C-reactive protein predicts colon cancer risk
The marker of inflammation known as C-reactive protein (CRP), which, when elevated, has emerged as a risk factor for cardiovascular disease, appears additionally to be predictive of one’s risk for developing colon cancer, according to a study published in the February 4 2004 issue of The Journal of the American Medical Association. Researchers at the Johns Hopkins Medical Institutions analyzed data obtained from 22,887 participants in the CLUE II ("Give Us a Clue to Cancer and Heart Disease") study who were followed from 1989 to 2000, and who had not been diagnosed with colorectal cancer at the study’s onset. Participants completed health questionnaires upon enrollment, and provided blood samples that were analyzed for C-reactive protein. The investigators identified 131 cases of colon cancer and 51 cases of rectal cancer that occurred during follow-up, and matched each of these subjects for age, gender, and other factors with two healthy controls.

It was discovered that median CRP levels were higher among individuals who developed colon cancer than in those who remained free of the disease. Subjects who had a median C-reactive protein of 2.44 milligrams per liter experienced a higher risk of developing colon cancer than participants whose median CRP was low at 1.94 milligrams per liter. Individuals in the top fourth of CRP levels had 2.5 the risk of developing colon cancer than that of those in the lowest fourth. There was no association found between levels of CRP and rectal cancer.

It was noted that participants who had taken aspirin or other nonsteroidal anti-inflammatory drugs with two days before having their blood drawn experienced a reduction in colon cancer risk. Another report published this week in the Annals of Internal Medicine (Feb 2004), found that women who reported taking two or more aspirin per day had half the risk of developing colon polyps than those who reported no aspirin use. Colon polyps are frequently a precursor of colon cancer.

Lead author and assistant professor of medicine at Johns Hopkins, Thomas P. Erlinger, MD, MPH, commented, "Higher levels of C-reactive protein are linked to an increased risk of several apparently distinct, chronic diseases: heart disease, stroke, diabetes, and now colon cancer. However, it's not clear yet how or whether measuring C-reactive protein would fit into current screening and prevention strategies for colorectal cancer. Further studies should help answer these questions and help clarify the mechanism by which inflammation increases the risk of cancer."

Colorectal Cancer
According to the Centers for Disease Control and Prevention, cancer of the colon and rectum affects nearly 150,000 Americans each year, with one out of every 20 individuals at risk for developing colorectal cancer at some point in their lifetime. It is the second most frequently diagnosed malignancy in the United States, causing approximately 56,000 deaths annually. However, early detection of colorectal cancer dramatically increases survival. For example, 92% of patients who receive early treatment are still alive after 5 years compared to 64% survival when adjacent organs or lymph nodes are affected. Only 7% of patients are alive after 5 years if the cancer is carried to distant organs (Dashwood 1999).

Curcumin has a number of biological effects within the body. However, one of the most important functions is curcumin's ability to inhibit angiogenic growth signals emitted by tumor cells eliciting angiogenesis (growth and development of new blood vessels).

In a study conducted by the International Institute of Anticancer Research in the 2001 edition of Anticancer Research, curcumin inhibited cell proliferation and induced G2/M (cell cycle phase) arrest in HCT-116 colon cancer cells. Furthermore, immunoblot analysis indicated that curcumin caused the induction of apoptosis as evidenced by cleavage of PARP, caspase-3, and reduction in Bcl-XL levels. Curcumin also stimulated the activity of caspase-8 which initiates the Ras signaling pathway of apoptosis. Curcumin therefore appears to exert its anticarcinogenic properties by inhibiting proliferation and inducing apoptosis in certain gastric and colon cancer cells.

The American Health Foundation's Nutritional Carcinogenesis and Chemoprevention Program investigated epidemiological data suggesting that dietary manipulations play an important role in the prevention of many human cancers. Curcumin has been widely used for centuries in the Asian countries without any toxic effects. Epidemiological data also suggest that curcumin may be responsible for the lower rate of colorectal cancer in these countries. Additionally, this data confirmed curcumin is a naturally occurring powerful anti-inflammatory medicine. Curcumin inhibits lipooxygenase activity and is a specific inhibitor of cyclooxygenase-2 (COX-2) expression. Curcumin has been shown to inhibit the initiation of carcinogenesis by inhibiting the cytochrome P-450 enzyme activity and increasing the levels of glutathione-S-transferase. Curcumin has also demonstrated inhibition of the promotion/progression stages of carcinogenesis. The antitumor effect of curcumin has been attributed in part to the arrest of cancer cells in S, G2/M cell cycle phase and to the induction of apoptosis. Curcumin has also inhibited the growth of DNA mismatch repair-defective colon cancer cells. Therefore, curcumin may have value as a safe chemotherapeutic agent for the treatment of tumors exhibiting DNA mismatch repair-deficient and microsatellite-unstable phenotype. The American Health Foundation suggests curcumin should be considered a safe, nontoxic, and easy-to-use chemotherapeutic agent for colorectal cancers in the setting of chromosomal instability as well as microsatellite instability.

https://www.lifeextension.com/protocols/cancer/colorectal

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Life Extension Magazine February 2004 issue

If you have questions or comments concerning this issue or past issues of Life Extension Weekly Update, send them to ddye@lifeextension.com or call 954 766 8433 extension 7716.

For longer life,

Dayna Dye
Editor, Life Extension Weekly Update
ddye@lifeextension.com
954 766 8433 extension 7716
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