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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some evidence suggests that diets high in animal fat or red meat may increase the risk of colon cancer, whereas high intake of fiber or vegetables may be protective. Frequently, intake of red meat has been a stronger risk factor than total fat. Because data from prospective cohort studies are sparse, we examined fat, meat, fiber, and vegetable intake in relation to risk of colon cancer in a cohort of 47,949 U.S. male health professionals who were free of diagnosed cancer in 1986. At baseline, these men, 40 to 75 years of age, completed a validated food frequency questionnaire and provided detailed information on other lifestyle and health-related factors. Between 1986 and 1992, 205 new cases of colon cancer were diagnosed in these men. Intakes of total fat, saturated fat, and animal fat were not related to risk of colon cancer. However, an elevated risk of colon cancer was associated with red meat intake (relative risk, 1.71; 95% confidence interval, 1.15-2.55 between high and low quintiles; P = 0.005 for trend). Men who ate beef, pork, or lamb as a main dish five or more times per week had a relative risk of 3.57 (95% confidence interval, 1.58-8.06; P = 0.01 for trend) compared to men eating these foods less than once per month. The association with red meat was not confounded appreciably by other dietary factors, physical activity, body mass, alcohol intake, cigarette smoking, or aspirin use. Other sources of animal fat, including dairy products, poultry, and fish as well as vegetable fat, were slightly inversely related to risk of colon cancer. No clear association existed between fiber or vegetable intake and risk of colon cancer. These data support the hypothesis that intake of red meat is related to an elevated risk of colon cancer.
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PMID:Intake of fat, meat, and fiber in relation to risk of colon cancer in men. 816 86

Using occupational data for over 2000 colon cancer cases diagnosed between 1980 and 1984 in Shanghai, and employment information from the 1982 census for the Shanghai population, standardized incidence ratios (SIR) were computed for occupational groups classified by job types and physical activity levels. Men employed in occupations with low physical activity levels had modest but significantly elevated risks of colon cancer. SIR for jobs with low activity based on sitting time was 121 (95% confidence interval, Cl: 108-135) and based on energy expenditure was 126 (95% Cl: 115-138). Corresponding SIR for women were 99 (95% Cl: 83-118) and 113 (95% Cl: 100-127). The data were also used to screen for specific occupations with elevated SIR to generate leads to occupational colon cancer. Increased incidence was observed for professional and other white collar workers, and male chemical processors and female textile workers. The findings add to the emerging evidence that workplace activity may influence the risk of this common cancer.
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PMID:Physical activity and occupational risk of colon cancer in Shanghai, China. 844 43

Folate derivatives are important in experimental colorectal carcinogenesis; low folate intake, particularly with substantial alcohol intake, is associated with increased risk. The enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR) catalyzes the conversion of 5,10-methylenetetrahydrofolate, required for purine and thymidine syntheses, to 5-methyltetrahydrofolate, the primary circulatory form of folate necessary for methionine synthesis. A common mutation (677C-->T) in MTHFR reduces enzyme activity, leading to lower levels of 5-methyltetrahydrofolate. To evaluate the role of folate metabolism in human carcinogenesis, we examined the associations of MTHFR mutation, plasma folate levels, and their interaction with risk of colon cancer. We also examined the interaction between genotype and alcohol intake. We used a nested case-control design within the Physicians' Health Study. Participants were ages 40-84 at baseline when alcohol intake was ascertained and blood samples were drawn. During 12 years of follow-up, we identified 202 colorectal cancer cases and matched them to 326 cancer-free controls by age and smoking status. We genotyped for the MTHFR polymorphism and measured plasma folate levels. Men with the homozygous mutation (15% in controls) had half the risk of colorectal cancer [odds ratio (OR), 0.49; 95% confidence interval (CI), 0.27-0.87] compared with the homozygous normal or heterozygous genotypes. Overall, we observed a marginal significant increased risk of colorectal cancer (OR, 1.78; 95% CI, 0.93-3.42) among those whose plasma folate levels indicated deficiency (<3 ng/ml) compared with men with adequate folate levels. Among men with adequate folate levels, we observed a 3-fold decrease in risk (OR, 0.32; 95% CI, 0.15-0.68) among men with the homozygous mutation compared with those with the homozygous normal or heterozygous genotypes. However, the protection due to the mutation was absent in men with folate deficiency. In men with the homozygous normal genotype who drank little or no alcohol as reference, those with the homozygous mutation who drank little or no alcohol had an 8-fold decrease in risk (OR, 0.12; 95% CI, 0.03-0.57), and for moderate drinkers, a 2-fold decrease in risk (OR, 0.42; 95% CI, 0.15-1.20); no decrease in risk was seen in those drinking 1 or more drinks/day. Our findings provide support for an important role of folate metabolism in colon carcinogenesis. In particular, these results suggest that the 677C-->IT mutation in MTHFR reduces colon cancer risk, perhaps by increasing 5,10-methylenetetrahydrofolate levels for DNA synthesis, but that low folate intake or high alcohol consumption may negate some of the protective effect.
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PMID:Methylenetetrahydrofolate reductase polymorphism, dietary interactions, and risk of colorectal cancer. 906 78

Previous studies indicate that physical activity is related inversely to colon cancer risk. However, details regarding that association--whether a dose-response relation exists, whether the relation differs between non-obese and obese persons, the effect of long-term physical activity--are unclear. We examined these issues in the Physicians' Health Study (United States). Physical activity was assessed at baseline among 21,807 men, aged 40 to 84 years, and again 36 months later. Men were followed for an average of 10.9 years (from baseline) during which 217 developed colon cancer. After adjusting for potential confounders (including age, obesity, and alcohol intake), the relative risks for colon cancer associated with vigorous exercise in times per week (< 1, 1, 2-4, 5+, at baseline) were 1.0 (referent); 1.1 (95% confidence interval [CI] = 0.7-1.7); 1.2 (CI = 0.8-1.6); and 1.1 (CI = 0.7-1.6), respectively; P trend = 0.6. Physical activity was not associated significantly with colon cancer risk either among non-obese or obese men. When we used physical activity assessments at baseline as well as at 36 months, physical activity again was unrelated to colon cancer risk. These data do not support the hypothesis that physical activity reduces the risk of colon cancer. Plausible alternate explanations for the null finding include misclassification of physical activity and the potential for increased surveillance for colon cancer ('screening effect') among those physically active.
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PMID:Physical activity and risk of colon cancer: the Physicians' Health Study (United States). 924 72

CHD is the number one killer of men and women. Men and women need to be educated about the warning symptoms of CHD and MI to assist in earlier diagnosis and treatment. Women need to be taught about the variety of factors that may affect their risk for CHD. All women should be counseled about the importance of primary and secondary prevention, as those with low probability of disease may some day have some form of cardiovascular illness, and those with high probability of disease may prevent or lessen the effects from an infarction. The Women's Health Initiative (WHI) is a study that may answer many of the unresolved questions about women and MI. The WHI was established by the National Institutes of Health (NIH) in 1993 to address negligence of women's health by the major federal research agencies. It is the largest study ever funded by NIH. Forty centers throughout the United States will follow 163,000 women for a 10-year-period to determine how to prevent heart disease, breast and colon cancer, and osteoporosis in postmenopausal women. The age range of women is from 50 to 79 years old. This study will have a major impact upon care of women for these varied conditions. While waiting for the answers to questions about treatment and prevention, we must use what information is available to us now. Women report for care later than men and often do not receive the same therapies and treatments, thus we need to become advocates for the female patient. We need to also assess the social support and caregiver availability that women have at home. If the situation is inadequate then community resources need to be accessed. In addition, follow-up care is essential. Because many women have complications of CHF and shock with their infarcts, we need to assure adequate follow-up. Transportation for the follow-up may also need to be provided or arranged since women's caregivers may be unable to drive their spouses to the doctor's office. Also, single, older women may be unable to use public transportation with ease. We can address the needs of the female population with CHD if we make a thorough assessment and individualize their plan of care. In today's world of health care, meeting an individual's needs is an ongoing challenge because the length of stay is shortened and resources are tighter. Creativity is often needed to adequately meet the assessed needs. In the future, MI may not be the number one killer of women. Preventing the onset of the disease or decreasing the risk of a reinfarction by empowering women may have an impact. It is hoped that the information given in this article could help the health care worker educate and empower women about this disease.
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PMID:Myocardial infarction. The number one killer of women. 944 72

A family history of prostate cancer has been associated with prostate cancer risk in most prior studies, and more limited data suggest that a family history of breast cancer may also be important; however, there are no data from a population-based cohort study of prostate cancer incidence that adjusts for major confounders. We conducted follow-up through 1995 on 1557 men, ages 40-86 years, who were randomly selected (81% response rate) as cancer-free controls for a population-based case-control study conducted in Iowa from 1987-1989. Family history of cancer in parents and siblings was obtained using a mailed questionnaire. Incident cancers and deaths were ascertained through linkages to state and national databases; 101 incident cases of prostate cancer were identified. At baseline, 4.6% of the cohort reported a family history of prostate cancer in a brother or father, and this was positively associated with prostate cancer risk after adjustment for age [relative risk (RR) = 3.2; 95% confidence interval (CI), 1.8-5.7] or after multivariate adjustment for age, alcohol, and dietary factors (RR = 3.7; 95% CI, 1.9-7.2). Risk was greater if a brother had prostate cancer (RR = 4.5; 95% CI, 2.1-9.7) than if a father had prostate cancer (RR = 2.3; 95% CI, 1.0-5.3). Also at baseline, 9.6% of the cohort had a family history of breast and/or ovarian cancer in a mother or sister, and this was positively associated with prostate cancer risk (age-adjusted RR = 1.7; 95% CI, 1.0-3.0; multivariate RR = 1.7; 95% CI, 0.9-3.2). Men with a family history of both prostate and breast/ovarian cancer were also at increased risk of prostate cancer (RR = 5.8; 95% CI, 2.4-14). There was no association with a family history of colon cancer. Exclusion of well-differentiated, localized tumors did not alter these findings. These data from an incidence study confirm that a family history of prostate cancer is a strong prostate cancer risk factor after adjustment for dietary and other risk factors, and suggest that selection and recall bias have not had an important influence on most case-control study results. These data also support the idea that a family history of breast cancer may also be a prostate cancer risk factor.
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PMID:Family history and prostate cancer risk in a population-based cohort of Iowa men. 995 Feb 40

It has been suggested that components of our diet play an essential role in carcinogenesis. Anthropometric indices, such as body weight and height, have often been considered as measurements of prevailing diet and nutrition in childhood respectively. To investigate to what extent height and body weight are associated with the risk of gastrointestinal cancer, data from a Norwegian screening programme for tuberculosis were analysed. More than 1,100,000 individuals, aged 30-69 years at the time of examination, were included in the study. Body weight, expressed as Quetelet's index (QI), and height records were linked with vital status data from Statistics Norway and the Cancer Registry of Norway. The analysis shows that individuals in the first quintile of height had a lower relative risk than later quintiles for colon cancer, independent of sex and stage of disease at completion of follow-up. The association between height and rectal cancer is similar, but weaker. Men in the fifth quintile of QI have a relative risk of 1.39 for colon cancer, compared with the first quintile, and they also have a slightly elevated risk for rectal cancer. Among women, the pattern is unclear, but we observed a significant relationship between high QI and cancer of the gallbladder. Our results indicate that prevailing diet and living conditions in early life do play a role, and seem to support the hypothesis that anthropometric indices could be of importance as indirect markers for the risk of colon cancer and, to some extent, for cancer of the rectum and gallbladder.
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PMID:Height, weight and gastrointestinal cancer: a follow-up study in Norway. 1033 56

Risk factors for colon cancer have essentially been considered in terms of relative risks. From a public health viewpoint, however, their impact depends not only on the strength of the association, but also on the distribution of exposures in the population. Thus we used data from a case-control study conducted in Italy between 1992 and 1996 to estimate the population-attributable risks (PARs) for colon cancer in relation to educational level, physical activity, energy and vegetable intake, eating frequency, and family history of colorectal cancer. Cases were 1,225 incident, histologically confirmed colon cancer patients admitted to the major teaching and general hospitals in six Italian areas; controls were 4,154 subjects with no history of cancer, admitted to hospitals in the same catchment areas for acute, nonneoplastic diseases. By use of the distribution of the risk factors in the cases and the multivariate relative risk estimates, PARs were computed, i.e., the proportion of colon cancer that would have been avoided if all subjects were moved to the lowest exposure level. The PARs were 12% for high education, 14% for low physical activity, 14% for high energy intake, 22% for low vegetable intake, 7% for high eating frequency, and 8% for a family history of colorectal cancer. These factors together accounted for 56% of colon cancer cases. PARs were similar across age strata. Men had higher PARs for education, physical activity, and their combination, but lower PARs for energy, eating frequency, vegetable intake, and their combination than women. The percentage of colon cancers attributable to all factors considered together was 50% in men and 67% in women. Even if the PAR estimates were based on several arbitrary assumptions on the exposure distribution for various risk factors, available knowledge could, in principle, explain > 50% of cases in this Italian population, thus indicating and quantifying the theoretical scope for prevention.
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PMID:Population-attributable risk for colon cancer in Italy. 1036 16

Obesity has been related to increased risk of colon cancer or adenomas, but the epidemiologic findings are not entirely consistent. We examined the relation of not only body mass index (BMI) but also waist-to-hip ratio (WHR) and weight gain to colon adenoma risk in men who received a preretirement health examination at the Japan Self Defense Forces (SDF) Fukuoka and Kumamoto Hospitals during the period from 1995 to 1996. In the series of 803 men at age 47-55 years, 189 cases of colon adenomas and 226 controls with normal total colonoscopy were identified. Weight at 10 years before was ascertained by referring to the recorded data. After allowance for hospital, rank in the SDF, smoking and alcohol use, weight gain over the past 10 years was significantly associated with increased risk of colon adenomas (odds ratio for > or = 6 kg versus < or =-2 kg = 2.2; 95% confidence interval 1.0-4.8). High BMI and high WHR were each associated with increased risk, but only WHR was related to the risk independently of weight gain. In particular, weight gain accompanied with a high WHR was associated with a significant increase in the risk. Men with high physical activity tended to have lower risk. Associations with obesity-related variables and physical activity were not materially differential as regards the location and size of adenoma. The findings indicate that weight gain in middle age leading to abdominal obesity increases the risk of colon adenomas, and consequently of colon cancer.
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PMID:Obesity, weight gain and risk of colon adenomas in Japanese men. 1054 50

Cigarette smoking has been identified as a risk factor for colon cancer, however, much less is known about the association between cigarette smoking and rectal cancer. The purpose of this article is to evaluate the associations between rectal cancer and active and passive cigarette smoking and other forms of tobacco use. We also evaluate how genetic variants of GSTM-1 and NAT2 alter these associations. A population-based case-control study of 952 incident rectal cancer cases and 1205 controls was conducted. Detailed tobacco use information was collected as part of an interviewer-administered questionnaire. DNA was extracted from blood to examine genetic variants of GSTM-1 and NAT2. Cigarette smoking was associated with an increased risk of rectal cancer in men [odds ratio (OR)=1.5, 95% confidence interval (CI), 1.1-2.1 for current smokers; OR=1.7, 95% CI, 1.3-2.3 for smoking >20 pack-years of cigarettes relative to never-smokers]. After adjusting for active smoking, exposure to cigarette smoke of others also was associated with increased risk among men (OR=1.5, 95% CI, 1.1-2.0). Neither GSTM-1 genotype nor NAT2-imputed phenotype was independently associated with rectal cancer. However, the risk associated with smoking cigarettes among those who were GSTM-1 null relative to those who never smoked and had the GSTM-1 present genotype was OR=2.0 (95% CI, 1.2-3.3). This interaction was of borderline significance (P=0.08). Men who had the combined GSTM-1 present genotype and who were rapid acetylators had no increased risk from cigarette smoking. There were no significant associations between cigarette smoking and rectal cancer among women. This study shows that men who smoke cigarettes, especially those who smoke >20 pack-years, are at increased risk of rectal cancer. This association may be influenced by GSTM-1 genotype. Furthermore, exposure to cigarette smoke of others may increase risk of rectal cancer among men who do not smoke.
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PMID:Associations between smoking, passive smoking, GSTM-1, NAT2, and rectal cancer. 1450 99


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