Fiber for reducing the risk of colorectal cancer -
Meals for all participants were provided and served in-house at a nutrition coordinating center to promote adherence to the study diet and accurate records of ingestion.
A colonoscopy was performed before and after the dietary switch to look for markers of colorectal cancer risk. After only two weeks of the dietary switch, there was decreased proliferation in the colonic epithelium of Americans given an Africanized, high-fiber diet and increased proliferation in the colonic epithelium of rural Africans fed a Westernized diet.
Figure 1. Proliferation in epithelial crypt cells, as indicated by Ki67 staining, in colonic mucosal biopsies from dietary-switch—study participants. Additionally, markers of inflammation increased in Africans and decreased in Americans after the dietary switch.
The high-fiber dietary switch resulted in increased saccharolytic fermentation and increased production of butyrate and other short-chain fatty acids and suppressed synthesis of secondary bile acids, which are inflammatory, in the colon of African American participants.
The inverse was observed in rural African participants. The study strongly suggested that the level of dietary fiber consumed can convert the colon from a cancer-promoting environment to a cancer-preventing environment in as little as two weeks.
The Alaskan Native diet consists almost exclusively of meat and fat. When the colonic microbiota and microbial metabolites in Alaskan Native individuals vs.
rural African individuals were compared, the profiles were completely different. In Dr. With African urbanization, there has been an increase in obesity, colon cancer, and other Westernized, noncommunicable diseases.
Not surprisingly, the gut microbiota is different between individuals living in urban Africa and in rural Africa. The best solution to this problem is to restore traditional foods, education, and exercise. Enhanced understanding of why this is happening and how to counteract it will have implications for managing similar, long-standing problems in developed countries.
These studies in rural and urban Africans and Alaskan Natives have important implications for all Americans and others living in Westernized societies. High-fiber diets can be used to treat obesity and may provide a novel way to manage type 2 diabetes by promoting intestinal microbiota that produce short-chain fatty acids.
The Pitt-Emory Legume Study will test the ability of high-fiber diets to reduce obesity, diabetes, and colon cancer NCT Participants in this randomized controlled trial will consume either a high-fiber diet with grams of dietary fiber per day from legumes or a healthy American control diet.
The participants will be between 40 and 75 years of age and at high risk for colon cancer due to being overweight or obese and having a history of a colon polyp in the past three years.
The primary endpoints of the study are body weight and proliferation of the colonic epithelium as a biomarker of colon cancer risk. Insulin resistance, biomarkers of systemic inflammation, the microbiome, and gut transit time will also be assessed.
Moreover, this important study will assess the long-term effects of the dietary intervention, with a follow-up in approximately three years, when participants undergo their next scheduled surveillance colonoscopy.
Colon cancer and other Westernized diseases can be attributed to microbiota-diet interactions, and there is increasing evidence that consuming at least 50 grams of fiber per day may prevent these diseases. High-fiber diets have the potential to resolve major public health concerns and allow Americans to live longer and have a better quality of life as they age.
Siegel RL, Miller KD, Goding Sauer A, et al. Colorectal cancer statistics, CA Cancer J Clin. Aune D, Keum N, Giovannucci E, et al. Whole grain consumption and risk of cardiovascular disease, cancer, and all cause and cause specific mortality: systematic review and dose-response meta-analysis of prospective studies.
Donohoe DR, Garge N, Zhang X, et al. The microbiome and butyrate regulate energy metabolism and autophagy in the mammalian colon. Cell Metab. Lancet Gastroenterol Hepatol. Fat, fibre and cancer risk in African Americans and rural Africans.
Nat Commun. Ocvirk S, Wilson AS, Posma JM, et al. A prospective cohort analysis of gut microbial co-metabolism in Alaska Native and rural African people at high and low risk of colorectal cancer. Am J Clin Nutr. Katsidzira L, Ocvirk S, Wilson A, et al. Differences in fecal gut microbiota, short-chain fatty acids and bile acids link colorectal cancer risk to dietary changes associated with urbanization among Zimbabweans.
Nutr Cancer. An inverse association among individuals with low fruit and vegetable consumption, if established, would be of considerable interest, since the implementation of targeted preventive measures within such populations would be feasible and cost-effective. Results from a meta-analysis of 13 case—control studies 19 have suggested that increased dietary fiber intake is associated with decreased risk of colorectal cancer, although prospective cohort studies 12 , 15 , 20 — 24 do not support such an association.
Nonetheless, evidence from animal studies and some clinical trials continues to suggest that cereals 9 , 16 , 25 — 29 , especially wheat bran, contain substances, such as fiber, phytic acid, various phenolic compounds, lignins, and flavonoids, that might lower the risk for colorectal cancers 9.
Cereal fiber might also bind carcinogens and modify glycemic index 9. The consumption of foods with a high glycemic index has been hypothesized to lead to colorectal cancer through the tumor-promoting effect of elevated levels of insulin, glucose, or triglycerides Nevertheless, two large prospective cohort studies 20 , 21 or two recent clinical trials of recurrent colorectal adenomas 31 , 32 found no association between colorectal cancer risk and cereal fiber consumption.
However, these findings have been criticized on the following grounds: Negative results from the large prospective study of U. nurses 20 have led some researchers to speculate that cereal fiber intake in this cohort was too low to observe an association; in contrast, in the clinical trials, the short-term study of recurrent adenomas 33 may have little relevance to the evolution of adenomas to colorectal cancer.
We prospectively analyzed data from a population-based cohort of 61 Swedish women with a relatively low consumption of fruit and vegetables and a high intake of cereal fiber, especially wheat fiber In addition to conducting traditional analyses of exposure quartiles, we also examined the risk of colorectal cancer among individuals who consumed the highest and the lowest amounts of fruit, vegetables, and cereal fiber.
From through , a population-based mammography screening program was introduced in two counties in central Sweden. Hence, completed questionnaires, which included items about age, weight kg , height cm , educational level, and diet, were obtained from 66 We excluded an additional women because their answers on the dietary portion of the questionnaire suggested that they had extreme energy intakes 3 standard deviations below or above the mean value for natural logarithm-transformed calories, with the use of cut points of and kcal or had carelessly completed the dietary questionnaire.
Thus, the study cohort comprised 61 women at the start of follow-up. Diet was assessed with the use of a self-administered food-frequency questionnaire FFQ that included 67 food items commonly eaten in Sweden.
For each food item, these frequencies were converted to frequency per day. In the FFQ, we asked how often such vegetables as cabbage, tomatoes, lettuce, spinach, potatoes, and carrots and beets were consumed. We did not obtain information on the consumption of cucumbers and onions, which made up only 5.
Specific fruit items included in the FFQ were citrus fruit, fruit juice, bananas, apples, and pears. We did not obtain information on the consumption of peaches, plums, grapes, and berries, each of which constituted a small percentage of the total fruit consumed but, when combined, constituted The average 4.
In terms of weight, the average serving sizes for fruit and vegetables were 95— g for fruit, 55 g for carrots and beets, 70 g for cabbage, 55 g for tomatoes, 30 g for spinach and lettuce, g for potatoes, and g for juice. We did not have information on supplement use in our data.
Nutrient calculations were based on the mean values of age-specific portion sizes 40—52, 53—65, and 66—74 years of scaled-weighed foods that were recorded for a total of days by women who were randomly selected from the study population.
Nutrient composition values obtained from Swedish National Food Administration data 37 were used for these calculations. The intake of dietary fiber and other nutrients was computed by multiplying the frequency of consumption of each unit of food by the nutrient content of the specified portions.
The main food sources for cereal fiber were whole-grain bread, crisp bread, oats, muesli as well as other breakfast cereal, pasta, and rice. Values for the fiber content of foods were derived from published measurements that were made with the use of a combination of enzymatic and gravimetric procedures The validity of nutrient estimates based on the self-reported food-consumption frequencies was evaluated for of the women who weighed and recorded what they consumed during four 7-day periods at 3- to 4-month intervals.
The validity estimates for fruit and vegetable intake were measured as a Pearson correlation coefficient r between the food questionnaire and food records r for individual items varied from. We identified incident cases of colon and rectal cancers that occurred in our study cohort through December 31, , by matching with two types of independent sources: 1 the computerized regional cancer registries that recorded all diagnoses of colon and rectal cancers in the two counties and 2 a list of all pathology reports from the two pathology departments covering the study area.
We identified colorectal cancers in total. Dates of deaths in the cohort were ascertained through the Swedish Death Registry.
The date that a study subject moved out of the study area was obtained by matching the cohort to the computerized and continuously updated Swedish Population Registry. This study was approved by the Ethics Committee at Uppsala University Hospital, Västerås, Sweden, and by the Regional Ethics Committee of the Karolinska Institute, Stockholm, Sweden.
Energy adjustment of nutrients was performed with the use of the residuals methodology recommended by Willett and Stampfer In the first step of the method, each nutrient is regressed on total energy both variables in continuous form.
Follow-up was censored at the date of death, the date of migration out of the study area, or at the end of the follow-up period December 31, For fruit and vegetable consumption, all multivariate risk-factor models were adjusted for age in 5-year age groups , consumption of red meat and dairy products in quartiles , and total energy as a continuous variable.
For dietary fiber consumption, all multivariate risk-factor models were adjusted for age in 5-year age groups , body mass index, educational level three categories , intake of energy as a continuous variable , and quartiles of alcohol, red meat, total fat, folic acid, vitamin D, vitamin C, and calcium.
For the trend tests, median values for each exposure category of a categorized variable were placed together in the model Variables were also analyzed in continuous form when the results from our categorized analyses were compatible with the assumption that the effects are linear.
During an average 9. The average age at diagnosis was 67 years for colon cancer patients and 68 years for rectal cancer patients. Median intakes of total fruit and vegetables varied widely in the cohort, ranging from 2. No appreciable difference was observed in median age, body mass index, or consumption of meat and alcohol among women in the various quartiles of fruit and vegetable consumption.
Consumption of fruit and vegetables was inversely associated with risk of colorectal cancer Table 2. Total consumption of fruit and vegetables combined was inversely associated with colon cancer and rectal cancer, but the association was stronger for the consumption of fruit, especially in relation to rectal cancer.
For colon cancer and, consequently, for total colorectal cancer, the reduction in risk appeared to be fairly small in all quartiles relative to the lowest quartile Table 2. We further explored the association between fruit and vegetable consumption and colorectal cancer risk among individuals in the lowest quartile by using the remainder of the cohort i.
With the use of a continuous variable to describe fruit and vegetable consumption, the RR for an increase of one serving per day in this restricted analysis was 0. We further examined fruit and vegetable consumption after categorization of the entire cohort into deciles.
Our results did not change when we examined fruit and vegetable consumption and adjusted either for age alone or for age and body mass index quartiles , educational level less than high school, high school, and university , and quartiles of total fat, dietary fiber, or alcohol.
The relationships between fruit and vegetable consumption and colon and rectal cancer risk were similar across different strata of alcohol consumption and body mass index. The median intake of cereal fiber ±standard deviation was 9. The median intake in the highest quartile was There was a greater than twofold difference in average cereal fiber intake between study subjects in the lowest versus the highest intake quartiles.
Cereal fiber intake was not associated with colorectal cancer risk Table 5. In age-adjusted and multivariate models, no trend in risk was observed over quartiles of energy-adjusted or unadjusted fiber intake.
Even higher levels of cereal fiber consumption showed no associations with colorectal cancer risk RR for the highest [median, When specific cancer sites were analyzed separately, no association was observed for either colon cancer total, proximal, or distal or rectal cancer.
Cereal fiber consumption was not related to the risk of colorectal cancer among the subgroups of our study population defined by categories of age, body mass index, and intakes of total fat, energy, alcohol, calcium, or folic acid.
In additional analyses, we observed no association between colorectal cancer and the consumption of foods high in whole grains or the total intake of sugar.
In contrast to our negative findings for cereal fiber consumption, we found that consumption of fiber from fruit showed an inverse association with colorectal cancer risk in a model adjusted only for age Table 6.
However, this association disappeared with multivariate adjustment. Neither intake of total dietary fiber nor intake of fiber from vegetables was associated with risk.
Early stages of cancer before diagnosis could make an affected individual less inclined to consume certain foods that might aggravate unpleasant symptoms.
To eliminate the possibility that undiagnosed preclinical colorectal cancer could influence our results, we reanalyzed the data after excluding cases of colorectal cancer that occurred within the first 3 years of follow-up.
Exclusion of such cases did not alter the results for fruit and vegetable consumption or for fiber consumed from any source. In this cohort of Swedish women, total fruit and vegetable consumption was inversely associated with colorectal cancer risk.
This association was driven mainly by fruit consumption and was strongest for the risk of rectal cancer. In contrast, risk reduction for colon cancer appeared to be relatively small in all quartiles of fruit and vegetable consumption except the lowest.
Thus, for total colorectal cancer risk, the inverse association was stronger and the dose—response effect was more evident among individuals who consumed very low amounts of fruit and vegetables. Four previous cohort studies have examined total fruit and vegetable consumption as an independent risk factor for colon and rectal cancers combined 11 , 14 or for colon cancer alone 15 , In a combined analysis of data from the Nurses' Health Study and the Health Professionals' Follow-up Study 11 , no association was observed between the risk for these cancers and consumption of fruit or vegetables.
Indeed, among health professionals who consumed one serving of fruit and vegetables or less per day, there was a suggestion that the women had an increased cancer risk compared with the men, probably because the majority of men took multivitamins.
Nonsupplement users in this cohort showed no clear association between cancer risk and fruit and vegetable consumption, even among individuals with low consumption.
However, the total number of individuals with cancer in that subanalysis was reduced to women and men, which may have limited its statistical power.
Other cofactors in the population may also modify the effect of fruit and vegetable consumption, such as the folic acid supplementation of breakfast cereals in the United States, which does not occur in Sweden.
The Iowa Women's Health Study 15 also reported no association between diet with the exception of garlic consumption and colon cancer risk.
Similar patterns of risk were observed in the Leisure World Study of an elderly cohort in California 17 and in The Netherlands Cohort Study on Diet and Cancer 14 : Women who consumed more fruit and vegetables than defined by the lowest consumption categories i.
In both cohorts, however, further reduction in risk with increasing fruit and vegetable consumption above the lowest category was minimal. Three other prospective cohort studies 12 , 13 , 16 have also examined whether the consumption of fruit and vegetables is associated with colorectal cancer risk, although none directly examined combined fruit and vegetable consumption.
An inverse association was observed among those in the American Cancer Society cohort who consumed large amounts of vegetables, citrus fruit, and high-fiber grains In the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort of male smokers in Finland 12 , neither fruit nor vegetable consumption showed any association with colorectal cancer risk.
As with most previous studies, however, associations in the lower range of consumption of these categories of vegetables were not examined closely.
In light of our findings, it is interesting to note that results of clinical trials of antioxidant supplements conducted in well-nourished populations have not shown reductions in the risk of any cancer 42 — 44 , whereas reductions in overall cancer rates were observed in a trial conducted in a nutritionally deficient population The former trials 42 — 44 did not, however, stratify their findings on baseline nutritional status.
Such an analysis might have shown an inverse association between antioxidants and cancer risk among individuals with low baseline nutritional status.
Dietary fiber intake was not associated with the risk of total colorectal cancer or cancer at any specific site in our cohort.
This lack of an association was most notable for cereal fiber consumption, which is considerably higher in our Swedish cohort than it is in the U.
cohorts Cereal fiber is thought to lower the risk of colorectal cancer, either by altering the site of resistant starch fermentation from the proximal to the distal colon 25 or by changing the absorption and metabolism of carcinogens in food We found that the median intake of cereal fiber in the highest quartile was Even when the Nurses' Health Study reassessed the diets of its participants with a more comprehensive FFQ 46 , the median cereal fiber intake in their highest consumption quintile 8.
It is important to note that our cohort differs from the nurses and male health professionals with respect to the composition of the fiber from cereal, fruit, and vegetables consumed. The total amount of fiber consumed by our cohort and the nurses and male health professionals was, however, similar in terms of total grams of fiber consumed per day because of the higher intake of fiber from fruit and vegetables by the nurses and health professionals.
We observed no decrease in colorectal cancer risk, even among subjects in the highest decile of cereal fiber consumption, in which the median intake was This amount exceeds the In addition, our average follow-up time of 9.
In total, these results suggest that high consumption of cereal fiber does not affect colorectal cancer risk. Although we observed an inverse association between colorectal cancer risk and fruit fiber consumption in age-adjusted models, that association disappeared after multivariate adjustment of the data for a wide range of other dietary factors.
Although the most recent analysis of dietary fiber in the Nurses' Health Study cohort 20 also showed no statistically significant association of colorectal cancer risk and intake of fiber from fruit or vegetables, a report on the health professionals cohort 47 did show an inverse association between intake of fruit fiber and risk of adenomas.
Our nutrient composition database did not allow us to directly assess the risk of colorectal cancer associated with intake of soluble or insoluble fiber. However, because fiber from fruit and vegetables is largely soluble and cereal fiber is largely insoluble, fiber from these different food sources can be used as crude measures of these two fiber types.
Nonetheless, we found no evidence that associations with fiber intake from any source varied as a function of age, body mass index, or various dietary factors. The strengths of our study include the large sample size and population-based character of our cohort, the diagnosis of colorectal cancer at specific subsites, the completeness of follow-up in the Swedish Cancer Registry system, and the availability of a large number of patients with colorectal cancers.
These features allowed us to examine associations within subgroups of our population with reasonable statistical power. In addition, the prospective assessment of diet in our study eliminates the potential for differential recall bias, which is of particular concern because preconceptions about the healthy effects of fruit, vegetables, and whole grains are common among the public.
It is also unlikely that undiagnosed early stages of colon or rectal cancer have altered the diets of our participants, because we observed the same associations when we restricted our analyses to individuals whose cancers occurred after the first 3 years of follow-up. Our study has four potential limitations.
First, we could not adjust our RR estimates for the potentially confounding effect of physical activity because that information was not collected at baseline.
However, we found that energy intake, which is a rough indicator of physical activity 48 , was not associated with colorectal cancer risk in our cohort and that our results did not change when we adjusted for the effects of energy intake or body mass index.
Because it has been suggested that physical activity is positively correlated with dietary fiber intake 20 , confounding from physical activity is predicted to drive risk estimates toward an inverse association, which we did not observe.
Adjustment for physical activity also did not alter cancer risk estimates associated with fruit and vegetable consumption in the Nurses' Health Study and Health Professionals' Follow-up Study data 11 or in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort Second, we did not reassess dietary information during the follow-up period.
Instead, we assumed that the relative ranking of subjects with respect to consumption of fruit, vegetables, and dietary fiber was maintained during the follow-up period. The validity of this assumption is supported by Goldbohm et al.
Third, we did not adjust our estimates for measurement error. However, the methods for this adjustment may not be appropriate for our study because the two instruments that were used to self-report diet, the 7-day diet records and the FFQ, are likely to generate similar reporting errors It is, therefore, doubtful that adjustment for measurement error would improve the validity of our estimates.
Fourth, our item FFQ may not allow an accurate estimation of energy intake. Therefore, the adjustments that we made for total caloric intake may not fully account for between-person variation in energy intake or physical activity; as a result, some residual effects due to these factors i.
Although we have no reason to suspect that such confounding would bias our findings only in the lower range of fruit and vegetable consumption, this possibility cannot be ruled out, especially since estimates of energy intake and fruit and vegetable consumption may be associated with measurement error that is not very well understood.
For example, misclassification of energy intake and physical activity can differ in different categories of self-reported fruit and vegetable consumption, producing bias toward or away from an estimate of no effect in the lower, middle, or upper ranges of fruit and vegetable consumption.
Greater misclassification among individuals in the middle and upper ranges of fruit and vegetable consumption compared with those in the lower range of consumption could, to some degree, account for the stronger inverse associations that we observed among individuals in the lower range. However, because nondifferential misclassification can attenuate any association that might exist toward no effect 41 , we cannot rule out the possibility that the inverse association between fruit and vegetable consumption and risk of colorectal cancers that we observed among individuals with low fruit and vegetable consumption would be even stronger in the absence of such measurement error.
However, it is also likely that the frequency of fruit and vegetables consumption that is adequate to decrease cancer risk, taking into account other health consequences, probably varies with individual factors and, perhaps, with other cofactors in the population, such as multivitamin use and whether foods are fortified with folic acid and other micronutrients.
Nevertheless, our data suggest that even moderate increases in fruit and vegetable consumption among persons with very low intake may confer benefits to this group.
Our data do not support the hypothesis that high consumption of cereal fiber decreases the risk of colon or rectal cancer, even though we examined a much broader range of cereal fiber intake than had been examined in previous cohort studies. The vast temporal and geographic differences in occurrence of colorectal cancer, however, suggest that some other environmental factors are indeed important.
Baseline characteristics of the study cohort according to total fruit and vegetable consumption. Baseline characteristics of the study cohort according to total dietary fiber intake.
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Some research suggests that dietary Pediatric orthodontic care may protect colorecyal colorectal cancer. However, more fot Fiber for reducing the risk of colorectal cancer needed to better understand the Oral care products between canced High-quality ingredients reducng colorectal cancer. Colorectal cancer refers to cancer that Fier in the colon or rectum. While the exact causes of colorectal cancer are unknown, some studies suggest that dietary habits may play a role. This article reviews the role that fiber may play in protecting against colorectal cancer, offers ways to get enough fiber, and discusses other tips for cancer prevention. Although we typically avoid language like this, specificity is key when reporting on research participants and clinical findings. Over the past few decades, several studies have analyzed the relationship between fiber intake and colorectal cancer risk.Video
What You Can Do to Reduce Risk of Colon Cancer Forgot Fiber for reducing the risk of colorectal cancer colorectak Enter Calorie intake control email address you used to create your account to initiate High-quality ingredients password reset. Coloorectal research was conducted by Stephen J. Westernized diseases, including colorectal cancer, diabetes, and cardiovascular disease, are a major threat to health care in the United States. The diet consumed by people living in high-income countries is a common underlying factor of these vastly different pathologies. The Westernized diet is low in fiber and high in meats, polyunsaturated fats, and simple carbohydrates.Fiber for reducing the risk of colorectal cancer -
Dietary fibre passes relatively unchanged into the large intestine, where it is fermented by bacteria—boosting gut health and reducing cancer risk.
As well as fruits, vegetables, nuts and seeds, other great sources of fibre include wholemeal or wholegrain breads or wraps, couscous, quinoa, brown rice, wholemeal pasta, high-fibre cereals, muesli and oats. Dietary fibre helps reduce colorectal cancer risk in four ways :. Keep up to date with the latest news and breakthroughs.
Skip to content. Are you getting enough dietary fibre? Every day, men should be aiming for 30g of dietary fibre and women should be aiming for 25g. Dietary fibre helps reduce colorectal cancer risk in four ways : It binds carcinogens to the stool and expels them from the body. Good bacteria in the colon convert fibre into short-chain fatty acids.
Results During 6 to 20 years of follow-up across studies, colorectal cancer cases were identified. Fiber intake from cereals, fruits, and vegetables was not associated with risk of colorectal cancer. The pooled multivariate RRs comparing the highest vs lowest study- and sex-specific quintile of dietary fiber intake were 1.
Conclusions In this large pooled analysis, dietary fiber intake was inversely associated with risk of colorectal cancer in age-adjusted analyses.
However, after accounting for other dietary risk factors, high dietary fiber intake was not associated with a reduced risk of colorectal cancer. Dietary fiber has been hypothesized to reduce the risk of colorectal cancer.
Potential mechanisms for a protective effect include dilution of fecal carcinogens and procarcinogens, reduction of transit time of feces through the bowel, production of short chain fatty acids, which promote anticarcinogenic action, and binding of carcinogenic bile acids.
Ecological correlation studies and many case-control studies have found an inverse association between dietary fiber intake and risk of colorectal cancer.
Because of these discordant results, the debate continues on whether dietary fiber consumption decreases colorectal cancer risk.
In this study, we evaluated the association between dietary fiber intake and risk of colorectal cancer by reanalyzing the primary data from 13 prospective cohort studies.
The Pooling Project of Prospective Studies of Diet and Cancer Pooling Project was established to summarize the association between dietary factors and risk of cancers, and the details of the Pooling Project have been described previously.
Studies including men and women 6 , 18 , 19 were separated into sex-specific cohorts. Each study provided baseline intake data of foods and nutrients that were assessed by a study-specific food frequency questionnaire. Pearson correlation coefficients between dietary fiber intake from the food frequency questionnaire and the reference method in the validation studies were higher than 0.
Incident colorectal cancer cases were identified by each cohort through self-administered questionnaires with subsequent medical record review, 3 , 22 , 25 linkage with a cancer registry, 4 , 17 - 21 or both. In addition to applying the exclusionary criteria used by each study, we also excluded individuals from the analyses who had a history of cancer other than nonmelanoma skin cancer at baseline and who reported implausible energy intakes beyond 3 SDs from the study-specific log e -transformed mean energy intake.
Data analyses comprised study- and sex-specific analyses and subsequent pooled analyses of the study-specific results.
Person-years of follow-up time were calculated from the date of the baseline questionnaire until the date of colorectal cancer diagnosis, death, or end of follow-up, whichever came first. The RRs of colorectal cancer were estimated according to study-specific quintiles, as well as to categories defined by absolute intake cut points that were identical across studies.
We performed study- and sex-specific age-adjusted and multivariate analyses. The test for trend across categories of intake was performed by assigning participants the median value of their category and entering those values as a continuous term in a regression model. Between-studies heterogeneity was tested by the Q statistic.
In addition, we evaluated whether dietary fiber intake was log-linearly associated with risk of colorectal cancer by comparing the nonparametric regression curve obtained using restricted cubic splines with the linear model using the likelihood ratio test and by visual inspection of the restricted cubic spline graphs.
The effect of misclassification of dietary fiber intake was evaluated by the method developed by Zucker and Spiegelman. During follow-up times of 6 to 20 years in 13 cohort studies, 7 person-years were accumulated and incident colorectal cancer cases were identified men and women; colon cancer and rectal cancer cases plus site unspecified.
The major source of dietary fiber varied across studies with cereals as a major contributor to dietary fiber intake in the European studies, and fruits and vegetables as the main sources in the North American studies Table 1.
This association was attenuated slightly but still remained statistically significant after adjusting for nondietary risk factors, multivitamin use, and total energy intake multivariate model I.
Additional adjustment for dietary folate intake further weakened the association multivariate model II. There was no statistically significant heterogeneity between studies for the highest quintile indicating that the differences in the study-specific results were compatible with random variation Figure 1.
The association between dietary fiber intake and risk of colorectal cancer was not significantly modified by sex or age at diagnosis; compared with the lowest quintile the pooled multivariate RR for the highest quintile was 0.
We also found no statistically significant differences in the association between dietary fiber intake and colorectal cancer risk by body mass index calculated as weight in kilograms divided by the square of height in meters , smoking, alcohol consumption, and red meat intake data not shown.
In addition, the results were similar in European and North American studies: the pooled multivariate RR in the highest quintile vs the lowest was 0. To examine whether the association between dietary fiber intake and risk of colorectal cancer was modified by length of follow-up, we performed separate analyses for cases diagnosed within the first 5 years of follow-up and for cases diagnosed at least 5 years after their baseline assessment.
In categorical analyses using identical absolute intake cut points across studies, the pooled age-adjusted RR was 0. For this comparison, the strongest confounder was smoking status. Dietary fiber from vegetables was not associated with risk of colorectal cancer in both the age-adjusted and multivariate models.
Comparing the highest vs the lowest quintile for fiber intake from cereals, the pooled multivariate RR was 0. For fiber intake from fruits and from vegetables, no significant differences by tumor site were observed data not shown.
Intakes of whole grain and refined grain food were each not statistically associated with risk of colorectal cancer: the pooled multivariate RR in the highest quintile vs the lowest were 0. In the analyses of grain foods, if dietary folate intake was not included as a covariate, the results did not change.
In this pooled analysis of 13 prospective cohort studies, we observed a statistically significant inverse association between dietary fiber intake and risk of colorectal cancer in the age-adjusted model.
However, the overall association was attenuated and no longer statistically significant after adjusting for other colorectal cancer risk factors. When intakes of dietary fiber were examined separately by specific food sources, none were associated with risk of colorectal cancer.
However, there was a suggestion that intake of dietary fiber from cereals and intake of dietary fiber from whole grain foods were both associated with a weak reduction in risk of rectal cancer. The association between dietary fiber intake and risk of colorectal cancer has been inconsistent among observational studies and several factors may explain the disparity: potential biases in each study, the failure to adjust for covariates in the multivariate models, and the range of dietary fiber intake.
Inconsistent results also have been reported from randomized clinical trials of dietary fiber supplementation on the recurrence of colorectal adenomas precursors of colorectal cancer ; most trials have found no reduced risk of adenoma recurrence with dietary fiber supplementation compared with placebo, 9 - 12 but one trial found a significantly increased risk of adenoma recurrence in the psyllium supplementation group.
A statistically significant reduction in risk of colorectal cancer with higher dietary fiber intake has been observed in most case-control studies. In addition, publication bias may contribute to the accumulation of literature with significant findings.
On the other hand, the Pooling Project is less susceptible to these biases because diet was assessed prior to diagnosis and the studies were not required to have published on the association between dietary fiber intake and risk of colorectal cancer.
The etiology of colorectal cancer has been studied extensively during the past few decades leading to the identification of many risk factors for colorectal cancer. Because earlier case-control studies did not adjust for recently identified colorectal cancer risk factors, reported associations with dietary fiber may have been confounded by factors for which no adjustment was made in the multivariate models.
The different results observed among recent studies also may be explained, in part, by the selection of the covariates that were included in the multivariate models. In our study, intake of folate was positively correlated with intake of dietary fiber, while intakes of red meat and total milk were inversely correlated with intake of dietary fiber, but the strength of correlations varied across studies.
Intake of alcohol was positively correlated with intake of dietary fiber in some studies, but showed an inverse correlation in other studies. Because the degree of confounding by other risk factors of colorectal cancer may vary depending on characteristics of a study population, thorough examination for selection of covariates to be included in a multivariate model is needed.
The range of dietary fiber intake reported within a study may be another factor that has contributed to different findings among studies.
If the range of intake of a nutrient in a study is very narrow, a null association may be more likely observed. However, lack of variation in dietary fiber intake is unlikely to have accounted for the null association we found.
This range is similar to the range observed in EPIC, which reported a statistically significant inverse association with dietary fiber intake.
Because the Pooling Project is a retrospectively planned pooled analysis of the primary data, the food frequency questionnaires that were used to assess diet varied across studies.
To take into account potential misclassification in dietary fiber intake that may arise from measurement error in energy intake, we calculated energy-adjusted intakes for each study. We also conducted analyses by categorizing dietary fiber intake using study-specific quintiles and identical absolute intake cut points across studies.
In the study-specific quintile analyses, true differences in population intakes were not taken into account, potentially resulting in misclassification of dietary fiber intake in the pooled results.
However, misclassification could also have occurred in the analyses based on identical absolute intake cut points because dietary fiber intakes may vary across studies due to differences in the accuracy in which the food frequency questionnaires estimated dietary fiber.
Despite the different potential for misclassification between these 2 analytic approaches, both showed no association between dietary fiber intake and risk of colorectal cancer above the lowest category of dietary intake. Several limitations of our analysis should be considered.
Fiber intake is likely to be measured with error because of errors in how study participants estimate their consumption of fiber-containing foods and by errors in the food composition databases.
A true association between dietary fiber intake and risk of colorectal cancer may be underestimated in our study. In addition, although we were able to correct for misclassification of dietary fiber intake at baseline, the single assessment of dietary fiber intake in our analysis may not reflect long-term usual intake as accurately as using repeated measurements of dietary intake during follow-up.
A strength of the Pooling Project is that the individual data from each cohort were reanalyzed using a standard approach, which provided more flexibility in examining dose-response relationships, confounding, and effect modification than meta-analyses of the published literature, which frequently summarize risk estimates obtained for heterogeneous exposure categories with different adjustment for potential confounders.
Also, we had high statistical power with over colorectal cancer cases, thus a substantial effect of fiber is unlikely to have been missed. In addition, in a subset of the studies we were able to correct for measurement error in dietary fiber intake using their validation study data.
In conclusion, we did not find support for a linear inverse association between dietary fiber intake and risk of colorectal cancer in a pooled analysis of 13 prospective cohort studies. Although high dietary fiber intake may not have a major effect on the risk of colorectal cancer, a diet high in dietary fiber from whole plant foods can be advised because this has been related to lower risks of other chronic conditions such as heart disease and diabetes.
Corresponding Author: Stephanie A. Smith-Warner, PhD, Department of Nutrition, Harvard School of Public Health, Huntington Ave, Boston, MA pooling hsphsun2. Author Contributions: Dr Smith-Warner had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design : Park, Spiegelman, van den Brandt, Giovannucci, Goldbohm, Graham, Krogh, Pietinen, Rohan, Willett, Smith-Warner. Acquisition of data : Berrino, van den Brandt, Buring, Colditz, Fuchs, Giovannucci, Goldbohm, Graham, Harnack, Hartman, Kato, Krogh, McCullough, Miller, Pietinen, Rohan, Schatzkin, Willett, Wolk, Zeleniuch-Jacquotte, Zhang, Smith-Warner.
Analysis and interpretation of data : Park, Hunter, Spiegelman, Bergkvist, Freudenheim, Fuchs, Giovannucci, Goldbohm, Graham, Harnack, Hartman, Jacobs, Kato, Leitzmann, Willett, Wolk, Zhang, Smith-Warner.
Critical revision of the manuscript for important intellectual content : Park, Hunter, Spiegelman, Bergkvist, Berrino, van den Brandt, Buring, Colditz, Freudenbheim, Fuchs, Giovannucci, Goldbohm, Graham, Harnack, Hartman, Jacobs, Kato, Krogh, Leitzmann, McCullough, Miller, Pietinen, Rohan, Schatzkin, Willett, Wolk, Zeleniuch-Jacquotte, Zhang, Smith-Warner.
Statistical analysis : Park, Spiegelman, Fuchs, Graham, Harnack, Willett, Smith-Warner. Obtained funding : Spiegelman, Bergkvist, Berrino, van den Brandt, Fuchs, Giovannucci, Graham, Pietinen, Schatzkin, Willett, Wolk, Smith-Warner.
Administrative, technical, or material support : Hunter, Colditz, Graham, Kato, McCullough, Pietinen, Willett, Wolk, Zhang. Role of the Sponsor: The sponsors were not involved in the study design, data analysis, interpretation of results, or writing of the report.
Acknowledgment: We thank Ruifeng Li, MS, Christine Rivera, MS, and Shiaw-Shyuan Yaun, MS, Harvard School of Public Health, for their assistance with data management and statistical analyses. full text icon Full Text. Download PDF Top of Article Abstract Methods Results Comment Article Information References.
Figure 1. Study-Specific and Pooled Multivariate Relative Risks RRs of Colorectal Cancer Comparing the Highest vs the Lowest Quintile of Dietary Fiber Intake View Large Download.
Figure 2. Nonparametric Regression Curve for the Association Between Dietary Fiber Intake and Risk of Colorectal Cancer View Large Download. Table 1. Description of Studies in the Analyses of Dietary Fiber and Colorectal Cancer in the Pooling Project View Large Download.
Table 2. Pooled Relative Risks of Colorectal Cancer for Quintiles of Dietary Fiber Intake View Large Download. Table 3. Pooled Relative Risks of Colorectal Cancer for Categories of Dietary Fiber Intake View Large Download. Table 4. Pooled Relative Risks of Colorectal Cancer by Sources of Dietary Fiber Intake View Large Download.
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Paul Terry, Edward Giovannucci, Karin B. Reduucing Several recent High-quality ingredients thr cohort studies have fo to demonstrate the Protein wraps protective Pediatric orthodontic care of fruit, vegetable, and dietary fiber consumption on colorectal cancer risk. To further explore this issue, we have examined these associations in a population that consumes relatively low amounts of fruit and vegetables and high amounts of cereals. Methods: We examined data obtained from a food-frequency questionnaire used in a population-based prospective mammography screening study of women in central Sweden. Women with colorectal cancer diagnosed through December 31,were identified by linkage to regional cancer registries.
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