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

The authors interviewed 428 pathologically confirmed cases of colon cancer and controls matched on age, sex, race, and neighborhood in the New York counties containing the cities of Buffalo, Niagara Falls, and Rochester. Risk of colon cancer in both males and females, studied separately, appeared to increase with the amount of total fats and total calories ingested. In addition, we found the risk to increase with increases in the Quetelet index of relative weight (weight (kg)/height (m)2). Dietary fiber was only equivocally associated with risk. Fats and Quetelet index were associated with increased risk in a regression analysis adjusting each factor for the other, as well as for fiber, age, and socioeconomic status. The same was true for calories and Quetelet index. Future efforts to clarify a possible protective role for fiber and to disentangle the effects of fats and calories need to be undertaken. The fact that calories ingested and obesity are each associated with increased risk suggests the importance of studying calorie expenditure.
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PMID:Dietary epidemiology of cancer of the colon in western New York. 284 38

A case-control study was conducted to assess the role of diet in the etiology of colon cancer. Diet was measured by means of a comprehensive quantifiable food frequency history instrument in 246 cases and 484 controls drawn from the general population of Utah. Each subject's diet was described by major nutrient groups and total energy based on the nutritional content of foods reported. Cases reported higher daily food intake 5 years preceding diagnosis than controls [men, rate ratio (RR) = 2.5; women, RR = 3.6], as measured by total energy content of the diet. Higher risk of colon cancer with increasing energy intake was independent of stage of disease at diagnosis and obesity, as measured by body mass. Fat, protein, and carbohydrate intake all had elevated RRs but could not be assessed as risk factors independent of energy intake because of their strong correlations with total calories. Due to the higher energy intake of the cases, odds ratios for the daily intake of dietary fiber and vitamins A and C were also greater than 1. However, adjusting for caloric intake removed this effect, and dietary fiber showed a weak protective effect. Total energy intake must be evaluated before attempting to assign a causal role to any food or nutrient that may be postulated to play a role in colon cancer.
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PMID:Energy intake: its relationship to colon cancer risk. 303 83

Comparisons of Hawaiian Japanese with Japanese living in Japan identify several differences between the 2 populations. The Hawaiian Japanese are heavier and taller; they consume more fat and protein; they have higher levels of serum cholesterol, more frequent fecal mutagens, and more frequent adenomatous polyps and diverticulae. These differences offer indirect support to the concept that the consumption of a Western diet favors the development of coronary heart disease and colon cancer which occur more frequently among the Japanese in Hawaii than in Japan. When assessed directly and prospectively, obesity, the serum cholesterol level, and dietary fat intake are positively associated with coronary heart disease. The serum cholesterol level and dietary fat intake are negatively associated with colon cancer, whereas the body mass index (height/weight) is positively related to this tumor in older men. The 2 diseases have shown dissimilar trends in the past 20 years, with coronary heart disease being stable at levels intermediate between the United States and Japan experience, whereas colon cancer has shown a steady increase with rates higher than those of whites in the United States. The differences in risk factors and trends displayed by the 2 diseases indicate that they affect different subsets of the westernized Japanese population. Additional studies are necessary if we are to establish the basis for these differences.
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PMID:Colorectal cancer in Hawaiian Japanese men: a progress report. 393 34

In a nine-year follow-up of a southern California community of 2,852 men and women aged 60-79 years, systolic blood pressure was a significant predictor of subsequent cancer mortality in men. This effect was independent of age, antihypertensive medication, smoking, obesity, and plasma cholesterol. Trends in women were similar but not statistically significant. Compared with those still alive, higher initial systolic blood pressure levels were apparent in those who died of colon cancer, stomach cancer, and all other cancers combined except for lung and prostate cancer. Possible mechanisms for this association and the implications of the data with regard to the benefits of measures to treat high blood pressure or lower population distribution of blood pressure are discussed.
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PMID:Systolic blood pressure and cancer mortality in an elderly population. 647 25

Some factors related to Westernization or industrialization increase risk of colon cancer. It is believed widely that this increase in risk is related to the direct effects of dietary fat and fiber in the colonic lumen. However, the fat and fiber hypotheses, at least as originally formulated, do not explain adequately many emerging findings from recent epidemiologic studies. An alternative hypothesis, that hyperinsulinemia promotes colon carcinogenesis, is presented here. Insulin is an important growth factor of colonic epithelial cells and is a mitogen of tumor cell growth in vitro. Epidemiologic evidence supporting the insulin/colon-cancer hypothesis is largely indirect and based on the similarity of factors which produce elevated insulin levels with those related to colon cancer risk. Specifically, obesity--particularly central obesity, physical inactivity, and possibly a low dietary polyunsaturated fat to saturated fat ratio--are major determinants of insulin resistance and hyperinsulinemia, and appear related to colon cancer risk. Moreover, a diet high in refined carbohydrates and low in water-soluble fiber, which is associated with an increased risk of colon cancer, causes rapid intestinal absorption of glucose into the blood leading to postprandial hyperinsulinemia. The combination of insulin resistance and high glycemic load produces particularly high insulin levels. Thus, hyperinsulinemia may explain why obesity, physical inactivity, and a diet low in fruits and vegetables and high in red meat and extensively processed foods, all common in the West, increase colon cancer risk.
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PMID:Insulin and colon cancer. 774 56

Intensive animal rearing, manipulation of crop production and food processing have altered the qualitative and quantitative balance of nutrients of foods consumed by Western society. This change, to which the physiology and biochemistry of man may not be presently adapted to, is thought to be responsible for the chronic diseases that are rampant in the Industrialised Western Countries. Agriculture production and food processing practices, dietary habits and lifestyle of the West is being fostered without any appraisal of the health implications by most developing countries. Consequently, a rising trend in the incidences of obesity, diabetes, high blood pressure, cardiovascular diseases, dental decay and appendicitis is apparent. Mediterranean countries are adopting the agriculture and food practices of northern Europe as the result of the harmonisation of European food and agriculture policy. It is predicted that the low incidence of morbidity and mortality from coronary heart disease, stroke, diabetes and breast and colon cancer of the Mediterranean countries would rise to the high northern European level in the foreseeable future. Most of these chronic diseases are lifestyle related and are preventable. This can be realised by tackling the root problem which is food production and processing practices and not by dispensing designer drugs or opening more hospital beds.
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PMID:Nutrition and health in relation to food production and processing. 806 63

Colon cancer was rare or uncommon in the past, and still is in traditionally-living third world populations. It now affects 3-5% of western populations. Epidemiological, case control, experimental and other studies suggest that proneness to colon cancer can be lessened by major dietary changes, principally decreasing fat intake by a third, and doubling the intake of fiber-containing foods, especially vegetables and fruit--recommendations similarly advocated for the avoidance of coronary heart disease and other degenerative diseases. Among nondietary factors, evidence indicates familiality, obesity and atmospheric pollution to be contributory, while parity, physical activity, solar radiation, high social class, estrogen use, and aspirin use, appear protective. Despite insufficiencies of knowledge of prevention, avoiding action should certainly be taken by those familially prone. For the rest, conceivably a prudent life-style could benefit a proportion avoiding colon cancer.
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PMID:Can the risk of colon cancer be lessened? 830 89

The role of obesity in the risk of colorectal cancer is uncertain. We investigated the association between height and weight and the risk of colorectal cancer in an 18-year follow-up of 5249 employed men aged 40-59 years (mean, 48 years). Cancer of the colon was diagnosed in 51 men, and cancer of the rectum in 42 (all were adenocarcinomas). Adjusted for weight and age, the tertile of men with shortest height had a relative risk (95% confidence limits) of rectum cancer of 3.1 (1.0-9.0, p = 0.04), compared with the tallest tertile. Compared with the tertile of men who weighed the most, the tertile of men who weighed the least had an increased risk of 2.5 (0.9-6.9, p = 0.08) after adjustment for age and height. Compared with men who were in the highest tertile of both height and weight, the men in the lowest tertile of both height and weight had and increased risk of 5.5 (1.2-24.9, p = 0.02). There were no significant differences in height and weight between colon cancer cases and non-cases, but colon cancer cases had a significantly lower body mass index (kg/m2), 24.4 versus 25.3 (p = 0.03). Potentially confounding factors, such as smoking, alcohol, coffee consumption, physical activity on the job and in leisure time, and social class, had no influence on the results. We conclude that low height and low weight were strong predictors of rectal cancer, and that the least obese men had the highest risk of colon cancer.
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PMID:Height, weight, and risk of colorectal cancer. An 18-year follow-up in a cohort of 5249 men. 844 55

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

Chemoprevention refers to the use of specific natural or synthetic chemical agents to reverse, suppress, or prevent the progression to invasive cancer. The ideal chemopreventive agent is safe and nontoxic over the long term. It should be easy to take and demonstrated to be effective in randomized trials in humans. Aspirin and NSAIDs meet many of the criteria for an ideal agent. The literature on aspirin and NSAIDs makes it clear that these agents can prevent colorectal cancer and precursor adenomas. That does not mean that we should make general recommendations for their use. First, we do not know the proper dose or duration. More important, these medications are accompanied by adverse effects that can be considerable. Indeed, the Medical Letter, an authoritative, unbiased publication on drugs and therapeutics, concluded that "for primary prevention in low-risk patients, more studies are required to establish whether the beneficial effect of aspirin is great enough to compensate for the possible increased risk of hemorrhagic stroke." These recommendations were directed at the use of these medications for prevention of myocardial infarction, but the same conclusions apply to colorectal cancer: although aspirin may prevent the disease, it may increase the risk of hemorrhagic strokes or cause other adverse effects. We must accurately balance the benefits and risks of these drugs, based on the results of ongoing randomized studies, before recommending aspirin for prevention of colorectal cancer. Is there anything that we can recommend to our patients for prevention of colorectal cancer? Based on observational epidemiologic studies, it is clear that individuals who consume a diet high in vegetables and natural fibers and low in fat have a reduced risk of colon cancer and polyps. Optimal nutrient intakes for the prevention of cancer might be more readily achieved via food fortification or supplementation, but this requires more research. Regular physical exercise and maintenance of normal body weight are also protective. Until the results of definitive studies of chemopreventive agents are available, we can recommend that our patients eat a sensible diet, exercise, and avoid obesity. Such an approach should protect them from cardiovascular disease, an even deadlier condition than colorectal cancer. In the future, we need randomized prevention trials that, for logistic reasons, may need to focus on the occurrence and progression of colorectal adenomas rather than carcinoma itself. Studies that test more than one compound at a time, using factorial designs, will be more efficient. We will need better information about duration and dose, adverse side effects, molecular mechanisms, and cellular sites of NSAID activity. Ultimately, we will need to know more about the biology and molecular biology of colorectal cancer and its precursors. That information will, perhaps, permit us to design agents to interrupt the pathway to cancer and to use intermediate markers more intelligently.
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PMID:Aspirin and other nonsteroidal anti-inflammatory agents in the prevention of colorectal cancer. 879 Nov 32


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