
People recently diagnosed with chronic fatigue syndrome – also known as myalgic encephalomyelitis or ME/CFS – have distinct differences in their gut microbiomes compared with people without the condition, suggesting that disruptions in gut bacteria may be related to the disease’s onset.
ME/CFS is a chronic disease affecting an estimated 17 million people worldwide. Symptoms include persistent fatigue, brain fog, pain and gastrointestinal complications. It is still unclear what causes the condition or its symptoms, though previous research has implicated gut bacteria, genetics, viral infections and even microscopic blood clots.
To investigate further, at Columbia University in New York and his colleagues analysed gut bacteria taken from stool samples from 106 people with ME/CFS and 91 people without the condition. They found significant differences in the quantities of nine microbes between the two groups even after adjusting for factors like age, body mass index (BMI) and sex.
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One of the most notable differences was in the abundance of a bacteria called Faecalibacterium prausnitzii. On average, people with ME/CFS had nearly 35 per cent less F. prausnitzii in their stool than people without the condition.
Participants completed a survey measuring fatigue symptoms at the time of stool collection. Comparing these fatigue scores with stool samples revealed a strong association between reductions in F. prausnitzii and fatigue severity. Together, these findings suggest F. prausnitzii – or more precisely, the lack thereof – may play a role in ME/CFS.
“One of the underpinnings of this illness is the amount of inflammation that these patients have on a day-to-day basis,” says at Nova Southeastern University in Florida. Since F. prausnitzii is a main producer of anti-inflammatory molecules called short-chain fatty acids, it is possible that decreases in F. prausnitzii may be contributing to the excess inflammation seen in ME/CFS, she says.
Another study conducted by at the Jackson Laboratory in Connecticut and her colleagues found similar associations. They analysed bacteria in stool samples from a separate cohort of people with ME/CFS, of whom 75 had been diagnosed with the condition in the last four years and 79 had been diagnosed more than 10 years ago.
They found that, on average, only those in the short-term disease group had significant decreases in microbes known to make short-chain fatty acids, including F. prausnitzii, compared with controls. In fact, those in the long-term disease group had gut microbiomes that closely resembled those of people without the condition.
One explanation could be that there is “an event happening early on in the disease process that eventually dissipates, but changed the gut environment”, says at Emory University in Georgia. For instance, many people with ME/CFS report that their symptoms began after a viral infection, which could have resulted in lasting disturbances to the gut microbiome. “You can think of it sort of like a hit and run,” says Sampson.
Other factors may also explain these findings. For example, people recently diagnosed with ME/CFS are more likely to experiment with unproven treatments, such as supplements, which could modify the composition of gut microbes, says Klimas. “We have to remember that just because the microbiome is altered in a disease does not mean that the microbiome is contributing to the disease,” says Sampson.
Even if ME/CFS doesn’t originate in the gut, understanding how it is affected in people with the condition may improve treatments. For example, supplements, faecal transplants or even just eating more leafy greens could help restore the number of short-chain fatty acid-producing bacteria in the gut, thereby decreasing inflammation associated with ME/CFS and its conditions, says Oh.
Cell Host & Microbe