What are the Risk Factors associated with Colorectal Cancer?
The exact causes of colorectal cancer are still unknown, but certain risk factors are known to increase the chances of developing this disease. Individuals who have cancer, including women with uterine, ovarian, and breast cancers, are at increased risk of colorectal cancer. Individuals who have been previously treated for colorectal cancer are at risk for recurrence.
- Personal history of adenomatous polyps
- Personal and/or family history of colorectal cancer
- Inflammatory Bowel Disease
- Irritable Bowel Syndrome
- Ulcerative Colitis
- Tobacco Use
- Age - over 50 at increased risk
- Physical inactivity
Colorectal cancer most commonly occurs inside of a polyp,which are usually benign growths that protrude from the mucous membrane forming in the colon and rectum. However, if polyps are left untreated they can become adenomatous polyps, which will eventually progress into cancer. As individuals age, their risk of developing polyps increases as does their risk for developing colorectal cancer. Proper screening for colorectal polyps is recommended to begin at 50 years old in the general population and sooner in individuals with a family history of colorectal cancer.
|Location of the colon in the body, with the corresponding cut-away section of a colon segment with polyps.|
Those with family members who have had colon cancer are at increased risk. Several genes are known to cause colon cancer, and there may be others not yet identified. Doctors say that a family has hereditary colorectal cancer when the exact gene causing the disease in that family has been pinpointed.
Colorectal cancer, or a predisposition to this disease, may be inherited. In particular, familial adenomatous polyposis (FAP) is an autosomal dominant disorder in which affected patients have 100 percent risk of colorectal cancer development. A mutation of the APC gene (adenomatous polyposis coli (APC)) on chromosome 5 causes this disease. Gene testing is available to identify patients with this genetic mutation. Sporadic colorectal cancer is the term given to those patients who are affected with the disease, but have no family history of this condition.
Hereditary nonpolyposis colorectal cancer (Lynch syndrome or HNPCC), an autosomal dominant disorder, is a disease in families where multiple members have colorectal and other forms of cancer. The syndrome causes right-sided colon cancer and may produce primary cancers in other sites. Researchers have isolated five mutated genes associated with HNPCC: human MutS homolog 2 gene (hMSh2), MutL homolog 1 gene (hMLh1), human PMS homolog 1 gene (hPMS1), and human PMS homolog 2 gene (hPMS2) and MSH6 (MS homolog 6 gene). Hereditary nonpolyposis colorectal cancer is characterized in families with at least three members with colorectal cancer (one must be a first degree relative of the other two), at least two successive generations.
Diet is considered a determinant of increased risk in the development of colorectal cancer. Although it is difficult to ascertain which components of the diet are most important in conferring cancer risk, compelling evidence suggests a strong dose-related association between red meat and fat intake and colorectal cancer.
While consumption of animal fat is positively associated with colon cancer, consumption of fish and skinless chicken is associated with lower risk. Higher cholesterol values (a reflection of total dietary fat intake) correlate significantly with later tumor development. Obesity in middle age is also associated with increased risk of colon cancer in men; increased physical activity appears to eliminate this risk.
Dietary fiber demonstrates a protective effect in the pathophysiology of colorectal cancer. Diets rich in vegetables and high fiber grains demonstrated significant protection against fatal colorectal cancer, as revealed in a prospective study of more than 760,000 people. Fiber appears to have a number of mechanisms responsible for its protective effects. First, fiber decreases the fecal transit time by increasing stool bulk. Fiber also appears to dilute the concentration of other colonic constituents, which tend to minimize contact between carcinogens and colon epithelium. In addition, fiber is not digested or absorbed in the small intestine but undergoes fermentation in the presence of the colonic flora. This reduces fecal pH and generates short-chain fatty acids (certain short-chain fatty acids can protect isolated colonic epithelial cells).
Diet appears to play a significant role in determining the incidence of colorectal cancers in the general population. Although the international incidence of colorectal cancer varies widely, groups migrating from low-risk to high-risk regions experience an increase in the incidence of the disease. Diets high in fat and low in fiber have consistent associations with increased colorectal cancer risk. Suggestions for diet modification to reduce cancer risk include: reduced caloric intake, reduction of dietary fat to less than 35% of caloric consumption, increased consumption of fresh fruit and vegetables with at least 25 g of fiber (see Lifestyle) (link to hereditary colon cancer web site Lifestyle section). Those using aspirin have less colorectal cancer than the rest of the population. Though the mechanism by which aspirin and NSAIDs exert a protective effect against tumor formation is speculative, studies have revealed a significant reduction in relative risk of colon cancer death among users (aspirin use more than 16 times per month).
Ulcerative Colitis and Crohn's Disease
Individuals with ulcerative colitis and Crohn's disease, among other inflammatory bowel diseases, are at increased risk of developing colorectal cancer.Ulcerative colitis and Crohn's disease are inflammatory conditions of the intestines; both are known risk factors for colorectal cancer. The risk of development of colorectal cancer is related to the severity and duration of the disease. Patients with ulcerative colitis and Crohn’s disease should undergo colonoscopic surveillance for epithelial dysplasia, a precursor to cancer, at routine intervals. Surveillance should be performed every 1–2 years in patients with 8-10 years duration of disease and annually in those with disease history of over 15 years.
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