Genetic polymorphisms of N-acetyltransferase 1 and 2 and risk of cigarette smoking-related bladder cancer.

Aromatic amines from cigarette smoking or occupational exposure, recognized risk factors for bladder cancer, are metabolized by N-acetyltransferases (NAT). This study examined the association of (NAT) 1 and 2 genotypes with the risk of smoking-related bladder cancer. A total of 74 pathologically confirmed bladder cancer patients and 184 controls were serially recruited from the National Taiwan University Hospital. History of cigarette smoking and other risk factors for bladder cancer was obtained through standardized questionnaire interview. Peripheral blood lymphocytes were collected from each subject and genotyped for NAT1 and NAT2 by DNA sequencing and polymerase chain reaction-restriction fragment length polymorphism methods. Allele frequency distributions of NAT1 and NAT2 were similar between cases and controls. There was a significant dose-response relationship between the risk of bladder cancer and the quantity and duration of cigarette smoking. The biological gradients were significant among subjects carrying NAT1*10 allele or NAT2 slow acetylators, but not among NAT2 rapid acetylators without NAT1*10 allele. The results are consistent with the hypothesis that NAT1 and NAT2 might modulate the susceptibility to bladder cancer associated with cigarette smoking.     

Meat consumption,cigarette smoking,and genetic susceptibility in the etiology of colorectal cancer: results from a Dutch prospective study

Objective: We evaluated the effect of meat consumption and cigarette smoking in combination with N-acetyltransferases 1 and 2 (NAT1 and NAT2), and glutathione S-transferase M1 (GSTM1) genotypes on colorectal cancer. Methods: From a Dutch prospective study, after 8.5 years of follow-up, data of 102 incident colorectal cancer cases and a random sample of 537 controls frequency-matched for gender and age were analyzed. Baseline information on dietary and smoking habits, as well as blood samples for DNA isolation and genotyping, were available. Results: Red meat intake increased colorectal cancer risk among men (OR 2.7; 95% CI 1.1–6.7 highest vs. lowest intake), whereas poultry and fish decreased risk among women (OR 0.5; 95% CI 0.2–1.07). Cigarette smoking for at least 16 years increased colorectal cancer risk among former smokers only (OR 2.7; 95% CI 1.0–7.4), compared to those having smoked for 15 years or less. NAT1 and NAT2 polymorphisms did not significantly modify these associations. High consumption of poultry and fish was inversely associated with colorectal cancer only in the presence of GSTM1. Conclusions: In this study meat consumption and former long-term smoking were associated with colorectal cancer. Associations of colorectal cancer with different types of meat were modified by gender and GSTM1 genotype.     

Cigarette smoking and risk of colorectal cancer among Norwegian women

Objective  The association between cigarette smoking and colorectal cancer (CRC) is still not established. In 2002, Norwegian women had the second highest incidence of CRC in the world. A large proportion of Norwegian women are ever smokers. We examined the association between cigarette smoking and CRC incidence among Norwegian women. Methods  We followed 68,160 women, aged 30–69 years, from the Norwegian Women and Cancer Study who completed a questionnaire in 1996 or 1998 by linkages to national registers through 31 December 2005. Rate ratios (RRs) and 95% confidence intervals (CIs) were estimated by fitting Cox proportional hazard models. Subsequently, we estimated the population attributable fraction. Results  Altogether, 425 incident cases of primary, invasive CRC were identified. Ever smokers had a 20% increased risk of CRC (RR = 1.2; 95% CI = 1.0–1.5), a 30% increased risk of colon (RR = 1.3; 95% CI = 1.0–1.7), and a 10% increased risk of rectal (RR = 1.1; 95% CI = 0.7–1.5) cancer compared to never smokers. The population attributable fraction was estimated to be 12% which indicated that approximately one in eight of the CRC cases could have been prevented at a population level. Conclusion  Our results support the hypothesis that cigarette smoking is a preventable cause of CRC among women.     

Passive smoking and lung cancer in Japanese non-smoking women: a prospective study

Although smoking is a major cause of lung cancer, the proportion of lung cancer cases among Japanese women who never smoked is high. As the prevalence of smoking in Japan is relatively high in men but low in women, the development of lung cancer in non-smoking Japanese women may be significantly impacted by passive smoking. We conducted a population-based prospective study established in 1990 for Cohort I and in 1993 for Cohort II. The study population was defined as all residents aged 40-69 years at the baseline survey. 28,414 lifelong non-smoking women provided baseline information on exposure to tobacco smoke from their husband, at the workplace and during childhood. Over 13 years of follow-up, 109 women were newly diagnosed with lung cancer, of whom 82 developed adenocarcinoma. Compared with women married to never smokers, hazard ratio (HR) [95% confidence interval (CI)] for all lung cancer incidence in women who lived with a smoking husband was 1.34 (95% CI 0.81-2.21). An association was clearly identified for adenocarcinoma (HR 2.03, 95% CI 1.07-3.86), for which dose-response relationships were seen for both the intensity (p for trend = 0.02) and amount (p for trend = 0.03) of the husband's smoking. Passive smoking at the workplace also increased the risk of lung cancer (HR 1.32, 95% CI 0.85-2.04). Moreover, a higher risk of adenocarcinoma was seen for combined husband and workplace exposure (HR 1.93, 95% CI 0.88-4.23). These findings confirm that passive smoking is a risk factor for lung cancer, especially for adenocarcinoma among Japanese women.     

Coffee consumption and risk of colorectal cancer in a population-based prospective cohort of Japanese men and women

We prospectively examined the association between coffee consumption and the risk of developing colorectal cancer in a large population-based cohort study (the JPHC Study) of Japanese men and women. Data were analyzed from a population-based cohort of 96,162 subjects (46,023 men and 50,139 women). A total of 1,163 incident colorectal cancers were identified during the follow-up period, including 763 cases of colon cancer and 400 of rectal cancer. We observed a significant inverse association between coffee consumption and the risk of developing invasive colon cancer among women. Compared with those who almost never consumed coffee, women who regularly consumed 3 or more cups of coffee per day had a RR of 0.44 (95% CI = 0.19-1.04; p for trend = 0.04) after adjustment for potential confounding factors. However, no significant association was found for rectal cancer in women. In men, no significant decrease was observed in any colorectal cancer site. Further, additional analyses on the association of green tea consumption with colorectal cancer risk found no significant association in men or women. These findings suggest that coffee consumption may lower the risk of colon cancer among Japanese women.     

Flame-broiled food, NAT2acetylator phenotype, and breast cancer risk among women with benign breast disease

Purpose The objective of this study was to examine the association between flame-broiled food consumption, a source of heterocyclic amine exposure, and the development of breast cancer among cohort of women with benign breast disease (BBD). The variation of the association by acetylation phenotype, as determined by the genotypes of selected N-acetyltransferase 2 (NAT2) enzymes, was also examined.Methods Among participants in an ongoing cohort study, 1187 women reported having a breast biopsy for BBD and completed a food frequency questionnaire. NAT2 G857A, NAT2 T341C, and NAT2 G590A genotypes were determined using DNA extracted from blood specimens collected in 1989. Incident cases of breast cancer were identified through linkage of the cohort participants with the Washington County Cancer Registry and the Maryland State Cancer Registry. Follow-up for the BBD cohort began at study entry in 1989 and ended on April 28, 2003.Results Of the women in this study, 77 subsequently developed breast cancer. Results showed that, among rapid acetylators, flame-broiled food intake was associated with a statistically significant increase in the risk of breast cancer (odds ratio (OR) 2.62; 95% confidence interval (CI) 1.06, 6.46). No association was observed between flame-broiled food intake and breast cancer among slow acetylators (OR 0.75; 95% CI 0.39, 1.43).Conclusions These findings suggest that flame-broiled food may be a modifiable risk factor for the progression of BBD to invasive breast cancer among women who have genotypes consistent with rapid acetylation.     

Prospective cohort study of cigarette smoking and colorectal cancer risk in women

Epidemiological studies have consistently found a positive association between cigarette smoking and risk of colorectal adenomas, so the absence of a clear association between smoking and colorectal cancer risk may seem paradoxical. However, if colorectal cancer develops only after an induction period of about 35 years, as has been proposed recently, then studies in which all subjects have fewer than about 35 years between smoking commencement and assessment of outcome would be unlikely to detect this association. Few studies have examined smoking of several decades' duration among women. Therefore, in the cohort study reported here, we used proportional hazards models to estimate hazard ratios relating cigarette smoking to colorectal cancer risk among 89,835 women aged 40-59 years at recruitment into the Canadian National Breast Screening Study, a randomized controlled trial of mammography screening for breast cancer. During an average 10.6 years of follow-up (936,433 person-years), a total of 527 women were diagnosed with incident colorectal cancer (363 colon and 164 rectal). We found that smoking was associated with increased risk of rectal cancer 30 years or more after commencement, and especially with smoking of 40 years' duration or longer (hazard ratio=3.14, 95% CI=1.33-7.42). There was little evidence for altered risk of colon cancer. These results, along with those of other recent studies, support the hypothesis that tobacco smoking is an initiator, rather than a promoter, of rectal cancer. However, the results do not support an association with colon cancer risk, even with smoking of very long duration and high intensity.     

Cumulative genetic defects in carcinogen metabolism may increase breast cancer risk (The Netherlands)

Variants in the metabolic genes NAT1, NAT2, GSTM1 or GSTT1, may cause differences in individual detoxifying capacity of possible carcinogens. We examined the cumulative effect of putative at risk genotypes on breast cancer risk and we examined the extent to which these polymorphisms modify the association between smoking and breast cancer. A case cohort study was conducted in the DOM cohort with 676 breast cancer cases and a random sample of 669 individuals. No effect of the NAT1, NAT2 or GSTM1 genotypes on breast cancer risk was observed. However, women with GSTT1 null genotype had a 30% increased breast cancer risk compared to women with GSTT1 present (RR = 1.30 (95% confidence interval (CI) 1.04–1.64)). Smoking did not influence breast cancer risk nor did genetic variations in NAT1, NAT2 or GSTM1 in combination with smoking. Compared to women who never smoked with GSTT1 present, women with GSTT1 null genotype and who formerly smoked showed an increased breast cancer risk (RR = 2.55 (95% CI 1.10–5.90)), but current smokers who smoked 20 cigarettes or more per day did not (RR = 1.06 (95% CI 0.51–2.18)). Increasing numbers of putative at risk genotypes increased breast cancer risk in a dose dependent manner (p for trend 0.01). The risk was more than doubled in women with all four risk genotypes, RR = 2.45 (95% CI 1.24–4.86), compared to women with zero putative at risk genotypes. In conclusion, the results of this study suggest that presence of three or more putative at risk genotypes increases breast cancer risk.     

Italian mediterranean index and risk of colorectal cancer in the Italian section of the EPIC cohort

Colorectal cancer is among the commonest cancers worldwide. Dietary factors have been linked to colorectal cancer risk, however, few studies have evaluated the relationship between a priori dietary patterns and colorectal cancer risk. We evaluated the effect of adherence to a Mediterranean dietary pattern, as measured by the Italian Mediterranean Index, on the risk of colorectal cancer in the 45,275 participants of the Italian section of the EPIC study who completed a dietary questionnaire. Hazard ratios (HRs) with 95% confidence intervals (CIs) for colorectal cancer in relation to categories of Italian Mediterranean Index score were estimated by multivariate Cox models adjusted for known risk factors, on the whole cohort, on men and women and according to cancer subsite. During a mean follow‐up of 11.28 years, 435 colorectal cancer cases were identified. The Italian Mediterranean Index was inversely associated with colorectal cancer risk (HR: 0.50; 95% CI: 0.35–0.71 for the highest category compared to the lowest, P‐trend: 0.043). Results did not differ by sex. Highest Italian Mediterranean Index score was also significantly associated with reduced risks of any colon cancer (HR: 0.54, 95% CI: 0.36–0.81), distal colon cancer (HR: 0.44, 95% CI: 0.26–0.75) and rectal cancer (HR: 0.41, 95% CI: 0.20–0.81), but not of proximal colon cancer. These findings suggest that adherence to a Mediterranean diet (as measured by the Italian Mediterranean Index) protects against colorectal cancer in general but not against cancer developing in the proximal colon.     

A prospective study of body mass,height, and smoking on the risk of colorectal cancer in women

Female registered nurses in the United States who responded to a questionnaire in 1976 that inquired about height, weight, and smoking history were followed for the development of colon or rectal cancers through May of 1984. Among the 118,404 respondents free of cancer in 1976, 191 colon cancers and 49 rectal cancers were observed during 916,170 person-years of follow-up. After omitting cases diagnosed within two years of weight report, we found little overall relation of body mass (Quetelet's) index to colon cancer risk; however there was a suggestion of elevated risk for the heaviest category of body mass index (29 kg/m², relative risk (RR)=1.5; 95 percent confidence interval = 0.8–2.7) relative to the lowest category (<21 kg/m²). Self-reported body mass index from adolescence had a slightly more pronounced, although not significant, association with risk of colon cancer. Increasing height was significantly associated with colon cancer (RR=1.6, 95 percent confidence interval = 1.1–2.5 for the tallest category [168 cm] vs the shortest [<160 cm], trend P=0.04). Measures of current or past smoking failed to demonstrate any consistent relationship with colon cancer.The Nurses Health Study has been supported by research grant CA-40356 from the National Institutes of Health. Dr Chute was supported by a National Research Service Award (T32-CA09001).     

Heterozygosity for the Cys282Tyr mutation in the HFE gene and the risk of colorectal cancer (Netherlands)

Background & Aims: Heterozygosity for the Cys282Tyr transition in the HFE-gene is associated with slightly increased iron levels and may therefore be a potential risk factor for colorectal cancer. Methods: We studied the relationship between Cys282Tyr-heterozygosity and colorectal cancer using a case–control design. The 240 colorectal cancer cases and 635 controls in our study were derived from a prospective cohort study of 12,242 postmenopausal women, who were invited for an experimental breast cancer screening program in Utrecht, the Netherlands. The women were age 51–69 at time of inclusion and were followed for a period of 20 years. HFE genotyping was performed by PCR and allele-specific oligonucleotide (ASO) hybridization. Results: The risk of colorectal cancer was higher for women who were heterozygous for the Cys282Tyr mutation, than for those who were Cys282Tyr-wildtypes, although this was not statistically significant (Age-adjusted OR = 1.2, 95% CI: 0.6–2.2). Cys282Tyr-heterozygotes who smoked seemed to be at higher risk of colorectal cancer, although the p-value for interaction was not significant (p-value 0.42). Conclusions: The Cys282Tyr mutation is not associated with an increased risk for colorectal cancer in postmenopausal women, although in combination with smoking a slightly increased risk cannot be excluded.     

Prospective study of NAT1 and NAT2 polymorphisms, tobacco smoking and meat consumption and risk of colorectal cancer

Heterocyclic amines in tobacco smoke and fried meat are activated or detoxified by N-acetyltransferases (NAT1 and NAT2). We identified 379 cases with colorectal cancer (CRC) and 769 sub-cohort members among a cohort of 57,000 members. There were no statistically significant associations between tobacco smoking, consumption of meat (red, processed and fried) and CRC risk. Preference for brown-dark pan-fried meat increased the CRC risk. NAT1 fast acetylators had a significantly higher risk of CRC than NAT1 slow acetylators, whereas NAT2 acetylator status did not affect the CRC risk. There were no statistically significant interactions between tobacco smoking and either NAT1 or NAT2 acetylator status in relation to CRC risk. However, smoking intensity increased CRC risk among carriers of both NAT1 and NAT2 fast. This indicates that N-acetylator status affects the relationship between smoking and CRC risk.     

Dietary fiber intake and subsequent risk of colorectal cancer: the Japan Public Health Center-based prospective study

Results on the association of dietary fiber intake with colorectal cancer risk were inconsistent among previous large prospective studies, but studies in non-Western populations are lacking. Consequently, the authors investigated the association between dietary fiber intake and the subsequent risk of colorectal cancer in a prospective cohort study of a Japanese population. Dietary fiber intake was estimated from food-frequency questionnaires comprising 44 or 52 items at the baseline survey and 138 food items at a 5-year follow-up survey. The authors identified 907 cases of colorectal adenocarcinoma diagnosed pathologically in 86,412 subjects during a 10-year follow-up from the baseline survey. After the 5-year follow-up survey, 522 cases were identified in 78,326 subjects during a 5.8-year follow-up. The authors estimated the multivariate-adjusted hazard ratios of colorectal cancer for dietary fiber intake using Cox's proportional hazards model. The authors found no statistically significant association between dietary fiber intake and colorectal cancer in analyses using data either from the baseline survey or from the 5-year follow-up survey. However, the risk of only the lowest quintile was high, compared with the second to the fifth quintiles. Furthermore, the lowest subtertile in the lowest quintile was associated with an increased risk in women (hazard ratio(Sub1 vs. Q5), 2.3; 95% confidence interval, 1.0-5.2). In conclusion, although a minor effect cannot be ruled out, the results did not support a hypothesis of a dose-dependent protective effect of dietary fiber intake against colorectal cancer.     

Influence of pre-diagnostic cigarette smoking on colorectal cancer survival: overall and by tumour molecular phenotype

Background:

Smoking is a risk factor for incident colorectal cancer (CRC); however, it is unclear about its influence on survival after CRC diagnosis.

Methods:

A cohort of 706 CRC patients diagnosed from 1999 to 2003 in Newfoundland and Labrador, Canada, was followed for mortality and recurrence until April 2010. Smoking and other relevant data were collected by questionnaire after cancer diagnosis, using a referent period of ‘2 years before diagnosis'' to capture pre-diagnosis information. Molecular analyses of microsatellite instability (MSI) status and BRAF V600E mutation status were performed in tumour tissue using standard techniques. Multivariate hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated with Cox proportional hazards regression, controlling for major prognostic factors.

Results:

Compared with never smokers, all-cause mortality (overall survival, OS) was higher for current (HR: 1.78; 95% CI: 1.04–3.06), but not for former (HR: 1.06; 95% CI: 0.71–1.59) smokers. The associations of cigarette smoking with the study outcomes were higher among patients with ⩾40 pack-years of smoking (OS: HR: 1.72; 95% CI: 1.03–2.85; disease-free survival (DFS: HR: 1.99; 95% CI: 1.25–3.19), those who smoked ⩾30 cigarettes per day (DFS: HR: 1.80; 95% CI: 1.22–2.67), and those with microsatellite stable (MSS) or MSI-low tumours (OS: HR: 1.38; 95% CI: 1.04–1.82 and DFS: HR: 1.32; 95% CI: 1.01–1.72). Potential heterogeneity was noted for sex (DFS HR: 1.68 for men and 1.01 for women: P for heterogeneity=0.04), and age at diagnosis (OS: HR: 1.11 for patients aged <60 and 1.69 for patients aged ⩾60: P for heterogeneity=0.03).

Conclusions:

Pre-diagnosis cigarette smoking is associated with worsened prognosis among patients with CRC.     

Incidence of colorectal cancer in BRCA1 and BRCA2 mutation carriers: results from a follow-up study

Background:

The BRCA1 and BRCA2 genes confer increased susceptibility to breast and ovarian cancer and to a spectrum of other cancers. There is controversy regarding the risk of colorectal cancer conferred by germline mutations in these two genes.

Methods:

We followed 7015 women with a BRCA mutation for new cases of colorectal cancer. Incidence rates in carriers were compared with population-specific incidence rates, and standardised incidence ratios (SIRs) were estimated. The expected numbers of cancers were computed by multiplying person–years at risk by the appropriate age-, sex- and country-specific incidence rates from the five countries.

Results:

Twenty-one incident colorectal cancer cases were observed among all mutation carriers, compared with 23.6 cases expected. The SIR for BRCA1 carriers was 0.92 (95% confidence interval (CI), 0.54–1.40, P=0.7) and for BRCA2 carriers was 0.82 (95% CI, 0.30–1.81, P=0.7). The SIR for colon cancer was 3.81 (95% CI 1.77–7.23) for women below the age of 50 years (both genes combined) and was 0.60 (95% CI 0.33–1.00) for women aged 50 years and above.

Conclusion:

The risk of colorectal cancer is increased in female carriers of BRCA1 mutations below the age of 50 years but not in women with BRCA2 mutations or in older women.     

Dietary and biomarker estimates of fatty acids and risk of colorectal cancer

The associations between intake of or circulating fatty acids and risk of colorectal cancer (CRC) are unclear. We examined prospectively the associations between dietary or biomarker fatty acids and CRC. For 41,514 men and women, aged 40–69 years, baseline (1990–94) dietary intakes of fatty acids were estimated using a food frequency questionnaire and plasma phospholipid (PPL) fatty acids were measured for 4,205 participants including 395 CRC cases, according to a case‐cohort design. Hazard ratios were computed using Cox regression adjusting for education, alcohol intake, smoking status, physical activity and total energy intake; and stratified for gender, ethnicity and family history of cancer, with age as the time scale. We assessed the heterogeneity of associations with colon and rectal cancers. PPL saturated fatty acids (SFAs) were positively associated with CRC risk, while total n‐3 polyunsaturated fatty acids (PUFA) and long chain marine n‐3 PUFAs showed inverse associations, significant only for 22:5 n‐3. No significant associations were observed for dietary fatty acid intakes but positive associations with CRC of borderline significance were seen for both dietary and PPL linoleic acid. Positive associations with dietary palmitic acid (16:0), MUFAs and n‐6 PUFAs were seen for rectal but not colon cancers. PPL 22:6 n‐3 was inversely associated with rectal cancer. Limiting intakes of SFAs and MUFAs could be assisted by following existing guidelines to limit red and processed meats which are important sources in the Australian diet. Our observations regarding linoleic acid should be examined further.     

Coffee consumption and the risk of colorectal cancer: a prospective cohort study in Japan

An inverse association between coffee consumption and the risk of colorectal cancer has been reported in several case-control studies, but results from prospective cohort studies have been inconclusive. We conducted a prospective cohort study among a Japanese population to clarify the association between coffee consumption and the risk of colorectal cancer incidence. We used data from the Miyagi Cohort Study for this analysis. Usable self-administered questionnaires about coffee consumption were returned from 22,836 men and 24,769 women, aged 40-64 years, with no previous history of cancer. We used the Cox proportional-hazard regression model to estimate hazard ratios and 95% confidence intervals. During 11.6 years of follow-up (425,303 person-years), we identified 457 cases of colorectal cancer. Coffee consumption was not associated with the incidence of colorectal, colon or rectal cancer. The multivariate-adjusted hazard ratio (95% confidence interval) of colorectal cancer incidence for 3 or more cups of coffee per day as compared with no consumption was 0.95 (0.65-1.39) for men and women (p for trend = 0.55), 0.91 (0.56-1.46) for men (p for trend = 0.53) and 1.16 (0.60-2.23) for women (p for trend = 0.996). Coffee consumption was also not associated with incidence of either proximal or distal colon cancer. We conclude that coffee consumption is not associated with the incidence risk of colorectal cancer in the general population in Japan.     

No association between fruit or vegetable consumption and the risk of colorectal cancer in Japan

In a pooled analysis of two prospective studies with 88,658 Japanese men and women, fruit and vegetable consumptions, were not associated with a lower risk of colorectal cancer (705 cases); multivariate relative risk (95% confidence interval) for the highest vs the lowest quartile of intake being 0.92 (0.70-1.19) and 1.00 (0.79-1.27), respectively.     

Dietary glycemic load, glycemic index and colorectal cancer risk: results from the Netherlands Cohort Study

Since hyperinsulinemia is implicated in the development of colorectal cancer, determinants of serum insulin levels, like the glycemic load and the glycemic index of the diet, could influence cancer risk. Our objective was to evaluate whether a diet with a high glycemic load or glycemic index is associated with increased colorectal cancer risk. In the Netherlands Cohort Study, 120,852 subjects completed a food frequency questionnaire in 1986. After 11.3 years of follow-up, 1,225 colon and 418 rectal cancer cases were available for analysis. A case-cohort approach was used to estimate multivariate adjusted rate ratios and 95% confidence intervals for quintiles of energy-adjusted glycemic load and glycemic index. The RR for colorectal cancer comparing the highest versus the lowest quintile levels of glycemic load and glycemic index were 0.83 (95% CI: 0.64-1.08) and 0.81 (95% CI: 0.61-1.08) for men and 1.00 (95% CI: 0.73-1.36) and 1.20 (95% CI: 0.85-1.67) for women. In general, no clear associations with cancer subsites were observed. Glycemic load and glycemic index were borderline significantly associated with an increased risk of proximal colon cancer in women (p-trend = 0.06 and 0.08, respectively), however, these associations were attenuated after exclusion of the first 2 years of follow-up (p-trend = 0.165 and 0.254, respectively). In men, glycemic index was associated with a reduced risk of distal colon cancer (p-trend = 0.03). Overall, our findings do not support the hypothesis that a diet with a high glycemic load or index is associated with a higher risk of colorectal cancer.     

The risk of colorectal cancer is associated with the frequency of meat consumption in a population-based cohort in Korea

Objective: To date, there have been few prospective cohort studies that have investigated the association between meat consumption and the risk of colorectal cancer (CRC) in Asian countries. A large, population-based cohort study was conducted to assess the effect of the frequency of meat consumption on the risk of CRC in Korean adults. Methods: The participants were Korean government employees, school faculty members, and their unemployed dependents, aged 30–80 years, who underwent health examinations between 1996 and 1997. In 2003, information on CRC incidence was obtained during the 6–7 year follow-up period. The final data analysis included 2,248,129 study subjects. The hazard ratio (HR) and 95% confidence interval (CI) of the HR were estimated using the Cox proportional hazards regression model. Results: During the follow-up period, CRC occurred in 4,501 men and 1,943 women (64.19 and 36.34 for age-standardized incidence rates per 100,000 person-years, respectively). In the total population, the estimated HRs and 95% CI for meat consumption of 2–3 times per week and more than 4 times per week compared with consumption of less than once per week were 1.06 (1.01–1.12) and 1.23 (1.13–1.35), respectively. In men only and women only groups, the HRs (95% CI) for consumption of more than 4 times per week compared with consumption of less than once per week were 1.13 (1.02–1.26) and 1.42 (1.21–1.66), respectively. Conclusion: The present findings suggest that frequency of meat consumption is positively associated with the risk of CRC.