Genetics versus Nutrition, Part Two
The saddest aspect of life right now is that science gathers knowledge faster than society gathers wisdom.
—ISAAC ASIMOV
We all get sick. Most of the time it’s no big deal. In the memorable words of physician and writer Lewis Thomas, “The great secret of doctors, known only to their wives, but still hidden from the public, is that most things get better by themselves; most things, in fact, are better in the morning.” Our bodies take care of any illness fairly quickly, no intervention needed (especially if we’re eating a WFPB diet). If not, we go to the doctor or, if it’s very serious, to a hospital. These are normal aspects of modern life that most of us take for granted. Yet most people don’t really understand disease and where it comes from: why we get sick and what role our DNA plays in letting or making that happen.
As we discussed briefly in chapter eight, genes are the starting point of both health and disease. They are the source for all our biological reactions that, in effect, lead to bodily form and function—what we call life. Some of our genes start reactions that lead to health. Others lead to disease.
The vast majority of our genes are the health-giving kind—otherwise, we wouldn’t last very long. These are the genes that form our cells, our organs, and our bones; that regrow skin after a cut or scrape; that make apples taste sweet and poisonous mountain buckthorn berries bitter. A small number of our genes, however, produce disease.
All disease starts with genes and gene combinations; what we call diseases are the end stages of interactions between our genes and elements from our environment, through the medium of our bodies. We get the flu, for example, because our genes produce certain symptoms in response to a particular microbe. We even bleed (and clot) when we get a paper cut because our genes have programmed that response into our physiologies. If our genes have made us hemophiliacs, it means that bleeding, once it’s started, is harder to stop. This interaction between genes and environment isn’t just the case for short-term illnesses like the flu or conditions like hemophilia. Our genes also trigger chronic diseases like cancer, heart disease, and diabetes in response to environmental stimuli (e.g., our diet, especially over a long period of time).
Our health-producing genes come from our parents. Where do our disease genes come from? There are two main sources. Some come from our parents and their ancestors before them; they are present in our initial germ or embryo. Other disease-causing genes may begin as health-giving genes that become damaged by mutation during our lifetimes.
These mutations are widely thought to be caused mostly by unnatural, synthetic chemicals that pollute our environment; we’ve already seen how oxidation reactions in our cells can produce such mutations. But these chemicals are not the only agents causing this kind of gene damage. Low levels of certain natural chemicals and other aspects of our environment (e.g., cosmic radiation, excessive sunlight, numerous chemicals in plants and microorganisms) can do the same thing. Together, these natural and unnatural chemicals cause continual low-level genetic damage during our lifetimes.
The good news is, our bodies have learned how to routinely repair such damage. Our cells have a repair capability that works remarkably well right after the damage occurs. They had to have developed such a capability, or our evolutionary ancestors, subject to the same exposure to natural chemicals that we are today (and much less medical care), would not have survived long enough to reproduce. But this process of repair is not perfect. A very small percentage of the genes damaged during our lifetime are not repaired and may spawn successive generations of damaged cells as our tissues are renewed.
Perhaps surprisingly, this small percentage may not be all that bad. Some mutated genes turn out to be beneficial, and contribute to human evolution as their carriers survive and reproduce in greater numbers than the non-mutated population. Mutations are how evolution works. But while that low level of damage is useful for humanity as a whole, it can be less beneficial to individuals, because often these mutated genes are the source of disease.
The aim of health professionals who focus on chronic disease caused by this long-term damage is therefore two-fold: to prevent as much of that damage as possible, and to treat as many of the effects of that damage—what we call disease—as possible. And genetics, at least right now and probably indefinitely, is not a very good place to begin either of these efforts.
As a research discipline, modern-day genetics addresses the consequences of that small percentage of disease-producing genes that we are born with in addition to those damaged genes that we acquire along the way. It operates from the assumption that one day we will be able to locate and identify damaged genes and use that information to more easily diagnose and treat disease. However, it largely fails to consider how to prevent genes from becoming damaged in the first place. And the field’s presumption that genetic engineering will be able to prevent disease from occurring by repairing or replacing specific genes that cause disease, is the height of hubris, given the unimaginable complexity of DNA.
The explanatory model long used by cancer researchers postulates that cancer begins either with an inherited gene or with a gene that has been damaged by a carcinogen or other factor during a person’s lifetime, with different cancer types having different genetic starting points. If the damaged gene or genes are not repaired or removed, the damage will become a permanent part of the cell’s genetic code, passed on to each successive generation of cells. This series of cell generations grow into cell masses, then tumor masses, theoretically at a somewhat faster or uninhibited rate. The presumption here is that this process is fixed, with virtually no opportunities for its reversal. If the cell and damaged gene replicate, there is nothing that can be done; the result is cancer. More damaged genes mean more cancer; fewer damaged genes mean less cancer (see Figure 9-1).
However, research has shown that there are other environmental factors involved in whether damaged DNA becomes cancer. During my laboratory work with AF, one line of research showed that even when we had genetically predisposed a mouse or rat to develop liver cancer by intentionally damaging its genes through exposure to hepatitis B or to a high dose of AF, the cancer would develop only in the presence of a high-animal-protein diet. In other words, nutrition trumped environment, even when the environment was particularly nasty. Although their DNA had been damaged, cancer did not inevitably result (see Figure 9-2).
FIGURE 9-1. Traditional explanatory model for cancer development
There’s also evidence from human subjects, which you can read in depth in The China Study, that supports the idea that the foods we eat and the nutrition they provide is far more important in determining cancer than our genetic backgrounds.1 Population studies begun forty to fifty years ago show that when people migrate from one country to another, they acquire the cancer rate of the country to which they move, despite the fact their genes remain the same. This strongly indicates that at least 80 percent to 90 percent—and probably closer to 97 percent to 98 percent—of all cancers are related to diet and lifestyle, not to genes. Also, comparisons of cancer rates among identical twins show that even though both members of a twin pair have the same DNA, most of the time they fail to get the same cancers. If genes alone were sufficient for cancer development, you’d expect them to get the same cancer nearly 100 percent of the time. (For those relatively few twins who do get the same cancer, their dietary similarities could be at least partly responsible.)
FIGURE 9-2. Revised explanatory model for cancer development
In short, proper nutrition doesn’t just prevent damage; it affects the way our bodies respond to already damaged genes, often mitigating disease symptoms as they arise or even preventing them completely, sometimes with no additional medication or other treatments needed. In experimental animal studies in my own laboratory, cancer progression could even be reversed by nutritional changes. And researchers are now producing evidence that WFPB nutrition can turn cancer-producing genes off altogether.
All this suggests that the way cancer works is a far cry from the way cancer researchers assume it works—and of course, how something works has major implications for the way we go about fighting it.
WEAPONS IN THE WAR ON CANCER
The more work I did with AF and diet, the more I became convinced that AF wasn’t the villain most scientists assumed it to be when it came to liver cancer. In fact, I started to see that none of the accepted “causes” of cancer, in the absence of a high-animal-protein diet, mattered that much. Not genetics, not chemical carcinogens like AF, not viruses. But the cancer industry, researchers, policy makers, the media, and the public focus almost exclusively on genes, chemicals, and viruses. Nutrition did not even make the list, even though it was becoming clear from my experiments and those of others that nutrition was cancer’s on-off switch.
Our offensive strategy in the War on Cancer primarily involves two main methods of prevention: controlling the expression of cancer-producing genes (by replacing or manipulating them), and getting rid of all environmental substances that might trigger genetic mutations. We saw in chapter eight why focusing on manipulating genes themselves will not be effective. But purging our environments of toxins isn’t the answer, either. First, it can’t be done. Even if we could remove all the human-made toxins from our environment (an effort I wholeheartedly support), nature still provides us with many mutagenic phenomena that we can’t regulate or engineer out of existence, like sunlight and radon. Second, and more to the point, the effect of these environmental mutagens (substances that cause mutations in DNA) is mostly trumped by good nutrition. Yet these findings haven’t stopped the government from spending far more time and money chasing after environmental carcinogens that are supposedly causing cancer by creating gene mutations than on promoting WFPB nutrition.
You can’t turn around without hearing about another potential source of cancer to avoid: toxic chemicals, viruses, cell phones, the sun . . . A recent New York Times article titled, “Is It Safe to Play Yet?” chronicles the almost paralyzing fears expressed by young parents trying to give their children a healthy start. Many of them purge their homes of makeup, shampoos, detergents, plastic cups and bottles, laminated furniture, and even rubber duckies.2
And every so often the media will gravitate toward a terrifying story of a cancer-causing agent in our midst. Alar, a common pesticide used on apples. Microwave ovens. Power lines near homes. Enormous public concern often arises. Then, adding fuel to the fire, we are reminded that an ever-increasing number of chemicals—some intentional, some not—are being added to our personal and public environments (food, water, cosmetics). And finally, we are told that only a tiny fraction (perhaps 2,000) of these chemicals (about 80,000 or so) have been tested for their carcinogenicity.
Social activists speak out, and rightly so, against “cancer clusters”: areas where there are abnormally high rates of particular cancers, presumably due to toxic dumping and other nasty practices that befall low-income communities but not their wealthier neighbors. Communities battle each other in NIMBY (not in my backyard) skirmishes that aim to move the toxic output as far away as possible. Movies like Erin Brockovich and A Civil Action convince us to buy bottled water or install kitchen filters to keep contaminants out of our homes.
The result of this constant onslaught is a pervasive sense of fear that either morphs into passivity (“I give up, there’s nothing I can do”) or obsessive action (“Let’s live in a bubble”). Ultimately, however, neither does much to reduce our cancer risk.
I’m not saying we shouldn’t work to block new onslaughts of toxicity. I should know; my speech suffered for decades from my exposure to dioxin, one of the most toxic chemicals known to humans, and one I helped discover when, as a postdoctoral researcher at MIT in the 1960s, I isolated it from oil used in poultry feed.3 As individuals, we should seek to minimize our exposure to carcinogens. And as a society, we should err on the side of over-caution before approving and disseminating new technologies and substances into our water, air, and soil.
But carcinogenic testing has become a self-perpetuating industry rather than a safeguard of public health. From its origins shortly after the discovery in the 1950s of a harmful chemical agent in a spray used on cranberries, this program has grown to a hundred-million-dollar program today. It is difficult to estimate the total costs for this program because of its secondary effects on regulatory and cancer control programs, but, in my estimation, it surely has amounted in total to tens of billions of wasted dollars. And although the goal of reducing environmental toxins is laudable, the government’s approach to this is ineffective and misleading.
The chief arm of the U.S. government’s war on “stuff that may cause cancer”—and the poster child for how our current approach wastes time and money—is the carcinogen bioassay program, a multimillion-dollar program that researches hundreds of chemicals in an attempt to figure out which ones cause cancer in humans.
THE CARCINOGEN BIOASSAY PROGRAM
In 1958, the U.S. government added a clause to the Food Additive Amendment of the Food and Drug Act that specified that no chemical should be added to our food supply if it was found to be carcinogenic. One natural outgrowth of the clause was that the government needed a way to determine which chemicals were, in fact, carcinogenic. So a program was set up to do just that. Known popularly as the carcinogen bioassay program (CBP), it seems at first blush like a very good thing: figure out what’s harmful and keep it out of our food supply.
The problem is, the reductionist assumptions that underpin the program, from the idea that environmental toxins inevitably lead to cancer, to the ill-considered design of the program’s research and testing methods, call its usefulness into question. The CBP distracts us from the significant and easily addressed causes of cancer, and directs us to secondary factors over which we have almost no control, thus accomplishing little and diverting resources from initiatives that could make a significant difference.
PROBLEMS WITH CBP RESEARCH METHODS
The CBP tests the ability of suspect chemicals to cause cancer in experimental animals (rats and mice) within their lifetimes (about two years). If enough of the lab animals get cancer while being dosed with a particular chemical, it is labeled a carcinogen. If supporting evidence shows a statistically significant (albeit usually contested) association with humans, it is labeled a human carcinogen. Some examples of human carcinogens identified by the CBP include dioxin, formaldehyde, asbestos, DDT (insecticide spray), polycyclic aromatic hydrocarbons (PAHs, in smoked foods and cigarettes), nitrosamines (in bacon and hot dogs), PCBs (used in the manufacture of electrical transformers), benzene (found in solvents, gasoline, and cigarette smoke), and of course the subject of my lab’s work, AF.
When the CBP selects a chemical for cancer risk evaluation, it starts with animal trials. First, the researchers select the animal (rat or mouse). Next, the rodents are dosed with levels of the suspected carcinogen about a thousand to ten thousand times higher than the equivalent doses that humans are expected to encounter. If a significant percentage of the animals develop cancer, the substance is classified as a carcinogen.
You may have noticed two gaping holes in this logic. First, there’s the assumption that if very high doses of a chemical cause cancer, then much lower doses must also cause cancer. Maybe not as often or as lethally, and maybe not as quickly, but cancer is still assumed to be the end result. In science-speak, this assumption is known as “high-dose to low-dose interpolation.” This is a very uncertain procedure because we don’t really know if the straight-line relationship seen at these exceptionally high doses continues to be linear all the way down to the much lower doses typically observed for human exposure. What if the high dose is like getting hit by a car, while the low dose is like getting hit by a Matchbox car? The high dose of the nonnutritive sweetener saccharin that caused a very small increase in bladder cancer in laboratory rats was equivalent to the human consumption of 1,200 cans of diet soda in a day. Silly? I think so. And it should be added, as already discussed, that the body is capable of repairing much of the damage that low levels of natural chemicals cause.
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!
CARCINOGENIC MISDIRECTION
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.
CBP CHEERLEADERS
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 CBP TODAY
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.4 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.5 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.