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Second, this method assumes that a response in one species (e.g., rat) is equivalent to the same kind of response in a second species (e.g., human). This is called “species-to-species extrapolation.” And it’s a huge leap of faith. Because we have laws that prevent human trials for carcinogens (and a good thing, too!), we can’t actually give benzene or PAHs to human subjects and see if they get more cancers. So we have to assume that what’s poison for the rat is poison for the human as well. The trouble is, it turns out that some substances that are carcinogenic for rats aren’t even necessarily carcinogenic for mice.

In 1980, I published in
Federation Proceedings,
a major journal, my concerns about the underlying rationale for this testing program, specifically the assumption that what’s poison for the rat is also poison for the human. To investigate the species-to-species extrapolation assumption, I compared the results in mice with the results in rats. At that time, 192 chemicals had been tested for carcinogenicity. A total of 76 of these chemicals were carcinogenic, but only 37 (49 percent) were carcinogenic for both species. I concluded, “If this is the limitation of correspondence between two presumably closely related species, how then could one expect any greater correspondence between a selected laboratory animal species and the more distant human species?” In other words, if fewer than half the carcinogenic chemicals affected both rats and mice, it’s likely that even fewer of them would have the same effect on humans.

Also, because the CBP focuses exclusively on the human-made chemicals, it ignores a significant source of environmental carcinogenicity: naturally occurring chemicals like AF. Such chemicals are not something we decide whether or not to add to our environment; they are already there. Since they cannot simply be legislated out of our food supply by ordering companies to stop using them, the CBP is forced to pretend that they do not exist.

What all this means, of course, is that we can’t trust the CBP’s findings, despite all the time and energy and money that the government has poured into testing all these suspected carcinogens. Instead of actionable knowledge, we’re left with free-floating anxiety that “everything out there
is dangerous and there’s almost nothing we can do about it.” Not exactly the sentiments of a well-informed and empowered population!

When a magician engages in misdirection, he attempts to distract his audience by focusing attention away from the main action of his trick. As he palms a card in his right hand, for example, he flourishes his left, or instructs a volunteer to shuffle the deck or open an envelope. As a result, the magician’s palming technique need not be flawless since nobody is watching that hand anyway.

The CBP is essentially a giant exercise, however unintentional, in misdirection away from what the evidence shows to have a much greater impact on the development of cancer: eating too much of the wrong kinds of foods. It’s based on the prevailing (but inadequate) theory that since chemical carcinogens are mutagenic, they are therefore primarily responsible for human cancer. In this model of cancer, nutrition is of little or no consequence. And with all available resources focused on doing reductionist research into the specific effects of specific chemicals on rats, without looking at the kind of wholistic evidence that would help determine whether or not those research studies were useful, there isn’t a lot of manpower or money left over to investigate other causes and solutions to the cancer problem. As we’ve seen before, reductionist research tends to create its own rabbit hole, into which researchers can plunge ever deeper as they move further and further away from usefulness and applicability.

The CBP, which focuses on a disproved hypothesis and annually costs hundreds of millions of dollars, has been a huge distraction from the more likely causes of cancer. But no one involved in this program really seems to care, either about the program costs or, more important, about the misleading message being sold to a fearful and seemingly helpless public.

During the 1980s and 1990s, I was one of the few voices shouting myself hoarse, “Don’t focus on the chemical carcinogens. Look at nutrition!” Our
lab was continuing to find evidence, in our own rodent experiments and in surveys of human populations like the China Study, that it was diet, not genes or carcinogens, that determined cancer development.

In the early 1980s, shortly after my presentations to the staff of the CBP’s predecessor, the National Toxicology Program (NTP) in North Carolina’s Research Triangle Park, the NTP organized a reasonably ambitious project at the carcinogen-testing laboratory in their Arkansas facility. One of the project goals was to investigate the role of nutrition in experimental cancer development, among other ideas. Dr. Ron Hart was put in charge, and he proceeded to focus his research program on the effect of calorie consumption on experimental cancer in a very large series of rodent studies. After some years, I invited Dr. Hart to present a seminar at Cornell to report some findings of that study. He brought along for me a large number of his publications. His findings were extensive and well done but, more important, they illustrated nutrition principles at work that were similar to those that we had found for protein. Both his research on calories and our work on protein and other nutrients clearly showed that it is the nutritional composition of the diet—not the chemical carcinogens in it—that primarily determines cancer occurrence.

During this same time, my lab was also turning out overwhelming evidence for the carcinogenic potential of nutrients like animal protein and fat. As I noted in that 1980
Federation Proceedings
article, for example, based on CBP’s own stated bioassay criteria, cow’s milk protein should be considered a carcinogen: consuming it leads to cancer, and cancer halts or goes into remission once milk protein consumption is stopped. My comments at that time were based both on others’ research studies on dietary protein and cancer from 1942 to 1979, and on our own laboratory’s early research findings (we had not yet done the most convincing studies to establish this protein effect, especially the intervention experiments in which cancer was turned on with cow’s milk protein and off when it was reduced or replaced).

In that article, I also pointed out the existence of a more reliable and less expensive way of testing chemicals for their cancer-producing potential: the Ames assay, developed by Professor Bruce Ames at the University of California, Berkeley. For a mere fraction of the dollars required for this Ames assay program (approximately 1 percent or less), we could evaluate chemicals for their mutagenicity and get more meaningful results.

In a nutshell, the Ames assay applies a suspected chemical carcinogen to an extract of rat liver, which is then incubated in a petri dish to see if mutations develop. A positive Ames assay indicates potential for cancer and other mutagen-initiated diseases. The recommendation for such chemicals would then be to avoid them and, if they were found capable of migrating into our food, water, and air, if possible, discontinue their use altogether.

Unsurprisingly, my views calling the CBP’s methods into question did not make me a popular figure in the cancer research community at the time. The agencies that had organized and invested hundreds of millions of dollars in the program didn’t agree with my views on its faults or nutrition’s potential for cancer prevention and treatment. Mixing ideas about nutritional practices with the occurrence of cancer in the same discussion has been like throwing gasoline on a fire, sprinkled with a pinch of TNT. I believe there are three main reasons for this.

First, the research community is trapped within the paradigm that chemical carcinogens are the main causes of human cancer and, further, that these carcinogens are best identified in rodent bioassay experiments, despite all the evidence that these experiments are very poor estimators of what is carcinogenic for humans. As we’ve seen, once scientists start operating within a paradigm, it’s very difficult for them to see, much less embrace, any evidence that calls that paradigm into question.

Second, unlike the attribution of cancer to genes and environmental toxins, linking cancer with poor nutrition smacks of “blaming the victim.” If genes and carcinogens account for human cancer, then cancer occurrence is due to something outside our control—to fate. We’re just lucky or unlucky; we bear no responsibility for either developing cancer or staying cancer-free. If nutrition imbalance is more important to causing cancer than chemical carcinogens—if our diets can turn cancer on and off—then cancer is something for which individuals possess some responsibility. Responsibility is not a bad thing; indeed, responsibility means empowerment. It means we have the power to control our health, through the simple act of choosing what we eat, rather than submit ourselves to random circumstance. But that power is not much comfort to those whose family and friends have already succumbed to disease.

Third, there are too many jobs, careers, and structures at stake. Three-fourths of the 75,000 experimental pathologists in the United States (an
estimate given to me at my North Carolina seminar by the director of the toxicology testing program) are involved in evaluating the results of bioassay-type carcinogen testing programs. These people have no interest in hearing that their efforts are misguided, and the money they are paid produces little or no return in improved public health.

Those who vigorously defend the carcinogen bioassay program tend to believe that cancer starts with genes (and even progresses because of genes) and that chemical carcinogens are the most important agents of genetic change. In contrast, nutritional influence is often considered a second-class idea because, at best, it only modifies the development of cancer; it doesn’t cause it. While that’s technically true, it’s like saying that grass seeds cause lawns, but watering, weeding, and providing sun only modifies lawns’ development. Yes, you need the seeds to grow a lawn, just as you need genetic mutations to start growing precancerous lesions. But as anyone who has ever tilled a field can tell you, if you leave it alone for long enough the birds and the wind will happily seed it for you. Likewise, we live in a world where carcinogenic mutations abound, many of them from natural sources like the sun, viruses, and molds. Unless you want to live in a hazmat bubble (which probably contains mutagenic agents in the plastic), you can’t avoid these carcinogens or the mutations they produce. The more effective method of prevention is to address what determines whether or not those mutations progress into cancer: nutrition.

The chief proponents of the CBP have continued that same drumbeat ever since those early days, against all the evidence to the contrary, and any serious dialogue on nutrition among these scientists is still missing. When CBP proponents do acknowledge that nutrition matters, they fall into the reductionist trap of identifying important individual nutrients. The emphasis on chemical carcinogens as the principal cause of cancer, especially their effects on genes, still predominates today.

Recently, one of this viewpoint’s longtime proponents, along with two public activists, even recommended expanding the existing animal bioassay program from two to three years. They suggested the inclusion of in-utero (i.e., during pregnancy) exposure plus an additional year to
observe the offspring in the hope that more chemical carcinogens might be discovered. In their 2008 paper, they claim as part of their justification that “chemical carcinogenesis bioassays in animals have long been recognized and accepted as valid predictors of potential cancer hazard to humans,” mostly quoting the publications of their own inner circle.
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Another author wants to refine and shorten the bioassay portion of this program by evaluating the so-called mode of action for each potential carcinogen.
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Both of these proposed testing modifications would require massive amounts of new funding. And the focus still remains on chemical carcinogens as the chief causes of human cancer.

Although the CBP’s methods are unreliable and wasteful, there’s still a basic good in its aim (if restructured to use short-term assays at a tiny fraction of its current costs): to identify and ban certain harmful chemicals. Certainly my life would have been healthier and less painful had I not encountered dioxin along the way! But this cannot be the only, or even the primary, weapon we use in our efforts to prevent cancer, because if it is, we will continue to fail.

We can’t solve problems by using the same kind of thinking we used when we created them.

—
ALBERT EINSTEIN

I
n the last few chapters, I’ve shown how reductionism distorts the way we do science, especially regarding the workings of our bodies. If the only victims of this distortion were biology textbooks and organic chemistry final exams, it would be sad, but not a great tragedy. The problem is, of course, that scientific theory and popular understanding of science determine the way our society teaches, funds, and rewards the practice of medicine. In this chapter, we’ll see reductionism’s fingerprints all over the way we view and treat disease.