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New study shows chronic fatigue syndrome may have to do with gut microbes


Chronic fatigue syndrome, perhaps more than any other disease, has a bad rap. It makes you debilitatingly tired from normal tasks but no amount of rest can help. There's no blood test or other easily read biomarkers, so many doctors are reluctant to diagnose the condition no matter how bad things get.

Scientists have finally shed some light on the condition, finding that your gut bacteria and inflammatory agents in the blood may have something to do with it.

In a study published this month in the journal Microbiome, Cornell University researchers looked at stool and blood samples of 48 people diagnosed with chronic fatigue syndrome (or more formally, myalgic encephalomyelitis) and at 39 healthy volunteers.

They found two main differences: Through DNA sequencing, they found the stool samples in the patients with the condition had less diversity in bacteria present in the gut and that there were fewer that were anti-inflammatory. The blood samples were also distinct: There were markers of inflammation that the researchers theorized may be due to a "leaky gut from intestinal problems that allow bacteria to enter the blood."

The researchers said that it was unclear whether these were causes or a consequences of the disease, but the discovery, despite the fact that it was only based on a small sample, is important for two reasons.

First, the indicators could be used in the future to help diagnose the condition, as they were present in 83 percent of the patients with chronic fatigue syndrome. Second, it suggests that diet and things like probiotics may be a way to help treat the disease by getting the gut microbiome back in balance.

“Our work demonstrates that the gut bacterial microbiome in chronic fatigue syndrome patients isn’t normal, perhaps leading to gastrointestinal and inflammatory symptoms in victims of the disease,” said Maureen Hanson, a professor of molecular biology and genetics at Cornell. “Furthermore, our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin.”

In an open letter to the National Institutes of Health's director, Francis Collins, last year, my former colleague Brian Vastag described the devastating toll that the condition has taken on his own life and decried the lack of progress in research:

In the past, you've shown a soft spot for certain orphan diseases. Well, the history of ME is akin to having locked an entire orphanage in a cellar and bulldozing the house.
On the list of illnesses the NIH studies, ME (listed as “ME/CFS”) is near the bottom in funding, ranked 231 out of 244. It received $5 million in 2014, less than hay fever, which cripples no one. That’s not enough money to equip a laboratory and run it for a year. This abject neglect — or sustained prejudice, or maybe both — stretches back a full three decades at the NIH (For a detailed history of how this sad state came to be, read Hillary Johnson’s deeply reported book "Osler’s Web.")
No one has a good count of ME patients in the United States — the Centers for Disease Control and Prevention misspent funds earmarked for this purpose — but there’s plausible evidence that several hundred thousand people are disabled by it. That’s comparable to the burden of multiple sclerosis — the illness ME most closely resembles. The NIH funds $110 million in MS research each year, and a sustained government investment has been crucial in the development of a dozen Food and Drug Administration-approved MS drugs. ME patients have no approved treatments. Diagnosis can be delayed for years, and misdiagnosis is common. (I was initially diagnosed with West Nile virus infection, a mistake due to a faulty blood test.)
But ME is finally emerging from the basement. Brand-name institutions and big-time researchers now recognize the huge burden ME places on society: tens of billions in medical expenses, lost productivity and missing tax revenue each year. Columbia University’s Ian Lipkin is searching for infectious triggers, and has reported severe immune problems in patients. Columbia received $150 million in NIH grants in 2015; Lipkin’s operation gets a big chunk of that not for ME/CFS research but for finding viruses such as those that cause SARS and MERS. But when the famous virus hunter applied for a trifling $1 million for ME research, the NIH turned him down, twice. So spurned, Lipkin and colleague Mady Hornig recently resorted to eating habanero peppers to raise money as part of a social media ME Chili Challenge inspired by the hugely successful ALS Ice Bucket Challenge.

Vastag may be happy to know that the Cornell study was NIH funded.

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