The cause of chronic fatigue syndrome has baffled researchers for decades, leaving patients to suffer a frustrating array of symptoms so varied it’s difficult to diagnose and treat.
But a recent study shows a connection between inflammation and the disease, offering promise for future diagnostics, studies, and potential clinical trials of immune-regulating drugs.
In 2004, Jose Montoya, MD, professor of infectious diseases who oversees the Stanford ME/CFS Initiative, encountered his first patient with chronic fatigue syndrome and never forgot it.
“I have seen the horrors of this disease, multiplied by hundreds of patients,” says Montoya, lead author of the study published online July 31 in the Proceedings of the National Academy of Sciences. “It’s been observed and talked about for 35 years now, sometimes with the onus of being described as a psychological condition. But chronic fatigue syndrome is by no means a figment of the imagination. This is real.”
He began exploring whether inflammation was key in diagnosing the syndrome after noticing the sporadic effectiveness of antiviral and anti-inflammatory drugs. He called in Mark Davis, PhD, senior author of the study, professor of immunology and microbiology, and director of Stanford’s Institute for Immunity, Transplantation and Infection.
Their teams analyzed blood samples from 192 of Montoya’s patients and 392 healthy control subjects. Results showed certain biomarkers, some of which cause inflammation, were higher in patients with severe symptoms and lower in those with milder symptoms.