For at least half a century, our thoughts about cancer—including its causes and treatments, plus the industry surrounding it—have mostly relied on an assumption: 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. Cancer-prone cells then grow into a cluster 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 intercept cancer development, in this context, 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.
The main reason we cannot “win” the War on Cancer is because we have failed to question this mutation theory of cancer.
A recent, highly publicized report relied on the mutation hypothesis to explain why some of our tissues have such higher rates of cancer.[1] They found that tissues with higher cancer rates 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 [HPV]). The other two-thirds of cancers are said to be random mutations (or stochastic mutations) with unknown causes (i.e., “bad luck” cancers).
This suggests we can do very little to prevent cancer except to avoid those known environmental factors, like smoking and excessive sunlight, and otherwise hope for the best. Importantly, the mutation theory of cancer serves as a fundamental rationale for the cancer industry of research, development, and clinical practice, irrespective of whether we assume cancers are random or not.
My laboratory began NIH-financed research on cancer causation over five decades ago that eventually led to a far more promising theory of cancer. Initially based on limited observations in humans, we investigated in laboratory rat experiments how cancer, once initiated by a mutation, was not further developed by a series of additional mutations. In our most thoroughly investigated experimental model, cancer was initiated by a gene mutation caused by a powerful chemical carcinogen (aflatoxin).[2–4] However, cancer development (in this case, primary liver cancer) was 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 suggests that although mutations prime cells for cancer development, progression to diagnosable cancer is nutritionally controlled by nonmutagenic 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 nonmutation mechanisms, acting collectively, or wholistically.
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, and 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 forty to fifty 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 nonmutation mechanisms (like nutrition) are often ignored, especially by professionals with little 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 futile because countless combinations of genes and cancer risk factors can change cancer development. Given this complexity, 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 or even reversed by nonmutagenic strategies like nutrition gives hope that we can control our own cancer destiny—if we know this information and how to apply it. Conversely, believing that cancer is mostly a random event beyond our control empowers only an already bloated industry, which we must rely on to come to our rescue with highly questionable, out-of-context pills and procedures that can cause more harm than good. The researchers of this recent “random cancer” report concluded that we must emphasize early testing, a mainstay of the failed War on Cancer. A more effective solution would direct more resources toward prevention.
I also question the researchers’ use of the word random, especially when they dismiss nutrition’s associations with cancer. Embellishing this concept with the more technical 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.
A nonmutagenic nutrition effect on cancer development closely resembles the same nutrition-based effects known to dramatically reverse advanced coronary heart disease and diabetes.[5][6] The dietary lifestyle that achieves 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.[7][8]
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 (and paid for all of mine) and suffer the consequences of marginally effective treatment protocols? Isn’t it time 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.
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