Mainstream Nutritional Science and the Unconventional Nutritional Cancer Therapies
What Science Says about Nutrition and Cancer: Macronutrients
Most physicians know little about the scientific literature on nutrition and cancer. Most patients who think they know about nutrition and cancer from popular health books actually know as little about the scientific nutrition literature as the physicians whose ignorance they decry.
When a cancer patient asks his doctor what he should do about diet, most oncologists simply advise that he “keep up his weight.” If the patient asks whether there is any evidence that diet or nutritional supplements might affect the course of the cancer, most oncologists would answer with an emphatic no.
When someone asks a nutritionally oriented alternative cancer therapist what to do about diet, the therapist will usually prescribe a detailed and often rigorous nutritional program. If the patient asks whether there is any evidence that the diet might affect the course of the cancer, the therapist is likely to answer emphatically yes.
Interestingly enough, the oncologist and the alternative cancer therapist often have something in common: neither has read the mainstream scientific literature on nutrition and cancer with any care. If, for instance, the oncologist had read that literature, he might give the patient who asked a much different answer: “You know, this is a frontier area in medicine that, frankly, I was not trained in. There are a lot of claims in the alternative therapies that I am cautious about, and I am convinced there are some dangers in some of the alternative therapies. But I have read enough in the literature to know that, at least in principle, diet and nutrition can affect the course of some cancers, either positively or negatively.
“If I were you, I would first try to eat a wholesome, nutritious diet, simply because you can use strength and energy to deal with both the cancer and the therapy. Take a few vitamin supplements–a multivitamin and perhaps some additional antioxidant vitamins C, E, and A–to ensure that your nutritional needs are met, especially as you go through hospitalization and treatment, which may cause nutrient deficiencies.
“As far as alternative nutritional therapies go, I have not studied them carefully but I would have to say to you that the evidence is mixed. Some patients apparently do well on those therapies, at least in terms of how they feel, but others do not. I would be particularly careful about any therapy if you begin to experience continuing weight loss and do not stabilize your weight at some reasonable level. Megavitamin therapy should only be done under expert supervision, since some nutrients may accelerate rather than retard the growth of a cancer. On the other hand, there is some positive evidence for the pharmacological uses of vitamins with cancer, both in support of radiation and chemotherapy and in cancer treatment. It will take some doing, but you and I should be able to look at the scientific studies or, even better, find a nutritionist familiar with this literature who can answer your questions.”
That would, I believe, be a fair and balanced answer for an oncologist to give a cancer patient who inquired about diet and cancer or about alternative nutritional therapies. It is better than the standard answer that there is “no evidence” that diet affects the course of a cancer because the scientific literature is filled with intriguing and often clearly important studies regarding not only cancer prevention but–far more important for the cancer patient–regarding cancer treatment as well.
The problem for both the cancer patient and the oncologist trying to research this area is that, in the scientific nutrition texts, the most intriguing studies are usually presented with so much caution–and are surrounded by so many legitimately countervailing findings–that the probability of a cancer patient or even a physician sorting out these studies is low. In the unconventional therapies, on the other hand, claims are repeatedly made, and often stated as authoritative, that either flatly contradict the scientific literature or ignore key problems, especially by overinterpreting isolated studies. For the health practitioner or cancer patient who wants to begin to understand these issues, the starting point I would recommend is the authoritative textbook by Maurice Shils and Vernon Young (in former editions Goodhart and Shils), Modern Nutrition in Health and Disease.1 The chapter by Shils on nutrition and cancer in this critical text is the place to start to see what the mainstream consensus is at this time.
In this and following chapters, I will walk in the no-man’s-land between the scientific literature and the unconventional literature on nutrition and cancer. I will do so as responsibly as I know how, although the fact remains that, despite years of study, I am not an authority in this field. So the reader should take my use of data and my interpretations cautiously and, of course, talk with his physician and, if at all possible, with a qualified nutritional scientist before embarking on any drastic program of self-care.
My excursion into the nutritional approaches to cancer represents a rough mapping of a field that I believe neither scientific nutritional texts nor unconventional nutritional texts have done real justice to. The maps may need correction as time goes on, but I hope that I describe the general contours clearly. This chapter and the following one are necessarily two of the most technically difficult chapters in this book. Some readers may wish to skim the subheads or simply go directly to the conclusion, which describes the major findings.
Four Categories of Dietary and Nutritional Approaches to Cancer
Dietary and nutritional approaches to cancer can be divided into the following major categories:
1. Recommendations given by various governmental and nongovernmental agencies on dietary and nutritional approaches to lowering the risk of cancer.
2. Recommendations given by these same governmental and nongovernmental agencies on dietary and nutritional guidelines for cancer patients. This advice is given to the patient directly or to oncologists and other professionals treating cancer. Interestingly enough, the first set of recommendations above for lowering cancer risk often directly contradict dietary recommendations given to cancer patients about how to maintain weight when diagnosed with cancer.
3. The epidemiological, experimental, and clinical research literature on nutrition and cancer, which very few oncologists or cancer patients are familiar with.
4. The claims and findings of a wide range of unconventional cancer therapists, researchers, and popularizers regarding dietary and nutritional approaches to cancer treatment.
The purpose of this chapter is to review the first two categories briefly and the third–the research literature on nutrition and cancer–in more detail. I have two reasons for this detailed treatment of the research literature on diet, nutrition, and cancer. First, there is a tremendous wealth of scientific information on nutritional approaches which is buried deep in the literature that has direct application for cancer treatment, appropriate self-care, and for future research. Second, only by carefully reviewing the scientific literature on nutrition can we be adequately prepared to review the claims of some of the major unconventional nutritional cancer therapies, which I will present in future chapters. This chapter considers macronutrients. The following chapter discusses micronutrients–vitamins and minerals.
Mainstream Recommendations for Cancer Prevention
Current views on nutrition and cancer prevention were shaped by the publication in 1982 of a report entitled Diet, Nutrition and Cancer by the National Academy of Sciences’s National Research Council. The report was written at the direction of the National Research Council’s Committee on Diet, Nutrition and Cancer, which was chaired by Clifford Grobstein, Professor of Biological Sciences and Public Policy at the University of California, San Diego. Based on its extensive review of the scientific literature, the committee issued a number of “interim dietary guidelines” to help Americans lower their risk of cancer. Among these were:
1. High fat consumption is linked to increased incidence of certain cancers (notably breast and colon cancer) and … low fat intake is associated with lower incidence of these cancers. The committee recommends that the consumption of both saturated and unsaturated fats be reduced in the average U.S. diet. An appropriate practical target is to reduce the intake of fat from its present level (approximately 40%) to 30% of total calories. The scientific data do not provide a strong basis for establishing fat intake at precisely 30% of total calories. Indeed, the data could be used to justify an even greater reduction [emphasis added]. However, in the judgment of the committee, the suggested reduction (i.e., one quarter of the fat intake) is a moderate and practical target, and is likely to be beneficial.
2. The committee emphasizes the importance of including fruits, vegetables, and whole grain cereal products in the daily diet. In epidemiological studies, frequent consumption of these foods has been inversely correlated with the incidence of various cancers. Results of laboratory experiments have supported these findings in tests of … fruits (especially citrus fruits) and vegetables (especially carotene3-rich and cruciferous vegetables).
These recommendations apply only to foods as sources of nutrients–not to dietary supplements of individual nutrients. … There is very little information on the effects of various levels of individual nutrients on the risk of cancer in humans. Therefore, the committee is unable to predict the health effects of high and potentially toxic doses of isolated nutrients consumed in the form of supplements [emphasis added].
3. In some parts of the world, especially China, Japan and Iceland, populations that frequently consume salt-cured (including salt-pickled) or smoked foods have a greater incidence of cancers at some sites, especially the esophagus and stomach. … The committee recommends that the consumption of [these] food[s] … be minimized.
4. Intentional additives (direct and indirect) should continue to be evaluated for carcinogenic activity before they are approved for use in the food supply.
5. Excessive consumption of alcoholic beverages, particularly combined with cigarette smoking, has been associated with an increased risk of cancer of the upper gastrointestinal and respiratory tracts. … The committee recommends that if alcoholic beverages are consumed, it be done in moderation.2
In 1984, the American Cancer Society added to these recommendations: “eat more high fiber foods; include foods rich in vitamins A and C; include cruciferous vegetables; and avoid obesity.”4
And in the most recent edition of Cancer: Principles and Practice of Oncology,5 much of the same basic information appears as dietary guidelines from the National Cancer Institute:
1. Reduce fat to 30% of calories or less.
2. Increase fiber intake to 20 to 30 gm/day, with an upper limit of 35êgm/day.
3. Include a variety of vegetables and fruit in the daily diet.
4. Avoid obesity.
5. Consume alcoholic beverages in moderation, if at all.
6. Minimize consumption of salt-cured, salt-pickled, and smoked foods.
Why the Silence on General Nutritional Guidance for Cancer Patients?
Since weight loss can be a basic problem for some cancer patients, physicians usually advise that these patients eat whatever they feel is tasty and will help them maintain weight. Shils summarizes the advice in this way: “For the patient with mild to moderate anorexia and taste changes, careful evaluation of food likes and dislikes and properly timed provision of attractive solid and liquid foods can make the difference between weight maintenance and loss.”6 A large professional literature also exists on specialized nutritional support for patients with specific complications due to radiation, surgery, drug treatment, or the development of the cancer itself.7
However, the textbooks are remarkably silent on the subject of nutritional guidelines for people who do not have specific needs resulting from complications of treatment or the progress of cancer. DeVita’s Cancer: Principles and Practice of Oncology, for example, devotes a large chapter to nutrition and cancer prevention, and a substantial section of a chapter to nutritional therapy for patients with disease or with treatment-related difficulties eating or digesting, but provides no general nutritional recommendations for the cancer patient who wants to eat a diet that will best support his general health, or support his resistance and recovery following cancer therapies.
On the face of it, this silence is curious, since a cancer patient might wonder whether he should try to follow the kind of healthy diet recommended for cancer prevention once he has cancer. The cancer patient might reasonably ask: If a specific diet, such as a low fat, high fiber whole-foods diet with an emphasis on fresh fruits and vegetables and whole grains lowers the incidence of some common cancers, might such a diet also slow or halt the development of one of these same existing cancers? And might a rigorous therapeutic diet along these same lines do even more to slow or reverse a cancer, or lower the chance of its recurrence, than a moderate diet that might be adequate for prevention?
None of these questions–the critical questions for cancer patients–were addressed in the National Academy of Sciences report on Diet, Nutrition and Cancer, nor, as I have said, are they addressed by the leading texts on oncology or nutrition. Nor have any of the other mainstream institutions that have issued guidelines for nutritional and dietary approaches to cancer prevention addressed these questions. Certainly, one of the reasons these critical questions of cancer patients are not addressed is because of the complexity of the scientific issues and the absence of adequate human clinical studies.
But there is also another reason for professional silence. In the sociology of American medicine, a mainstream nutritionist faces a great professional risk in studying the role of nutrition in the progress and treatment of cancer in areas that go beyond the current institutional consensus. The same dangers exist for an academic psychologist who chooses a career commitment to study the effects of psychological interventions on the progress of cancer. Therefore the mainstream nutritionist, like his psychologist colleague, risks powerful professional sanctions if he ventures into this field, even though the reasonable implications of nutritional research point inevitably to the question of whether or not the cancer patient, alone or with the aid of a physician or nutritionist, can do anything to slow or reverse the course of the cancer, or to protect himself from the side effects of treatment by altering his dietary and nutritional regimen.
Like his psychologist colleague, the nutritionist is sociologically marginal to the medical professions in charge of cancer treatment. Furthermore, like his psychologist colleague, he is often unable to get physicians to practice good nutritional interventions when there is unimpeachable scientific evidence of their efficacy. So why should the nutritionist venture into one of the most professionally forbidden zones in modern medicine, where the evidence is so complex and contradictory, when all of the professional sanctions are so high? From the nutritionist’s perspective, working in these controversial fields will destroy his credibility as an advocate of nutritional treatment in areas that modern nutrition is sure of, but that mainstream medicine continues to neglect or ignore.
So, while the nutritionists and the oncologists are largely silent on the issue of therapeutic nutrition for reasonably healthy cancer patients, the research literature is filled with highly provocative studies that bear directly on the critical questions of diet and nutrition in cancer treatment as well as cancer prevention.
Again, a remarkable parallel exists between the studies that support nutritional approaches to cancer and the studies that support psychological approaches. As we will see in the next chapter, there is now significant evidence that nutritional support, like psychological support, can decrease the side effects of conventional therapies, and even in some instance support conventional therapies. There is also evidence that nutritional support can in some instances enhance chemotherapy and radiotherapy, while in other cases it can diminish their effectiveness. In addition, good evidence exists that diet and nutrition may enhance or reduce some measures of immunocompetence, whether or not enhanced immunocompetence effectively combats cancer. In animal and laboratory studies there is good evidence that diet and nutrition can also have a direct effect on cancer growth and regression, raising the question of whether or not this is also true for humans.
But controlled clinical trials of the radical therapeutic diets have simply not been done. And while it appears unlikely to me that any of the nutritional approaches represent anything approaching a definitive cure for cancer, the critical question is whether they may not contribute both to quality of life and life extension, especially when integrated with other health-promoting complementary therapies and the judicious use of conventional therapies.
Because these studies have not been done, mainstream statements that “there is no evidence that these therapies cure cancer” are doubly misleading: (1) the real issue is probably not cure but contribution to effective cancer management and treatment, and (2) the absence of evidence at this point represents an absence of scientific study, not a negative assessment based on extensive study.
“Underfeeding” and Caloric Restrictions
Nutritionists differentiate between “caloric restriction,” which involves the restriction of a major contributor to calories in the diet, usually carbohydrates, and “underfeeding,” in which all elements in the diet are restricted. Individual micronutrients, including vitamins and minerals, can also be selectively restricted.8
One of the most significant nutritional findings in cancer is the relationship between high caloric intake and the incidence of cancer. This is found in the epidemiological literature on the hormone-related cancers–breast, prostate, colon, and ovarian cancer. In Diet, Nutrition and Cancer, the National Academy of Sciences notes, “Berg (1975) pointed out that the international distribution of hormone-dependent cancers has generated suspicion that these cancers may be related to affluence. He suggested that diets typical of affluent populations, when ingested since childhood, could overstimulate the endocrine system, lead to aberrations in metabolic processes, and result in cancer.”9
When Armstrong and Doll did a correlational study of cancer incidence and total caloric intake in 32 countries, they found significant correlations between the total calories ingested and the incidence of rectal cancer and leukemia in men, and mortality from breast cancer in women.10
The suspicion about the relationship of many common cancers to diets of affluence is well grounded in experimental research. Maurice Shils writes, “It is well established that experimental animals who have been deprived of food to the point of weight loss have a lower incidence of spontaneous tumors and a slower rate of growth of transplanted tumors.” Not only does nutritional restriction slow the development of cancer and the rate of growth of transplanted tumors but: “Repletion with a complete diet of previously protein-deprived tumor-bearing rats also appreciably increases the ratio of tumor weight to host tissue weight.”11
Lawrence Kushi, Ph.D., a knowledgeable nutritional epidemiologist who is presently an assistant professor in the Division of Human Development and Nutrition at the University of Minnesota School of Public Health, recasts the question of excessive nutrient intake and the potential benefits of nutrient restriction in the terms of appropriate balance:
The key in this area is balance between physical activity and nutrient intake. The message from animal studies regarding underfeeding is not that caloric restriction may be a worthwhile approach for management of cancer. … Rather, I believe the interpretation is that an adequate physical activity and energy balance to maintain health may be an important part of the prevention of and recovery from many diseases, including cancer. … For humans living in our society, this may include reductions in the consumption of certain kinds of foods (e.g., meat) but perhaps an overall increase in food intake that is a direct result of increased physical activity in some cases.12
Research studies have shown that the extent of the inhibiting effect of “underfeeding” depends on the tumor type, the degree of diet restriction, and the presence of carcinogenic agents. According to Shils:
When a commercial diet was compared to four purified diets varying in protein (casein), carbohydrate (sucrose) or in total calories in male rats, total tumor risk was found to be directly and exponentially related to caloric intake. Within each dietary group, rats of heavier weight had greater tumor risk than lighter rats … Lowest incidence, greatest time in delay of occurrence, absence of malignant epithelial tumors and greatest life expectancy were observed when intakes of protein, carbohydrate and total calories were low. [emphasis added].13
These findings would suggest, of course, that “underfeeding” (or the induction of macronutrient or micronutrient deficiencies) has potential therapeutic benefit for cancer patients. And as Shils notes:
The rationale for attempting inhibition or actual reversal of established neoplastic growth by induction of nutritional deficiencies is based on the possibility that certain tumor cells may be more sensitive to such depletion than are normal tissues. An increased sensitivity may reside in the … differences in the requirements for certain nutrients so that depletion by dietary means … will adversely affect tumor cells to a greater degree than host cells.
It has been concluded that caloric intake can retard the establishment and growth of transplanted tumor cells only when the host weight diminishes. Similarly, protein deprivation and other deficiencies are inhibitory only when associated with poor growth or weight loss [emphasis added].14
As we shall see, these scientific findings are of critical interest with respect to assessing the therapeutic claims of many of the alternative cancer therapies, which often restrict protein and total caloric intake, and which are often accompanied by significant patient weight loss. The question is, to the degree that alternative therapies employing these kinds of restrictions are beneficial for some patients, to what extent are the caloric and protein restrictions responsible for this effect?
Shils clearly states above–in a passage worth remembering–that the rationale for attempting to inhibit or reverse cancer nutritionally is that cancer cells may be more sensitive to nutritional “deficiencies” created by therapeutic diets than are healthy cells. The striking concept is that–as with chemotherapy–the diet will inhibit or reverse the cancer without too severely compromising the patient in terms of nutritional depletion. But it is important to add that, while Shils describes this rationale for such nutritional approaches, he does not endorse it.
If cancer cells may be more sensitive to nutritional restriction than normal cells, they also often have–in common with fetal growth tissue–a greater ability than normal cells to obtain their energy and nutrient needs in the face of nutritional deprivation. In other words, nutritional deprivation does inhibit the development of cancer in some experimental models at the point associated with weight loss. But does the cancer, in spite of this inhibition, still maintain a relative advantage over healthy cells in claiming whatever nutrients are available?
This is obviously a critical point for people with cancer. If a highly restrictive diet causes weight loss, with the result that the patient ends up stabilized at a healthy lower weight, and the cancer has been inhibited from further growth, that is a decisive clinical victory. If the patient temporarily stabilizes at a lower weight, but the tumor retains an advantage in nutrient uptake, it will grow–albeit more slowly because of nutrient restriction–and progressive weight loss will continue. If the patient fails to stabilize at a lower weight, it could either be because the diet is inadequate for that particular person to sustain healthy life or because the tumor has a great enough advantage in nutrient uptake that weight stabilization is unachievable. These are the hypothetical possibilities.
Researchers have also tried restricting intake of specific micronutrients (vitamins and trace minerals) as opposed to the macronutrients (fat, protein, and carbohydrate) we discussed above. For example, they have restricted different specific amino acids to see if it is possible to inhibit the development of cancers without excessive host weight loss. Phenylalanine and tyrosine restriction inhibited the growth of S91 melanoma in mice, for example.15 As Shils points out, vitamins have also been restricted: “Deficiencies of folic acid, of pyridoxine, or of riboflavin have each been found to result in significant inhibition of the growth of certain tumors beyond the effect of vitamin deficiency per se.”16
Immune status also has a complex relationship to restriction of diet or specific nutrients. While depressed immune function was initially believed to be a result of the cancer itself, numerous studies have now demonstrated that altered immune responses can result from malnutrition. According to Shils:
Efforts can be made to improve immunity either by improving nutritional status or, alternatively, by inducing certain deficiencies in an effort to slow tumor growth and enhance immune responses [emphasis added]. In 1949 Stoerk and Emerson found that induction of riboflavin deficiency in C3H mice at 6 to 14 days after implantation of lymphosarcoma 6C3H-CD resulted in marked to complete regression of the tumor within 10 days and in a 30 to 37 per cent cure rate; tumor reinoculated into “cured” mice with or without riboflavin in the diet failed to “take.” The authors believed that the [riboflavin] deficiency slowed tumor growth and permitted immune defenses to become effective.17
On the other hand, cellular immunity can also be depressed by protein restriction. And Shils, having set forth a provocative case for exploring “underfeeding” in cancer therapy, simply concludes:
There is increasing clinical evidence that reestablishment of cellular immunity by nutritional means, together with control of infection, plays an important role in decreasing morbidity and mortality. A number of nutritional deficiencies can adversely affect the various parameters of immune mechanisms. The importance of optimum defenses against infection in the cancer patient emphasizes the need for providing adequate nutrition.18
The National Academy of Sciences report adds an additional caveat–that it is not clear in many caloric restriction studies whether reduction in total caloric intake is the key variable or whether the critical factor is the reduction in dietary fat.19
In a 1988 contribution to Cancer, Ludwik Gross, M.D., reviewed pertinent literature on the inhibition of tumors and leukemia in rats and mice with underfeeding. He found that by restricting food intake, tumor incidence in rats exposed to total body gamma radiation was reduced from 93% to 35% in females and from 59% to 7% in males. In a similar study with mice, radiation-induced leukemia dropped from 50% to 4% after food restriction:
If the results of experiments carried out on rats and mice are extrapolated to humans, it would follow that all of us (particularly those who have had multiple cases of cancer or leukemia among family members) should aim at holding our weight below the limits considered normal for our age, sex and height. This appears particularly important for persons that have been exposed to large doses of ionizing radiation.20
And, as Gross points out, American Cancer Society data show that men and women who are overweight have an almost 50% higher incidence of cancer than those of similar sex and age who are not overweight.21 His recommendation for restricting caloric intake seems particularly important for relatively young people with good survival potential who are undergoing radiotherapy for cancer and who have long lives ahead during which radiation-induced cancers might occur.
In summary, important research evidence exists on both sides of the critical question of whether total caloric restriction or restriction of specific macronutrients or micronutrients will enhance or diminish the patient’s chances of recovery. Without question, populations with lower caloric intake have a lower incidence of some cancers. But whether dietary restriction will inhibit or reverse an established cancer–whether there is a significant nutritional margin at which human life and immunocompetence is sustained while the cancer is inhibited or reversed–has not yet been established scientifically.
Many alternative nutritional therapies–including the Gerson diet, the macrobiotic diet, the Hippocrates diet, and the Livingston-Wheeler diet, to name only a few–frequently result in weight loss. They restrict intake of some nutrients and increase intake of others. Many healthy people who try these diets stabilize at a lower weight, often their weight in high school or college. Some cancer patients, especially those with slow-growing cancers, also clearly stabilize on many of these diets. In experimental studies, this weight loss is the point at which cancer inhibition or reversal is also sometimes demonstrated. At the same time, ignorant or incautious use of alternative nutritional therapies has also been associated with continuing weight loss and with demonstrable diminished immunocompetence. Even more significant is the question of whether or not stabilizing at a lower weight on an alternative nutritional therapy is a net gain for the cancer patient, because of the possible competitive advantage in nutrient uptake of the tumor over the host and because of the high energy requirements of many cancers. On the one hand, the patient may have temporarily stabilized his weight, and even possibly slowed the growth of the tumor. On the other hand, he has lowered his body weight and energy reserves that are known to extend life with many cancers because of the energy uptake advantage that cancers often have. A study of small cell lung cancer patients, for example, found their level of energy expenditure was 37% above that of normal controls.22
Simplistic positions on both sides of this issue are simply not warranted. The question of whether dietary and nutritional therapies that restrict intake of some nutrients along the lines of many unconventional therapies are helpful or hurtful to people with some cancers remains unanswered scientifically. But, in my judgment, there is good reason to believe that both help and hurt are possible consequences of using these selectively nutrient-restricting therapies.
Dietary Fat, Proteins, and Carbohydrates
“Of all the dietary factors that have been associated epidemiologically with cancers of various sites, fat has probably been studied most thoroughly and produced the greatest frequency of direct associations,” wrote the authors of the National Academy of Sciences Study, Diet, Nutrition and Cancer.23 In epidemiological studies, correlations with high dietary fat have been reported for gastrointestinal cancers (especially of the large bowel) and endocrine cancers–breast, prostate, ovarian, and testicular cancers.24
Dietary fats are generally regarded as a promoter, rather than an initiator, of cancer. In experimental animal studies, increasing the level of dietary fat from 5% to 20% increases both the incidence and the rate of growth of chemically induced breast cancer. But the breast cancer levels increase only if the high fat diet is fed after, rather than before, the chemical initiation of the tumor.25
A study by Goodman et al. at the University of Hawaii, which compared the historical dietary fat and cholesterol intake of lung cancer patients with that of controls, showed that men in the highest quartile of cholesterol intake had a 2.2 times greater risk of lung cancer than those in the lowest quartile. The effect was not demonstrated for women, however, and was restricted to heavy smokers. Similar results were found for total fats, saturated fats, and, to some extent, unsaturated fats, but the high correlation between fat and cholesterol made it impossible to separate the effects of these nutrients.26 This result could be interpreted as lending credence to the possible role of dietary fat as a promoter, rather than initiator, of lung cancer.
Finally, in a study of the relationship between dietary fat intake and disease progression and survival in breast cancer patients by Gregorio et al., at State University of New York, it was estimated that the risk of death at any time was increased 1.4-fold for each 1,000 gm in monthly fat intake, with the association strongest for patients with advanced disease.27 This finding is consistent with that of P.I. Tartter and his associates at Mount Sinai who concluded that a lower preoperative serum cholesterol level (and lower weight) is associated with longer disease-free survival.28
Although the data are very strong, the mechanisms by which fat acts as a tumor promoter are not understood. But, says the National Academy of Sciences report:
Of all the dietary components … studied, the combined epidemiological and experimental evidence is most suggestive for a causal relationship between fat intake and the occurrence of cancer … particularly [of] the breast and colon. Data from studies in animals suggest that when total fat intake is low, polyunsaturated fats are more effective than saturated fats in enhancing tumorigenesis [emphasis added], whereas the data on humans do not permit a clear distinction to be made between the different components of fat.29
This last point is surprising: in animal studies, polyunsaturated fats have a greater cancer-producing capacity than saturated fats when fat intake is low. On the other hand, in epidemiological studies, animal fats are correlated with increased cancer incidence when total fat consumption is relatively high.
Six years after the National Academy of Sciences report, Tim Byers reviewed progress on the fat-cancer question since the release of the report. He concluded: “There continues to be evidence, although it is inconsistent, that dietary fat may be an important factor in colon cancer. … However, the hypothesized relationship between dietary fat and breast cancer [has] been less consistently supported by new findings.”30 And Shils echoes Byers’ caution: “A definite positive relationship remains to be demonstrated in view of mounting negative evidence.”31
The research literature on dietary proteins and cancer is ambiguous. In a relatively short discussion, the National Academy of Sciences concluded: “Protein intake may be associated with an increased risk of cancer at some sites,” but “because of the relative paucity of data on protein compared to fat, and the strong correlation between intakes of fat and protein in the Western diet, the committee is unable to arrive at a firm conclusion about protein.”32
Similarly, the academy found data too sparse to reach any conclusions about the role of carbohydrates (with the possible exception of fiber) in cancer, except insofar as high carbohydrate intake contributes to high total caloric intake which, as we have seen, is associated with increased risk of cancer.33
Dietary fiber includes indigestible carbohydrates and some carbohydrate-like elements. They provide bulk in food and are found in vegetables, fruits, and whole grains. Dietary fiber consumption often decreases with the consumption of a Western-style diet. Based on epidemiological studies, Burkitt and Trowell proposed in 1975 that the increased incidence of some cancers and other chronic illnesses may result from a low intake of dietary fiber.34 Extensive research studies followed. The National Academy of Science report in 1982 stated that there was no conclusive evidence that dietary fiber protects against colorectal cancer, but that some specific components of fiber might have a protective effect.35 The years that followed the publication of Diet, Nutrition and Cancer have borne out its prediction that some types of fiber have protective effects and that others do not, and still others may enhance tumor growth.
Lucien R. Jacobs of the University of California School of Medicine, Davis, reviewed the experimental literature and found that “most experiments with wheat bran and cellulose have shown evidence of a significant protective effect. In contrast, numerous other fiber supplements have been shown to enhance tumor development. These include pectin, corn bran, undegraded carrageenan, agar, Metamucil , and alfalfa.”36
David M. Klurfeld and David Kritchevsky extensively reviewed the literature on human gastrointestinal cancer and fiber. They reported that the strongest correlations between dietary fiber consumption and gastrointestinal cancers are found in international studies “in which numerous environmental variables differ. Studies on smaller groups within a culture have not given strong support to the findings of international comparisons. Colon cancer rates within regions of the U.S. vary with sufficient magnitude that diet is unlikely to account for more than a minor proportion of risk. … It would be premature to suggest that a high fiber diet will confer protection against gastrointestinal cancer.”37 But investigators are divided, and the protective effects of fiber have been suggested for both breast and prostate cancer, as well as colon cancer.38
Epidemiological studies, laboratory research, and clinical research support the fundamental proposition that nutritional interventions hold great promise in cancer prevention, in reducing side effects of treatment, and in moderating or reversing the progress of some cancers.
What is shocking is that the same timidity characterizing psychological research on controlling cancer progression–which has not been aggressively pursued–is also characteristic of nutritional research. In laboratory studies, nutritional researchers are fairly bold in studying the effects of nutrients on cancer progression, and in protecting against the side effects of treatment or enhancing treatments. But, when it comes to testing these provocative animal and cell-line laboratory studies in humans, they are constrained by perceived professional sanctions, just as the psychological researchers have been constrained in studies designed to test whether psychological interventions extend life with cancer.
In recent years, the atmosphere at the National Cancer Institute (NCI) and American Cancer Society has changed somewhat with respect to nutritional therapies–almost to the same degree that it has changed with respect to psychological therapies. Yet the NCI clinical intervention trials currently under way focus primarily on preventing cancer–or at most preventing the recurrence of cancer–and they primarily test individual nutrients, or small combinations of nutrients.39 The nutritional interventions that are actually examined are characteristically puny in comparison with the vigor of alternative nutritional interventions, where fundamental dietary change–sometimes in combination with multivitamin therapy (see next chapter)–is used with existing cancers as well as in prevention.
This failure to assess comprehensive nutritional interventions in existing cancers is all the more distressing because nutritional interventions, like psychological interventions, are characteristically nontoxic and generally enhance the quality of life, and researchers could readily find volunteers among cancer patients to participate in such clinical trials.
Neither the psychological studies nor the nutritional studies answer the real question of exceptional cancer patients, which is whether or not a combination of vigorous psychological, nutritional, and (often) other interventions can cascade into cancer inhibition or actual reversal. There is absolutely no scientific reason why these combined modalities–like combined chemotherapies or combined programs of radiation, chemotherapy, and other interventions–cannot and should not be assessed together.
Many researchers believe, for instance, that in early-stage metastatic breast cancer, patients have little, if anything, to gain by early initiation of chemotherapy or radiotherapy. This is also true for many non-small cell lung cancer patients, metastatic colon cancer patients, and metastatic prostate cancer patients. Hence we are in a position where all the major American cancers–colon, prostate, breast, and lung–do not, at certain important points in the illness, require immediate conventional interventions. Many of those patients–certainly a significant minority–would like nothing better than to be involved in vigorous clinical trials of less toxic or nontoxic therapies.
It is evident, therefore, that while both the nutritional and psychological literatures point to the potential benefits of vigorous interventions, the combined interventions that interest exceptional cancer patients most–and that most resemble the alternative therapies for which some successes are clinically reported–are simply not being tested in clinical trials. There is no legitimate scientific reason why evaluation of such combined therapies to determine whether or not they have a role in enhancing quality of life or extending life should not be a national research priority.
So what can we conclude from this somewhat complex and confusing data? Some practical guidelines:
1. For cancer prevention, dietary fat should be kept as low as possible–at least to 30% of total caloric intake, according to the National Academy of Sciences. This applies to all fats–including vegetable or polyunsaturated fats as well as animal fats. The controversy continues over the relationship of dietary fat to common cancers such as colon, prostate, and breast cancer, with the correlation clearest in international epidemiological studies (in which there may be confounding factors) and conflicted in studies within countries.
2. Ideally, weight should be kept within normal range–both for pre-vention and treatment. The unanswered question is whether or not caloric restriction (as well as the restriction of other nutrients) that is prescribed by some alternative nutritional therapies results in a state of health where the cancer is underfed and inhibited but the body retains adequate nutrition.
3. For cancer prevention, fresh fruits and vegetables should be eaten daily.
4. For cancer prevention, alcohol should be consumed in moderation, if at all. Smoking should be completely terminated.
5. Fiber–wheat bran and cellulose–have been shown in animal stud-ies to have some protective effect against cancer, while corn, Metamucil, and alfalfa fiber may promote cancer.
In reviewing this nutritional literature, the most striking impression is that nutrition appears to hold considerable promise in cancer prevention, in reducing the side effects and augmenting the benefits of conventional treatment, in enhancing general health and quality of life, and in some instances in extending life with cancer. It is imperative that research in this area be accelerated.
Notes and References
1 Maurice E. Shils and Vernon R. Young, eds., Modern Nutrition in Health and Disease (Philadelphia: Lea & Febiger, 1988), especially M.E. Shils, “Nutrition and Diet in Cancer”; D.H. Hornig et al., “Ascorbic Acid”; and Q.N. Myrvik, “Nutrition and Immunology.”
2 National Academy of Sciences, National Research Council, Committee on Diet, Nutrition and Cancer, Diet, Nutrition and Cancer (Washington, DC: National Academy Press, 1982), 1-15-1-16.
3 A precursor of vitamin A.
4 Marion Nestle, Nutrition in Clinical Practice (Greenbrae, CA: Jones Medical Publications, 1985), 183.
5 Vincent T. DeVita, Jr., ed., Cancer: Principles and Practice of Oncology, third edition (Philadelphia: J. B. Lippincott Company, 1989), 177.
6 Maurice E. Shils, “Nutrition and Diet in Cancer.” In Shils and Young, eds., Modern Nutrition in Health and Disease, 1415.
7 Ibid.; see especially chart “Consequences of cancer treatment predisposing to nutrition problems,” 1408.
8 Ibid., 1380-1.
9 National Academy of Sciences, Diet, Nutrition and Cancer, 4-1.
10 Ibid., 4-2.
11 Maurice E. Shils, “Nutrition and Neoplasia.” In Robert S. Goodhart, and Maurice E. Shils, eds., Modern Nutrition in Health and Disease (Philadelphia: Lea & Febiger, 1980), 1187.
12 Lawrence Kushi, Ph.D., personal communication with the author, 25 January 1991.
13 Shils, “Nutrition and Neoplasia,” 1153-4.
14 Ibid., 1159.
15 Ibid., 1160.
16 Ibid., 1160-1.
17 Ibid., 1161.
18 Ibid., 1162-3.
19 National Academy of Sciences, Diet, Nutrition, and Cancer, 4-4.
20 Ludwik Gross, “Inhibition of the Development of Tumors or Leukemia in Mice and Rats After Reduction of Food Intake: Possible Implications for Humans,” Cancer 62:1463-5 (1988).
21 Ibid., 1464.
22 D. Russell et al., “Effects of Total Parenteral Nutrition and Chemotherapy on the Metabolic Derangements in Small Cell Lung Cancer,” Cancer Research 44:1706 (1984). Cited in Moshe Shike and Murry F., Brennan, “Supportive Care of the Cancer Patient.” In DeVita, ed., Cancer: Principles and Practice of Oncology, 2031.
23 National Academy of Sciences, Diet, Nutrition and Cancer, 5-1.
24 Ibid., 5-17.
25 Ibid., 5-19.
26 M.T. Goodman et al., “The Effect of Dietary Cholesterol and Fat on the Risk of Lung Cancer in Hawaii,” The American Journal of Epidemiology 128(6):1241-55 (1988).
27 D.I. Gregorio, “Dietary Fat Consumption and Survival Among Women with Breast Cancer,” Journal of the National Cancer Institute 75(1):37-41 (1986).
28 P.I. Tartter, “Cholesterol and Obesity as Prognostic Factors in Breast Cancer,” Cancer 47(9):2222-7 (1981).
29 National Academy of Sciences, Diet, Nutrition and Cancer, 5-20-5-21.
30 Tim Byers, “Diet and Cancer: Any Progress in the Interim?” Cancer 62:1713-24 (1988).
31 Maurice Shils, “Nutrition and Diet in Cancer.” In Shils and Young, Modern Nutrition in Health and Disease, 1396.
32 National Academy of Science, Diet, Nutrition, and Cancer, 6-11.
33 Ibid., 7-5.
34 Ibid, 8-1.
35 Ibid., 8-5.
36 Lucian R. Jacobs, “Modification of Experimental Colon Carcinogenesis by Dietary Fiber.” In Lionel A. Poirier, Paul M. Newberne, and Michael W. Pariza, eds., Essential Nutrients in Carcinogenesis (New York: Plenum Press, 1986), 105-18.
37 David M. Klurfeld and David Kritchevsky, “Dietary Fiber and Human Cancer: Critique of the Literature.” In Poirier et al., Essential Nutrients in Carcinogenesis, 119.
38 Melvyn R. Werbach, M.D., Nutritional Influences on Illness (Tarzana, CA: Third Line Press, 1987), 100.