Several new studies into colon cancer have identified early changes that turn on wrong gene switches that in turn cause colon cancer. One study links obesity to colon cancer¹, the other study links digestive inflammation to colon cancer². The good news is that by taking proactive steps these adverse changes can be easily stopped.

For the first time a clear gene-related link explains how obesity causes colon cancer. Adiponectin, like leptin, is a hormone signal that comes from fat cells. It maintains normal levels when leptin is working properly. When leptin levels elevate during obesity (leptin resistance) then adiponectin levels improperly drop. This leads directly to insulin resistance and Type II diabetes. Some individuals have a gene alteration that enables higher than normal production of adiponectin, which also confers significant protection against colon cancer. The research, published in JAMA, showed that low adiponectin significantly elevated colon cancer risk. Earlier research has also pointed to low adiponectin³ as a factor in various cancers, especially breast cancer.

Other research shows that during digestive inflammation a gene called P-Cadherin malfunctions, leading to the spreading of inflamed digestive tissue and setting the stage for colon cancer. The malfunctioning gene was suffering from hypomythelation, meaning it lacked methyl donors.

Collectively, these studies mean that a person with a history of digestive problems who is also overweight has multiple factors of colon cancer risk. Since cancer would take 10-15 years to form as a result of these stressors. That gives many people ample warning and time to take action. Colon cancer is the second deadliest form of cancer (behind lung cancer) and only ½ the people treated survive.