Colorectal Cancer Health Center

continued...

Obesity

At least three large cohort studies have found an association between obesity and CRC incidence or mortality.[29,30,31] The Nurses' Health Study found that women with a body mass index (BMI) of more than 29, compared with women with a BMI of less than 21, had an adjusted RR for CRC incidence of 1.45 (95% CI ,1.02-2.07).[29] In the CPS II [31], men and women with a BMI of 30 to 34.9 had an adjusted RR for CRC mortality (compared with people with a BMI of 18.5-24.9) of 1.47 (95% CI, 1.30-1.66), with a statistically significant dose-response effect.[31] The effects were similar in men and women.

Factors associated with a decreased risk of colorectal cancer

Physical activity

A sedentary lifestyle has been associated in some [32,33] but not all [34] studies with an increased risk of CRC. Numerous observational studies that have examined the relationship between physical activity and colon cancer risk.[35] Most of these studies have shown an inverse relationship between level of physical activity and colon cancer incidence. The average RR reduction is reportedly 40% to 50%. Large U.S. cohort studies have found statistically significant adjusted RR of 0.54 (95% CI, 0.33-0.90) [29] and 0.53 (95% CI, 0.32-0.88) [30] when comparing people with high versus low average energy expenditure. A meta-analysis of 52 observational studies found an overall adjusted RR of 0.76 (95% CI, 0.72-0.81), with similar results for men and women.[36]

Interventions associated with a decreased risk of colorectal cancer: Benefits and harms

Nonsteroidal anti-inflammatory drugs

Although evidence is currently inadequate to determine whether nonsteroidal anti-inflammatory drugs (NSAIDs) reduce CRC incidence, proponents suggest that any effect of these drugs results from their ability to inhibit the activity of cyclooxygenase (COX). COX is important in the transformation of arachidonic acid into prostanoids, prostaglandins, and thromboxane A2. NSAIDs include not only aspirin (acetylsalicylic acid [ASA]) (which is considered separately here) and other, first-generation nonselective inhibitors of the two functional isoforms of COX, termed COX-1 and COX-2, but also newer second-generation drugs that inhibit primarily COX-2. Normally, COX-1 is expressed in most tissues and primarily plays a housekeeping role (e.g., gastrointestinal mucosal protection and platelet aggregation). COX-2 activity is crucial in stress responses and in mediating and propagating the pain and inflammation that are characteristic of arthritis.[37]

Nonselective COX inhibitors include indomethacin (Indocin); sulindac (Clinoril); piroxicam (Feldene); diflunisal (Dolobid); ibuprofen (Advil, Motrin); ketoprofen (Orudis); naproxen (Naprosyn); and naproxen sodium (Aleve, Anaprox). Selective COX-2 inhibitors include celecoxib (Celebrex), rofecoxib (Vioxx), and valdecoxib (Bextra). Rofecoxib and valdecoxib are no longer marketed because of an associated increased risk of serious cardiovascular events.