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The Fires Within #5/8 ( By TIME - Feb. 23. 2004 )

What they have discovered is a complex interplay between inflammation, insulin and fat--either in the diet or in large folds under the skin. (Indeed, fat cells behave a lot like immune cells, spewing out inflammatory cytokines, particularly as you gain weight.) Where inflammation fits into this scenario--as either a cause or an effect--remains unclear. But the case for a central role is getting stronger. Dr. Steve Shoelson, a senior investigator at the Joslin Diabetes Center in Boston, has bred a strain of mice whose fat cells are supercharged inflammation factories. The mice become less efficient at using insulin and go on to develop diabetes. "We can reproduce the whole syndrome just by inciting inflammation," Shoelson says.

That suggests that a well-timed intervention in the inflammatory process might reverse some of the effects of diabetes. Some of the drugs that are already used to treat the disorder, like metformin, may work because they also dampen the inflammation response. In addition, preliminary research suggests that high CRP levels may indicate a greater risk of diabetes. But it's too early to say whether reducing CRP levels will actually keep diabetes at bay.

CANCER: THE WOUND THAT NEVER HEALS

Back in the 1860s, renowned pathologist Rudolf Virchow speculated that cancerous tumors arise at the site of chronic inflammation. A century later, oncologists paid more attention to the role that various genetic mutations play in promoting abnormal growths that eventually become malignant. Now researchers are exploring the possibility that mutation and inflammation are mutually reinforcing processes that, left unchecked, can transform normal cells into potentially deadly tumors.

How might that happen? One of the most potent weapons produced by macrophages and other inflammatory cells are the so-called oxygen free radicals. These highly reactive molecules destroy just about anything that crosses their path--particularly DNA. A glancing blow that damages but doesn't destroy a cell could lead to a genetic mutation that allows it to keep on growing and dividing. The abnormal growth is still not a tumor, says Lisa Coussens, a cancer biologist at the Comprehensive Cancer Center at the University of California, San Francisco. But to the immune system, it looks very much like a wound that needs to be fixed. "When immune cells get called in, they bring growth factors and a whole slew of proteins that call other inflammatory cells," Coussens explains. "Those things come in and go 'heal, heal, heal.' But instead of healing, you're 'feeding, feeding, feeding.'"

Sometimes the reason for the initial inflammatory cycle is obvious--as with chronic heartburn, which continually bathes the lining of the esophagus with stomach acid, predisposing a person to esophageal cancer. Other times, it's less clear. Scientists are exploring the role of an enzyme called cyclo-oxygenase 2 (COX-2) in the development of colon cancer. COX-2 is yet another protein produced by the body during inflammation.



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