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Carcinomas of the gastrointestinal tract (GI) are among the most common malignancies with regard to their incidence and mortality. Nutritional factors play an important role in the tumor development. The strength of their influence varies with the localization in the GI tract. Epidemiological studies focusing on GI cancer incidence or mortality as an endpoint necessitate large numbers of subjects to achieve significant results. Generally, a low energy and fat intake and a high intake of antioxidative vitamins (vitamin C, E, beta-carotene) and secondary plant metabolites (especially polyphenols) appear to be protective in GI carcinogenesis. Moderate drinking of alcohol and increased consumption of whole grain products, as opposed to highly refined carbohydrates, may help to reduce the risk of colon cancer. The recommended type of diet is low in fat, especially in saturated fatty acids, includes monounsaturated fatty acids, and includes moderate amounts of polyunsaturated fatty acids (no more than 10% of calories). Moderate consumption of salt and of highly salted, smoked, and barbecued foods should be encouraged. Obesity should be avoided by trying to match energy intake with expenditure while increasing physical activity levels. The mechanisms by which nutritional factors act especially on molecular events still remain to be examined. The use of molecular biomarkers will help us better understand cancer development as well as the role and significance of nutritional factors in this process.
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PMID:Basis and consequences of primary and secondary prevention of gastrointestinal tumors. 889 41

Epidemiologic evidence in humans and controlled trials in animal models indicate that total dietary fat increases the risk of cancer. The animal evidence indicates that the greatest efficacy in promoting carcinogenesis is achieved with omega-6 fatty acids with little or no effect from either the omega-3 or monounsaturated fatty acid families. Epidemiologic studies in humans indicate a positive association between meat intake and colon cancer, but a negative association with chicken and fish. There is also a negative association between non-steroidal anti-inflammatory drug (NSAID) intake and colon cancer. Red meat is a potentially significant source of dietary arachidonic acid, which is the primary substrate for the eicosanoids whose production is blocked by NSAIDs. Thus there is a positive association between carcinogenesis and dietary intake of both the omega-6 fatty acid precursor linoleic acid and its product arachidonic acid, and a negative association with use of a drug blocking its metabolism to eicosanoids. Another potentially important factor in arachidonate metabolism is variation in its endogenous distribution. We have recently reported abnormal distribution of arachidonic acid between lipid fractions in human obesity, and parallel abnormalities in animal models of genetic obesity. This implies a potential role for variation in the endogenous distribution of arachidonic acid in the etiology of cancers which have increased incidence in human obesity. This paper addresses the role of arachidonate intake, its endogenous production, and its distribution within lipid fractions in carcinogenesis.
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PMID:Metabolism of exogenous and endogenous arachidonic acid in cancer. 893 50

In populations in sub-Saharan Africa, transitional changes in patterns of morbidity and mortality are taking place, with decreases in the diseases of poverty and infection, but rises in chronic diseases of prosperity, associated, however, with greater longevity. Remarkably, bowel diseases - appendicitis, diverticular disease, colon cancer - while nearly absent in rural areas, have very low incidences in urban dwellers, despite rises in risk factors, including a decreasing intake of fibre-containing foods. Currently, there is no explanation for the phenomenon, which stands in marked contrast to the considerable rises which have occurred in dental caries, obesity in women and diabetes.
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PMID:Effects of transition on bowel diseases in sub-Saharan Africans. 905 36

Physical inactivity increases the risk for heart disease, diabetes, colon cancer, high blood pressure, obesity, osteoporosis, muscle and joint disorders, and symptoms of anxiety and depression. However, approximately one third of adults in the United States report no leisure-time physical activity, and rates of inactivity have been higher in January than in June. Among adults, the prevalence of leisure-time physical inactivity is highest among those who are older, Hispanic, and residing in southern states. A national health objective for the year 2000 is to reduce to < or = 15% the proportion of persons reporting no leisure-time physical activity (objecive 1.5). To assist in monitoring efforts to achieve this objective, CDC analyzed data from the 1994 Behavioral Risk Factor Surveillance system (BRFSS) and estimated for each month the proportion of adults from selected demographic groups who reported no leisure-time physical activity. The findings indicate seasonal patterns in the prevalence of reported leisure-time physical inactivity; however, monthly rates of inactivity were higher and more stable among older persons, Hispanics, and residents of southern states.
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PMID:Monthly estimates of leisure-time physical inactivity--United States, 1994. 915 73

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

A high correlation between national per capita disappearance of fat and national rates of colon cancer led to the hypothesis that consumption of fat, especially from animal sources, increases risk for colon cancer. Over the past two decades, this hypothesis has been tested in numerous case-control and cohort studies. In general, neither case-control nor cohort studies find that the total fat composition of the diet increases risk of colon cancer. Case-control studies frequently find that total energy consumption is related to a higher risk of colon cancer, but this result is difficult to interpret because physical activity appears to be protective whereas obesity increases risk. In contrast with the results for total fat, epidemiologic data regarding the role of specific fatty acids are sparse. Nonetheless, useful information regarding major fatty acids may be inferred from the numerous studies that have examined major source of various fats in relation to colon cancer. Intake of red meat or beef has been related to colon cancer risk in most case-control and cohort studies, whereas dietary fat from sources other than red meat, including dairy, poultry, and vegetable oils, does not increase risk of colon cancer. The apparent influence of red meat does not appear to be mediated through its total lipid content, suggesting that other factors such as heterocyclic amines formed during cooking may be critical. Mechanisms whereby fat or red meat may influence colon carcinogenesis are discussed, although none appear compelling.
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PMID:The role of fat, fatty acids, and total energy intake in the etiology of human colon cancer. 939 16

The aim of the study was to evaluate the results of surgical treatment of colorectal cancer during 45 years of existence of the Department. In this time 1478 cases of rectal cancer and 1008 cases of colon cancer were operated on. Most commonly the diseases occurred between the sixth and seventh decade of live (32.8%). Histology revealed tubular adenocarcinoma in 83.3% of the cases, mucinous adenocarcinoma in 13.5% and other types in 3.2%. The choice of the surgical procedure was based on the individual characteristics of each case, including: localisation of the tumor, histological type, clinical staging, sex of the patient, obesity and overall operative risk. The tumor was localised less then 10 cm above the anal verge in 70% of the patients with rectal cancer. Well differentiated carcinomas (G1) were seen in 32% of the patients, moderately differentiated carcinomas (G2) in 57% and poorly differentiated (G3) in 11%. Curative resections were performed in 64.7% of the patients (1608 cases) and palliative procedures in 35.3% of the patients (878 cases). The mortality rate after curative surgery was 6% and after palliative procedures 5%. The use of combined therapy consisting of surgical treatment and chemo- or radiotherapy allowed for obtaining five years survival rate of 57.4%, local recurrences were seen in 21% of patients. Analysing our own material we evaluated the radicality of different types of operations and the possibility of preserving the sphincter apparatus.
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PMID:[45 years of experience in surgical treatment for cancer of the large intestine]. 944 33

Few studies have examined the long-term effects of childhood obesity on adult disease. Nonetheless, obesity present in childhood or adolescence seems to increase the likelihood of adult morbidity and mortality. In men who were obese during adolescence, all-cause mortality and mortality from cardiovascular disease and colon cancer were increased. In both men and women obese during adolescence, rates of cardiovascular disease and diabetes were increased. Among women but not men obese during adolescence, obesity has a variety of adverse psychosocial consequences. These include completion of fewer years of education, higher rates of poverty, and lower rates of marriage and household income. These effects seem related both to the persistence of obesity and to the effects of childhood or adolescent obesity on the quantity and location of body fat deposition. Approximately 50% of obese adolescents with a body mass index at or above the 95th percentile become obese adults. Furthermore, the risk factors for adult disease that are associated with obesity in children and adolescents persist into adulthood or increase in prevalence if weight gain occurs. Although both total body fat and regional fat deposition could account for the association of childhood or adolescent obesity with adult disease, no studies to date have examined cardiovascular risk factors and related them to visceral fat, controlled for total body fat.
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PMID:Childhood weight affects adult morbidity and mortality. 947 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

Obesity is a known risk factor for a number of diseases with serious mortality and morbidity implications. Thus, obesity is an economic burden to communities, since it reduces quality of life and leads to premature mortality; in addition, healthcare resources are used to manage obesity-related disease. It was estimated that in 1989, management of disease due to obesity (defined as body mass index greater than 30) cost A$395 million. This estimate covers the healthcare costs for the management of obesity, non-insulin-dependent diabetes mellitus (NIDDM), gallstones, hypertension, coronary heart disease (CHD), breast cancer (among postmenopausal women), and colon cancer. As this estimate excludes the costs of some disease attributable to obesity, it is an underestimate of the true costs. Nonetheless, the estimated cost of the management of obesity-related conditions represents 86% of the healthcare costs used for the management of alcohol-related diseases in Australia. Healthcare costs attributable to obesity have not yet been estimated for countries elsewhere in Asia and the Pacific. However, it is acknowledged that obesity is a major problem in the Pacific, with exceptionally high prevalence rates and concomitant high rates of diseases for which obesity is a major risk factor, particularly NIDDM and CHD. It would, therefore, be useful to explore the cost of disease attributable to obesity in healthcare systems in these communities, and the potential for preventive programmes to reduce these costs.
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PMID:The cost of obesity: the Australian perspective. 1014 49


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