Commentaries, Health October 5, 2015

Why Cancer Research Has Stalled

by Jonathan Latham

By T. Colin Campbell (Jacob Gould Schurman Professor Emeritus, Cornell University)

A recent publication, which received sustained media attention, claimed that most cancers are just “bad luck” (Tomasetti and Vogelstein 2015). Its authors stated that only about one-third of cancer mutations are caused by known lifestyle or environmental factors (smoking, alcohol use, UV light and human papilloma virus). The other two-thirds of cancers, said the authors, are random (stochastic or chance) mutations with no known cause. Therefore, we can do very little to prevent cancer except to avoid these known risk factors.

But such conclusions fail to explain changes in the rates of cancer over time, or the wide variation in cancer prevalence between different human populations. They are flawed for a very fundamental reason: they assume that most types of cancer are caused by DNA mutations. This is the mutation theory of cancer. It serves as a fundamental explanation of cancer development and thus is a central focus of cancer research and clinical practice.

T Colin Campbell (Cornell Professor Emeritus)
T Colin Campbell (Cornell Professor Emeritus)

For at least a half-century, our thoughts about cancer—its causes, its treatments, even its business—have mostly relied on this underappreciated assumption. We assume that cancer begins when an environmental chemical carcinogen or some type of radiation causes a genetic mutation, and this converts a normal cell to a cancer prone one. Although the body normally repairs most of these mutations, a few become fixed during cell division. The resulting cancer-prone cells then grow into a cluster of next generation cells through a series of additional mutations, ultimately giving rise to a mass of cells that become diagnosed as cancer. Such is the mutation theory of cancer.

In line with this theory, to avoid or to intercept cancer means avoiding the agents that cause these mutations. This is prevention. Failing this, treatments are applied to find ways to selectively kill these cancer cells with surgery, chemotherapy or radiation. We do not, however, expect diseased cells to revert to normality because mutations, once established, are not considered reversible.

I disagree with this theory. I suggest that failing to question the mutation theory of cancer is the underlying scientific reason the War on Cancer is not being won.

A nutritional theory of cancer

My laboratory began NIH-financed research on cancer causation over five decades ago. It eventually led to a far more promising theory of cancer development. This theory was initially based on limited observations in humans; but further investigations with laboratory rats showed how cancer, although initiated by a mutation, was not subsequently dependent on the accumulation of additional mutations.

In our most thoroughly investigated experimental model, cancer is initiated by a gene mutation caused by a powerful chemical carcinogen called aflatoxin (Appleton and Campbell 1983a; Appleton and Campbell 1983b; Youngman et al., 1992). Then, cancer development (primary liver) is predominantly promoted by feeding protein at levels typical of the protein content of most human diets, which are substantially above the levels necessary for good health. We believed cancer development in our studies was not caused by additional mutations because 1) the original mutation-producing chemical was no longer present during promotion and 2) dietary protein is not directly mutagenic. This suggested that, although mutations prime cells for cancer development, further progression to diagnosable cancer is typically nutritionally controlled. No mutations are necessary.

Consistent with this, when protein consumption was decreased to the amount adequate for good health, cancer growth was reversed. Remarkably, cancer growth could be turned on, then off, then on, then off again by a nutrition protocol that did not involve mutations (Schulsinger et al., 1989). Further research showed that promotion of cancer growth occurred with animal-based protein but not plant-based protein.

In follow-up studies we found many other non-mutation mechanisms that promoted cancerous growth. Each of these mechanisms acts interdependently. Animal-based protein increases levels of a growth hormone that encourages cancer growth (insulin-like growth factor), compromises the body’s natural killer cells that normally destroy cancer cells and favors calories being used for cancer growth, among many other non-mutation dependent mechanisms. Thus, initial mutations prime cells for cancer development but then these mutations may lie dormant for relatively long periods of time with a low protein diet. Later, they can be activated to support new cancer growth when higher levels of animal protein consumption are reached. Much like a rash returning when an allergen is reintroduced.

Human evidence strongly supports these experimental animal studies (and refutes the “bad luck theory”). For example, cancer rates for different populations vary widely, being close to nil in some populations for some cancer types. Rates for major cancers (e.g., breast, colon, prostate) correlate with animal protein-based diets. Most of these studies refer to total or saturated fat, but this is a surrogate measure for animal-based food. Other studies, conducted 40-50 years ago, clearly showed that people migrating from one country to another assumed, within a generation or so, the cancer risk of the country to which they moved, without changing their genetics and only changing their nutritional practices.

The mutation theory of cancer has long been the Holy Grail of most cancer research, so much so that hypotheses that rely on promoting cancer by non-mutation mechanisms (like nutrition and chemical contaminants) are often ignored, especially by professionals with little or no knowledge of the science of nutrition.

The consequences of this mutation theory of cancer are deadly. Wrongly assuming that cancer is primarily a product of genetic mutations implies that cancer progression is unstoppable. It implies that cancer control will depend on identifying and selectively killing specific cancer cells and blocking their responsible genes with targeted drugs. This strategy has been and will continue to be severely limiting because countless combinations of genes and their products can change cancer development. But understanding and accepting a new paradigm would mean accepting that funding research to identify new cancer drugs, especially targeted drugs with certain but unpredictable side effects, is the wrong priority for cancer research.

Knowing that cancer can be controlled or reversed by non-mutagenic strategies like nutrition gives hope that we can control our own cancer destiny. Believing that cancer is mostly a random event beyond our control gives hope only to an already bloated industry to come to our rescue, by developing highly questionable, out of context pills and procedures that cause more harm than good. The researchers of this recent ‘random cancer’ publication concluded, for example—now that they believe that cancers are random events—that we must emphasize “developing better tests to find cancers early enough to cure them”. This is a failed strategy and a mainstay of the War on Cancer.

I also question the researchers’ use of the word ‘random’, especially when they dismiss nutritional associations with cancer. These researchers are personally unaware of the vast and convincing evidence on the effects of nutrition on cancer, therefore they should simply admit their ignorance without invoking the concept of randomness and using it to justify searches for responsible genes and treatments with often gruesome drugs.

The non-mutagenic nutrition effects we observed in our research on cancer development closely resemble the nutrition-based effects known to dramatically reverse other diseases, including advanced coronary heart disease and diabetes (Esselstyn 2014 and Barnard 2009). These nutrition-based effects have been observed as a result of the dietary lifestyle composed of whole plant-based foods without added oil and refined carbohydrates. The benefits are truly remarkable, broad in scope, and surprisingly rapid in response (Campbell and Campbell 2005; Campbell 2013).

Isn’t it time that we question the long-held assumption that cancer is mostly developed by a series of mutations and is not related to diet? Isn’t it time that we share these ideas with the public who pay for this research (including all of mine) and who suffer the consequences of marginally effective treatment protocols? Isn’t it time that we let the public know that the progression of cancer is not as random as widely believed? It’s more than mutation – it’s also nutrition…which we have the power to control.

*This article is adapted from one that originally appeared on


Appleton, B. S. & Campbell, T. C. Effect of high and low dietary protein on the dosing and postdosing periods of aflatoxin B1-induced hepatic preneoplastic lesion development in the rat. Cancer Res. 43, 2150-2154 (1983).

Appleton, B. S. & Campbell, T. C. Dietary protein intervention during the post-dosing phase of aflatoxin B1-induced hepatic preneoplastic lesion development. J. Natl. Cancer Inst. 70, 547-549 (1983).

Barnard, N. et al. A low-fat vegan diet elicits greater macronutrient changes, but is comparable in adherence and acceptability, compared with a more conventional diabetes diet among individuals with type 2 diabetes. J. Am. Diet. Assoc. 109, 263-272 (2009).
Campbell, T. C. & Campbell, T. M., II. The China Study, Startling Implications for Diet, Weight Loss, and Long-Term Health. (BenBella Books, Inc., 2005).
Campbell, T. C. Whole. Rethinking the science of nutrition (with H. Jacobson). (BenBella Books, 2013).
Esselstyn, C. B. J., Gendy, G., Doyle, J., Golubic, M. & Roizen, M. F. A way to reverse CAD? J Fam. Pract. 63, 356-364b (2014).
Schulsinger et al. (1989) Effect of Dietary Protein Quality on Development of Aflatoxin B1 -Induced Hepatic Preneoplastic Lesions. J. Natl. Cancer Institute 81: 1241-1245.
Tomasetti, C. & Vogelstein, B. Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science 347, 78-81 (2015).
Youngman, L. D. & Campbell, T. C. Inhibition of aflatoxin B1-induced gamma-glutamyl transpeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets: evidence that altered GGT+ foci indicate neoplastic potential. Carcinogenesis 13, 1607-1613 (1992).

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Comments 6
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  • Dear Jonathan,

    Good piece on cancer without mutations!

    There is, however, one “irreversible” alternative, namely cancer as a form of speciation (PD et al. “Is carcinogenesis a form of speciation? Cell Cycle (2011).

    Are by chance related to Harriet Latham-Robinson?


    Peter Duesberg

  • Very interesting article, but there is an alternative theory that cancer is not caused by mutations, yet “irreversible”.

    According to this theory cancer is a form of speciation (PD, et al. Cell Cycle, 2011).

    BTW Is Latham related to Harrier Latham-Robinson?


    Peter Duesberg

  • Here are some resources:


    By Samuel S. Epstein, M.D.


    Apart from well-documented evidence on control and manipulation of health and environmental information, industry has used various strategies to con the public into complacency and divert attention from their own recklessness and responsibility for the cancer epidemic. Key among these is the “blame-the-victim” theory of cancer causation, developed by industry scientists and consultants and a group of conservative pro-industry academics, and tacitly supported by the “cancer establishment.” This theory emphasizes the faulty lifestyle-smoking, a fatty diet, sun bathing, and genetic susceptibility, as the major causes of preventable cancer. And at the same time it trivializes the role of involuntary exposures to occupational and environmental carcinogens. Another misleading diversion is their claim that there is no evidence of recently increasing cancer rates other than lung cancer, for which smoking is given the exclusive credit. While the role of lifestyle is obviously important and cannot be ignored, the scientific and exclusionary basis of this theory is as unsound as it is self-serving. Certainly, smoking is a major, but not the only, cause of lung cancer. Evidence such as the following clearly incriminates the additional role of exposure to occupational carcinogens and carcinogenic community air pollutants: some 20 percent of lung cancers occur in non-smokers; there have been major recent increases in lung cancer rates in non-smokers; an increasing percentage of lung cancer is of a histological type (adenocarcinoma) not usually associated with smoking; high lung cancer rates are found with certain occupational exposures independent of smoking; and excess lung cancer rates are found in communities where certain major industries are located. The chemical industry clearly uses tobacco as a smoke screen to divert attention from the role of carcinogenic chemicals in inducing lung cancer as well as other cancers.

    What To Do About It

    The cancer epidemic poses a grave and growing crisis of enormous cost to health, life and economy for the nation. The Politics of Cancer (Sierra Club Books, Samuel Epstein, M.D., 1978) concluded with the following specific recommendations designed to reduce the toll of preventable cancer:

    Cancer must be regarded as an essentially preventable disease.

    The hidden political and economic factors which have blocked and continue to block attempts to prevent cancer must be recognized.

    The ineffective past track record of government in cancer prevention must be recognized.

    The critical roles in cancer prevention that public interest groups and informed labor leadership have exercised must be recognized and their further efforts fully encouraged and supported.

    Congress must resolve the major inconsistencies in a wide range of legislation on environmental and occupational carcinogens.

    Substantially higher federal priorities for the prevention of cancer must be developed.

    Policies of the various federal agencies with responsibilities in cancer prevention must be effectively integrated and coordinated.

    Top business management must recognize the essential similarities between their long-term interests and goals and those of society. Prevention of occupational cancer and cancer in the community-at-large is of primary importance to both.

    The American Cancer Society must be influenced to balance its preoccupation with treatment with activist programs designed to prevent cancer.

    The medical and scientific community must accept a higher degree of responsibility and involvement in the prevention of cancer by actions on both the professional and political levels.

    Medical schools and schools of public health must be persuaded to massively reorient their educational and training programs from the diagnosis and treatment of disease and cancer to prevention.

    Chemicals in consumer products and in the workplace must be clearly and simply identified and labelled.

    Additional new approaches must be developed for obtaining and for retaining honest and scientifically reliable data on the carcinogenicity and toxicity of new chemicals already in commerce; such data must be made accessible to public scrutiny. Maximum legal penalties should be directed against all those responsible, directly and indirectly, for distortion or manipulation of toxicological and epidemiological data on the basis of which decisions on human safety and risk are based.

    Apart from actions on a political level, there are limited personal options. To some extent, it may be possible to reduce the chances of developing cancer by making informed changes in lifestyle, use of consumer products and work.

    The major determinants of preventable cancer are political and economic, rather than scientific, and as such must be addressed in the open political arena. Cancer prevention must be made, at least, to rank with inflation on the next local, state and national political tickets.

    The Politics of Cancer, Revisited
    By Samuel S. Epstein, M.D.

    Cancer: It’s a Growth Industry

    David Ross interviews Dr. Samuel Epstein

    Dr. Samuel Epstein’s 20 Year Fight Against Biotech, Cancer-Causing Milk

  • Models framed by looking “within the body” at disease avoid the messier economic, political and cultural changes of looking “outside the body” for causal factors.

    Campbell’s summary describes how this happens for cancer; I have previously described the same for ALS and Alzheimer’s. Autism too is showing signs of moving from the genetic model to an enviro-genetic model. For diseases with an environmental component, limiting the inquiry and the intervention to within the body obviously allows all of us to be exposed, creating a roulette kind of situation. This is a curious modern practice, which anthropologists have compared with primitive human sacrifice. Back then, the act of sacrifice was conscious and public and driven by beliefs; in so called “developed” societies, the sacrifice is anonymous for most of us, semi-random and hidden (for epidemiologists to uncover) while consciousness of sacrifice is muted by consumerism and corporate greed.

    Genetics now, and in the future genetic-specific interventions, offer the temptation to narrow-modelled scientists to look deeper into and keep intervening “inside the body”. All the time celebrating the wonderful science being accomplished and giving the public a sense of hope and expectation for the next “breakthrough”. The public and patients hit by the disease remain at a level of consciousness that this disease’s dynamic is only “within me” because the intervention is within my body!! Sociologists call this a self-fulfilling prophecy at the societal level.

    Two strategies come to mind:

    a) link this reluctance to look at environment for its impact on health with the denial that what and how we produce material objects and live has an impact on climate change;

    b) quantify the reluctance, at least in one way, by calculating the total $ going into enviro or environ-human body research, as compared with “within the body” research, including drug interventions.

    Thoughts on any of this are welcome.

    Mark McGuire
    M.Sc. Health Research Methods M.A. Social & Health Policy

  • I am a big fan of the eloquent Professor Campbell. My work on the nutritional value of the wild foods of Indigenous Australians in traditional times takes an additional twist to his research and position.

    While nutrition and low animal protein intake and very low to no dairy consumption may indeed stop and often reverse cancers, we do need to look at the make up of what we call food today.

    I see evidence that modern produce has evolved with our demands for high-yield, bullet-proof harvests, cold-chain hardy and transport-ripened fruits and vegetables. We have bred high sugar (sucrose and fructose), low fibre, juicy, nutritionally deplete foods that are a shadow of their former selves in terms of micro-nutrients; antioxidants, anti-inflammatories, enzyme regulators, adaptogens, minerals and micro-sugars. I write about this in my book, Wild Foods: Looking back 60,000 years for clues to our future survival (New Holland Publishing, 2015).

    While ‘super-foods’ are often presented as a holy grail to health, what Indigenous Australians had to eat (a super-food arsenal) facilitated and supported what is the world’s longest living culture. Their foods are now being researched (my own work in this field began in 1983) and results show vastly different foods in number (by a factor of 10) and quality (orders of magnitude) provided for long term survival and strategic planning, heightened memory recall of these strategies and tactical frameworks across generations and access to a work-life balance of which we can only dream.

    Many wild fruits, herbs and spices contain micro-nutrients that are pro-apoptotic, anti-proliferative and anti-mutagenic against cancer cells as well as supportive of normal cellular metabolism. While we certainly can and possibly should reduce our domesticated animal protein intake, we need to simultaneously assess the deterioration in the quality of our food supply and vastly improve the dietary range. We also need to include wild foods wherever possible and if this ensures better preservation and conservation of wild areas, all the better.

    The good news is that here in Australia and in other wild places such as the Amazon, parts of Asia and Africa, we still can find wild foods. Perhaps re-engineering some of our foods to re-introduce wild qualities while also broadening the range of foods we have available may be strategies for the cancer industry to consider. It will need to be a selfless activity as in time they will work themselves out of a job as our cumulative health improvement might just make them redundant.

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