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

Colorectal cancer is the third most common malignant neoplasm worldwide. Epidemiological and laboratory animal studies have established a link between various nutritional factors and the etiology of this cancer. Recent studies in genetic epidemiology and molecular biology have shown that inherited genetic factors also play an important role in colorectal carcinogenesis. Thus, genetic-nutritional interactions may form the basis for the development of this cancer. Nutritional factors that appear to promote or attenuate the carcinogenic process in the colon include fat, excess calories, fibre, calcium, selenium, and various vitamins. Strategies for primary prevention of colorectal cancer should therefore be targeted to all populations who are at risk because of dietary and hereditary predisposition. Based on current knowledge, recommended nutrition guidelines for reducing the risk of colon cancer include decreased fat consumption, adequate amounts of fruits, vegetables, and calcium, and avoidance of overweight. Research to further elucidate the role of diet in colorectal carcinogenesis should include randomized studies in humans, testing of various nutritional regimens, and the use of colonic adenomas and markers of cell proliferation and differentiation as end-points.
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PMID:Primary prevention of colorectal cancer. The WHO Collaborating Centre for the Prevention of Colorectal Cancer. 220 51

The associations between colorectal cancer and body weight (expressed as body mass index) and between colorectal cancer and physical activity were examined in 715 histologically confirmed cases of colorectal adenocarcinoma and 727 age- and sex-matched controls. The data were obtained from a large, population-based study, The Melbourne Colorectal Cancer Study, which was conducted in Melbourne, Australia. There was a statistically significant increase in the risk of rectal cancer but not of colon cancer in overweight and obese males but not in females. This association for males remained statistically significant after adjustment was made for dietary risk factors previously established for this study (Nutr Cancer 9, 21-42, 1987), with the exception of sodium intake, which produced a downward modification of the relative risk close to unity. The increased risk of rectal cancer in overweight and obese males was modified by beer intake, which was previously found to be a risk for rectal cancer in males in this study. Various levels of physical activity were not statistically significantly associated with the risk of colorectal cancer in either males or females. Also, the colorectal cancer risks associated with the body mass index were not significantly altered by adjustment for the physical activity level.
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PMID:Body weight and physical activity as predictors of colorectal cancer risk. 230 Apr 99

Associations between fatal colon or colorectal cancer and frequency of use of meat, cheese, milk, eggs, green salad, and coffee, as well as percent desirable weight, are described with the use of 21 years of follow-up for 25,493 white California Seventh-Day Adventists. Associations are presented in terms of relative risk (RR) of colorectal cancer for heavy or light exposure versus rare exposure. There were no clear relationships evident between colon or rectal cancer and meat, cheese, milk, or green salad use. Egg use was positively associated with risk of fatal colon cancer in both males (RR = 1.6) and females (RR = 1.7). Coffee use was positively associated with both colon and rectal cancer mortality in males and females, particularly for colon cancer during the last 11 years of follow-up (male RR = 3.5; female RR = 1.9). Overweight (percent of desirable weight greater than or equal to 125) was associated with an increased risk of fatal rectal cancer in both sexes combined (RR = 2.8) and colon cancer in males only (RR = 3.3). Furthermore, eggs, coffee, and overweight appear to be independently associated with risk of both colon and colorectal cancer. These three factors may explain a substantial portion of the colorectal cancer mortality differential between Adventists and U.S. whites (62% for males; 30% for females).
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PMID:Dietary relationships with fatal colorectal cancer among Seventh-Day Adventists. 385 44

In 1994, there were approximately 160,000 new cases of colon cancer in the United States with 58,000 fatalities, making this form of cancer the second most common cause of cancer deaths. Up to 50% of colon cancers may have a strong inherited factor, but in the remaining cases, diet and lifestyle factors are thought to play essential roles in the carcinogenic process. Various epidemiologic studies have examined the relation between obesity and colon cancer. The largest prospective study of 750,000 men showed that mortality from colorectal cancer was significantly elevated in men who were > or = 40% overweight. No such increase was found in women. Subsequent studies reported conflicting results. Overweight is likely a surrogate. Other risk factors include a high-fat, energy-dense diet; inadequate consumption of fruit and vegetables; and lack of physical activity, which have been associated with a high incidence of colon cancer.
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PMID:Body weight and colon cancer. 861 38

This study was undertaken to update and revise the estimate of the economic impact of obesity in the United States. A prevalence-based approach to the cost of illness was used to estimate the economic costs in 1995 dollars attributable to obesity for type 2 diabetes mellitus, coronary heart disease (CHD), hypertension, gallbladder disease, breast, endometrial and colon cancer, and osteoarthritis. Additionally and independently, excess physician visits, work-lost days, restricted activity, and bed-days attributable to obesity were analyzed cross-sectionally using the 1988 and 1994 National Health Interview Survey (NHIS). Direct (personal health care, hospital care, physician services, allied health services, and medications) and indirect costs (lost output as a result of a reduction or cessation of productivity due to morbidity or mortality) are from published reports and inflated to 1995 dollars using the medical component of the consumer price index (CPI) for direct cost and the all-items CPI for indirect cost. Population-attributable risk percents (PAR%) are estimated from large prospective studies. Excess work-lost days, restricted activity, bed-days, and physician visits are estimated from 88,262 U.S. citizens who participated in the 1988 NHIS and 80,261 who participated in the 1994 NHIS. Sample weights have been incorporated into the NHIS analyses, making these data generalizable to the U.S. population. The total cost attributable to obesity amounted to $99.2 billion dollars in 1995. Approximately $51.64 billion of those dollars were direct medical costs. Using the 1994 NHIS data, cost of lost productivity attributed to obesity (BMI> or =30) was $3.9 billion and reflected 39.2 million days of lost work. In addition, 239 million restricted-activity days, 89.5 million bed-days, and 62.6 million physician visits were attributable to obesity in 1994. Compared with 1988 NHIS data, in 1994 the number of restricted-activity days (36%), bed-days (28%), and work-lost days (50%) increased substantially. The number of physician visits attributed to obesity increased 88% from 1988 to 1994. The economic and personal health costs of overweight and obesity are enormous and compromise the health of the United States. The direct costs associated with obesity represent 5.7% of our National Health Expenditure in the United States.
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PMID:Current estimates of the economic cost of obesity in the United States. 954 25

Energy balance results from the exact equilibrium between caloric intake and caloric expenditure. A caloric intake larger than caloric expenditure results in overweight, even obesity, but other determinants, like hormonal dysfunction and/or genetic traits may play a part in obesity syndrome. Obesity, and even overweight, have been recognized as risk factors for the development of cancers. Human epidemiological studies, which have tended to establish the nature of the relationship between energy balance and cancer, are summarized first, with the influence of the various factors which act both on obesity and on cancer risk. Among these factors are the macronutrients responsible for the caloric intake, and some lifestyle factors (physical activity, drinking habits and tobacco use). Second, the animal studies help to distinguish between different relevant factors, and to understand some of the underlying mechanisms. However, the insulin-resistance syndrome, which appears to underlie the relationship between obesity and hormone-dependent cancers, and possibly colon cancer, is only relevant to human physiology because hormonal alterations are part of it. Prevention of hyperinsulinemia, insulin resistance and the accompanying visceral obesity appears to be a major public health task for the prevention of cancers.
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PMID:Energy balance and cancers. 1033 54

Epidemiological studies on risk factors for CRC have focused mainly on diet. In any case, the results of these studies show several inconsistencies, except for the beneficial role of high intake of vegetables and, to some lesser extent, of fruit. Weight and height have also been studied, partly because they reflect the balance between energy intake and expenditure in different age periods. Energy intake, body size and physical activity will be reviewed in this paper focusing mostly on recent data coming from Italian, English and Scandinavian studies. Overweight has long been recognized as a risk factor for hormone related and other cancers and this is confirmed not simply from case-control studies but from large cohort studies as well. The major findings of recent Italian studies are that excessive weight at various ages predicts colorectal cancer risk in men while in women, abdominal obesity, as indicated by a high WHR, represents a more reliable risk indicator. If all men could reduce their BMI below 25, about 9% of male colorectal cancer might be avoided in Italy. A decrease of WHR below 0.82 might reduce colorectal cancer in women by 19%. In addition, the epidemiological evidence consistently shows that physical activity reduces the risk of colon cancer. On the contrary, evidence on rectal cancer is less impressive. Some uncertainty still exists in relation to the intensity and duration of physical activity. In conclusion, body size control along all life and physical activity represent important factors to prevent colon cancer and a wide range of chronic conditions. Therefore, strategies to favour these goals through counselling from health-care providers, regulatory changes and programs aimed at individuals and communities should be implemented.
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PMID:Energy intake, overweight, physical exercise and colorectal cancer risk. 1077 19

The INSEE national surveys in 1980 and 1991, and the OBEPI study in 1997, allowed to study the prevalence of overweight and obesity in France, as well as its increase during these past years. The number of adult obese individuals remained stable between 1980 and 1991. The 1997 estimation suggests a moderate increase. By contrast, the number of obese children has increased between 1980 and 1991, whatever the level of study of the mother. Several diseases are strongly linked with obesity, such as hyperuricemia, hypertension, coronary heart disease, diabetes mellitus. Thus the declared prevalence of diabetes is 2% when BMI ranges from 18.5 to 25 kg/m2, and reaches 20% at a BMI > 34 kg/m2 with age ranging 40-70 years old. The presence of obesity during childhood is also correlated with an increased mortality, with an enhanced prevalence of coronary heart disease, hyperuricemia, colon cancer in men, and joint disease in women during adulthood. An increase in the prevalence of diabetes is expected in the near future: demography, as children born after the war will reach age of 55-75, the lowering of glycemic threshold for the diagnosis of diabetes, increased prevalence of obesity are the main explanations. Our health care system will need to evolve in order to deal with this increased number of patients, and measures have been recently set for that purpose.
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PMID:[Update on the epidemiology of obesity and type 2 diabetes in France]. 1094 46

There is growing evidence that excess body weight increases the risk of cancer at several sites, including kidney, endometrium, colon, prostate, gallbladder and breast in post-menopausal women. The proportion of all cancers attributable to overweight has, however, never been systematically estimated. We reviewed the epidemiological literature and quantitatively summarised, by meta-analysis, the relationship between excess weight and the risk of developing cancer at the 6 sites listed above. Estimates were then combined with sex-specific estimates of the prevalence of overweight [body mass index (BMI) 25-29 kg/m(2)] and obesity (BMI > or = 30 kg/m(2)) in each country in the European Union to obtain the proportion of cancers attributable to excess weight. Overall, excess body mass accounts for 5% of all cancers in the European Union, 3% in men and 6% in women, corresponding to 27,000 male and 45,000 female cancer cases yearly. The attributable proportion varied, in men, between 2.1% for Greece and 4.9% for Germany and, in women, between 3.9% for Denmark and 8.8% for Spain. The highest attributable proportions were obtained for cancers of the endometrium (39%), kidney (25% in both sexes) and gallbladder (25% in men and 24% in women). The largest number of attributable cases was for colon cancer (21,500 annual cases), followed by endometrium (14,000 cases) and breast (12,800 cases). Some 36,000 cases could be avoided by halving the prevalence of overweight and obese people in Europe.
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PMID:Overweight as an avoidable cause of cancer in Europe. 1116 69

Recent epidemiology indicates that unopposed oral estrogen replacement therapy has a surprisingly small impact on breast cancer risk--little if any in overweight women--whereas combined regimens featuring synthetic progestins are attended by a much larger increase in this risk. These findings may reflect the fact that oral estrogen acts on the liver to down-regulate systemic IGF-I activity, whereas concurrent administration of androgens--including the androgenic progestins often used in replacement therapy--abrogates this effect. Increased systemic IGF-I activity has been linked to increased breast cancer risk, and may be largely responsible for the greater incidence of breast cancer in overweight postmenopausal women--who thus should have the most to gain from suppression of IGF-I activity by oral estrogen. Down-regulation of IGF-I may likewise account for the marked reduction in colon cancer risk associated with current estrogen replacement therapy. Fortunately, natural progesterone--now available in micronized oral preparations--does not oppose the hepatic effects of oral estrogen, and moreover may be preferable to androgenic progestins with respect to vascular function. Oral replacement therapy featuring micronized progesterone, if administered throughout postmenopausal life, can be expected to have a highly positive impact on vascular health, bone density, and risks for Alzheimer's disease and colon cancer--benefits which, in most women, may vastly outweigh the associated increase in risk for breast and endometrial cancers.
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PMID:Androgenic progestins amplify the breast cancer risk associated with hormone replacement therapy by boosting IGF-I activity. 1142 89


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