Information about the prevention of cancer and the science of screening appropriate individuals at high risk of developing cancer is gaining interest. Physicians and individuals alike recognize that the best “treatment” of cancer is preventing its occurrence in the first place or detecting it early when it may be most treatable.
Colorectal cancer is the second leading cause of cancer death in the United States. The disease strikes both men and women, with more than 140,000 cases diagnosed each year. Approximately 50,000 people die from colorectal cancer each year.
The chance of an individual developing cancer depends on both genetic and non-genetic factors. A genetic factor is an inherited, unchangeable trait, while a non-genetic factor is a variable in a person’s environment, which can often be changed. Non-genetic factors may include diet, exercise, or exposure to other substances present in our surroundings. These non-genetic factors are often referred to as environmental factors. Some non-genetic factors play a role in facilitating the process of healthy cells turning cancerous (i.e. the correlation between smoking and lung cancer) while other cancers have no known environmental correlation but are known to have a genetic predisposition. A genetic predisposition means that a person may be at higher risk for a certain cancer if a family member has that type of cancer.
People with a personal or family history of adenomatous polyps or familial adenomatous polyposis (FAP) are at an increased risk for developing colorectal cancer. Adenomatous polyps are non-cancerous tumors that grow in the colon or rectum and can become cancerous, ultimately developing into colorectal cancer. Familial adenomatous polyposis (FAP) is a genetic disease that causes hundreds of adenomatous polyps to form in the colon or rectum. FAP most often affects adolescents and young adults, many of whom develop colorectal cancer at an early age.
Hereditary nonpolyposis colorectal cancer (HNPCC) is a genetic syndrome caused by mutation in one of several genes. HNPCC accounts for about 3-5% of all colorectal cancer. With HNPCC, people generally develop a single colorectal cancer rather than an unusual number of polyps, as in FAP. Individuals with the HNPCC gene mutations have an 80% lifetime risk of developing colorectal cancer.
Individuals with a family history of colorectal cancer or colorectal adenomas (polyps) also have an increased risk of developing colorectal cancer, as do those with a personal history of either of these conditions. In addition, people suffering from inflammatory bowel disease have a greater chance of developing colorectal cancer.
Diet: Some, but not all, research indicates that a high-fat diet, as well as a diet low in fiber and folic acid, may play a role in the development of colorectal cancer. Three recently published clinical studies, however, have failed to produce evidence to support the theory that a diet low in fiber leads to colorectal cancer.1 There is considerable evidence, however, that a high intake of red meat increases the risk of colorectal cancer.
In a study involving 76,402 women, researchers at the Harvard School of Public Health in Boston found that a “western” diet increases the risk of colon cancer, compared to a “prudent” diet. A “western” diet was defined as including higher levels of red and processed meats, sweets and desserts, French fries, and refined grains while the “prudent” diet consisted of higher intakes of fruits, vegetables, legumes, fish, poultry and whole grains. After the data was adjusted for additional risk factors (which can skew statistical results), the researchers reported that women on a Western diet were 46% more likely to develop colon cancer than women who ate a prudent diet.2
Another dietary factor that has consistently been linked with an increased risk of colorectal cancer is alcohol intake.3,4 Alcohol – regardless of the type (beer, wine, or spirits) — appears to increase the risk of colorectal cancer in both men and women. The risks of moderate alcohol intake must, however, be balanced with the potential benefits; moderate alcohol intake reduces the risk of heart disease.
Obesity: Obesity has consistently been linked with an increased risk of colon cancer in men.5 The extent to which obesity influences colon cancer risk in women is less clear, although larger waist circumference has been linked with increased colon cancer risk in both men and women.6
Smoking: Studies of the link between tobacco and risk of colorectal cancer have been inconsistent. A pooled analysis of the Women’s Health Initiative studies found an increased risk of rectal cancer among smokers, but no increased risk of colon cancer.7 Some previous studies, however, have reported a link between smoking and colon cancer.
Researchers have estimated that more than 50% of colon cancers could be prevented through healthy lifestyle choices.8
Talk with your doctor before starting an exercise program. If your doctor decides that it’s appropriate for you, you may benefit from following exercise guidelines such as those provided by the American Cancer Society.12 Developed for the general population (and not specifically for cancer survivors), the guidelines recommend that adults engage in at least 30 minutes of moderate-to-vigorous physical activity on five or more days per week. A longer duration of exercise (45 to 60 minutes) may provide additional benefits.
Moderate-intensity activity includes brisk walking and cycling on level terrain. Vigorous activity includes cycling or walking up hills and jogging. For more information, visit the physical activity Web site of the Centers for Disease Control and Prevention.
Detection and Treatment of Precancerous Polyps: For cancers such as breast cancer, screening does not prevent the development of the cancer; rather, screening detects the cancer at an early stage when treatment is most likely to be successful. In the case of colon cancer, however, screening can sometimes prevent the development of cancer by identifying precancerous colon polyps. Removing these polyps can prevent the later development of cancer. Colorectal cancer screening tests are described in more detail below.
Diet: There is convincing evidence that excess body fat substantially increases the risk for many types of cancer. While much of the cancer-related nutrition information cautions against a high-fat diet, the real culprit may be an excess of calories. Studies indicate that there is little, if any, relationship between body fat and fat composition of the diet. These studies show that excessive caloric intake from both fats and carbohydrates lead to the same result of excess body fat. The ideal way to avoid excess body fat is to limit caloric intake and/or balance caloric intake with ample exercise.
Studies suggest that high intake of red meat may increase the risk of colorectal cancer. One strategy for positive dietary change is to replace red meat with chicken, fish, nuts and legumes.
For many years, researchers speculated that the low incidence of colorectal cancer in parts of Africa could be linked to a high-fiber diet; however, several studies have failed to support this theory. In 1999, three pivotal clinical studies evaluating the effects of a high-fiber diet on colorectal cancer failed to establish a correlation between high fiber consumption and reduction in the incidence of colorectal cancer. In two of these studies, researchers directly compared 2 groups of individuals with either high or low fiber consumption and found an equal number of polyps in each group. There are many reasons to eat a diet high in fiber, particularly to help reduce the risk for coronary artery disease; however, such a diet does not appear to help prevent the development of colorectal polyps or cancer.
There is strong evidence that moderate to high alcohol consumption increases the risk of certain cancers. One reason for this relationship may be that alcohol interferes with the availability of folic acid. Alcohol in combination with tobacco may create an even greater risk.
Nonsteroidal Anti-inflammatory Drugs (NSAIDS): NSAIDS are used to reduce inflammation and pain; they include drugs such as aspirin and ibuprofen. Studies have suggested that NSAIDS reduce the risk of colorectal cancer.13 The potential benefits of regular use of these drugs, however, must be weighed against the potential risks. In 2007, the U.S. Preventive Services Task Force (USPSTF) recommended against routine use of aspirin or other NSAIDS for the prevention of colorectal cancer in individuals at average risk of colorectal cancer.14
The following points contributed to this decision:
The USPSTF notes, however “These recommendations do not apply to patients with a personal history of colorectal cancer or other conditions that put them at high risk for the disease.” It is also important to note that these recommendations do not alter previous recommendations about the use of low-dose aspirin in people at increased risk of cardiovascular disease.
Patients at high risk for colorectal cancer as a result of personal or family history may wish to talk with their doctor about steps they can take to reduce their risk.
Calcium: Researchers have demonstrated a link between high calcium intake and a reduction in the development of colorectal adenomas. One study showed that patients taking 1200 mg of calcium daily demonstrated a 20% reduction in colorectal adenoma formation and a 45% reduction in advanced adenoma formation.15 Physicians surmise that a reduction in adenoma formation would lead to a reduction in cancer rates. Furthermore, calcium and Vitamin D may work synergistically to decrease adenoma formation.16
Vitamin D: Vitamin D is a fat-soluble vitamin that comes from dietary supplements, foods such as fortified milk and cereal, certain kinds of fish (including salmon, mackerel, and tuna), and exposure to sunlight. Vitamin D is hypothesized to play a role in the prevention of some types of cancer, including colon cancer. According to results from two large studies – the Health Professionals Follow-up Study and the Nurses’ Health Study – individuals with higher blood levels of vitamin D may have a reduced risk of developing colon cancer.17
For many types of cancer, progress in cancer screening has offered promise for earlier detection and higher cure rates. The term screening refers to the regular use of certain examinations or tests in persons who do not have symptoms of cancer.
Screening is crucial for the prevention and early detection of colorectal cancer. The American Cancer Society currently recommends that people at average risk of colorectal cancer begin being screened for colorectal cancer at the age of 50. Screening may need to begin at a much earlier age for people with a personal or family history of adenomatous polyps, FAP, HNPCC, colorectal cancer, or chronic inflammatory bowel disease.
Several screening strategies are currently available. These include the fecal occult blood test (FOBT), flexible sigmoidoscopy, colonoscopy and double contrast barium enema. The frequency of screening depends on the method. In general, FOBT is performed every year, sigmoidoscopy is performed every five years, and colonoscopy is performed every 10 years. Individuals interested in colorectal cancer screening should discuss the options with their physician in order to determine the most appropriate procedure.
According to recommendations from the U.S. Preventive Services Task Force (USPSTF), routine colorectal cancer screening should continue until the age of 75.18 Patients over this age may wish to talk with their physician about the need for continued screening.
Fecal Occult-Blood Test (FOBT): The fecal occult-blood test checks for hidden blood in the stool. Recently, results from an 18-year study indicated that annual or biannual FOBT could significantly reduce the incidence of colorectal cancer. If positive, this test indicates the presence of bleeding polyps and the need for further screening, such as colonoscopy. The further screening tests allow the identification and removal of polyps, which results in a reduced incidence of colorectal cancer.
Fecal Immunochemical Test (FIT): Fecal immunochemical tests are a newer type of fecal occult-blood test. Unlike traditional FOBT, FIT does not require drug or dietary restrictions on the part of the patient.
Flexible sigmoidoscopy: During this procedure, a physician uses a lighted tube to look inside the rectum and the lower part of the colon (sigmoid colon) for polyps or areas suspicious for cancer. The physician may perform a biopsy in order to collect samples of suspicious tissues or cells for closer examination. This is an outpatient procedure that does not require sedative anesthesia or pain medication. There are no or few complications associated with this procedure.
Colonoscopy: During this procedure, a longer flexible tube that is attached to a camera is inserted through the rectum, allowing physicians to examine the internal lining of the colon for polyps or other abnormalities. The physician may perform a biopsy in order to collect samples of suspicious tissues or cells for closer examination. This is a more difficult procedure than sigmoidoscopy to perform, requiring anesthesia or heavy sedation, but it allows the entire colon to be viewed. Significant complications occur in 0.1-0.3% of patients or less.19
Double-contrast barium enema: A chalky substance called barium is inserted through the rectum and into the colon and rectum. The patient then undergoes x-rays of the colon and rectum so that the physician can evaluate the area for polyps or other abnormalities. The barium helps open the colon so that the x-rays are more detailed and clear.
While these screening strategies help to monitor for the development of adenomatous polyps and colorectal cancer, other tests exist which may allow physicians to identify patients who are at risk for the development of colorectal cancer.
Predictive genetic testing: A predictive test for hereditary colorectal cancer is now available. This test detects disease-causing mutations in two genes, MLH1 and MSH2, which are responsible for the majority of hereditary non-polyposis colorectal cancer (HNPCC). This test may allow patients who are identified to be at a high risk for HNPCC to have earlier and more frequent exams and to have pre-cancerous polyps removed. Individuals interested in genetic testing should consult with their physicians about the risks and benefits of this procedure.
The potential for earlier detection and higher cure rates increases with the advent of more refined screening techniques. In an effort to provide more screening options and perhaps more effective prevention strategies, researchers continue to explore new techniques for the screening and early detection of cancer.
Several new strategies for the screening of colorectal cancer have recently emerged. Despite progress in this area, it is still important that individuals continue to utilize the standard screening procedures in an effort to maintain health and detect colorectal cancer early when it is most treatable. However, these new procedures hold promise for earlier and more reliable detection of colorectal cancer and some individuals may be interested in participating in clinical trials that will help to determine the effectiveness of these new techniques.
DNA stool test: This new screening procedure involves looking for abnormal DNA in stool samples. Changes in DNA occur as tumors develop in the colon. The tumors shed cells into the intestine, which makes it possible to detect the abnormal DNA cells in stool samples. This simple, non-invasive screening procedure has proven effective in some clinical studies20 but is expensive to perform. Research is ongoing to determine the feasibility of using this as a standard screening procedure.
Virtual colonoscopy: In virtual colonoscopy (also called CT colonography), spiral CT scanners scan the entire colon to produce a 3-D image. The procedure allows for the complete visualization of the colon more quickly and less invasively than with conventional colonoscopy, although patients who have polyps detected will still need to undergo conventional colonoscopy to have the polyps removed. Virtual colonoscopy is a promising new technique, but more research may be needed before it becomes a standard screening procedure for colorectal cancer.
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2 Fung T, Hu FB, Fuchs C, et al. Major dietary patterns and the risk of colorectal cancer in women. Archives of Internal Medicine. 2003; 163:309-314.
3 Cho E, Smith-Warner SA, Ritz J et al. Alcohol intake and colorectal cancer: a pooled analysis of cohort studies. Annals of Internal Medicine. 2004;140:603-13.
4 Ferrari P, Jenab M, Norat T et al. Lifetime and baseline alcohol intake and risk of colon and rectal cancers in the European prospective investigation into cancer and nutrition (EPIC). International Journal of Cancer. 2007;121:2065-72.
5 Thygesen LC, Gronbaek M, Johansen C et al. Prospective weight change and colon cancer risk in male US health professionals. International Journal of Cancer. 2008:123:1160-5.
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7 Paskett ED, Reeves KW, Rohan TE et al. Association between cigarette smoking and colorectal cancer in the Women’s Health Initiative. Journal of the National Cancer Institute. 2007;99:1729-35.
8 Harvard Report on Cancer Prevention. Volume 3: Prevention of Colon Cancer in the United States. Cancer Causes and Control. 1999;10:167-180.
9 Howard RA, Freedman DM, Park Y, Hollenbeck A, Schatzkin A, Leitzmann MF. Physical activity, sedentary behavior, and the risk of colon and rectal cancer in the NIH-AARP Diet and Health Study. Cancer Causes and Control. 2008;19:939-53.
10 Nilsen TI, Romundstad PR, Petersen H, Gunnell D, Vatten LJ. Recreational physical activity and cancer risk in subsites of the colon (the Nord-Trondelag Health Study). Cancer Epidemiology Biomarkers & Prevention. 2008;17:183-8.
11 Friedenreich C, Norat T, Steindorf K et al. Physical activity and risk of colon and rectal cancers: the European prospective investigation into cancer and nutrition. Cancer Epidemiology Biomarkers & Prevention. 2006;15:2398-407.
12 Doyle C, Kushi LH, Byers T et al. Nutrition and physical activity during and after cancer treatment: an American Cancer Society Guide for informed choices. CA: A Cancer Journal for Clinicians. 2006;56:323-353.
13 Jacobs E, Thun M, Bain E, et al. A large cohort study of long-term daily use of adult-strength aspirin and cancer incidence. Journal of the National Cancer Institute. 2007; 99: 608-615.
14 U.S Preventive Services Task Force. Routine Aspirin or Nonsteroidal Anti-inflammatory drugs for the primary prevention of colorectal cancer: U.S. preventive services task force recommendation statement. >Annals of Internal Medicine. 2007;146:361-364.
15 Baron JA, Beach M, Mandel JS, van Stolk RU, Haile RW, Sandler RS, Rothstein R, Summers RW, Snover DC, Beck GJ, Bond JH, Greenberg ER. Calcium supplements for the prevention of colorectal adenomas. Calcium Polyp Prevention Study Group. New England Journal of Medicine. 1999;340:101-107
16 Grau MV, Baron JA, Sandler RS, Haile RW, Beach ML, Church TR, Heber D. Vitamin D, calcium supplementation, and colorectal adenomas: results of a randomized trial. Journal of the National Cancer Institute. 2003; 95: 1765-1771.
17 Wu K, Feskanich D, Fuchs CS, Willett WC, Hollis BW, Giovannucci EL. A nested case-control study of plasma 25-hydroxyvitamin D concentrations and risk of colorectal cancer. Journal of the National Cancer Institute. 2007;99:1120-9.
18 U.S. Preventive Services Task Force. Screening for Colorectal Cancer: U.S. Preventive Services Task Force Recommendation Statement. Annals of Internal Medicine. Early online publication October 7, 2008.
19 Zubarik R, Fleisher DE, Mastropietro C, et al. Prospective analysis of complications 30 days after outpatient colonoscopy. Gastrointestinal Colonoscopy. 1999;50:322-8.
20 Itzkowitz SH, Brand R, Jandorf L, et al. A simplified, noninvasive stool DNA test for colorectal cancer detection. American Journal of Gastroenterology. Early online publication August 27, 2008.
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