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, 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.”

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