A landmark genetic study reveals a far stronger link between genetics and chronic fatigue syndrome (ME/CFS) than previously understood. Researchers have identified over 250 genes potentially involved in the condition – six times more than earlier estimates – opening new avenues for treatment and a clearer understanding of its relationship to long COVID. The findings underscore the biological reality of ME/CFS, which has long been dismissed or misunderstood by some medical communities.
The Genetic Basis of ME/CFS
The study, conducted by Precision Life in Oxford, analyzed genomic data from over 10,500 people diagnosed with ME/CFS, comparing it to the UK Biobank’s database of individuals without the condition. Researchers focused on single nucleotide polymorphisms (SNPs), subtle variations in the genome, but took a novel approach by analyzing groups of SNPs rather than individual markers. This is crucial because chronic illnesses rarely stem from single genes; they arise from complex interactions between multiple genetic factors.
The researchers found 22,411 SNP groups linked to ME/CFS risk, composed of 7,555 SNPs overall. The more of these groups a person carries, the higher their risk of developing the condition. This builds on previous research, including an August study identifying 43 relevant genes; the new work expands that list to 259 “core” genes with the strongest connections. The sheer scale of the study provides confidence in these findings, overcoming issues with underpowered earlier research.
Differentiating ME/CFS from Long COVID
The study also sheds light on the overlap between ME/CFS and long COVID, both characterized by debilitating post-exertional malaise (PEM). Roughly 42% of the genes linked to long COVID also appear in ME/CFS, suggesting the conditions share underlying biological mechanisms. However, researchers caution that this may be an underestimate due to differences in how participants were analyzed. Further investigation is needed to precisely delineate the genetic and biological distinctions between the two.
Implications for Treatment and Research
Currently, there are no specific medications for ME/CFS, forcing patients to rely on symptom management tools like painkillers or antidepressants. The new genetic insights, however, could revolutionize treatment. By identifying high-prevalence, high-impact genetic variants, scientists can prioritize drug development and repurposing efforts.
“If you’re really interested in druggability and wanting to benefit as many patients as possible, the [variants] with the higher prevalence and the higher effect size are obviously the ones that you would choose to investigate first,” says Steve Gardner of Precision Life.
Additional research, including a £1.1 million project led by Imperial College London, will explore the interplay between genetics, immune responses, latent viruses, and gut microbiomes in ME/CFS and long COVID. The goal is to move beyond symptom management toward targeted therapies that address the root causes of these chronic conditions.
Ultimately, the growing body of genetic evidence surrounding ME/CFS demands increased recognition and investment in research. The condition is not simply a psychological or behavioral issue, but a biologically-rooted illness with clear genetic underpinnings.
