Turning Off Cancer

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AMERICANS DREAD CANCER more than any other disease. Slowly and pain- fully being consumed by cancer for months, even years, before passing away is a terrifying prospect. This is why cancer is perhaps the most feared of the major diseases.
So when the media reports a newly found chemical carcinogen, the public takes notice and reacts qUickly. Some carcinogens cause outright panic. Such was the case a few years ago with Alar, a chemical that was routinely sprayed on apples as a growth regulator. Shortly after a report from the Natural Resources Defense Council (NRDC) titled "Intoler- able Risk: Pesticides in Our Children's Food,"l the television program 60 Minutes aired a segment on Alar. In February 1989 a representative of NRDC said on CBS's 60 Minutes that the apple industry chemical was "the most potent carcinogen in the food supply." 2,3
The public reaction was swift. One woman called state police to chase down a school bus to confiscate her child's apple.4 School systems across the country, in New York, Los Angeles, Atlanta and Chicago, among others, stopped serving apples and apple products. According to
John Rice, former chairman of the U.S. Apple Association, the apple in- dustry took an economic walloping, lOSing over $250 million.s Finally, in response to the public outcry, the production and use of Alar came to a halt in June of 1989.3
The Alar story is not uncommon. Over the past several decades, sev- eral chemicals have been identified in the popular press as cancer-caus- ing agents. You may have heard of some:
• Aminotriazole (herbicide used on cranberry crops, causing the "cranberry scare'" of 1959)
• DDT (widely known after Rachel Carson's book, Silent Spring)
• Nitrites (a meat preservative and color and flavor enhancer used in hot dogs and bacon)
• Red Dye Number 2
• Artificial sweeteners (including cyclamates and saccharin)
• Dioxin (a contaminant of industrial processes and of Agent Or- ange, a defoliant used during the Vietnam War)
• Aflatoxin (a fungal toxin found on moldy peanuts and corn)
I know these unsavory chemicals quite well. I was a member of the National Academy of Sciences Expert Panel on Saccharin and Food Safety Policy (1978-79), which was charged with evaluating the poten- tial danger of saccharin at a time when the public was up in arms after the FDA proposed banning the artificial sweetener. I was one of the first scientists to isolate dioxin; I have firsthand knowledge of the MIT lab that did the key work on nitrites, and I spent many years researching and publishing on aflatoxin, one of the most carcinogenic chemicals ever discovered-at least for rats.
But while these chemicals are Significantly different in their proper- ties, they all have a similar story with regard to cancer. In each and ev- ery case, research has demonstrated that these chemicals may increase cancer rates in experimental animals. The case of nitrites serves as an excellent example.
THE HOT DOG MISSILE
If you hazard to call yourself "middle-aged" or older, when I say, "Ni- trites, hot dogs and cancer," you might rock back in your chair, nod your head, and say, "Oh yeah, I remember something about that." For the younger folks-well, listen up, because history has a funny way of repeating itself.
The time: the early 1970s. The scene: the Vietnam War was begin- ning to wind down, Richard Nixon was about to be forever linked to Watergate, the energy crisis was about to create lines at gas stations and nitrite was becoming a headline word.
Sodium Nitrite: A meat preservative used since the 1920s.6 It kills bacteria and adds a happy pink color and desirable taste to hot dogs, bacon and canned meat.
In 1970, the journal Nature reported that the nitrite we consume may be reacting in our bodies to form nitrosamines.7
Nitrosamines: A scary family of chemicals. No fewer than seven- teen nitrosamines are "reasonably anticipated to be human car- cinogens" by the U.S. National Toxicology Program.8
Hold on a second. Why are these scary nitrosamines "anticipated to be human carcinogens"? The short answer: animal experiments have shown that as chemical exposure increases, incidence of cancer also increases. But that's not adequate. We need a more complete answer.
Let's look at one nitrosamine, NSAR (N-nitrososarcosine). In one study, twenty rats were divided into two groups, each exposed to a differ- ent level of NSAR. The high-dose rats were given twice the amount that the low-dose rats received. Of rats given the lower level of NSAR, just over 35% of them died from throat cancer. Of rats given the higher levels, 100% died of cancer during the second year of the experiment.9- 11
How much NSAR did the rats get? Both groups of rats were given an incredible amount. Let me translate the "low" dose by giving you a little scenario. Let's say you go over to your friend's house to eat every meal. This friend is sick of you and wants to give you throat cancer by exposing you to NSAR. So he gives you the equivalent of the "low" level given to the rats. You go to his house, and your friend offers you a bologna sandwich that has a whole pound of bologna on it! You eat it. He offers you another, and another, and another . .. .You'll have to eat 270,000 bologna sandwiches before your friend lets you leave.9, 12 You better like bologna, because your friend is going to have to feed you this way every day for over thirty years! If he does this, you will have had about as much exposure to NSAR (per body weight) as the rats in the "low"-dose group.
Because higher cancer rates were also seen in mice as well as rats, us- ing a variety of methods of exposure, NSAR is "reasonably anticipated" to be a human carcinogen. Although no human studies were used to make this evaluation, it is likely that a chemical such as this, which consistently causes cancer in both mice and rats, can cause cancer in humans at some level. It is impossible to know, however, what this level of exposure might be, especially because the animal dosages are so astronomical. Nonetheless, animal experiments alone are considered enough to conclude that NSAR is "reasonably anticipated" to be a human carcinogen.9
So, in 1970, when an article in the prestigious journal Nature con- cluded that nitrites help to form nitrosamines in the body, thereby im- plying that they help to cause cancer, people became alarmed. Here was the official line: "Reduction of human exposure to nitrites and certain secondary amines, particular1y in foods, may result in a decrease in the incidence of human cancer."7 Suddenly nitrites became a potential killer. Because we humans get exposed to nitrites through consump- tion of processed meat such as hot dogs and bacon, some products came under fire. Hot dogs were an easy target. Besides containing addi- tives like nitrites, hot dogs can be made out of ground-up lips, snouts, spleens, tongues, throats and other "variety meats."13 So as the nitrite! nitrosamine issue heated up, hot dogs weren't looking so hot. Ralph Nader had called hot dogs "among America's deadliest missiles."14 Some consumer advocacy groups were calling for a nitrite additive ban, and government officials began a serious review of nitrite's potential health problems. 3
The issue jolted forward again in 1978, when a study at the Massa- chusetts Institute of Technology (MIT) found that nitrite increased lym- phatic cancer in rats. The study, as reported in a 1979 issue of Science, 15 found that, on average, rats fed nitrite got lymphatic cancer 10.2% of the time, while animals not fed nitrite got cancer only 5.4% of the time. This finding was enough to create a public uproar. Fierce debate ensued in the government, industry and research communities. When the dust settled, expert panels made recommendations, industry cut back on ni- trite usage and the issue fell out of the spotlight.
To summarize the story: marginal scientific results can make very big waves in the public when it comes to cancer-causing chemicals. A rise in cancer incidence from 5% to 10% in rats fed large quantities of nitrite caused an explosive controversy. Undoubtedly millions of dollars were spent follOwing the MIT study to investigate and discuss the findings. And NSAR, a nitrosamine possibly formed from nitrite, was "reasonably anticipated to be a human carcinogen" after several animal experiments where exceptionally high levels of chemical were fed to animals for al- most half their lifespan.
BACK TO PROTEIN
The point isn't that nitrite is safe. It is the mere possibility, however un- likely it may be, that it could cause cancer that alarms the public. But what if researchers produced conSiderably more impressive scientific results that were far more substantial? What if there was a chemical that experimentally turned on cancer in 100% of the test animals and its rela- tive absence limited cancer to 0% of the animals? Furthermore, what if this chemical were capable of acting in this way at routine levels of intake and not the extraordinary levels used in the NSAR experiments? Finding such a chemical would be the holy grail of cancer research. The implica- tions for human health would be enormous. One would assume that this chemical would be of considerably more concern than nitrite and Alar, and even more significant than aflatoxin, a highly ranked carcinogen.
This is exactly what I saw in the Indian research paper16 when I was in the Philippines. The chemical was protein, fed to rats at levels that are well within the range of normal consumption. Protein! These results were more than startling. In the Indian study, when all the rats had been predisposed to get liver cancer after being given aflatoxin, only the ani- mals fed 20% protein got the cancer while those fed 5% got none.
Scientists, myself included, tend to be a skeptical bunch, especially when confronted with eye-popping results. In fact, it is our responsibil- ity as researchers to question and explore such provocative findings. We might suspect that this finding was unique to rats exposed to aflatoxin and for no other species, including humans. Maybe there were other unknown nutrients that were affecting the data. Maybe my friend, the distinguished MIT professor, was right; maybe the animal identities in the Indian study got mixed up.
The questions begged for answers. To further study this question, I sought and received the two National Institutes of Health (NIH) research grants that I mentioned earlier. One was for a human study, the other for an experimental animal study. I did not "cry wolf' in either application by suggesting that protein might promote cancer. I had everything to lose and nothing to gain by acting like a heretic. Besides, I wasn't convinced that protein actually might be harmful. In the experimental animal study, I proposed to investigate the "effect of various factors [my italics] on aflatoxin metabolism." The human study, mostly focused on aflatoxin's effects on liver cancer in the Philippines, was briefly reviewed in the last chapter and was concluded after three years. It was later renewed in a much more sophisticated study in China (chapter four).
A study of this protein effect on tumor development had to be done ex- tremely well. Anything less would not have convinced anyone, especially my peers who would review my future request for renewed funding! In hindsight, we must have succeeded. The NIH funding for this study con- tinued for the next nineteen years and led to additional funding from other research agencies (American Cancer Society, the American Institute for Cancer Research and the Cancer Research Foundation of America). On these experimental animal findings alone, this project gave rise to more than 100 scientific papers published in some of the best journals, many public presentations and several invitations to participate on expert panels.
ANIMAL RIGHTS
The rest of this chapter concerns experimental animal research, all of which included rodents (rats and mice). I know well that many oppose the use of experimental animals in research. I respect this concern. I respectfully suggest, however, that you consider this: very likely, I would not be advocating a plant-based diet today if it were not for these animal experiments. The findings and the principles derived from these animal studies greatly contributed to my interpretations of my later work, including the China Study, as you will come to see.
One obvious question regarding this issue is whether there was an alternative way to get the same information without us- ing experimental animals. To date, I have found none, even after seeking advice from my "animal rights" colleagues. These experi- mental animal studies elaborated some very important principles of cancer causation not obtainable in human-based studies. These principles now have enormous potential to benefit all of our fel- low creatures, our environment and ourselves.
THREE STAGES OF CANCER
Cancer proceeds through three stages: initiation, promotion and progres- sion. To use a rough analogy, the cancer process is similar to planting a lawn. Initiation is when you put the seeds in the soil, promotion is when the grass starts to grow and progression is when the grass gets completely out of control, invading the driveway, the shrubbery and the sidewalk.
So what is the process that successfully "implants" the grass seed in the soil in the first place, i.e., initiates cancer-prone cells? Chemicals that do this are called carcinogens. These chemicals are most often

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