For years, infectious disease expert Jose Montoya, MD, has been frustrated by the mysteries of chronic fatigue syndrome (also known as myalgic encephalomyelitis) and the unexplainable and often debilitating symptoms of the many patients who come through his clinic at Stanford. But earlier this year, Montoya’s perseverance was rewarded and his optimism soared following a seven-year study he led that showed that the disease has a clear link to 17 immune system proteins, including 13 proteins that are pro-inflammatory.
This proved what scientists had suspected — that inflammation is the prime driver behind the disease, which affects between one and four million people, often with devastating effects. When the finding first came to light, Montoya told me he was “ecstatic.”
“This is telling the world that we have finally a biological correlate for these patients’ symptoms,” he said to me in a recent Q&A for Stanford Medicine News. “These patients are not crazy. Our findings validate their symptoms — that their illness is real and has a biological basis. Now that we know that this is something real, ingrained in the biology of the body and the immune system that explains why these patients are so sick, we could end up with a blood test, but equally or more exciting, now we can find drugs to conquer the disease.”
In the study, the researchers analyzed blood samples from 200 patients, comparing them to 400 controls. Among the CFS patients, they found 17 immune system molecules known as cytokines that tracked the patients’ symptoms and the severity of their illness. Some of these cytokines were associated with inflammation. In recent years, scientists have developed the ability to measure this kind of inflammation, meaning it may be possible to produce a blood test for the disease, Montoya said.
Even more important, he said, is that these patients might ultimately be offered some form of treatment for the illness, which currently isn’t available. Montoya noted that other inflammatory conditions, such as lupus and rheumatoid arthritis, are treatable, so there’s no reason to believe CFS is any different.
“Now that the study has established that it’s inflammatory, we can look for those drugs that treat inflammation,” Montoya said. “I could die happy if I knew that was the door that was opened.”
Montoya collaborated in the study with Mark Davis, MD, PhD, director of Stanford’s Institute for Immunity, Transplantation and Infection.
Previously: Blood test: Scientists crack code of chronic fatigue syndrome’s inflammatory underpinnings, Stanford researcher develops tools to understand chronic fatigue syndrome, A look at the fight against chronic fatigue syndrome and Unbroken: A chronic fatigue syndrome patient’s long road to recovery
Photo by Steve Fisch