The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally

Dr. Jason Fung, a Toronto-based nephrologist (kidney specialist), argues that type 2 diabetes is not a chronic and progressive disease but a fully reversible dietary condition caused by excessive sugar consumption and the resulting overproduction of insulin. Drawing on decades of clinical experience treating diabetic patients whose health deteriorated despite standard medication, he builds a case that conventional treatment treats only the symptom, high blood glucose, while ignoring the root cause: too much insulin in the body. The book traces the history of diabetes, explains the biological mechanisms driving the disease, critiques existing therapies, and presents an alternative approach centered on low-carbohydrate diets and intermittent fasting.

In a foreword, investigative journalist Nina Teicholz frames the institutional context, noting that 45 international medical societies endorsed bariatric surgery (weight-loss surgery that shrinks the stomach or reroutes digestion) as a first-line treatment in 2016 rather than exploring dietary solutions. She credits science journalist Gary Taubes's 2007 book Good Calories, Bad Calories with reviving the carbohydrate-insulin hypothesis, the theory that refined carbohydrates raise insulin and thereby drive weight gain and diabetes. She identifies two structural barriers: Pharmaceutical companies fund most major medical associations and have no interest in a dietary cure, and experts face cognitive dissonance in confronting the possibility that decades of low-fat dietary advice fueled the epidemics it aimed to prevent.

Fung opens with a history of diabetes stretching from the ancient Egyptian Ebers Papyrus (c. 1550 BC) through early dietary treatments, including physician John Rollo's all-meat diet in 1797 and diabetology pioneer Apollinaire Bouchardat's strategy forbidding sugars and starches. He recounts the 1921 discovery of insulin at the University of Toronto by Frederick Banting, Charles Best, and John Macleod, which transformed type 1 diabetes from a death sentence into a manageable condition but overshadowed earlier dietary approaches. By 1936, researcher Harold Percival Himsworth had distinguished two forms of the disease: type 1, caused by autoimmune destruction of insulin-producing cells, and type 2, characterized by insulin resistance, in which the body produces abundant insulin but cells no longer respond effectively. Fung stresses these are polar opposite conditions requiring fundamentally different treatments.

He traces the modern epidemic to the demonization of dietary fat beginning in the 1950s. The 1977 Dietary Goals for the United States encouraged raising carbohydrate consumption to 55 to 60 percent of the diet while decreasing fat. Obesity rates climbed immediately, and diabetes followed a decade later, quadrupling worldwide from 108 million cases in 1980 to 422 million by 2014.

The book catalogs the devastating damage diabetes causes, from blindness and kidney failure to heart attacks, amputations, Alzheimer's disease, and cancer. Fung argues that the worsening of these complications despite treatment advances proves the current paradigm is flawed. The root cause is not high blood glucose but insulin resistance.

Fung dismantles the caloric model of obesity, citing the Women's Health Initiative, a study of nearly 50,000 women showing that more than seven years of calorie counting produced virtually no weight loss. He argues obesity is a hormonal imbalance driven by excessive insulin, which signals the body to store energy as glycogen (chains of glucose stored in the liver) or, when glycogen stores are full, as new fat through a process called de novo lipogenesis. Fasting lowers insulin and burns stored energy. Weight remains stable as long as eating and fasting periods are balanced.

The book's central mechanistic argument concerns how insulin resistance develops. Fung presents it as an overflow phenomenon: just as passengers cannot board a subway train already jammed with people, glucose cannot enter cells already overstuffed with sugar. The body produces more insulin to force glucose inside, but this only worsens the overflow, creating a vicious cycle. Experiments in which continuous insulin infusions in healthy people increased insulin resistance by 15 to 40 percent within days confirm that insulin itself causes the condition.

Fung identifies two phases of disease development. In phase one, excessive glucose and fructose consumption drives chronically elevated insulin, which forces the liver to produce new fat. This fat accumulates in the liver, a condition called non-alcoholic fatty liver disease (NAFLD), which precedes clinical diagnosis by a decade or more. Fat also accumulates in muscles, worsening whole-body insulin resistance. In phase two, fat clogs the pancreas and impairs its ability to produce insulin. When compensatory production fails, blood glucose spikes and diabetes is diagnosed. Fung rejects the theory that pancreatic cells are permanently damaged, citing evidence that caloric restriction and surgery restore function by removing small amounts of excess fat.

A key chapter focuses on fructose. Unlike glucose, which every cell can metabolize, fructose can only be processed by the liver, making it approximately 34 times more likely to cause fatty liver. Experiments showed that seven days of fructose overfeeding worsened insulin sensitivity by 25 percent, while glucose overfeeding did not. Fung explains China's diabetes explosion, from 1 percent in 1980 to 11.6 percent by 2013, as the result of adding sugar to a traditionally high-carbohydrate but low-sugar diet.

These mechanisms converge in metabolic syndrome, a cluster of conditions including abdominal obesity, high triglycerides, low HDL cholesterol, high blood pressure, and high blood glucose. First named by Dr. Gerald Reaven in 1988, the syndrome affects nearly one-third of North American adults. Fung argues all its components share a single root cause: chronically elevated insulin.

The book critiques existing treatments. The ACCORD study (1999 to 2008) was stopped early because intensively treated patients were dying 22 percent faster than those receiving standard care. By contrast, metformin, which lowers blood glucose without raising insulin, reduced diabetes-related death by 42 percent in the UKPDS study. Fung categorizes oral diabetes medications as "good" (those that lower insulin, such as SGLT2 inhibitors), "bad" (weight-neutral drugs like metformin), and "ugly" (those that raise insulin, such as sulfonylureas and thiazolidinediones). He critiques insulin therapy separately, presenting population data linking insulin use to dramatically increased mortality. Only medications that lower insulin show cardiovascular benefits. He also dismisses low-fat diets and exercise as adequate treatments, noting that exercise benefits skeletal muscles but does not address the fatty liver at the disease's core.

In the final section, Fung presents his solutions. He draws lessons from bariatric surgery, which often reverses diabetes quickly with high remission rates, frequently within weeks and before significant weight loss. He argues the mechanism is sudden caloric restriction that forces the body to burn fat stored inside the liver and pancreas. Since these benefits can be achieved without surgery, he advocates two dietary interventions. First, a low-carbohydrate diet that eliminates added sugars and refined carbohydrates while embracing natural fats such as olive oil, nuts, eggs, and fatty fish. Second, intermittent fasting, which he distinguishes from continuous caloric restriction. Chronic calorie reduction fails because the body compensates by lowering its metabolic rate, but fasting studies show metabolism actually increases by 12 percent over four days. Fasting triggers hormonal adaptations: Insulin drops sharply, noradrenaline rises to keep metabolism high, and growth hormone rises to maintain lean mass. His Intensive Dietary Management program typically prescribes 36-hour fasts three times per week combined with a low-carbohydrate diet under medical supervision.

Throughout the book, Fung includes patient case studies illustrating successful reversal: Simon, 66, achieved a nondiabetic hemoglobin A1C (a measure of average blood sugar over three months) of 5.9 percent and maintained a 45-pound weight loss; Bridget, 62, stopped 210 units of daily insulin after a 21-day fast; Ravi, 40, stopped 102 units of daily insulin within two weeks. He also cites prevention studies, including the China Da Qing study, which reduced diabetes incidence by 43 percent over six years using lifestyle interventions.

In an afterword, Fung recounts his journey from conventional training to establishing his Intensive Dietary Management program in 2011 with colleague Megan Ramos. He frames the book as fundamentally about hope: the hope that type 2 diabetes can be eradicated within a generation through dietary knowledge alone, without drugs or surgery.