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Intake of Fat, Meat, and Fiber in Relation to Risk of Colon Cancer in Men
Edward Giovannucci, Eric B. Rimm, Meir J. Stampfer, Graham A. Colditz, Alberto Ascherio and Walter C. Willett
Edward Giovannucci
Eric B. Rimm
Meir J. Stampfer
Graham A. Colditz
Alberto Ascherio
Walter C. Willett
DOI: Published May 1994
Some evidence suggests that diets high in animal fat or red meat may increase the risk of colon cancer, whereas high intake of fiber or vegetables may be protective. Frequently, intake of red meat has been a stronger risk factor than total fat. Because data from prospective cohort studies are sparse, we examined fat, meat, fiber, and vegetable intake in relation to risk of colon cancer in a cohort of 47,949 U.S. male health professionals who were free of diagnosed cancer in 1986. At baseline, these men, 40 to 75 years of age, completed a validated food frequency questionnaire and provided detailed information on other lifestyle and health-related factors. Between 1986 and 1992, 205 new cases of colon cancer were diagnosed in these men. Intakes of total fat, saturated fat, and animal fat were not related to risk of colon cancer. However, an elevated risk of colon cancer was associated with red meat intake (relative risk, 1.71; 95% confidence interval, 1.15–2.55 between high and low quintiles; P = 0.005 for trend). Men who ate beef, pork, or lamb as a main dish five or more times per week had a relative risk of 3.57 (95% confidence interval, 1.58–8.06; P = 0.01 for trend) compared to men eating these foods less than once per month. The association with red meat was not confounded appreciably by other dietary factors, physical activity, body mass, alcohol intake, cigarette smoking, or aspirin use. Other sources of animal fat, including dairy products, poultry, and fish as well as vegetable fat, were slightly inversely related to risk of colon cancer. No clear association existed between fiber or vegetable intake and risk of colon cancer. These data support the hypothesis that intake of red meat is related to an elevated risk of colon cancer.
↵1 Supported by Grants CA 55075 and HL 35464 from the NIH and Special Institution Grant 18 from the American Cancer Society. G. A. C. is supported by a Faculty Research Award (FRA-398) from the American Cancer Society.
↵2 To whom requests for reprints should be addressed, at Channing Laboratory, 180 Longwood Avenue, Boston, MA 02115.
Received December 6, 1993.
Accepted March 3, 1994.
©1994 American Association for Cancer Research.
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