Stanford scientists have linked auto immune inflammation to Myalgic encephalomyelitis also known as chronic fatigue syndrome, a debilitating disease with no known cure.
Researchers at the Stanford University School of Medicine have linked ME/CFS to variations in 17 immune-system signalling proteins, or cytokines, whose concentrations in the blood correlate with the disease’s severity.
The findings, published in the Proceedings of the National Academy of Sciences, could be used to improve the diagnosis and treatment of the disorder, which has eluded doctors for decades.
More than 250,000 people in the UK suffer from ME/CFS, a disease with no known cure or effective treatments which typically persists for decades.
“Chronic fatigue syndrome can turn a life of productive activity into one of dependency and desolation,” said Jose Montoya, MD, professor of infectious diseases, who is the study’s lead author.
‘Solid basis for a diagnostic blood test’
“There’s been a great deal of controversy and confusion surrounding ME/CFS — even whether it is an actual disease,” said Davis. “Our findings show clearly that it’s an inflammatory disease and provide a solid basis for a diagnostic blood test.”
“Many ME/CFS patients experience symptoms common in inflammation-driven diseases, But because its symptoms are so diffuse —sometimes manifesting as heart problems, sometimes as mental impairment nicknamed “brain fog,” other times as indigestion, diarrhea, constipation, muscle pain, tender lymph nodes and so forth — it often goes undiagnosed, even among patients who’ve visited a half-dozen or more different specialists in an effort to determine what’s wrong with them.” Montoya said.
“I have seen the horrors of this disease, multiplied by hundreds of patients,” he said. “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.”
The study’s senior author is Mark Davis, PhD, professor of immunology and microbiology and director of Stanford’s Institute for Immunity, Transplantation and Infection. Davis helped create the Human Immune Monitoring Center.
“I have seen the horrors of this disease, multiplied by hundreds of patients.”
The researchers found that only two of the 51 cytokines they measured were different in comparison to healthy subjects. Tumor growth factor beta was higher and resistin was lower in ME/CFS patients. However, the investigators found that the concentrations of 17 of the cytokines tracked disease severity. Thirteen of those 17 cytokines are pro-inflammatory.
ME/CFS patients have a higher than normal incidence of lymphoma, and Montoya speculated that TGF-beta’s elevation in ME/CFS patients could turn out to be a link.
Leptin is a cytokine whose levels corresponded to disease severity. Leptin is secreted by fat tissue is known for telling the brain when somebody’s stomach is full. Leptin is also an active pro-inflammatory substance and is more abundant in women’s blood than in men’s, which may be why more women than men have ME/CFS.
“For decades, the ‘case vs. healthy controls’ study design has served well to advance our understanding of many diseases,” Montoya said. “However, it’s possible that for certain pathologies in humans, analysis by disease severity or duration would be likely to provide further insights.”
Other Stanford co-authors of the study are clinical research coordinator Jill Anderson; Tyson Holmes, PhD, senior research engineer at the Institute for Immunity, Transplantation and Infection; Yael Rosenberg-Hasson, PhD, immunoassay and technical director at the institute; Cristina Tato, PhD, MPH, research and science analyst at the institute; former study coordinator Ian Valencia; and Lily Chu, MSHS, a board member of the Stanford University ME/CFS Initiative.