(4 of 5)
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.
Over the past few years, researchers have shown that folks who take daily doses of aspirin — which is known to block COX2 — are less likely to develop precancerous growths called polyps. The problem with aspirin, however, is that it can also cause internal bleeding. Then in 2000, researchers showed that Celebrex, another COX-2 inhibitor that is less likely than aspirin to cause bleeding, also reduces the number of polyps in the large intestine.
So, should you be taking Celebrex to prevent colon cancer? It's still too early to say. Clearly COX-2 is one of the factors in colon cancer. "But I don't think it's the exclusive answer," says Ray DuBois, director of cancer prevention at the Vanderbilt-Ingram Cancer Center in Nashville, Tenn. "There are a lot of other components that need to be explored."
Asprin for Alzheimer's Disease?
When doctors treating Alzheimer's patients took a closer look at who seemed to be succumbing to the disease, they uncovered a tantalizing clue: those who were already taking anti-inflammatory drugs for arthritis or heart disease tended to develop the disorder later than those who weren't. Perhaps the immune system mistakenly saw the characteristic plaques and tangles that build up in the brains of Alzheimer's patients as damaged tissue that needed to be cleared out. If so, the ensuing inflammatory reaction was doing more harm than good. Blocking it with anti-inflammatories might limit, or at least delay, any damage to cognitive functions.
The most likely culprits this time around are the glial cells, whose job is to nourish and communicate with the neurons. Researchers have discovered that glial cells can also act a lot like the mast cells of the skin, producing inflammatory cytokines that call additional immune cells into action. "The glial cells are trying to return the brain to a normal state," explains Linda Van Eldik, a neurobiologist at Northwestern University Feinberg School of Medicine in Chicago. "But for some reason, in neurodegenerative diseases like Alzheimer's, the process seems to be out of control. You get chronic glial activation, which results in an inflammatory state."