For at least a half-century, our thoughts about cancer—its causes, its treatments, even its business—have mostly relied on a relatively little known assumption. We assume that cancer begins with an environmental chemical carcinogen or some type of radiation that causes a genetic mutation that converts a normal cell to a cancer prone cell. Although the body normally repairs most of these mutations, a few become fixed during cell division into the genes of a new generation of cells. The new 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.
To avoid or to intercept cancer development means avoiding the offending agents that cause these mutations (i.e., prevention) or, failing this, finding ways to selectively kill these cancer cells, by treatments like surgery, chemotherapy or radiation (i.e., treatment). We don’t expect diseased cells to revert to normality because mutations, once established, are not reversible. I suggest that failing to question this mutation theory of cancer is the main reason we cannot ‘win’ the War on Cancer.
A recent highly publicized report relied on this hypothesis to explain why some of our tissues have such higher rates of cancer. They found that high rate cancer tissues experience a higher rate of cell divisions (r=0.81) when mutations are more likely to occur. They also concluded that only about one-third of these mutations are caused by known lifestyle or environmental factors (smoking, alcohol use, UV light and human papilloma virus). The other two-thirds of cancers are said to be random (stochastic or chance) mutations with no known cause, i.e., “bad luck” cancers. Therefore, we can do very little to prevent cancer except to avoid smoking and excessive sunlight. Importantly, whether random or purposeful, both types of cancer rely on this mutation theory of cancer, which serves as a fundamental rationale for the “cancer industry” of research, development, and clinical practice.
I disagree, as follows.
My laboratory began NIH-financed research on cancer causation over five decades ago that eventually led to a far more promising theory for cancer. Initially based on limited observations in humans, we investigated in laboratory rat experiments how cancer, once initiated by a mutation, is not further developed by a series of additional mutations. In our most thoroughly investigated experimental model, cancer is initiated by a gene mutation caused by a powerful chemical carcinogen (aflatoxin). Then, cancer development (primary liver) is predominantly promoted by feeding protein at levels exceeding the amount required for good health but nonetheless typical of the protein content of most human diets. Cancer development 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 nutritionally controlled by non-mutagenic mechanisms.
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. Further, promotion of cancer growth occurred with animal-based protein, not plant-based protein.
We found many non-mutation mechanisms, acting collectively, or wholistically. Animal-based protein increases a growth hormone that encourages cancer growth (insulin-like growth factor), compromises the body’s natural killer cells that normally destroy cancer cells and minimizes calories being used for cancer growth, among many other mechanisms. Initial mutations that prime cells for cancer development may lie dormant for relatively long periods of time with a low protein diet, but later can be activated to support new cancer growth when higher levels of animal protein consumption are restored. This is rather like the spring rain, sunlight and warmth rejuvenating the growth of plants that lie dormant during dry, cold conditions.
Human evidence strongly supports these experimental animal studies. Cancer rates for different populations vary widely, being close to nil in some populations for different cancer types. Rates for major cancers (e.g., breast, colon, prostate) correlate with animal protein based diets, although most of these studies referred to total or saturated fat, 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) 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, once started, 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 futile because countless combinations of genes and cancer risk factors can change cancer development. Understanding and accepting this complexity means that funding research to identify new cancer drugs, especially targeted drugs with certain but unpredictable side effects is the wrong priority.
Knowing that cancer can be controlled, even reversed by non-mutagenic strategies like nutrition, gives hope that we can control our own cancer destiny—if we know this information and are properly informed how to apply it. Believing that cancer is mostly a random event beyond our control only gives hope 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’ report 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. A more effective solution would direct resources toward prevention before developing better tests.
I also question the researchers’ use of the word ‘random’, especially when they dismiss nutrition associations with cancer. Embellishing this concept with the adjective ‘stochastic’, does not make it any more intellectually appealing. 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 treating their activities with gruesome drugs.
A non-mutagenic nutrition effect on cancer development closely resembles the same nutrition-based effects known to dramatically reverse advanced coronary heart disease and diabetes. The dietary lifestyle that does this is 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.
Isn’t it time that we question the long-held assumption that cancer, although initiated by a mutation, is subsequently developed by a series of additional mutations? Isn’t it time that we share these ideas with the public who pay for this research (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.
- 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).
- 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).
- 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).
- 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).
- 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).