Monday, September 2, 2019
Prevention of Colon Cancer through Proper Nutrition Essay
Incidence            Colon cancer is the third most often diagnosed cancer and is the second primary cause of cancer deaths in North America. The incidence is approximately 650,000 cases every year worldwide and has been increasing in the past few years. However, the mortality rate has decreased in 2002; the worldwide incidence was 278,000 male and 251,000 female cases every year (Landis, Murray, Bolden, & Wingo, 1999). In people 65 years or older, the incidence rate of colon cancer is 70% (Parkin, Whelan, Ferlay, Raymond, & Young, 1997). In people not more than 65 years old, the incidence is about 120 new cases for every 100,000 inhabitants every year; in people aged 55-75, the incidence of colon cancer is approximately 200 for every 100,000 inhabitants every year (Jemal et al., 2004)            The lifetime risk of colorectal cancer in the general population is 2.5% to 5%, which means that 25-50 out of 100 people will get colon cancer in their lifetimes (Adrouny, 2002). This risk is increased two- or threefold if there is a first-degree relative who has had an adenomatous polyp or cancer. Mortality is about 90 for every 100,000 inhabitants per year (Jemal et al., 2004). The male-to-female ratio varies from 1.0 to 1.4 depending on the tumor registry that is reporting the data (Adrouny, 2002). The risk of colon cancer increases with age. The majority of cases occur in people over the age of sixty. In people between the ages of forty and fifty years the incidence of colon cancer is 15 new cases per 100,000 persons (Adrouny, 2002). Modifiable Risk Factors            While many mechanisms remain ambiguous, many studies have indicated that a number of lifestyle and dietary factors are likely to have significant consequences on the risk of colon cancer. Smoking early in life, probably in combination with a diet that has no or low in some micronutrients like methinine and folate, is likely to increase the risk of colon cancer. Other environmental exposures, such as smoking, are also likely to be involved in causing colon cancer. Moreover, overeating, weight gain in adulthood, and obesity are strongly implicated as risk factors for colon cancer. Not only are obesity and weight gain associated with the presence of adenomatous polyps, but so is weight variability over a period (Adrouny, 2002). Physical inactivity or sedentary occupation is also a major risk factor for colon cancer.            According to Giovannucci (2002), processed meats, red meat, and possibly refined carbohydrates may increase colon cancer risks. Also, more recent evidence show that chronic hyperinsulinemia is likely to have an influence on colon cancer risks. As insulin resistance and subsequent hyperinsulinemia is induced by excess energy intake and some characteristics of the Western diet, such as refined carbohydrates and saturated fats, insulin may contribute to colon cancer (Giovannucci, 2002). In addition, agents with chemopreventive properties like postmenopausal estrogens and aspirin are likely to have unpleasant effects, thus making general recommendations require a cautious consideration of the risk-benefit ratio. Non-Modifiable Risk Factors            Although the genetic and biochemical mechanisms of colon cancer may still be incompletely understood, it is acknowledged that the anatomic precursor of colon cancer is the adenomatous polyp. Basically, adenoma is a benign growth from a glandular tissue; a polyp is a growth protruding from a mucous membrane. People who have adenomatous polyps in the colon are at increased risk of developing cancer. One major non-modifiable risk factor is the familial adenomatous polyposis (FAP). Here, an affected individual develops hundreds or thousands of polyps by his or her teen years, any one of which may develop into a cancer. Preventive action, usually consisting of repeated examination or removal of the colon, is necessary, along with careful screening of family members for this disorder. The Gardner syndrome is probably a variant of FAP; it occurs about half as frequently and has similar clinical features. It may affect the small intestine as well as the colon.            Oldfield and Turcot syndromes might be related to FAP. While the former is associated with sebaceous cysts, the latter is associated with tumors of the central nervous system and may be transmitted by an autosomal recessive gene. Another risk factor for colon cancer is hereditary nonpolyposis colorectal cancer (HNPCC). Although these forms of colon cancer arise from polyps, individuals do not have an abundant proliferation of polyps as in the abovementioned polyposis syndromes. The polyps that are found in family members have an extraordinarily high likelihood of progressing to cancer. Prevention            The large body of evidence shows that it is feasible to prevent colon cancer. In their study, Emmons et al. (2005) approximate that a significant fraction of the colon cancer risk in the middle-aged men in the United States might be avoidable with optimal common lifestyle and dietary behaviors. National recommendations and clinical practice and for adult men and women in the US already promoted the following for the prevention of cancer in general, and colon cancer in particular: controlling of obesity, quitting smoking, limiting alcohol intake, increasing physical activity, consuming more fruits and vegetables and diets that are low in saturated fat (American Cancer Society, 1996). The following prevention practices are specifically aimed at middle aged (30-50 years) American men. As mentioned earlier in this paper, there is a higher incidence rate of colon cancer in men than women, and that this age bracket is highly at risk for colon cancer. The focus is the primary prevention of colon cancer by consuming more fruits and vegetables.            The consumption of fruits and vegetables as a measure in preventing colon cancer has been supported in many studies (e.g., Smith-Warner, Genkinger, & Giovannucci, 2006). It was found that for total vegetables, 75% of the results reported in 22 case-control studies suggested that colon cancer risk was reduced by at least 20% for those in the highest compared with the lowest intake category, with 33% of the estimates indicating that the reduction in risk exceeded 50%. For total fruits, the results have been less consistent among 19 case-control studies; 48% of the risk estimates suggested at least a 20% reduction in risk and only 11% showed more than a 50% lower risk for the highest versus the lowest intakes (Kousnik et al., 2007). Furthermore, in an earlier review of 21 case-control and four cohort studies by an international panel, credible evidence was found that vegetable consumption indeed reduces colon cancer risks (World Cancer Research Fund, 1997).            Studies have also suggested that dietary calcium plays a role in protecting against colon cancer; it may do so by binding fatty acids and bile acids and directly inhibiting abnormal growth of colon epithelial cells. Fruits and vegetables are thought to reduce the risk of colon cancer because they have a higher composition of fiber compared to other diets. On the other hand, diets low in fiber and high in fat intake are thought to increase the risk of the cancer. Thus, it is not surprising that, in Africa and Asia, where dietary customs place emphasis on high-fiber, low-fat foods, fruits, and vegetables, people have lower incidence of colon cancer compared to the United States and Europe.            The major explanation for the protective effect of cereal fiber is not known. One of the most convincing theories is that fiber has a dilutional effect on fecal ingredients which may cause development of cancer. It also has an effect on the faster passage of stool through the bowel, thus reducing cell damage and contact time (Adrouny, 2002). In general, however, more recent epidemiologic research has tended not to support the strong influence of fiber in preventing colon cancer; instead, some phytochemicals or micronutrients in foods rich in fiber may be important. Folate is one nutrient that has of late been receiving much attention and is increasingly being studied in randomized intervention trials. Recent research suggests that persons who supplement their diet with at least 800 micrograms of the vitamin folic acid on a daily basis have a reduced incidence of colon cancer (Adrouny, 2002). References  American Cancer Society. (1996). Guidelines on diet, nutrition, and cancer prevention. Cancer Journal for Clinicians, 46, 325-341. Giovannucci, E. (2002). Modifiable risk factors for colon cancer. Gastroenterology Clinic North America, 31, 925-43. Jemal, A., Clegg, L. X., Ward, E., Ries, L. A., Wu, X., Jamison, P. M. et al. (2004). Annual report to the nation on the status of cancer, 1975–2001. Cancer, 101, 3–27. Koushik, A., Hunter, D. J., Spiegelman, D., Beeson, W. L., van den Brandt, P. A., Buring, J. E. et al. (2007). Fruits, Vegetables, and Colon Cancer Risk in a Pooled Analysis of 14 Cohort Studies. Journal of National Cancer Institute, 99, 1471-1483. Landis, S.H., Murray, T., Bolden, S., & Wingo, P. A. (1999). Cancer statistics 1999, Cancer Journal for Clinicians, 49, 8–31 Parkin, D. M., Whelan, S. L., Ferlay, J., Raymond, L., &Young, J. (Eds.). (1997), Cancer Incidence in Five Continents. Lyon: IARC Press. Smith-Warner, S. A., Genkinger, J., & Giovannucci, E. (2006). Fruit and vegetable intake and cancer. In D. Heber, G. L. B;ackburn, V. L. Go, & J. Milner (Eds.), Nutritional oncology (97-173). Burlington, MA: Elsevier. World Cancer Research Fund. (2007). Food, nutrition and the prevention of cancer: a global perspective. Washington (DC): American Institute for Cancer Research. Â
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