These data indicated that being tall or overweight is associated with an increased risk of colon cancer in men, while alcohol consumption was associated with colon cancer risk in both sexes.
Six other prospective studies (
Albanes et al, 1988;
Chute et al, 1991;
Bostick et al, 1994;
Giovannucci et al, 1995;
Robsahm and Tretli, 1999;
Smith et al, 2000), but not all, support our finding that being tall significantly elevates the risk of colorectal cancer. One possibility is that taller people may have longer intestines (
Hirsch et al, 1956) and have a greater rate of cell division within the tissue (
Albanes and Winick, 1988); thus, more colon cells may be at risk. Greater exposure to mitogenic factors, such as growth hormone, insulin, insulin-like growth factors, and sex steroids, could also result in increased cancer risk. Height has been related to elevated risk of several specific cancers, including breast (
Swanson et al, 1988) and prostate (
Smith et al, 2000). Animal experiments have shown that low-energy diets from early age shorten overall animal length and reduce cancer risk (
Kritchevsky, 1995). In humans, wartime food deprivation for pubescent women was associated with lower breast cancer rates than in younger and older cohorts (
Tretli and Gaard, 1996). Furthermore, an association has been reported between higher caloric intake during childhood and higher rates of cancer (
Frankel et al, 1998). Height is partly determined by total caloric intake during childhood and adolescence; so its association with colon cancer may indicate that total caloric intake during childhood is relevant for a later colon cancer risk.
Evidence has long suggested that people with excess body weight are at higher risk of colorectal cancer (
Lew and Garfinkel, 1979;
Nomura et al, 1985;
Albanes and Taylor, 1990). Our study, as well as others (
Garfinkel, 1985;
Wu et al, 1987;
Russo et al, 1998;
Robsahm and Tretli, 1999;
Murphy et al, 2000), shows a positive association between the risk of colon cancer of BMI in men but not in women. Other case–control studies (
Slattery et al, 1997;
Caan et al, 1998) and a cohort study (
Ford, 1999) have shown a significant positive association between the risk of colon cancer and BMI in both sexes, although this was weaker among women in the two case–control studies. Central obesity, which may increase colon cancer risk by acting as a tumour-growth promoter or mitogen (
Giovannucci, 1995;
Bjorntorp, 1991), is more common among males. Thus, BMI may simply be a more accurate indicator of central obesity for men than for women (
Murphy et al, 2000). Another possibility is a protective effect of oestrogen.
Our study also shows a significant positive dose–response relation between alcohol consumption and colon cancer risk in both sexes, although not significant in women as found in other studies. In a prospective study in California, the RR of colorectal cancer was 2.42 (95% CI=1.3–4.5) in men who drank more than 30

ml

day
−1 compared to nondaily alcohol drinkers, while the RR among women who consumed more than 30

ml

day
−1 relative to the same group was weaker and not significant (RR=1.45, CI=0.8–2.6) (
Wu et al, 1987). Similar results were obtained when the cases of rectal cancer were omitted.
Klatsky et al (1988) prospectively studied and found a positive relation between the risk of colon cancer and total alcohol intake in both sexes, although the results in women but not men were statistically significant. On the other hand, a meta-analysis (
Longnecker et al, 1990) including both prospective and case–control studies showed that the RR of colorectal cancer was 1.10 (95% CI=1.05–1.14), and the association did not vary according to gender or site within the large bowel. In almost all case–control studies, the use of hospital controls, among which proportions of alcohol-related disease were high, may have biased the results.
There was no association between BMI and rectal cancer risk in both the sexes. Similar finding was obtained in a case–control study reported by
Dietz et al (1995), that body weight was positively associated with colon cancer but not with rectal cancer. Positive association between BMI and rectal cancer has been reported in some studies (
Phillips and Snowdon, 1985;
Russo et al, 1998), but not in others (
Dietz et al, 1995;
Howe et al, 1997). A significant association between alcohol consumption and rectal cancer risk has been reported (
Klatsky et al, 1988;
Hirayama, 1989), but in our study, the association was weak in men. We must mention that the number of cases of rectal cancer might be too small to have meaningful analyses.
Recent prospective studies have suggested a positive association between long-term and heavy smoking and colon cancer (
Giovannucci et al, 1994;
Hsing et al, 1998;
Terry et al, 2001). In our present study, no significant association was observed in relation to the quantity of cigarettes smoked except for rectal cancer risk in men.
A major advantage of our study is that it is population based and prospective, thereby minimising recall bias. Incidence rather than mortality can avoid bias because of a progress of medical treatment as well as effect of disease. Furthermore, the data were analysed adjusting for physical activity, nutrition, and years of education.
However, several limitations must be considered. Firstly, height was self-reported and not measured. Although the intraclass correlation coefficient between self-reported height and measured height in a subsample was relatively high, self-reported information may result in misclassification. However, since the height information was collected before the development of cancer, any misclassification would be nondifferential with respect to the disease. Such random misclassification would tend to attenuate RR estimates, and, thus, would not explain the association between height and colon cancer.
Secondly, height was reported at the baseline. Stature has been reported to be at its peak at the end of the third decade of life (
Friedlander et al, 1977). Our subjects were 35 years old or over, so their height at the baseline might have been already reduced by ageing or disease and may not have represented their highest. However, age was adjusted for in our analysis, while additional adjustment for pre-existing disease, such as hypertension and diabetes mellitus, did not substantially alter the results.
Another limitation is incomplete detection of colorectal cancers, although details from the two study hospitals appear to cover around 90% of the colorectal cancers in the city reported by the prefectural cancer registry. Some colorectal cancer patients must therefore have been classified as subjects without colorectal cancer. However, it is unlikely that taller or heavier patients were selectively included in the present study. In addition, the study was so large that the effect of misclassification of true cases was minimal.
In summary, this cohort study provides evidence that height and overweight may be associated with an increased risk of colon cancer for Japanese men, and heavy alcohol consumption may increase the risk of colon cancer in both sexes.