Chronic fatigue syndrome seems to have a very strong genetic element
The largest study so far into the genetics of chronic fatigue syndrome, or myalgic encephalomyelitis, has implicated 259 genes – six times more than those identified just four months ago
Chronic fatigue syndrome doesn’t have a single cause, but the role of genetics is starting to come to light
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We’re starting to get a handle on the role that genetics plays in the onset of chronic fatigue syndrome, or myalgic encephalomyelitis (ME/CFS). According to the largest study of its kind to date, more than 250 genes are involved – six times the number identified earlier this year. Not only could this help us develop treatments that tackle ME/CFS at its roots, but the study also adds to our knowledge of how it differs from long covid, a very similar condition.
“It’s opening up a huge number of new avenues, either for novel therapy development or for drug repurposing,” says team member Steve Gardner at Precision Life in Oxford.
ME/CFS is a chronic condition that is often disabling. It has many symptoms, but a core feature is post-exertional malaise, where even small amounts of activity lead to prolonged exhaustion. ME/CFS is generally triggered by an infection, but it is unclear why many people can get such an infection but not develop the condition.
To learn more, Gardner’s team examined genomic data from more than 10,500 people who had been diagnosed with ME/CFS. This data was previously gathered by a project called DecodeME, which revealed in August that people with ME/CFS have key genetic differences from those without the condition.
Now, Gardner and his colleagues have compared this data with that of people without ME/CFS from the UK Biobank. They focused on genetic variants called single nucleotide polymorphisms (SNPs), in which a single letter of the genome is changed.
A standard analysis would look at one SNP at a time, but “complex disease biology just isn’t like that”, says Gardner. “There are multiple genes involved, and they’re interacting with each other. Some are amplifying each other’s effects, some are inhibiting each other’s effects.”
Instead, the researchers looked for groups of SNPs associated with ME/CFS risk. They found 22,411 such groups, composed of combinations of 7555 SNPs, out of the more than 300,000 they identified overall. The researchers also found that the more of these SNP groups a person had, the greater their chances of developing ME/CFS.
“That’s where they start to take the thing forward,” says at Brunel University of London.