LETTER TO THE EDITOR

Prevention of Colonic Neoplasms? Is It forReal or Just a Hoax?

To the Editor:

We would like to respond to the article by McNeil et al.1 Therecent reports of the Polyp Prevention Trial2 and the ArizonaCancer Center fiber trial,3 along with the accompanying edito-rial by Dr. Byers,4 imply that prevention of colorectal cancer(CRC) is still well beyond our reach; yet migration studies ofpopulations moving from low-incidence to high-incidence lo-cales (such as Japan to Hawaii) suggested that exogenous factorsexisted that altered CRC risk. The rapid increase in the inci-dence of CRC throughout the first 13 years (1973 to 1986) ofthe SEER (Surveillance, Epidemiology, and End Results) pro-gram (a National Center for Health Statistics program thatmonitors cancer incidence and outcomes in the United States,beginning in 1973) added urgency to define these factors.5 Inaddition, underdeveloped countries, which once had vanish-ingly small rates of CRC and whose lifestyles we had hoped, insome degree, to emulate to reduce CRC incidence, were playinga rapid game of catch-up in CRC. Whereas there was in 1978 a50-fold difference between mortality in highest risk and lowestrisk countries, by 1992 this had narrowed to only a 12-folddifference.6,7

What has been conspicuous in its absence in the study ofCRC prevention was any natural population in which CRCincidence had declined. Was it possible to reverse the trend? Itseemed that only social cataclysm could create such a popula-tion, that rising risk of CRC was an inevitable result of peaceand prosperity; yet such a population has appeared where it wasleast expected—in the United States. SEER reported that therapidly rising incidence of CRC in the United States suddenlyreversed in 1986, and the incidence has declined since then at arate greater than 1% per year.5 Over a 25% drop in distal CRCincidence occurred in white men and women from 1986 to1994 (Fig. 1). Proximal patterns are most remarkable for thelesser decline in both white genders, and a steady rise in inci-dence among African American men. Prevention of CRC isclearly occurring here in the United States.

This reversal in trend provided a unique opportunity to de-termine what happened in the United States to cause thischange. Therefore, choosing a different perspective than theintervention studies discussed by Drs. McNeil, Weiss and Mar-tin,1 a time trend study of all suspected risk factors for CRCfocused on a data collection representative of the whole UnitedStates population, beginning 15 years before the change in can-cer trend in 1971. This was done because there is a considerablelag time from exposure to tumor formation and diagnosis andbecause at that time the most nationally representative databecame available through the National Health and Nutrition

Examination Surveys.8 All suspected risk factors for which timetrend data were available were included in that report. Thisbroad focus was necessary because no proven paradigm of CRCprevention yet existed (compared with, for example, smokingcessation in lung cancer), despite 40 years of intensive research.The dietary factor most supportive of the decline in CRC inci-dence was fiber. Other factors clearly played a role, the mostimportant being the increasing use of colonoscopic polypec-tomy.

The findings of this analysis have important implicationsrelated to screening for CRC. The apparent success of polypec-tomy in reducing CRC incidence in the general populationsuggests that cancer control might be more effectively achievedif the emphasis in screening would shift towards technologiesthat are effective in detecting adenomas. The feasibility of inci-dence reduction is also established and should encourage fur-ther attempts to accelerate this through primary prevention.Increased fiber consumption may already have played a role inthis reduction, and current trends in the use of estrogen, aspirin,and calcium may accelerate this decline in CRC risk over thenext decade. Altered caloric balance (eating less fat and moreexercise), so heavily emphasized in recent reports, is apparentlymore difficult to achieve in this society than CRC reduction.

RICHARD NELSON, MDVICTORIA PERSKY, MD

MARY TURYK, MPHDepartment of Surgery and

Epidemiology/Biometry DivisionUniversity of Illinois at Chicago

School of Public HealthChicago, Illinois

REFERENCES

1. McNeil JJ, Weiss WB, Martin RR. Prevention of colonicneoplasms? Is it for real or just a hoax? Curr Surg 2000;57:532-538.

2. Schatzkin A, Lanza E, Corle D, et al. Lack of effect of alow-fat, high-fiber diet on the recurrence of colorectal ade-nomas. N Engl J Med 2000;342:1149-1155.

3. Alberts DS, Martinez ME, Roe DJ, et al. Lack of effect of ahigh-fiber cereal supplement on the recurrence of colorectaladenomas. N Engl J Med 2000;342:1156-1162.

4. Byers T. Diet, colorectal adenomas, and colorectal cancer.N Engl J Med 2000;342:1602-1603.

5. Surveillance, Epidemiology, and End Results (SEER) program

CURRENT SURGERY • © 2001 by the Association of Program Directors in Surgery 0149-7944/01/$20.00Published by Elsevier Science Inc. PII S0149-7944(00)00416-5

4

[CD-ROM]. Bethesda, Md: National Cancer Institute,DCPC, Surveillance Program, Cancer Statistics Branch,1997.

6. Segi M. Age adjusted death rates for cancer for selected sites in46 countries. Nagoya, Japan: Segi Institute of Cancer Epi-demiology, 1984.

7. Landis SH, Murray T, Bolden S, Wingo PA. Cancer statis-tics 1998. CA Cancer J Clin 1998;48:6-29.

8. Nelson RL, Persky V, Turyk M. Determination of factorsresponsible for the declining incidence of colorectal cancer.Dis Colon Rectum 1999;42:741-752.

FIGURE 1. Age-adjusted colorectal cancer incidence from 1973 to 1994 in the distal colorectum by race and gender (Surveillance, Epidemiology, andEnd Results program). Distal cancer was defined as adenocarcinoma in the sigmoid colon to the rectum, excluding the anal canal. ■ 5 white males; }5 white females; Œ 5 African American males; ● 5 African American females. (Reprinted with permission from Nelson et al.8)

CURRENT SURGERY • Volume 58/Number 1 • January/February 2001 5