Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a persistent and debilitating illness characterized by extreme fatigue lasting for at least 6 months, along with problems in thinking and memory, chronic pain, and un refreshing sleep, among other symptoms. According to the Mayo Clinic, as of 2023, the exact cause of ME/CFS remained unknown. Experts believed it likely resulted from a combination of factors, including certain infections, physical or emotional trauma, and possible dysfunctions in the ATP production system. But among the most popular of these factors, was the fact that they saw evidence of a genetic component involved in the condition, since many people noticed it seemed to run in families. This theory got a major boost from a landmark study called DecodeMe, which conducted the largest DNA analysis of ME/CFS to date. Researchers compared single nucleotide polymorphisms (SNPs), or tiny differences in DNA code, between 15,579 individuals diagnosed with ME/CFS and 259,909 controls.
The study identified eight genomic regions significantly associated with ME/CFS. Some of these regions are near genes involved in immune response (suggesting vulnerability to infections), and others are connected to the nervous system. One particularly interesting gene is CA10, which has been previously linked to chronic pain, which interestingly enough is a symptom many people with ME/CFS patients report. Importantly, the study found no overlap between these ME/CFS genetic signals and variants associated with depression or anxiety, which strengthens the argument that ME/CFS has a distinct biological basis. That said, these genetic differences are not exclusive to people with ME/CFS because many of these SNPs are also seen in people without the illness.Putting everything together, the DecodeMe study gives strong, objective evidence to the idea that genetics make people more vulnerable to ME/CFS, rather than the condition being purely psychological. Some of the risk variants may impair the body's ability to fight off infections, or they may influence pain sensitivity, but the study's authors warn that having a risk variant doesn't guarantee someone gets the illness. These new insights help validate the patients' lived experiences while also offering concrete starting points for future biological research. Unfortunately, the researchers emphasize that progress could be hindered by lack of funding. More work is needed to understand exactly how these genetic signals translate into biological processes, and to see whether they could help build diagnostics or even guide treatments in the future.
Sources:
“Initial Findings from the DecodeME Genome-Wide Association Study of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.” MedRxiv, 8 Aug. 2025, www.medrxiv.org/content/10.1101/2025.08.06.25333109v1.full.pdf.
“Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).” Mayo Clinic, Mayo Foundation for Medical Education and Research, 11 May 2023, www.mayoclinic.org/diseases-conditions/chronic-fatigue-syndrome/symptoms-causes/syc-20360490.
Offord , Catherine. “Possible Genetic Clues to Me/Chronic Fatigue Syndrome Identified in Massive Study | Science | AAAS.” Science, 6 Aug. 2025, www.science.org/content/article/possible-genetic-clues-me-chronic-fatigue-syndrome-identified-massive-study.

Very interesting. You mention that some of the risk variants include the body's ability to fight off infections therefore I wonder what parallel that draws to the count of white blood cells in the body of the patient. Hopefully the scientists involved receive the funding needed to expand their research.
ReplyDeleteI really like how you explained the DecodeME study and highlighted why its findings matter. The connection between immune genes, nervous-system pathways, and symptoms like chronic pain makes the genetic basis of ME/CFS feel much clearer. I also liked that you pointed out how the study separates ME/CFS from mental-health conditions. It’s cool that this research offers real scientific direction, even if funding challenges could slow progress.
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