People with chronic fatigue syndrome (CFS) often go years without a diagnosis—and even after getting one, the “realness” of their condition may be questioned by friends, family members, and even doctors. That’s partially because there are no tests to determine whether a person has CFS (also known as myalgic encephalomyelitis or ME/CFS) and because symptoms can vary widely from person to person.
But new research is offering hope to CFS sufferers, and to doctors who diagnose and treat the condition. In a study published in the Proceedings of the National Academy of Sciences, Stanford University researchers identify 17 proteins whose levels in the blood appear to be related to CFS severity. They say the discovery is an important step in proving that CFS does have a physical cause, and hopefully in developing a diagnostic test for the condition, as well.
For the study, researchers analyzed blood samples from 186 chronic fatigue patients who’d been experiencing symptoms for more than 10 years on average, and 388 healthy people. They tested for levels of 51 different cytokines, or proteins that are secreted by immune cells and circulate in the blood.
When the researchers compared average cytokine levels in CFS patients versus the healthy control samples, they found that only 2 of the 51 substances they tested for were significantly different: One, called tumor growth factor beta, was higher in CFS patients, while the other, called resistin, was lower.
But when they looked more closely at CFS patients—and began to compare those with mild cases to those with more serious ones—they found more cytokine connections. In total, the levels of 17 different cytokines seemed to fluctuate with symptom severity: They were lower in people with mild symptoms when compared to the control group, but higher in people with severe symptoms.
The fact that these cytokine levels were high in some CFS patients but low in others explains why, in the overall analysis, the findings canceled each other out. It could also be why previous studies have failed to find such associations, the authors wrote in their paper. The differences could be due to genetics, they say, and may be a clue as to why some patients only develop mild symptoms while others fare much worse.
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Researchers have long suspected that CFS is related to inflammation, and these results support that theory. Of the 17 cytokines linked to symptom severity, 13 are known to promote inflammation. One of those cytokines is leptin, a satiety hormone secreted by fat tissue, which women tend to have more of than men. This could help explain why three quarters of CFS patients are women, the authors say.
But the biggest takeaway from this study, they say, is that the identification of these 17 biomarkers (substances that indicate the presence of disease) could lead to the development of a laboratory test to diagnose CFS.
“There’s been a great deal of controversy and confusion surrounding ME/CFS—even whether it is an actual disease,” said senior author Mark Davis, professor of immunology and microbiology, in a press release. “Our findings show clearly that it’s an inflammatory disease and provide a solid basis for a diagnostic blood test.”
It could also pave the way for future research into treatments that can target these specific cytokines, suggests Anthony Komaroff, an epidemiologist at Harvard University and author of a forthcoming commentary to be published with the new study. It is now clear that there are real abnormalities in patients with CFS, Komaroff wrote in his commentary—although he also points out that these abnormalities should be confirmed with further research.
“Fortunately, the National Institutes of Health has announced it intends to increase its intramural and extramural investment in CFS research, and many laboratories outside the United States are also actively investigating the illness,” Komaroff wrote. “Hopefully, a decade from now, doctors will know better what to measure and, more importantly, what to do to ease the suffering caused by this illness.”
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