Fruit and vegetable intakes and risk of colorectal cancer and incident and recurrent adenomas in the PLCO cancer screening trial

The roles of fruits and vegetables in colorectal cancer development are unclear. Few prospective studies have assessed the association with adenoma, a known precursor to colorectal cancer. Our aim was to evaluate the association between fruit and vegetable intake and colorectal cancer development by evaluating the risk of incident and recurrent colorectal adenoma and colorectal cancer. Study participants were identified from the intervention arm of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Fruit and vegetable intake was measured using a self‐reported dietary questionnaire. Total fruit and vegetable intake was not associated with reduced incident or recurrent adenoma risk overall, but a protective association was observed for multiple adenomas (Odds ratio _{3rd tertile vs. 1st tertile} = 0.61, 95% confidence interval (CI): 0.38, 1.00). Higher fruit and vegetable intakes were associated with a borderline reduced risk of colorectal cancer (Hazard ratio (HR) _{3rd tertile vs. 1st tertile} = 0.82, 95% CI: 0.67, 1.01), which reached significance amongst individuals with high processed meat intakes (HR = 0.74, 95% CI: 0.55, 0.99). Our results suggest that increased fruit and vegetable intake may protect against multiple adenoma development and may reduce the detrimental effects of high processed meat intakes on colorectal cancer risk.     

Adiponectin and colorectal adenomas: Self Defense Forces Health Study

Adiponectin is an adipocyte-derived protein with an insulin-sensitizing action. Circulating levels of adiponectin are inversely correlated with obesity, especially abdominal obesity. Some studies have suggested that low levels of circulating adiponectin might be related to increased risk of colorectal cancer and adenomas. The present study examined the relationship between total and high-molecular-weight (HMW) adiponectin to colorectal adenomas in the Self Defense Forces (SDF) Health Study. The study subjects comprised 656 cases of colorectal adenomas and 648 controls with normal colonoscopy among men receiving a preretirement health examination at two Self Defense Forces hospitals. Total and HMW adiponectin were slightly lower in adenoma cases than in controls; geometric means of total adiponectin were 5.42 µg/mL in cases and 5.63 µg/mL in controls ( P =  0.13), and the corresponding values of HMW adiponectin were 2.47 µg/mL and 2.57 µg/mL, respectively ( P =  0.29). Regardless of adjustment for body mass index and other lifestyle factors, total adiponectin was unrelated to the risk of colorectal adenomas. Total adiponectin levels were inversely related to the risk of large adenomas (≥ 5 mm), but not of small adenomas, with a nearly statistically significant decreasing trend ( P =  0.06). However, the inverse association was largely ascribed to body mass index and other lifestyle factors. HMW adiponectin showed no clear association with either overall or size-specific risk of colorectal adenomas. The study provided suggestive evidence for a protective association between adiponectin and large adenomas, but did not indicate a protective association independent of adiposity. ( Cancer Sci 2008; 99: 781–786)     

C-reactive protein and colorectal adenomas: Self Defense Forces Health Study

Chronic inflammation has been implicated in colorectal carcinogenesis. Several studies have investigated the relationship between C-reactive protein (CRP), a biomarker of inflammation, and colorectal cancer and adenomas, resulting in inconsistent findings. The present study examined the relationship between circulating levels of high-sensitivity CRP and colorectal adenomas. The study subjects comprised 646 cases of colorectal adenoma and 635 controls of normal total colonoscopy among men receiving a preretirement health examination at two hospitals of the Self Defense Forces. Statistical adjustment was made for cigarette smoking, alcohol use, body mass index, physical activity, and other potential confounders. The multivariate-adjusted geometric means showed no measurable differences between adenoma cases and controls, but were higher among cases with larger adenomas (trend P  = 0.03). Likewise, although the prevalence odds of colorectal adenomas did not differ according to CRP levels as categorized at the 30th, 60th, and 90th percentiles in the controls, higher levels of CRP were associated with a statistically significant increase in the prevalence odds of large adenomas (≥5 mm), but not of small adenomas (<5 mm). The multivariate-adjusted odds ratios of large adenomas for the lowest to highest categories of CRP were 1.00 (referent), 1.81 (95% confidence interval 1.17–2.80), 1.61 (95% confidence interval 1.03–2.52), and 2.21 (95% confidence interval 1.28–3.84), respectively (trend P  = 0.01). A positive association between CRP and prevalence odds of large adenomas was not modified by either smoking or overweight. These findings suggest that inflammation is linked to the growth of colorectal adenomas. ( Cancer Sci 2009; 100: 709–711)     

Tea consumption, apoptosis, and colorectal adenomas.

Induction of apoptosis has been suggested as a mechanism for the anti-carcinogenic effect of tea constituents in animals and in vitro studies. We addressed this hypothesis in a human study. Study participants were consecutive patients who underwent colonoscopy at the UNC Hospitals (August 1998 to March 2000). Biopsies were taken from normal rectal mucosa. Apoptosis was scored by the terminal deoxyribonucleotide transferase-mediated digoxigenin dUTP nick end labeling (TUNEL) method and by standard morphological criteria. The analysis included 171 patients with adenomas (cases) and 323 adenoma-free controls. After adjusting for sex, age, race, and BMI, apoptotic score was inversely associated with adenoma: the odds ratios (ORs) for linear trend associated with tertiles were 0.3 (0.3-0.5) for morphologic score and 0.5 (0.4-0.6) for the TUNEL score, respectively. Tea consumption (2-3 and >3 versus <2 servings/day) showed a weak negative association with adenoma: the ORs were 0.7 (0.3-1.4) and 0.5 (0.2-1.1), respectively. Neither measurement of apoptotic score changed by the level of tea consumption (P value for Kruskal-Wallis test > or =0.5). We did not find statistical interaction between apoptotic score and tea consumption. Tea exposure is not associated with apoptosis in normal rectal tissue in vivo.     

Epoxide hydrolase polymorphisms, cigarette smoking and risk of colorectal adenoma in the Nurses' Health Study and the Health Professionals Follow-up Study

Microsomal epoxide hydrolase (mEH) is involved in the bioactivation and detoxification of polycyclic aromatic hydrocarbons derived from tobacco smoke and charred meat intake. Two coding region mEH variants located in exon 3 (Tyr113His) and exon 4 (His139Arg) have been described and may affect the enzyme's specific activity. We investigated these polymorphisms and tested interactions with smoking and charred meat intake in relation to risk of colorectal adenoma in two case-control studies nested in the Nurses' Health Study (NHS) and Health Professionals Follow-up Study (HPFS) cohorts. mEH exon 3 and exon 4 polymorphisms were not associated with overall risk of adenoma among 556 incident cases and 557 controls from the NHS or 376 prevalent cases and 725 controls from the HPFS. A statistically significant interaction was found between the exon 4 polymorphism and smoking for men (P = 0.03) and a borderline significant interaction was found between the exon 3 polymorphism and smoking for women (P = 0.06). Women having the exon 3 'rapid' Tyr/Tyr genotype were at increased risk when exposed to either > or =25 pack-years smoking [relative risk (RR) = 2.43, 95% confidence interval (CI) 1.47-4.01] or <25 pack-years of smoking (RR = 1.73, 95% CI 1.10-2.73) relative to non-smokers. Men with the exon 4 'slow' His/His genotype were at increased risk when exposed to > or =25 pack-years smoking (RR = 2.21, 95% CI 1.43, 3.41) or <25 pack-years smoking (RR = 1.71, 95% CI 1.13-2.59) relative to non-smokers. Charred meat intake was not associated with adenoma risk and there was no significant interaction with either mEH polymorphism. Our results indicate that individuals exposed to > or =25 pack-years smoking were at increased risk for colorectal adenoma and that risk is related to dose of tobacco carcinogens and mEH activity level, but the results were not consistent between men and women.     

Fruit and vegetable consumption in the prevention of oesophageal and cardia cancers.

The incidence of adenocarcinoma of the oesophagus has increased rapidly in recent decades. In order to appreciate the potential for prevention by means of dietary modification, we estimated the aetiological fractions and the increments in absolute risk attributable to low intake of fruit and vegetables for adenocarcinoma and squamous cell carcinoma of the oesophagus and for adenocarcinoma of the gastroesophageal junction. We conducted a nationwide population-based case-control study in Sweden, with participation of 608 cases and 815 controls. We used unconditional logistic regression to estimate relative risks, from which we calculated aetiological fractions. Individuals in the highest exposure quartile (median 4.8 servings/day) versus the lowest (median 1.5 servings/day) showed approximately 50% lower risk of oesophageal adenocarcinoma and 40% lower risk of oesophageal squamous cell carcinoma, but no risk reduction for gastric cardia adenocarcinoma. Approximately 20% of oesophageal adenocarcinoma, and likewise squamous cell carcinoma, in Sweden was attributed to consuming less than three servings of fruit and vegetables per day. A very large number of individuals (over 25,000) would need to increase their fruit and vegetable consumption moderately in order to prevent one oesophageal cancer per year. Moderate relative risk reductions translate into weak absolute risk reductions for oesophageal cancers in Sweden.     

Large-scale evaluation of genetic variants in candidate genes for colorectal cancer risk in the Nurses' Health Study and the Health Professionals' Follow-up Study

Advances in genomics offer new strategies for assessing the association of common genetic variations at multiple loci and risk of many diseases, including colorectal cancer. Low-penetrance alleles of genes in many biological pathways, such as DNA repair, metabolism, inflammation, cell cycle, apoptosis, and Wnt signaling, may influence the risk of nonfamilial colorectal cancer. To identify susceptibility genes for colorectal cancer, we designed a large-scale case-control association study nested within the Nurses' Health Study (190 cases and 190 controls) and the Health Professionals' Follow-up Study (168 cases and 168 controls). We used a custom GoldenGate (Illumina) oligonucleotide pool assay including 1,536 single nucleotide polymorphisms (SNP) selected in candidate genes from cancer-related pathways, which have been sequenced and genotyped in the SNP500Cancer project; 1,412 of the 1,536 (92%) of the SNPs were genotyped successfully within 388 genes. SNPs in high linkage disequilibrium (r(2) >/= 0.90) with another assayed SNP were excluded from further analyses. As expected by chance (and not significant compared with a corrected Bonferroni P = 0.00004), in the additive model, 11 of 1,253 (0.9%) SNPs had a P(trend) < 0.01 and 38 of 1,253 (3.0%) SNPs had a P(trend) >/= 0.01 and P(trend) < 0.05. Of note, the MGMT Lys(178)Arg (rs2308237) SNP, in linkage disequilibrium with the previously reported MGMT Ile(143)Val SNP, had an inverse association with colorectal cancer risk (MGMT Lys(178)Arg: odds ratio, 0.52; 95% confidence interval, 0.35-0.78; unadjusted P(trend) = 0.0003 for the additive model; gene-based test global P = 0.00003). The SNP500Cancer database and the Illumina GoldenGate Assay allowed us to test a larger number of SNPs than previously possible. We identified several SNPs worthy of investigation in larger studies.     

Twenty-four non-synonymous polymorphisms in the one-carbon metabolic pathway and risk of colorectal adenoma in the Nurses' Health Study

Dietary folate and alcohol consumption as well as polymorphic variants in one-carbon metabolism genes may modulate risk of colorectal adenoma through aberrant DNA methylation and altered nucleotide synthesis and repair. We assessed the association of 24 non-synonymous single nucleotide polymorphisms (nsSNPs) in 13 genes in the one-carbon metabolism pathway and risk of colorectal adenoma in 556 incident cases and 557 controls nested in the Nurses' Health Study. Most of the SNPs were not associated with risk of colorectal adenoma. We did, however, observe a modest increased risk among carriers of the transcobalamin (TCN) II 259 Pro/Arg + Arg/Arg variant (odds ratio 1.48, 95% confidence interval 1.09-2.02) for colorectal adenoma. The TCN II Pro259Arg polymorphism may affect TCN binding and transport of vitamin B(12) and thus warrants further investigation of its biological function. In addition, the methionine synthase reductase (MTRR) Arg415Cys and MTRR Ser284Thr variant carriers, also in the vitamin B(12) pathway, have suggestive associations with advanced colorectal adenoma (defined as being larger than 1 cm, villous, tubular-villous or carcinoma in situ histology). We observed significant evidence for departure from multiplicative interaction for the betaine-homocysteine methyltransferase (BHMT) Arg239Gln with dietary methyl status (based on intake of dietary folate, methionine and alcohol intake) in relation to colorectal adenoma; no such interaction was observed for the other 23 SNPs. Further investigation is required to validate the association of the polymorphisms in the one-carbon metabolic genes and risk of colorectal adenoma.     

Mediators of fruit and vegetable consumption among colorectal cancer survivors

Introduction  

Due to early detection and treatment, survival from colorectal cancer (CRC) diagnosis has been steadily increasing. A CRC diagnosis could be considered a “teachable moment,” a time when interventionists might successfully promote dietary changes. CRC interventions with tailored print communication (TPC) and telephone motivational interviewing (TMI) have been shown to be effective in promoting fruit and vegetable consumption (FVC) among CRC survivors. However, little is known about how these interventions work to exert their effect. This study investigated whether information processes mediate the relationship between a CRC intervention and FVC among CRC survivors.     

Periodontal disease,tooth loss and colorectal cancer risk: Results from the Nurses' Health Study

Periodontal diseases including tooth loss might increase systemic inflammation, lead to immune dysregulation and alter gut microbiota, thereby possibly influencing colorectal carcinogenesis. Few epidemiological studies have examined the association between periodontal diseases and colorectal cancer (CRC) risk. We collected information on the periodontal disease (defined as history of periodontal bone loss) and number of natural teeth in the Nurses' Health Study. A total of 77,443 women were followed since 1992. We used Cox proportional hazard models to calculate multivariable hazard ratios (HRs) and 95% confidence intervals (95% CIs) after adjustment for smoking and other known risk factors for CRC. We documented 1,165 incident CRC through 2010. Compared to women with 25–32 teeth, the multivariable HR (95% CI) for CRC for women with <17 teeth was 1.20 (1.04–1.39). With regard to tumor site, the HRs (95% CIs) for the same comparison were 1.23 (1.01–1.51) for proximal colon cancer, 1.03 (0.76–1.38) for distal colon cancer and 1.48 (1.07–2.05) for rectal cancer. In addition, compared to those without periodontal disease, HRs for CRC were 0.91 (95% CI 0.74–1.12) for periodontal disease, and 1.22 (95% CI 0.91–1.63) when limited to moderate to severe periodontal disease. The results were not modified by smoking status, body mass index or alcohol consumption. Women with fewer teeth, possibly moderate or severe periodontal disease, might be at a modest increased risk of developing CRC, suggesting a potential role of oral health in colorectal carcinogenesis.     

Fruit and vegetable consumption is inversely associated with having pancreatic cancer

Objective

Studies on fruit, vegetable, fiber, and grain consumption and pancreatic cancer risk are inconclusive. We used a clinic-based case?Ccontrol study specifically designed to address limitations of both cohort and case?Ccontrol studies to examine the relationship.

Methods

Participants were excluded who reported changing their diet within 5 years prior to study entry. And 384 rapidly ascertained cases and 983 controls (frequency matched on age (±5 years), race, sex, and residence) completed epidemiologic surveys and 144-item food frequency questionnaires. Odds ratios (OR) and 95% confidence intervals were calculated using logistic regression adjusted for age, sex, smoking, body mass index, energy intake, and alcohol consumption.

Results

Comparing highest to lowest quintiles, we observed significant inverse associations (OR < 0.8) with significant trends (p _trend < 0.05) for citrus, melon, and berries, other fruits, dark green vegetables, deep yellow vegetables, tomato, other vegetables, dry bean and pea, insoluble fiber, soluble fiber, whole grains, and orange/grapefruit juice, and an increased association with non-whole grains. Results were similar after adjusting for diabetes or total sugar intake.

Conclusions

We provide evidence that lower consumption of fruits, vegetables, whole grains, and fiber is associated with having pancreatic cancer. This may have a role in developing prevention strategies.     

Fruit and vegetable consumption in relation to ovarian cancer incidence: the Swedish Mammography Cohort

We prospectively examined the incidence of epithelial ovarian cancer and its subtypes in relation to baseline fruit and vegetable consumption in the Swedish Mammography Cohort, a population-based cohort study of 61 084 women aged 38-76 years in 1987-1990. During an average follow-up of 13.5 years, 266 incident cases of invasive epithelial ovarian cancer were diagnosed. After adjustment for potential confounders, we observed a statistically significant inverse association between consumption of vegetables and ovarian cancer risk (P-value for trend=0.01); the multivariate rate ratio (RR) for the comparison of three or more servings of vegetables per day with one or fewer servings per day was 0.61 (95% confidence interval (CI), 0.38-0.97). For fruit consumption a modest, not statistically significant, positive association was found (P-value for trend=0.07); the multivariate RR for the highest compared with the lowest category of consumption being 1.37 (95% CI, 0.90-2.06). The associations with fruit and vegetable consumption did not vary by subtype of ovarian cancer. These findings suggest that high consumption of vegetables, but not of fruits, may reduce the risk of ovarian cancer.     

Alcohol consumption, alcohol dehydrogenase 3 polymorphism, and colorectal adenomas.

Alcohol is a probable risk factor with regard to colorectal neoplasm and is metabolized to the carcinogen acetaldehyde by the genetically polymorphic alcohol dehydrogenase 3 (ADH3) enzyme. We evaluated whether the association between alcohol and colorectal adenomas is modified by ADH3 polymorphism. We recruited 433 cases with adenomatous polyps and 436 polyp-free controls among Caucasians undergoing endoscopy between 1995 and 2000. Frequency and amount of habitual alcohol consumption were assessed by beverage type, using a validated self-administered food frequency questionnaire. All participants provided blood for genotyping of ADH3. Multivariate analyses adjusting for gender, age, and indication for endoscopy showed that alcohol increased the risk of colorectal adenomas among women [odds ratio (OR), 1.8; 95% confidence interval (CI), 1.0-3.2, >/=10 versus <1 drink/week]. Among men, the risk of adenomas was increased only for those consuming > 21 drinks/week (OR, 1.8; 95% CI, 0.9-3.8, compared with men drinking < 1 drink/week). Among subjects in the highest tertile of alcohol consumption, those with the ADH3*1/*1 genotype were at higher risk (OR, 1.8; 95% CI, 1.0-3.1) than those with other ADH3 genotypes (OR, 1.2; 95% CI, 0.7-1.9) when compared with those in the lowest tertile with ADH3*1/*2 or ADH3*2/*2 genotypes. In conclusion, our findings are consistent with results of other studies, suggesting that alcohol consumption elevates the risk of adenomatous colorectal polyps. ADH3 polymorphism may modify the association between alcohol consumption and colorectal adenomas.     

Epoxide hydrolase and CYP2C9 polymorphisms, cigarette smoking, and risk of colorectal carcinoma in the Nurses' Health Study and the Physicians' Health Study

Microsomal epoxide hydrolase (mEH) and cytochrome P450 2C9 (CYP2C9) are involved in the bioactivation and detoxification of polycyclic aromatic hydrocarbons (PAHs) derived from tobacco smoke. Two coding-region mEH variants (Tyr113His, His139Arg) and CYP2C9 variants (Arg144Cys, Ile359Leu) have been described and affect enzyme specific activity. We investigated these polymorphisms and tested interactions with smoking in relationship to risk of colorectal carcinoma in two case-control studies nested in the Nurses' Health Study (NHS) and Physicians' Health Study (PHS) cohorts. mEH Tyr113His and His139Arg polymorphisms were not associated with the risk of cancer among 197 incident cases and 490 controls from the NHS. Among 273 incident cases and 453 controls from the PHS, carrying one or two copies of the 'rapid' 139Arg allele was associated with a significantly reduced risk of colorectal cancer (OR=0.70, 95% CI 0.49--0.99) when compared with His139 wild-type individuals. Risk of colorectal cancer was significantly reduced among men carrying the CYP2C9 *1/*2 genotype (OR=0.62, 95% CI 0.42--0.92) or at least one CYP2C9 variant allele (OR=0.72, 95% CI 0.52--1.00) when compared with *1/*1 wild-type individuals. For women, carrying at least one variant CYP2C9 allele was inversely associated with the risk of colorectal cancer (OR=0.85, 95% CI, 0.57--1.27) when compared with *1/*1 wild-type individuals. No statistically significant genotype-smoking or gene-gene interactions were found in this study. Our results indicate that individuals exposed to tobacco carcinogens were at increased risk of colorectal cancer and that overall risk is related to mEH and CYP2C9 genotype, although the results were not consistent between men and women.     

Vitamin B2 intake and colorectal cancer risk; results from the Nurses' Health Study and the Health Professionals Follow‐Up Study cohort

Vitamin B2 serves as a cofactor to enhance one‐carbon metabolism, maintain mucous membranes, and has been implicated in lowering colorectal cancer (CRC) risk. However, few prospective studies have examined the association between vitamin B2 intake and CRC. In this study, we estimated the associations between vitamin B2 intake and CRC risk using the Nurses' Health Study (NHS) and the Health Professionals Follow‐Up Study (HPFS) cohorts. Vitamin B2 intake was measured by a validated food frequency questionnaire every 4 years. Among 100,033 women in the NHS and 44,007 men in the HPFS we documented a total of 3,037 incident CRC cases (2,093 women and 944 men) during 24–26 years of follow‐up until 2010. Intakes of total (from food and supplements), dietary (from food only), and supplemental vitamin B2 were inversely related to CRC risk in age‐adjusted analysis in NHS. However, the association was attenuated and no longer statistically significant in multivariate analysis (p‐trend ≥0.08). The pooled multivariate relative risks (95% confidence interval) comparing individuals in the extreme quintiles of intakes were 0.93 (0.81–1.06) for total vitamin B2, 0.89 (0.61–1.28) for dietary vitamin B2 and 0.94 (0.81–1.08) for supplemental vitamin B2. These associations of total vitamin B2 intake were similar for risk of CRC with varying lag‐time periods (0–4, 4–8, 8–12 or 12–16 years), for risk of CRC subtypes by tumor location, and across strata of intake of folate or alcohol. Our prospective data do not support a beneficial role of vitamin B2 intake in lowering incidence of CRC.     

Fruit and vegetable consumption and squamous cell carcinoma of the esophagus in Japan: the JPHC study

Epidemiological studies have consistently demonstrated a decrease in the risk of esophageal squamous cell carcinoma (SCC) associated with higher fruit and vegetable intake, although the association has been examined predominantly in case-control studies. Here, we conducted a population-based prospective cohort study among middle-aged Japanese men. Lifestyle characteristics were investigated using a self-administered questionnaire, which included a validated food frequency questionnaire with 138 food and beverage items. We followed a total of 38,790 men aged 45-74 years. A Cox proportional hazards model was used to estimate the hazard ratios (HRs) and 95% confidence intervals (95% CIs) for esophageal SCC, with adjustment for potential confounders. During 297,651 person-years of follow-up, a total of 116 men were newly diagnosed with esophageal SCC. An increase in consumption of total fruit and vegetables by 100 grams per day (g/day) was associated with an 11% decrease in the incidence of esophageal SCC (95% CI: 1-21%). In particular, a higher intake of cruciferous vegetables was associated with a significant decrease in risk (HR per 100 g/day: 0.44; 95% CI: 0.23-0.82). Stratified analyses revealed that the beneficial effect of fruits and vegetables was not able to completely offset the harmful effect of tobacco and alcohol. Our findings provide further evidence for the protective role of fruits and vegetables in the development of esophageal SCC. To effectively reduce the burden of this disease, however, priority should be placed on smoking and drinking cessation. Finally, cruciferous vegetables deserve further investigation as foods possibly effective in the prevention of esophageal SCC.     

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.     

Fruit and vegetable consumption and risk of bladder cancer: a prospective cohort study

Fruit and vegetable consumption has been inconsistently associated with risk of bladder cancer. We used data from a prospective population-based cohort study of 82,002 Swedish women and men to examine the association between fruit and vegetable consumption and bladder cancer incidence. Diet was assessed with a validated food frequency questionnaire. During a mean follow-up of 9.4 years, 485 incident cases of bladder cancer were identified in the Swedish cancer registries. We found no statistically significant association between intakes of total fruits and vegetables, total fruits, or total vegetables and bladder cancer risk after adjustment for age, sex, education, and cigarette smoking. The multivariate rate ratios (95% confidence intervals) comparing the highest with the lowest quartile of intake were 0.80 (0.60-1.05) for total fruits and vegetables, 0.93 (0.69-1.25) for fruits, and 0.89 (0.67-1.19) for vegetables. Likewise, no associations were observed for citrus fruits, cruciferous vegetables, or green leafy vegetables. The associations did not differ by sex or smoking status. In conclusion, findings from this prospective study suggest that fruit and vegetable intakes are not likely to be appreciably associated with the risk of bladder cancer.     

Fruit and vegetable consumption and incidence of gastric cancer: a prospective study.

BACKGROUND: Whether fruit and vegetable consumption may confer protection from gastric cancer remains controversial. METHODS: We prospectively investigated the association between consumption of fruits and vegetables and the incidence of gastric cancer among participants from two population-based cohort studies: 36,664 women in the Swedish Mammography Cohort and 45,338 men in the Cohort of Swedish Men. Participants completed a food-frequency questionnaire in 1997 and were followed up for cancer incidence through June 2005. Cox proportional hazards models were used to estimate multivariate hazard ratios (HR) and 95% confidence intervals (95% CI). RESULTS: During a mean follow-up of 7.2 years, we ascertained 139 incident cases of gastric cancer. Vegetable consumption was inversely associated with risk of gastric cancer, whereas no significant association was observed for fruit consumption. After controlling for age and other risk factors, women and men who consumed > or =2.5 servings/d of vegetables had a HR of 0.56 (95% CI, 0.34-0.93) for developing gastric cancer compared with those who consumed <1 serving/d. The respective HR for fruit consumption was 0.86 (95% CI, 0.52-1.43). Among specific subgroups of vegetables, consumption of green leafy vegetables and root vegetables was inversely associated with risk of gastric cancer; the multivariate HRs comparing > or =3 servings/wk with <0.5 serving/wk were 0.64 (95% CI, 0.42-0.99) for green leafy vegetables and 0.43 (95% CI, 0.27-0.69) for root vegetables. CONCLUSIONS: Frequent consumption of vegetables may reduce the risk of gastric cancer.