The Cancer Code: Jason Fung's Evolutionary Theory of Cancer

Table of Contents

1. The Book and the Blog Series Behind It
2. Cancer Paradigm 1.0, 2.0 and 3.0
3. His Case Against the Somatic Mutation Theory
4. Seed and Soil
5. Convergent Evolution and the Shared Traits of Cancer
6. Atavism: Cancer as a Return to Ancient Life
7. Obesity as the Soil: The Epidemiology He Draws On
8. Insulin, Insulin-Like Growth Factor 1 and Mechanistic Target of Rapamycin as Growth Signals
9. Hallmarks of Cancer and the Warburg Effect
10. Fasting and Cancer: What the Studies Tested
11. Key Research Papers
12. Connections
13. Featured Videos

1. The Book and the Blog Series Behind It

The Cancer Code is the third of Fung’s “Code” books, after The Obesity Code (2016) and The Diabetes Code (2018). It was published by Harper Wave in 2020 with the subtitle A Revolutionary New Understanding of a Medical Mystery. Unlike the first two books, it does not come out of his own clinic: Fung is a kidney specialist, not an oncologist; in his post on the physicists who took up cancer research, he praises the fresh questions that outsiders to a field can ask.

Most of the book’s argument appeared first as a numbered blog series on cancer, written in 2017 and 2018 and still published on the website of the fasting program he co-founded. The series opens with “Obesity and Cancer” (August 2017) and runs through posts on cancer as an endocrine disease, convergent evolution, seed and soil, and, in February 2018, “Beyond the Somatic Mutation Theory of Cancer”. In that last post he wrote that he was pausing the series because of the coming release of The Diabetes Code; the book that followed two years later gathers the same ideas into one argument.

The central claim, in his blog wording, is blunt: “Cancer, as a whole, is almost certainly NOT a genetic disease.” He does not deny that cancer cells carry mutations. His argument is about what drives and selects those mutations, and he answers that question with evolution and metabolism rather than with genetics alone.

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2. Cancer Paradigm 1.0, 2.0 and 3.0

Fung organises the history of cancer research into three “paradigms”, a framing he set out in his post on convergent evolution and carries into the book:

• Cancer Paradigm 1.0 — cancer as unbridled growth. In his account this was the working view until molecular biology took over the field.
• Cancer Paradigm 2.0 — cancer as a collection of random genetic mutations that cause unbridled growth: the somatic mutation theory. He writes that it dominated research for decades, and that large tumour-sequencing efforts such as The Cancer Genome Atlas, a United States government project, were in his view what finally undermined it.
• Cancer Paradigm 3.0 — cancer seen through an evolutionary lens. Something, he argues, is driving the mutations that drive the growth; the cancer cell is being selected for survival by its surroundings.

In the 2017 post he closes the paradigm passage by naming his candidate for that “something”: mitochondrial damage and metabolic health. In a 2025 podcast on the book, the program’s summary describes him calling cancer “an evolutionary and metabolic condition deeply connected to insulin, diet, and lifestyle”, with high insulin, obesity and processed foods creating fertile “soil”.

The rest of the book, and the rest of this page, follows that order: first his reasons for leaving Paradigm 2.0, then the evolutionary ideas that make up Paradigm 3.0, and finally the metabolic “soil” he connects to his earlier work on insulin.

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3. His Case Against the Somatic Mutation Theory

Fung uses “somatic mutation theory” (SMT) for the view that a cancer begins when a single body cell slowly collects random mutations in oncogenes and tumour-suppressor genes until it can grow without limit, evade the immune system, build its own blood supply and spread. In his third cancer post he writes: “You must approach is [sic] as an endocrine (hormonal) disease.”

His objections, as he states them, are these:

• Improbability. He finds it implausible that random mutations would hand one cell the whole set of abilities a cancer needs, and compares it to people mutating until they could shoot lasers from their eyes.
• Environment and migration. He points to migration studies in which people who move from a low-risk country to a high-risk one take on the cancer rates of their new home within a generation or two, while their genes stay the same. To him this shows that diet and environment, not inherited genes, explain much of the difference between countries.
• Obesity. Obesity is linked to many cancers, yet, he writes, fat cells are not mutagenic; becoming heavier does not mutate DNA. That link, in his view, “opens the door” to a hormonal and metabolic explanation.
• Return on research. He argues that decades of gene-by-gene work have produced too little progress in adult cancers, and describes the field as missing the forest for the trees.

The genetic paradigm he argues against is summarised in a 2013 review in Science by Bert Vogelstein and colleagues, “Cancer genome landscapes”, which describes the mutated “driver” genes found by sequencing many tumours. Fung also discusses a 2015 paper by Cristian Tomasetti and Vogelstein, often called the “bad luck” paper. Its abstract reports that the lifetime risk of cancer in different tissues correlated strongly (0.81) with the total number of stem-cell divisions in those tissues, and the authors concluded that only about a third of the variation in cancer risk among tissues was attributable to environmental factors or inherited predispositions, the majority being due to random mutations during normal DNA copying. That paper is a statistical modelling study across tissues, and its reading of “bad luck” is the opposite pole from Fung’s emphasis on the environment.

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4. Seed and Soil

To shift attention from the cancer cell to its surroundings, Fung returns to one of the oldest ideas in oncology. In 1889 the English surgeon Stephen Paget, studying where breast cancer spreads, proposed that a cancer cell is like a seed that only grows where the soil suits it; the paper was reprinted in 1989 as a seminal article. Fung writes:

“If you drop a grass seed in the desert – it does not grow. But drop that same grass seed into your lawn – it may grow extremely well.”

His point is that the seed is identical in both places, so studying the seed’s genes alone cannot explain why one grows and the other does not. He applies this to the body: the ability to turn cancerous lies, in his view, in nearly every cell, since oncogenes are altered forms of normal growth genes. What decides whether a cell becomes a cancer, he argues, is largely the “soil” — the growth signals, nutrient sensors and hormones around it. He lists cigarette smoke on lung cells, human papillomavirus in the cervix, asbestos on the lining of the lung and obesity for breast tissue as examples of soils that make cancer more likely.

He draws on the tissue organisation field theory, which looks at cancer at the level of tissues rather than single cells, and on evolution: single-celled organisms, he notes, grow and move by default until nutrients run out, while the cells of a multicellular body are held in check by signals from their neighbours. As an example of treating the soil rather than the seed, he points to imatinib, a drug for chronic myeloid leukaemia that blocks a growth-signalling enzyme rather than repairing the genetic defect itself.

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5. Convergent Evolution and the Shared Traits of Cancer

Fung’s second evolutionary idea is convergent evolution: unrelated species that live in similar environments come to look alike. He uses the flying squirrels of North America and the gliding marsupials of Australia, which share a body plan but not the genes that built it, and Darwin’s finches, whose beaks matched their food. The lesson he draws is that the environment, the selective pressure, explains the result better than any list of the particular mutations involved.

Applied to cancer, he writes that two breast cancers can carry completely different sets of mutations and still look and behave the same, with the same core traits. “There is nothing random about cancer’s mutations because they all develop the same features,” he writes. If mutations were truly random, he argues, the results would be random too; the fact that so many different genetic routes arrive at the same destination tells him that something in the body is selecting them. That observation is the core of what he names Cancer Paradigm 3.0.

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6. Atavism: Cancer as a Return to Ancient Life

The third idea, and the one that gives the book its “evolutionary theory”, comes from two physicists. Fung tells how the National Cancer Institute, a United States government agency, set up physical-science oncology centres to bring researchers from outside biology into cancer research. The physicist Paul Davies, who by his own account had no prior knowledge of cancer, and the astrobiologist Charles Lineweaver came to cancer through that effort.

Their 2011 paper, “Cancer tumors as Metazoa 1.0”, states the hypothesis in its abstract: the genes of cellular cooperation that evolved with multicellular life about a billion years ago are the same genes that malfunction in cancer, and cancer is an “atavistic” condition in which an ancient “toolkit” of pre-existing adaptations is unlocked, bringing back an earlier layer of genes that once ran loose colonies of only partly specialised cells, much like tumours. They argue this would explain how cancer acquires a whole suite of abilities so quickly. Fung summarises the idea in his own words:

“Cancer was a targeted de-evolution to a more primitive form of life. The origins of cancer are the origins of life itself.”

The same authors developed the model further. A 2014 paper by Lineweaver, Davies and Mark Vincent proposes, as a theoretical strategy, aiming treatment at the newer abilities that cancer cells lose first, such as the support of adaptive immunity, rather than at their main strength, cell division. A 2021 paper by Lineweaver, Kimberly Bussey, Alison Blackburn and Davies proposes that cancer progresses through a series of reversions rather than a single step back, and sets out new predictions to test, including ones tied to the evolution of oxidative phosphorylation (the energy-making process in mitochondria). All three papers are theoretical models with proposed tests, not clinical studies.

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7. Obesity as the Soil: The Epidemiology He Draws On

Fung opens his cancer series with obesity, because it is where his earlier work and his cancer theory meet. He describes a 2003 study in the New England Journal of Medicine as the one that firmly established the link. That study, by Eugenia Calle and colleagues at the American Cancer Society, followed more than 900,000 United States adults who were free of cancer when they enrolled in 1982; over 16 years there were 57,145 deaths from cancer. Its abstract reports that the heaviest group (body-mass index of at least 40) had death rates from all cancers combined 52 percent higher in men and 62 percent higher in women than people of normal weight, and the authors estimated that overweight and obesity could account for 14 percent of cancer deaths in men and 20 percent in women. This is an observational cohort, which shows association rather than proof of cause.

In 2016 a working group of the International Agency for Research on Cancer, the cancer agency of the World Health Organization, reviewed the evidence and listed 13 cancers linked to excess body fat. Fung’s reading of such findings is that obesity cannot cause cancer by mutating genes, so it must act through hormones and metabolism — the soil.

A 2017 matched cohort study by Daniel Schauer and colleagues looked at the reverse direction: 18,355 people who had weight-loss (bariatric) surgery compared with 40,524 matched people who did not. Its abstract reports that average weight loss at one year was 27 percent after surgery against 1 percent without it, and that each 10 percent of weight lost was associated with a lower risk of any cancer (hazard ratio 0.897); the surgery itself showed no effect separate from the weight lost. It too is observational.

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8. Insulin, Insulin-Like Growth Factor 1 and Mechanistic Target of Rapamycin as Growth Signals

For Fung, the common thread between obesity, type 2 diabetes and cancer is insulin. He describes insulin, the related hormone insulin-like growth factor 1 (IGF-1), and the cell’s nutrient sensor mechanistic target of rapamycin (mTOR) as growth signals that tell cells food is plentiful and growth is safe; high and constant levels, in his view, make a fertile soil for cancer. This is where The Cancer Code connects to his earlier books.

The research he draws on, by type:

• Review. Michael Pollak’s 2008 review “Insulin, insulin-like growth factors and neoplasia” sets out how these hormones act on cancer cells and why that matters for cancer risk and treatment.
• Human cohort. In a 2009 case-cohort study within the Women’s Health Initiative, Marc Gunter and colleagues measured fasting insulin in postmenopausal women without diabetes. The abstract reports that women in the highest quarter of insulin levels had a higher risk of breast cancer than those in the lowest (hazard ratio 1.46), and among women not using hormone therapy the figure was 2.40 after adjusting for estradiol. The link between obesity and breast cancer weakened once insulin was accounted for, and the authors concluded that high insulin may be an independent risk factor that helps explain the obesity–breast cancer link.
• Mouse and cell work. A 2018 Nature paper by Benjamin Hopkins, Lewis Cantley and colleagues studied drugs that block PI3K, an insulin-activated enzyme often mutated in cancer. In several tumour models in mice, the rise in insulin that the drugs provoke re-activated the same pathway in the tumours; preventing that insulin rise with dietary or drug approaches made the drugs work better in the mice. These were animal findings.
• Human observational. A 2005 BMJ report by Josie Evans and colleagues in Scotland compared people with type 2 diabetes taking metformin, a drug that does not raise insulin, with those who were not, and found metformin use associated with a lower risk of cancer. This is an observational comparison.

Fung presents this body of work as supporting his view that hyperinsulinemia (too much insulin) is part of cancer’s soil. The studies themselves are a mix of association and laboratory work, and none of them tested lowering insulin as a way to prevent cancer in people.

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9. Hallmarks of Cancer and the Warburg Effect

Two classic papers frame the middle of Fung’s argument. The first is the “hallmarks of cancer” scheme of Douglas Hanahan and Robert Weinberg, updated in 2011 as “Hallmarks of cancer: the next generation”, which lists the abilities that cancer cells share, such as unregulated growth, new blood-vessel growth and spread, with reprogrammed energy metabolism among its newer additions. Fung uses the list as evidence for his convergent-evolution point: very different tumours end up with the same set of traits.

The second is Otto Warburg’s 1956 paper “On the origin of cancer cells” in Science. Warburg observed that cancer cells rely heavily on fermenting glucose even when oxygen is present, and proposed that damage to cell respiration lies at the origin of cancer. This is now called the Warburg effect. Fung discusses it in his series as part of the metabolic side of cancer, and it fits the “mitochondrial damage and metabolic health” he names as the likely selecting force in Paradigm 3.0.

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10. Fasting and Cancer: What the Studies Tested

Fung is best known for therapeutic fasting, and in The Cancer Code and later talks he links his cancer theory to diet and insulin. His argument concerns lowering the growth signals of the soil; he does not claim that fasting cures cancer, and this site does not present it as a treatment. The research on fasting and cancer so far is mostly early and of different kinds:

• Mice and cell studies. A 2012 paper by Changhan Lee, Valter Longo and colleagues reported that short-term starvation made 15 of 17 mammalian cancer cell lines more sensitive to chemotherapy drugs, and that in mouse models of neuroblastoma, fasting cycles combined with chemotherapy — but neither alone — led to long-term cancer-free survival. These findings are in mice and cell cultures.
• Human observational. A 2016 study by Catherine Marinac and colleagues followed 2,413 women with early-stage breast cancer and without diabetes. Their mean overnight fast was 12.5 hours. Fasting less than 13 hours a night was associated with a higher risk of breast cancer recurrence than fasting 13 hours or more (hazard ratio 1.36); the differences in breast cancer deaths and in deaths from any cause did not reach statistical significance. Each 2-hour increase in overnight fasting was associated with lower hemoglobin A1c, a long-term blood-sugar marker.
• Human randomised trial. The Dutch DIRECT trial, reported in 2020 by Stefanie de Groot and colleagues, randomised 131 women with HER2-negative stage II or III breast cancer to a fasting-mimicking diet or their regular diet for 3 days before and during chemotherapy given before surgery. The abstract reports no difference in side effects between the groups, even though a steroid usually given with chemotherapy was left out in the fasting-mimicking group, and more frequent tumour responses on imaging with the diet (odds ratio 3.168). The trial excluded women with diabetes and those with a body-mass index of 18 or below. It is a phase 2 trial, and the authors called for further study.

A safety fact matters here. Advanced cancer often causes cachexia, a loss of appetite, muscle and weight that Fung himself describes in his cancer series. In his fasting writing he states that “patients that are severely underweight or malnourished should not fast”, because of the risk of refeeding syndrome, a dangerous shift in blood minerals when food is restarted after starvation. In the DIRECT trial, the fasting-mimicking diet was given under trial supervision to women chosen to meet set weight and health limits.

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Key Research Papers

1. Paget S. The distribution of secondary growths in cancer of the breast. 1889. Cancer Metastasis Rev. 1989;8(2):98-101. — PubMed PMID: 2673568
2. Davies PC, Lineweaver CH. Cancer tumors as Metazoa 1.0: tapping genes of ancient ancestors. Phys Biol. 2011;8(1):015001. — PubMed PMID: 21301065
3. Lineweaver CH, Davies PC, Vincent MD. Targeting cancer’s weaknesses (not its strengths): Therapeutic strategies suggested by the atavistic model. Bioessays. 2014;36(9):827-35. — PubMed PMID: 25043755
4. Lineweaver CH, Bussey KJ, Blackburn AC, Davies PCW. Cancer progression as a sequence of atavistic reversions. Bioessays. 2021;43(7):e2000305. — PubMed PMID: 33984158
5. Vogelstein B, Papadopoulos N, Velculescu VE, Zhou S, Diaz LA Jr, Kinzler KW. Cancer genome landscapes. Science. 2013;339(6127):1546-58. — PubMed PMID: 23539594
6. Tomasetti C, Vogelstein B. Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science. 2015;347(6217):78-81. — PubMed PMID: 25554788
7. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646-74. — PubMed PMID: 21376230
8. Warburg O. On the origin of cancer cells. Science. 1956;123(3191):309-14. — PubMed PMID: 13298683
9. Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med. 2003;348(17):1625-38. — PubMed PMID: 12711737
10. Lauby-Secretan B, Scoccianti C, Loomis D, Grosse Y, Bianchini F, Straif K, et al. Body Fatness and Cancer—Viewpoint of the IARC Working Group. N Engl J Med. 2016;375(8):794-8. — PubMed PMID: 27557308
11. Schauer DP, Feigelson HS, Koebnick C, Caan B, Weinmann S, Leonard AC, et al. Association Between Weight Loss and the Risk of Cancer after Bariatric Surgery. Obesity (Silver Spring). 2017;25 Suppl 2:S52-S57. — PubMed PMID: 29086527
12. Pollak M. Insulin, insulin-like growth factors and neoplasia. Best Pract Res Clin Endocrinol Metab. 2008;22(4):625-38. — PubMed PMID: 18971123
13. Gunter MJ, Hoover DR, Yu H, Wassertheil-Smoller S, Rohan TE, Manson JE, et al. Insulin, insulin-like growth factor-I, and risk of breast cancer in postmenopausal women. J Natl Cancer Inst. 2009;101(1):48-60. — PubMed PMID: 19116382
14. Hopkins BD, Pauli C, Du X, Wang DG, Li X, Wu D, et al. Suppression of insulin feedback enhances the efficacy of PI3K inhibitors. Nature. 2018;560(7719):499-503. — PubMed PMID: 30051890
15. Evans JM, Donnelly LA, Emslie-Smith AM, Alessi DR, Morris AD. Metformin and reduced risk of cancer in diabetic patients. BMJ. 2005;330(7503):1304-5. — PubMed PMID: 15849206
16. Lee C, Raffaghello L, Brandhorst S, Safdie FM, Bianchi G, Martin-Montalvo A, et al. Fasting cycles retard growth of tumors and sensitize a range of cancer cell types to chemotherapy. Sci Transl Med. 2012;4(124):124ra27. — PubMed PMID: 22323820
17. Marinac CR, Nelson SH, Breen CI, Hartman SJ, Natarajan L, Pierce JP, et al. Prolonged Nightly Fasting and Breast Cancer Prognosis. JAMA Oncol. 2016;2(8):1049-55. — PubMed PMID: 27032109
18. de Groot S, Lugtenberg RT, Cohen D, Welters MJP, Ehsan I, Vreeswijk MPG, et al. Fasting mimicking diet as an adjunct to neoadjuvant chemotherapy for breast cancer in the multicentre randomized phase 2 DIRECT trial. Nat Commun. 2020;11(1):3083. — PubMed PMID: 32576828

PubMed Topic Searches

1. Atavistic model of cancer
2. Hyperinsulinemia and cancer risk
3. Tissue organization field theory of cancer
4. Obesity and cancer incidence: cohort studies
5. Fasting alongside chemotherapy: randomised trials

Further Reading

• Open Library: The Cancer Code (2020)
• Jason Fung, “Obesity and Cancer – Cancer 1” (August 2017)
• Jason Fung, “Cancer as an endocrine disease – Cancer 3” (August 2017)
• Jason Fung, “Convergent Evolution and Cancer – Cancer 9” (November 2017)
• Jason Fung, “Cancer’s Seed and Soil – Cancer 11” (January 2018)
• Jason Fung, “Beyond the Somatic Mutation Theory of Cancer – Cancer 15” (February 2018)
• Podcast episode 231: The Cancer Code, with Jason Fung (November 2025)

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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 Diabetes Code: Jason Fung on Type 2 Diabetes
• Jason Fung: Books, Clinic and Legacy
• Contemporary Practitioners
• Cancer
• Cancer and Parasites
• Fasting Around Chemotherapy
• Obesity
• Metformin

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