Hormone the culprit between obesity and colon cancer

A team of scientists from the University of California, San Diego say they believe a chemical produced by fat cells encourages colon cancers to grow faster; they say this may explain why severely overweight people appear to be at far greater risk of the disease.

The research team say obese people are up to three times more likely to develop colorectal cancer and the hormone leptin could be the culprit.

The hormone apparently triggers an increased growth in human colon cancer cells as the more fat cells a person has, the more leptin appears in their bloodstream.

Previous research has already established that some colon cancer cells appear to be organised to respond to leptin, with "receptors" for the chemical on their surfaces.

The San Diego team were eager to discover further evidence of the link by watching what happened to human cancer cells exposed to the hormone in the laboratory, so they added the hormone to different varieties of cancer cells.

Dr. Kim Barrett who led the research, says growth was stimulated in all the cell lines and in two out of three tested, the hormone also hampered the usual process of programmed death that allows the body to replace normal cells, but which often malfunctions in cancers.

Dr. Barrett says the results may explain why obesity increases a person's risk of colonic cancer and could lead to drug companies developing new treatments against the disease.

According to the study colon cancer patients suffer from cancerous growths in the colon, rectum and appendix.

Britain is currently the most obese country in Europe with one in five men and a quarter of all women catergorised as obese.

As many as 30,000 people a year die prematurely from obesity-related conditions, including cancers.

The latest research suggests that severely obese men double their risk of dying from prostate cancer and obesity is also believed to increase the chance of developing breast cancer.

The study is published in the British Journal of Surgery.