© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 10, 791-792,
May 16, 2001
© 2001 Oxford University Press
CORRESPONDENCE |
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Affiliation of authors: Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.
Correspondence to: Arthur Schatzkin, M.D., Dr.P.H., National Institutes of Health, Executive Plaza North, 6130 Executive Blvd., Rm. 211, Rockville, MD 20852. (e-mail: Schatzkina{at}exchange.nih.gov).
Nelson et al. argue that, even though some recent observational (1) and experimental (2) epidemiologic studies have yielded null results, pessimism about diet and cancer is unwarranted because colorectal cancer incidence has been declining in the United States. Ecologic (aggregate) studies, including those of time trends (3), international correlations, and migration, do indeed suggest a causal relationship between diet and colorectal cancer risk. These studies are far from conclusive, however, because of the possibility of confounding: Many potential etiologic factors (besides diet) change over time, from country to country, and with migration.
It was at least partially in recognition of the promising ecologic data on diet and colorectal cancer risk that investigators around the world initiated individual-level observational and experimental epidemiologic studies. Some of these studies are consistent with the ecologic data on fiber/fruits and vegetables and colorectal cancer; some, including some recent ones, are not.
Animal experiments clearly show that diet modulates colorectal tumorigenesis, but it has been a challenge to move beyond the ecologic data and demonstrate comparable causal relations in humans. Because we are likely dealing with modest relative risks for most foods and nutrients, inconsistencies in the epidemiologic evidence—for fiber and fruits/vegetables vis-a-vis colorectal cancer, for example—are not surprising. Moreover, we need to acknowledge potential limitations of our observational and experimental epidemiology. Perhaps dietary assessment instruments do not measure the intake of key foods and nutrients with sufficient accuracy to discern important but modest alterations in cancer risk. Maybe traditionally assessed "fiber" and "fruits and vegetables" only partially capture the central functional role of nutritional exposures such as chronic insulin stimulation (4) and methyl group availability (5). Perhaps null adenoma recurrence trials followed people for too short a time or evaluated the wrong part of the neoplastic process.
The recent null studies can be seen as a source of pessimism, but they are better taken as indicators of the complexity of the diet and cancer field and the difficulties inherent in identifying precisely what dietary factors, singly or in combination, modulate carcinogenesis in people. Perhaps the most constructive stance is to regard the recent studies as incentives to identify and address the limitations in our individual-level epidemiologic research.
The actual cause of the declining cancer rates in the United States has been a source of some controversy (6,7). In addition to diet, colonoscopic polypectomy has been cited as a potential determinant of the falling rate. In fact, Nelson et al., in their ecologic analysis (3), cite increased use of colonoscopic polypectomy as the one factor "most consistent with the observed pattern of [colorectal cancer incidence] change." It is particularly noteworthy—if ironic—that in the past few years colorectal cancer incidence in the United States has ceased its decline and is actually increasing. One hopes that this recent upward "blip" reflects increased screening rather than some deleterious dietary practice.
REFERENCES
1
Michels KB, Giovannucci E, Joshipura KJ, Rosner BA, Stampfer MJ, Fuchs CS, et al. Prospective study of fruit and vegetable consumption and incidence of colon and rectal cancers. J Natl Cancer Inst 2000;92:1740–52.
2
Schatzkin A, Lanza E, Corle D, Lance P, Iber F, Caan B, et al. Lack of effect of a low-fat, high-fiber, diet on the recurrence of colorectal adenomas. Polyp Prevention Trial Study Group. N Engl J Med 2000;342:1149–55.
3 Nelson RL, Persky V, Turyk M. Determination of factors responsible for the declining incidence of colorectal cancer. Dis Colon Rectum 1999;42:741–52.[CrossRef][Web of Science][Medline]cancerlit;99304943
4 Bruce WR, Wolever TM, Giacca A. Mechanisms linking diet and colorectal cancer: the possible role of insulin resistance. Nutr Cancer 2000;37:19–26.[CrossRef][Web of Science][Medline]
5
Giovannucci E, Rimm EB, Ascherio A, Stampfer MJ, Colditz GA, Willett WC. Alcohol, low-methionine–low-folate diets, and risk of colon cancer in men. J Natl Cancer Inst 1995;87:265–73.
6
Kuller LH, Schoen RE. Re: Temporal patterns in colorectal cancer incidence, survival, and mortality from 1950 through 1990 [letter]. J Natl Cancer Inst 1994;86:1554–5.
7
Chu KC, Tarone RE. Response to re: temporal patterns in colorectal cancer incidence, survival, and mortality from 1950 through 1990 [letter]. J Natl Cancer Inst 1994;86:1555–6.
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