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Eating to Die

In response to:

Death for Dinner from the February 21, 1974 issue

To the Editors:

I have read your periodical since its inception, and have found it consistently interesting. I have assumed that your reviewers and essayists have always been expert, and sometimes authoritative (even though they frequently make no pretense at balance and dispassion).

Now I wonder. For you have just published a piece concerning issues with which I am familiar, and it is a laugher (“Death for Dinner,” NYR, February 21). I suppose that the society which supports the AMA and the food industry deserves an equal and opposite level of misinformation, hysteria, and just plain nonsense.

The author states “We suffer climbing rates of cancer and other degenerative disease, mental retardation, and birth defects.” There are no data to suggest that the incidence of either retardation or birth defects has risen for the past few decades.

Enclosed you will find a copy of authoritative death rates from cancer for the years 1930 to 1969, by site, and by sex, for the United States. There have been precipitous falls in death rates for cancer of the stomach for both men and women; since about 1950, rates for colon and rectal cancer have been rapidly decreasing in females and, less so, in males. The cancer sites that have been experiencing sharp rises are lung and pancreas, and also leukemia, There is no evidence from these data that cancer most likely to be related to diet (i.e., that of the gastrointestinal tract) is on the increase in our population.

The facts are that an association between fiber content of food and intestinal cancer is a probable nonsense. There is no proof that such an association does not exist, but there is no evidence for the association, either.

Another quote: “Children with iron deficiencies, one witness explained to the Senate Committee, often have decreased attention spans, ‘the time during which they can pay close attention to the teacher.’ No wonder the antihyperactivity drug Ritalin is so popular.” The psychophysiological consequences of iron deficiency anemia, except at extreme levels, are very poorly understood. The pioneering work of Elwood and his colleagues in Britain has shown that no physiological or emotional changes could be detected in a group of women with iron deficiency anemia whose anemia was corrected by iron treatment compared to a randomized control group given placebo treatment.

Again: “Our daily diets of processed foods, rich in refined sugar and modified carbohydrates like white flour, are probably major causes of diabetes, heart and arterial disease, and intestinal cancer—among other ailments.” For an author who later implies that we would be better off with real butter and eggs in our bread, rather than substitutes, this is nonsense. There is no reason to believe that diabetes is “caused” by processed foods, or in fact, any other sort of foods. When a person is genetically predisposed to diabetes, obesity can precipitate clinical symptoms. There is good data to suggest that heart and arterial disease can be caused by improper diet: too many calories, and too much cholesterol and saturated fat, of which “real butter and eggs” would be a rich source….

David Rush, M. D.

Associate Professor of Public Health (Epidemiology) and Pediatrics

Columbia University

School of Public Health

New York City

Daniel Zwerdling replies:

Rush’s letter is valuable. It manages in just a few paragraphs to hurtle us into that Mary Poppins world in which so many public health professionals reside: no nasty thoughts about food, totally oblivious to any destructive relationship between products the food industry sells us and our health. Does Rush live on some other planet? I scarcely know where to begin a necessarily brief reply, except to urge Rush, when he has time off from his professional duties, to consult a medical library. There, for example, he would find the Report on the Third International Cancer Survey, by Sidney J. Cutler, Associate Chief of Biometry Branch at the National Cancer Institute, analyzing how cancer incidence rates, in general, are increasing. Cutler: “Among males, incidence of and mortality from cancer have been increasing continuously. The increase has been particularly large among blacks…. it is likely that a substantial fraction of the reported increase reflects the impact of environmental factors, e.g., …changes in eating…” (my italics). Cutler lists other environmental factors too, of course. Cancer incidence among females is “either decreasing…or leveling off,” Cutler notes, but he explained in a phone interview that, everything averaged out, incidence of cancer is increasing society-wide.

Now, why, why, why did Rush present statistics on death rates of cancer? For an article about progress in surgical, radiation, and drug therapy techniques, I’d be grateful; but for an article referring to possible causes of cancer, we want statistics on cancer incidence. So Rush’s figures are, at best, worthless, and deceptive. Let’s talk about colon cancer. From Cutler at the National Cancer Institute: Among white males, incidence of cancer of the colon increased 27 percent between 1947 and 1969. Among white females, incidence decreased just 1 percent during that period, but only after a 16 percent increase between 1937 and 1947. Incidence of cancer of the colon among black males increased 90 percent between 1947 and 1969, and 129 percent among black females.

As for other kinds of cancer, I’ve never heard Rush’s Rule that carcinogens in the food, or cancer-inducing properties of a total diet, must do their nasty work only in the stomach and intestines. Indeed, food additives have caused cancer, in the laboratory animals, in a wide variety of locations—like the bladder (cyclamates). Cutler: “The survey data point to increases in incidence (of bladder cancer) in both white and black males.” Or: “The marked increase in the incidence of esophageal cancer in both male and female blacks suggests the influence of changes in eating and drinking practices….”

About fiber content in foods and intestinal cancer: can someone who specializes in epidemiology really not have read the various epidemiological studies over the past few years, showing that populations who eat fiber-poor diets have high rates of intestinal cancer while populations who eat fiber-rich diets have practically none? Such studies have focused on Japanese (whose rates of colon cancer have been rapidly increasing as their diet becomes more Westernized), Africans and Asians, among others. As Denis Burkitt, a leading English epidemiologist, writes in Cancer, “No other form of cancer is so closely linked to the alterations in dietary habits” as intestinal cancer is. There are different theories on why low-fiber diets might cause intestinal cancer—Burkitt suggests it’s because fiber-low foods pass so slowly through the bowels and therefore bacteria living in the gut have a much greater opportunity to convert food substances to cancer-causing chemicals.

While he’s talking about the relation of fiber to intestinal disease, why doesn’t Rush even mention diverticulitis—a painful intestinal inflammation which hospitalizes about 200,000 mostly elderly Americans each year? Few gastroenterologists will challenge the evidence that diets low in fiber cause diverticulitis. One especially interesting study in the British Medical Journal, April 15, 1972, by Painter et al., describes how diets high in fiber helped cure patients suffering from the painful disease.

Even Dr. Jean Mayer, Harvard nutritionist and chairman of the White House nutrition conference a few years ago, writes that “It now appears possible—indeed, likely—that if you don’t eat sufficient vegetable fiber you very much increase your chances of developing at least three diseases: appendicitis, diverticulitis, and the dreaded cancer of the colon” (The Washington Post, August 30, 1973). But for more information, Rush might find interesting reading in the following articles, which discuss evidence relating to the effect of fiber in the diet on intestinal diseases, including cancer: The American Journal of Clinical Nutrition, December 25, 1972; Gut, 1973; The British Medical Journal, May 22, 1971, and February 3, 1973; Lancet, June 16, 1971, December 30, 1972, and June 9, 1973; papers before the October, 1971, meeting of the American Dietetic Association, on “Rationale for Diet in Gastrointestinal Disease”; and various National Cancer Institute monographs.

Now, iron deficiency and its effect on children. Why does Rush turn to the “pioneering work” on iron deficiency in women? The Senate witness I quoted—Dr. Walter Mertz, chairman of the USDA Human Nutrition Institute—had turned to studies like “Extent and Meanings of Iron Deficiency in the US,” Summary Proceedings of a Workshop, March 8-9, 1971, by the Food and Nutrition Board, National Academy of Sciences. For example, the study “Consequences of Mild Deficiency in Children,” by Dr. Doris Howell, Department of Pediatrics, Medical College of Pennsylvania: “Children with iron deficiency anemia…show very markedly decreased attentiveness, more aimless manipulation, less complex and purposeful activity, narrower attention span, and perceive fewer stimuli in the presence of dominant stimuli.” Or “Effects of Iron Deficiency on Psychological Tests in Children,” by Dr. Jefferson L. Sulzer, Early Childhood Research Center, Tulane University: Children classified as iron deficient, he reported, “were more frequently identified as inattentive because more easily distracted, hyper-or hypo-active, lacking persistence in solving problems, and having less sense of competence.”

As for Rush’s final paragraph, distressed about links between “processed foods” and diabetes—a growing volume of ongoing research suggests strongly that high sugar consumption causes diabetes and heart disease, in those who are genetically sensitive to sucrose. Again, Rush can go himself to a medical library. Just one reference, from Dr. Aharon M. Cohen, Head, Diabetic Unit and Isotope Laboratory for Endocrine Research, Hadassah University Hospital in Israel: “We have proved that sucrose feeding causes diabetes and its vascular complications in the experimental animal.” Cohen, among other researchers, is currently conducting years-long research in humans, but he notes, “As in many other cases, the results in the experimental animal are also applicable to man.”

In any case, all this research focusing on how food causes disease is rather recent—and many health-related professionals educated some years ago have not had the time to catch up on it. But beyond his trivial peckings, what is Rush really trying to tell us in this confusing letter? That too much butter and eggs aren’t good for us? I agree. But that otherwise, the food we eat has little effect on our health? As a member of the public who wishes that someone had taught my family how to eat healthfully years ago, I shrink to imagine that that is the vital message from the public health profession. With that kind of mind set, it must be a short hop indeed from the philosophy of the classroom to the kitchens of Betty Crocker.

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