Diet Connection

Does Scientific Data Support the Idea that Diet Can Affect Colon Cancer Risk?

For centuries, it has been suspected that diet influences cancer development. This is particularly true for colon cancer. Among the first modern evidence for this came from studies of Japanese citizens who emigrated to the US earlier this century. Investigators observed that Japanese natives developed colon cancer less often than US citizens did. However, after living in the US for many years, these migrants developed colon cancer at rates similar to other US citizens. This change was likely due to abandoning the traditional low fat Japanese diet and adopting a colon cancer-promoting Western diet.

Other studies suggest a connection between colon cancer and the amount of meat and fat a person consumes. The amount of meat and fat eaten was compared in different countries worldwide; the more meat and fat was consumed in a certain country, the more colon cancer would be observed there. Denis Burkitt, a famous British surgeon working in Africa as a medical missionary, made the keen observation that Africans consume a large amount of dietary fiber and rarely develop colon cancer. These two observations formed the foundation for modern theory of the effect of diet on colon cancer.

Intensive work has been done to verify these landmark observations and to identify other factors affecting colon cancer development. Possible elements include: a) daily energy intake (i.e., the number of calories one eats per day); b) abundance or deficiency of specific nutrients; c) abundance or deficiency of nutrients from selected sources (such as meats or vegetables); or d) the presence of cancer-causing substances in foods. It is possible that any or all of these are important in the development of colon cancer. Selected key factors are briefly discussed below.
 

Key Research Areas
Calories: Total daily caloric intake (also known as total energy intake) may be important in colon cancer development. In animal studies, it has been shown that cutting calories reduces the formation of colon tumors. Human studies also have suggested but not proven this. Obesity has also been linked with increased colon cancer risk. Consumption of more calories than are burned off causes weight gain and obesity.

Fat: Much scientific evidence (from studies in people and animals) suggests that the greater the amount of fat in the diet, the greater the risk for colon cancer. Animal fat, particularly that derived from red meats, is a prime offender. Experiments in animals have found that certain fats are worse than others. Saturated or certain polyunsaturated fats (such as corn and safflower oils) promote colon cancer, whereas other fats, such as those derived from cold water fish (fish oils), prevent it. These observations need to be confirmed in humans before they can be fully accepted. The ways that dietary fat influences colon cancer are not entirely known but are currently under intense laboratory investigation such as in our clinical research studies at The Rockefeller University Hospital Clinical Research Center (http://www.rucares.org).

Cholesterol: Dietary cholesterol intake has been linked to colon cancer. However, since evidence for this association has not been consistent, this association must be viewed as indefinite until more evidence is available.

Fiber: Fiber, the indigestible, mostly plant-based material in the food we eat, has been accepted as preventing colon cancer. This has recently been called into question, particularly the ability of fiber alone to reduce colon cancer development. The relationship between fiber and cancer risk demonstrates that the link between diet and disease is very complex. Translating dietary information into nutrient information is difficult, since measurement of "doses," determination of fiber content of foods, and influence of co-variables such as fat and vitamin intake are hard to assess. Furthermore, the study of diet as a risk factor is difficult due to problems relating to the recall of diet (e.g., patients with cancer are more likely to recall having had a "bad" diet than are healthy subjects), and in the "selection" of patients (e.g., sicker patients may not survive long enough to enter a clinical study). Moreover, the study population itself may not represent the population as a whole (e.g., the nurses followed in the previously mentioned Harvard study may have other health habits that protect them from colon cancer).

Regardless, there are many reasons to suspect that a fiber-rich diet can prevent colon cancer. Dietary fiber acts as a bulking agent, diluting the levels of harmful and potentially cancer-causing chemicals in the colon and rectum. It also speeds the passage of stool through the colon, thereby reducing the exposure time to potential cancer-causing chemicals, and enhancing excretion. Fiber may effect a "tumor suppression" gene (a gene that protects against abnormal growth of cells). Additionally, fiber may be digested by colonic bacteria into beneficial chemicals, such as butyric acid, which may protect the colon and rectum against developing pre-cancerous polyps (nodules arising from the lining of the colon) and cancers.

Fruits and Vegetables: These foods reduce the risk of developing pre-cancerous polyps as well as full-blown colon cancers. Most are rich in fiber and both groups contain little fat; however, there is more convincing evidence about the beneficial effects of vegetables than of fruits. The ability of either food group to prevent colon cancer is most likely through the action of wide variety of natural compounds they contain (such as vitamins, phenolics, isoflavanoids, etc.). The combination of these beneficial anticancer ingredients in their natural form may be crucial to the effectiveness of these foods in cancer prevention. Some of these compounds are also under investigation in our research studies at the Rockefeller University Hospital.

Calcium: Calcium has been reported to inhibit colon cancer development. A recent double-blind placebo-controlled clinical study found that 1200 mg of calcium per day, given as a dietary supplement, reduced the reappearance of pre-cancerous colon polyps in patients who had polyps removed from their colon or rectum previously. Calcium may bind to and inactivate cancer-promoting substances, such as bile acids, within the colon.

Vitamins and Minerals: Folic acid, the antioxidant vitamins A, C, D, E, and the mineral selenium have all been reported to prevent colon cancer. However, there is not enough data to declare that each unequivocally possesses colon cancer preventive properties. Vitamins A, C, E, and selenium may work by preventing damage to the cells the lining the colon.

Alcohol and Coffee:The majority of studies indicate that high alcoholic beverage intake increases the risk for colon cancer, while recent data suggest that coffee consumption may reduce colon cancer risk.

Aspirin and Colon Cancer:Nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin are among the most commonly used drugs. Aspirin, which recently celebrated its one-hundredth birthday, is the model NSAID. Many studies suggest that regular long-term aspirin intake can reduce the risk of colon cancer by as much as 50%. Aspirin also seems to reduce the incidence of pre-cancerous colon polyps. However, NSAIDs have well-known adverse side effects, (such as abdominal discomfort and gastrointestinal ulceration and bleeding), and thus should not be used casually for colon cancer prevention. One should never take NSAIDs for this purpose without being under the care of a physician. Efforts have focused on development of safer NSAIDs. New aspirin-like agents are being investigated to determine if they are safe and effective for the prevention of colon cancer.

Therefore, it is clear that a number of simple dietary changes may indeed reduce one's risk of colon cancer. Recommended dietary guidelines regarding these factors along with typical quantities found in common foods are discussed in the article, "Practical Dietary Advice to Reduce Colon Cancer Risk."

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