Chronic Fatigue Syndrome Is a Physical Illness

People with chronic fatigue syndrome often have trouble explaining why they feel exhausted and in pain.

Much like a mental illness, many people suffering from the illness have had their symptoms dismissed as being “all in their heads.”

But that’s not necessarily true.

New research shows the first “robust” evidence that chronic fatigue syndrome (CFS) — medically known as myalgic encephalomyelitis (ME) — is a physical disorder that may be kick-started by an infection.

We now have evidence confirming what millions of people with this disease already know, that ME/CFS isn’t psychological.”
Dr. Mady Hornig, Center for Infection and Immunity

“We now have evidence confirming what millions of people with this disease already know, that ME/CFS isn't psychological,” Dr. Mady Hornig director of translational research at the Center for Infection and Immunity and associate professor of epidemiology at Columbia's Mailman School, said in a press release.

Researchers at Columbia published a study identifying changes in a person’s immune system that then lead to the disorder.

“This study delivers what has eluded us for so long: unequivocal evidence of immunological dysfunction in ME/CFS and diagnostic biomarkers for disease,” Dr. W. Ian Lipkin, director of the Center for Infection and Immunity and professor of neurology and pathology at Columbia’s Mailman School, said.

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Infection Could Trigger Lasting Immune Response

The Columbia team says their research supports the hypothesis that CFS may be triggered in a “hit-and-run” fashion following a common infection, such as infectious mononucleosis.

The cross-sectional study, published in the journal Science Advances, involved analyzing the blood plasma samples of 298 CFS patients and 348 people without the disease.

The researchers found distinct biomarkers created by the immune system in those with the disease. They also found differences in those who have had the disease for less than three years and those who have had it more than three years.

Those who had the disease for a shorter extent of time had higher amounts of different types of cytokines, or molecules that regulate your body’s defensive response to inflammation and infection.


Specifically, the Columbia team reports, early-stage CFS patients have elevated levels of interleukin-17A, a known biomarker of a faulty immune system.

The researchers added the elevated biomarker levels seem to subside after three years because the immune system has become exhausted after failing to calm itself after an infection. They compared it to an engine running at high gear for an extended period of time.

"Our results should accelerate the process of establishing the diagnosis after individuals first fall ill as well as discovery of new treatment strategies focusing on these early blood markers," Hornig, lead author of the study, said.

Proper diagnosis for CFS has been historically troublesome. The Institute of Medicine (IOM) estimate that up to 91 percent of the 2.5 million people who have chronic fatigue have not yet been diagnosed.

Earlier this month, an expert panel at the IOM recommended chronic fatigue be labeled as a systemic exertion intolerance disease (SEID) and established diagnostic criteria that better reflect scientific research.

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A Common Culprit in Autoimmune Disorders

Interleukin-17A doesn’t only affect people with CFS.

High levels of this specific cytokine are associated with many chronic inflammatory conditions, such as multiple sclerosis, psoriasis, and rheumatoid arthritis.

Interleukin-17A is a potential target for biologic treatments designed to dampen the body’s immune system to relieve symptoms of these conditions.

In January, the U.S. Food and Drug Administration approved Cosentyx (secukinumab), a psoriasis drug that targets interleukin-17A to quiet the body’s immune response.

Psoriasis, an autoimmune disorder, can also be triggered by an infection. CFS is a common complaint of people with psoriatic arthritis, an inflammatory joint condition that can develop in people in late-stage psoriasis.

But before researchers would test existing or experimental drugs on CFS patients to target interleukin-17A, they say they need to replicate their results in a study that follows patients to observe how their cytokine levels differ over time.

Before there can be effective treatments for CFS, there must be a better understanding of CFS so it can be diagnosed earlier.

“Early diagnosis may provide unique opportunities for treatment that likely differ from those that would be appropriate in later phases of the illness,” Hornig said.

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