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      Lack of Effect of a Low-Fat, High-Fiber Diet on the Recurrence of Colorectal Adenomas

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          Abstract

          We tested the hypothesis that dietary intervention can inhibit the development of recurrent colorectal adenomas, which are precursors of most large-bowel cancers. We randomly assigned 2079 men and women who were 35 years of age or older and who had had one or more histologically confirmed colorectal adenomas removed within six months before randomization to one of two groups: an intervention group given intensive counseling and assigned to follow a diet that was low in fat (20 percent of total calories) and high in fiber (18 g of dietary fiber per 1000 kcal) and fruits and vegetables (3.5 servings per 1000 kcal), and a control group given a standard brochure on healthy eating and assigned to follow their usual diet. Subjects entered the study after undergoing complete colonoscopy and removal of adenomatous polyps; they remained in the study for approximately four years, undergoing colonoscopy one and four years after randomization. A total of 1905 of the randomized subjects (91.6 percent) completed the study. Of the 958 subjects in the intervention group and the 947 in the control group who completed the study, 39.7 percent and 39.5 percent, respectively, had at least one recurrent adenoma; the unadjusted risk ratio was 1.00 (95 percent confidence interval, 0.90 to 1.12). Among subjects with recurrent adenomas, the mean (+/-SE) number of such lesions was 1.85+/-0.08 in the intervention group and 1.84+/-0.07 in the control group. The rate of recurrence of large adenomas (with a maximal diameter of at least 1 cm) and advanced adenomas (defined as lesions that had a maximal diameter of at least 1 cm or at least 25 percent villous elements or evidence of high-grade dysplasia, including carcinoma) did not differ significantly between the two groups. Adopting a diet that is low in fat and high in fiber, fruits, and vegetables does not influence the risk of recurrence of colorectal adenomas.

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          Most cited references18

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          Whole-grain consumption and risk of coronary heart disease: results from the Nurses' Health Study.

          Although current dietary guidelines for Americans recommend increased intake of grain products to prevent coronary heart disease (CHD), epidemiologic data relating whole-grain intake to the risk of CHD are sparse. Our objective was to evaluate whether high whole-grain intake reduces risk of CHD in women. In 1984, 75521 women aged 38-63 y with no previous history of cardiovascular disease or diabetes completed a detailed, semiquantitative food-frequency questionnaire (SFFQ) and were followed for 10 y, completing SFFQs in 1986 and 1990. We used pooled logistic regression with 2-y intervals to model the incidence of CHD in relation to the cumulative average diet from all 3 cycles of SFFQs. During 729472 person-years of follow-up, we documented 761 cases of CHD (208 of fatal CHD and 553 of nonfatal myocardial infarction). After adjustment for age and smoking, increased whole-grain intake was associated with decreased risk of CHD. For increasing quintiles of intake, the corresponding relative risks (RRs) were 1.0 (reference), 0.86, 0.82, 0.72, and 0.67 (95% CI comparing 2 extreme quintiles: 0.54, 0.84; P for trend < 0.001). After additional adjustment for body mass index, postmenopausal hormone use, alcohol intake, multivitamin use, vitamin E supplement use, aspirin use, physical activity, and types of fat intake, these RRs were 1.0, 0.92, 0.93, 0.83, and 0.75 (95% CI: 0.59, 0.95; P for trend = 0.01). The inverse relation between whole-grain intake and CHD risk was even stronger in the subgroup of never smokers (RR = 0. 49 for extreme quintiles; 95% CI: 0.30, 0.79; P for trend = 0.003). The lower risk associated with higher whole-grain intake was not fully explained by its contribution to intakes of dietary fiber, folate, vitamin B-6, and vitamin E. Increased intake of whole grains may protect against CHD.
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            Colorectal cancer: molecules and populations.

            J D Potter (1999)
            The epidemiology and molecular biology of colorectal cancer are reviewed with a view to understanding their interrelationship. Risk factors for colorectal neoplasia include a positive family history, meat consumption, smoking, and alcohol consumption. Important inverse associations exist with vegetables, nonsteroidal anti-inflammatory drugs (NSAIDs), hormone replacement therapy, and physical activity. There are several molecular pathways to colorectal cancer, especially the APC (adenomatous polyposis coli)-beta-catenin-Tcf (T-cell factor; a transcriptional activator) pathway and the pathway involving abnormalities of DNA mismatch repair. These are important, both in inherited syndromes (familial adenomatous polyposis [FAP] and hereditary nonpolyposis colorectal cancer [HNPCC], respectively) and in sporadic cancers. Other less well defined pathways exist. Expression of key genes in any of these pathways may be lost by inherited or acquired mutation or by hypermethylation. The roles of several of the environmental exposures in the molecular pathways either are established (e.g., inhibition of cyclooxygenase-2 by NSAIDs) or are suggested (e.g., meat and tobacco smoke as sources of specific blood-borne carcinogens; vegetables as a source of folate, antioxidants, and inducers of detoxifying enzymes). The roles of other factors (e.g., physical activity) remain obscure even when the epidemiology is quite consistent. There is also evidence that some metabolic pathways, e.g., those involving folate and heterocyclic amines, may be modified by polymorphisms in relevant genes, e.g., MTHFR (methylenetetrahydrofolate reductase) and NAT1 (N-acetyltransferase 1) and NAT2. There is at least some evidence that the general host metabolic state can provide a milieu that enhances or reduces the likelihood of cancer progression. Understanding the roles of environmental exposures and host susceptibilities in molecular pathways has implications for screening, treatment, surveillance, and prevention.
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              Dietary fiber and the risk of colorectal cancer and adenoma in women.

              A high intake of dietary fiber has been thought to reduce the risk of colorectal cancer and adenoma. We conducted a prospective study of 88,757 women, who were 34 to 59 years old and had no history of cancer, inflammatory bowel disease, or familial polyposis, who completed a dietary questionnaire in 1980. During a 16-year follow-up period, 787 cases of colorectal cancer were documented. In addition, 1012 patients with adenomas of the distal colon and rectum were found among 27,530 participants who underwent endoscopy during the follow-up period. After adjustment for age, established risk factors, and total energy intake, we found no association between the intake of dietary fiber and the risk of colorectal cancer; the relative risk for the highest as compared with the lowest quintile group with respect to fiber intake was 0.95 (95 percent confidence interval, 0.73 to 1.25). No protective effect of dietary fiber was observed when we omitted, adjustment for total energy intake, when events during the first six years of follow-up were excluded, or when we excluded women who altered their fiber intake during the follow-up period. No significant association between fiber intake and the risk of colorectal adenoma was found. Our data do not support the existence of an important protective effect of dietary fiber against colorectal cancer or adenoma.
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                Author and article information

                Journal
                New England Journal of Medicine
                N Engl J Med
                Massachusetts Medical Society
                0028-4793
                1533-4406
                April 20 2000
                April 20 2000
                : 342
                : 16
                : 1149-1155
                Article
                10.1056/NEJM200004203421601
                10770979
                e7385d13-074a-4d9b-9d8d-43d3c2c9dba2
                © 2000
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