The infection connection
Microbial triggers of chronic inflammation
What is the spark that lights the fires of chronic inflammation? Is it defective genes? Too many bacon-cheeseburgers? Toxic chemicals in our air, water and food?
Genetic and environmental factors certainly may contribute to inflammatory conditions, but there is another, albeit controversial explanation for them—persistent, and often silent, infections.
One of the most outspoken proponents of this theory, Paul Ewald, Ph.D., of the University of Louisville, argues that defective genes are an unlikely cause of chronic diseases because, over evolutionary time, they should have disappeared from the human population. Although there are exceptions in which a mutation may be beneficial (such as the mutation for sickle cell anemia which provides resistance to malaria), Ewald thinks that infectious agents are more likely culprits.
“Bad genes and bad environments have often been falsely accused, or, at least, they have taken more than their share of the blame. Viruses and bacteria are the primary offenders,” he writes in his 2002 book Plague Time: The new germ theory of disease.
Perhaps the most convincing evidence for his argument comes from the example of ulcer disease. For years, the medical community believed that stress and spicy food caused most ulcers. However, in the 1980s a team of researchers led by Barry Marshall, M.D., at the University of Western Australia made a radical proposal—that a curiously curvy bacterium called Helicobacter pylori was the primary cause of gastric ulcers.
Marshall proved that this bacterium was the cause of ulcers by guzzling an H. pylori cocktail. He subsequently developed gastritis, an inflammation of the stomach lining and precursor to ulcer disease, which was cured by a course of antibiotics.
Marshall’s revolutionary idea didn’t catch on immediately. “It probably took five or six years for the medical community to grasp the concept that ulcer disease was indeed an infectious disease,” says Richard Peek, M.D., chief of the Division of Gastroenterology, Hepatology and Nutrition at Vanderbilt University Medical Center.
According to the U.S. Centers for Disease Control and Prevention, H. pylori is now considered to be responsible for 80 percent to 90 percent of ulcers and is associated with a two- to six-fold increased risk of gastric cancers. Approximately two-thirds of the world’s population is infected with the bacterium.
Yet most people who are infected never develop ulcers or gastric cancers. Why not? Peek believes the body’s inflammatory response to the infection may be the answer.
“It appears that disease results from the dynamic interactions between a particular virulent strain (of H. pylori) and a susceptible host,” he says. “Most of these host genetic differences we are finding are within inflammatory genes.”
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