I have only been ill since 2022, so I am still relatively new to the history of ME/CFS — although, in my experience, every month spent severely ill can sometimes feel like several months in the moderate stage, simply because the level of suffering and restriction is so extreme.
I often wonder what ME/CFS research was really like before 2020. My own research only began in March 2025, when I finally understood what was happening to me.
At the time, I kept coming across the same names and the same hypotheses: the Davis family, the Itaconate Shunt, Klaus Wirth’s work around mitochondrial dysfunction, viral persistence with Putrino, PolyBio and others. I completely missed the whole BC007 episode — and, looking back, perhaps that was not such a bad thing.
I have the impression that 2025 was an important year. There was DecodeME, the work published by Fluge and Mella and several other studies that I found particularly interesting, including the study involving autopsies of the brains of severely affected patients.
But one question keeps bothering me, and perhaps it is a naive one : why do some of the best-known researchers sometimes seem to pursue their own particular avenue almost independently of what is happening elsewhere ?
I was struck, for example, by how little attention DecodeME sometimes seems to receive in the public discourse of otherwise highly influential researchers: Scheibenbogen, Wirth, Davis, PolyBio, West, Putrino, Iwasaki, Lipkin, Klimas... I remember reading an interview with Nancy Klimas and getting the impression that she remained very focused on her own therapeutic trials — Sipavibart, probiotics, and so on — without really integrating what DecodeME might change in the way the disease is understood.
And yet the DecodeME findings seem robust enough to deserve a much broader mobilisation of the field. Of course, a genetic association is not a mechanistic explanation, let alone an immediate therapeutic target. But it provides objective anchors. It should, it seems to me, encourage teams to work collectively on the implicated genes, biological pathways and cell types, rather than continuing to pursue their own theories in isolation.
That is probably what has surprised me most since I started discovering how research actually works. Before becoming severely ill, I naively imagined biomedical science as a kind of vast collective construction, where every new solid piece of evidence would immediately reshape everyone’s hypotheses.
Instead, I am discovering something far more human : laboratories with their own areas of expertise, funding streams, long-standing hypotheses, trials already underway, collaborations, and sometimes rivalries — and therefore a certain degree of intellectual inertia.
Meanwhile, severe and very severe patients continue to live in conditions that I find profoundly undignified. There is a lot of discussion about biomarkers, mechanisms, trials and models, but much less about the absolute urgency of the situation facing people who sometimes can no longer wash themselves, speak, tolerate light or sound, and whose lives may be reduced to a single room for years.
Perhaps this is stating the obvious, but I increasingly feel that we will not get very far if every research team continues to play its own instrument alone.
What we need is an orchestra.
Researchers need to be willing to abandon hypotheses more quickly when they no longer fit the emerging evidence.
I am probably stating things that are obvious to people who have followed this field for years. But having discovered all of this only after becoming severely ill, I remain deeply surprised by the way biomedical research actually functions.
I thought I was entering the world of the “hard sciences.”
What I am discovering instead is that, even when the data are hard, the people interpreting them are still human.
