, et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. Lancet. 2018;391(10120):541-551. — PubMed PMID: 29221645
16. Lean MEJ, Leslie WS, Barnes AC, Brosnahan N, Thom G, McCombie L, et al. Durability of a primary care-led weight-management intervention for remission of type 2 diabetes: 2-year results of the DiRECT open-label, cluster-randomised trial. Lancet Diabetes Endocrinol. 2019;7(5):344-355. — PubMed PMID: 30852132
17. Carter S, Clifton PM, Keogh JB. Effect of Intermittent Compared With Continuous Energy Restricted Diet on Glycemic Control in Patients With Type 2 Diabetes: A Randomized Noninferiority Trial. JAMA Netw Open. 2018;1(3):e180756. — PubMed PMID: 30646030
18. Hallberg SJ, McKenzie AL, Williams PT, Bhanpuri NH, Peters AL, Campbell WW, et al. Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study. Diabetes Ther. 2018;9(2):583-612. — PubMed PMID: 29417495

PubMed Topic Searches

1. Hyperinsulinemia as a cause of insulin resistance
2. The twin-cycle hypothesis: liver and pancreatic fat in type 2 diabetes
3. Remission of type 2 diabetes with weight loss
4. Intermittent fasting, type 2 diabetes and hypoglycemia

Further Reading

• Open Library: The Diabetes Code (2018)
• Open Library: The Diabetes Code Cookbook (2021)
• Jason Fung, “Fatty Pancreas – T2D34” (2017)
• Jason Fung, “Towards a Cure – T2D35” (2017)
• Jason Fung, “Losing a single gram of fat can reverse diabetes? – T2D 9” (2015)

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Connections

• Dr. Jason Fung: Fasting, Insulin and The Obesity Code
• Jason Fung: Life and Career
• The Obesity Code: Jason Fung’s Hormonal Theory of Obesity
• Jason Fung on Intermittent and Therapeutic Fasting
• The Cancer Code: Jason Fung’s Evolutionary Theory of Cancer
• Jason Fung: Books, Clinic and Legacy
• Contemporary Practitioners
• Type 2 Diabetes
• Diabetes Remission and Reversal Strategies
• Insulin Resistance
• Non-Alcoholic Fatty Liver Disease
• Fasting

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