⚠️After seeing the response from patients, clinicians and scientists, I think this needs to be said clearly: Re-promoting an article that has caused so much harm to the Long COVID community is not brave journalism. It is irresponsible. This article did not simply “open a difficult conversation.” It amplified a deeply damaging frame: that maybe patients are rejecting the uncomfortable truth that CBT, exercise and “mind-body” approaches are the way forward. But when you present a complex post-infectious disease through that lens, without properly separating psychological support from biological treatment, you are not helping patients. You are making their lives harder. These narratives do not stay inside an article. They reach families. They reach employers. They reach disability assessors. They reach doctors who already know very little about Long COVID. They reach people who are looking for an excuse to say: “maybe it is just anxiety,” “maybe you are afraid of exercise,” “maybe you are keeping yourself sick.” That has consequences. Social consequences. Medical consequences. Workplace consequences. Psychological consequences. Patients with Long COVID are already fighting disbelief, lack of biomarkers in routine care, lack of approved treatments, disability, isolation and medical neglect. Using their suffering to generate clicks while repackaging old psychosomatic narratives in modern “mind-body” language is not courageous. It is cruel. The problem is not talking about the nervous system. The problem is turning nervous system involvement into a story about beliefs, fear, trauma or patients refusing to accept recovery. The problem is using recovery anecdotes as if they establish causality. The problem is ignoring those who worsened with exercise. The problem is presenting PEM caution as dogma. The problem is being much more generous with “brain retraining” narratives than with the biomedical evidence already showing immune, vascular, autonomic, metabolic and muscular abnormalities in Long COVID. If a journalist wants to write about Long COVID, they have a responsibility to understand the history of harm done to post-infectious patients. Because this is not new. ME/CFS patients have lived this for decades. “Unexplained” became “psychological.” “Normal routine tests” became “nothing is wrong.” “Supportive care” became “cure.” “Exercise” became “rehabilitation,” even when patients were crashing. And now the same mistake is being repeated with Long COVID. Patients are not angry because they reject science. They are angry because they recognize the pattern. They have seen what happens when medicine turns biology it cannot yet measure into psychology. So no, this is not “a way forward.” A way forward would be stratification, biomarkers, mechanistic trials, antivirals, immunology, dysautonomia research, PEM-safe protocols, autoantibody studies, vascular biology, tissue persistence, metabolism and serious clinical phenotyping. A way forward would be listening to all patients, including those harmed by exercise and psychologizing narratives. A way forward would be scientific humility: admitting what we still do not know without turning unexplained biology into psychology. Not click-driven repetition of the same ideas that have already harmed post-infectious patients for decades.

‼️⚠️Please read this until the end. A widely shared article has presented a deeply misleading view of Long COVID, suggesting once again that cognitive behavioral therapy, exercise, and “mind-body” approaches may be the uncomfortable truth patients refuse to accept. This needs to be challenged. Not because the nervous system does not matter. Not because psychological support cannot help. But because confusing support with cure, physiology with psychology, and heterogeneity with “it might be in your head” is exactly how medicine has harmed post-infectious patients for decades. There are articles about Long COVID that look like science journalism, but in reality they repackage, in modern language, a very old idea: if we do not fully understand a disease, maybe the problem is in the patient’s mind. And that is not science. That is repeating history. The article begins with a striking sentence: “There isn’t a single approved pharmaceutical treatment, not even a test to verify the presence of the illness.” This may sound forceful, but it is a very misleading way of presenting the problem. The fact that there is still no drug specifically approved for Long COVID, or a single diagnostic test, does not mean that “nothing has been found.” It means that we are dealing with a heterogeneous disease, probably with several biological subgroups, and that medicine has not yet converted those findings into validated clinical tools. “No single diagnostic biomarker” is not the same as “no biology.” In just a few years, immunological, vascular, neurological, endocrine, and metabolic abnormalities have been described in subgroups of Long COVID patients: autonomic dysfunction, herpesvirus reactivations such as EBV/HHV-6, alterations in the cortisol axis, autoantibodies against GPCR receptors — including adrenergic and muscarinic receptors — persistent viral antigens, endothelial damage, muscle abnormalities after exertion, mitochondrial dysfunction, persistent inflammation, and differential immune changes. Is everything settled? No. Does that mean it is psychological? Also no. Science does not work like that. Multiple sclerosis did not stop existing before we had MRI. Many autoimmune diseases do not show up in routine blood tests. If a complete blood count, a basic biochemistry panel, or an X-ray comes back “normal, normal, normal,” that does not prove the absence of disease. It only proves that you are looking with inadequate tools. One of the article’s most serious mistakes is this: it confuses the absence of a simple clinical test with the absence of organic disease. And that mistake has caused harm for decades. The article also says: “Almost $2 billion and half a decade of international effort have yielded little more than hypotheses about micro blood clots and spike proteins and mitochondrial dysfunction.” No. That is not correct. A hypothesis is a provisional explanation. But when you compare patients and controls and find significant differences in muscle tissue, metabolism, response to exertion, immune biomarkers, viral antigens, autoantibodies, or vascular dysfunction, you are no longer talking about “little more than hypotheses.” You are talking about lines of biomedical evidence that still need to be organized, replicated, stratified, and translated into treatments. That is not scientific failure. That is research into a complex and new disease. 🔵Continued in the next post.👇🏻 (1/6)