[GER]Myalgic encephalomyelitis/chronic fatigue syndrome: the enigma of a disturbance of bodily resonance and predictive processing, 2026, Zipper et al

Chandelier

Senior Member (Voting Rights)
ME/CFS: das Enigma einer Störung leiblicher Resonanz und predictive processing

Zipper, Stephan

Zusammenfassung​

Die durch das Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) ausgelöste Pandemie stellte einen verstörenden Einschnitt in unser biopsychosoziales Gefüge dar. Ein namentlicher Teil der an SARS-CoV-2-Erkrankten zeigte anhaltende und/oder im zeitlichen Verlauf nach der Akutinfektion neu aufgetretene Beschwerden, die häufig als Long- bzw. Post-COVID bezeichnet werden. Neben unbestreitbar bestehenden organisch-biologischen Ursachen für eine Persistenz von Beschwerden nach durchgemachter akuter SARS-CoV-2-Infektion gilt es, auch soziopsychologische Faktoren, die zum Fortbestehen leiderzeugender Symptome führen, zu berücksichtigen. Nach einem Abriss neurobiologischer Grundlagen werden psychodynamische Hypothesen als mögliche Ursache für eine Symptompersistenz bzw. -ausweitung aufgestellt und systematische psychodynamisch orientierte Untersuchungen angeregt.

Abstract​

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a syndrome in which the causes and pathophysiology are not yet fully understood. This often leads to epistemic conflicts: those affected feel their symptoms are not taken seriously and lose trust in the medical system.

There is therefore a call for a form of medicine that takes subjective experience seriously and communicates scientific uncertainties transparently. Questions regarding the “body-mind problem” are discussed using the predictive processing model, through which ME/CFS can be understood as a miscalibration of interoceptive predictions. From a phenomenological and hermeneutic perspective, the condition can be viewed as a disturbance of bodily resonance and of the relationship between the self and the world.

Web | DOI | PDF | Die Psychotherapie | Paywall
 
An expanded biopsychosocial view of post-COVID, 2025, Zipper et al

Ein erweiterter biopsychosozialer Blick auf Post-COVID

Zipper, Stephan

Zusammenfassung​

Die durch das Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) ausgelöste Pandemie stellte einen verstörenden Einschnitt in unser biopsychosoziales Gefüge dar. Ein namentlicher Teil der an SARS-CoV-2-Erkrankten zeigte anhaltende und/oder im zeitlichen Verlauf nach der Akutinfektion neu aufgetretene Beschwerden, die häufig als Long- bzw. Post-COVID bezeichnet werden. Neben unbestreitbar bestehenden organisch-biologischen Ursachen für eine Persistenz von Beschwerden nach durchgemachter akuter SARS-CoV-2-Infektion gilt es, auch soziopsychologische Faktoren, die zum Fortbestehen leiderzeugender Symptome führen, zu berücksichtigen. Nach einem Abriss neurobiologischer Grundlagen werden psychodynamische Hypothesen als mögliche Ursache für eine Symptompersistenz bzw. -ausweitung aufgestellt und systematische psychodynamisch orientierte Untersuchungen angeregt.

Abstract
The pandemic triggered by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) represented a disturbing intrusion in our normal biopsychosocial system. A significant proportion of those suffering from SARS-CoV‑2 infections showed persistent and/or new symptoms over time after the acute infection, which are often referred to as long-COVID or post-COVID.

In addition to indisputable organic and biological causes for the persistence of symptoms after an acute SARS-CoV‑2 infection, sociobiological factors which lead to the persistence of symptoms and cause suffering must also be taken into account. Following an outline of neurobiological principles, psychodynamic hypotheses are put forward as possible causes of symptom persistence or expansion. Systematic psychodynamically oriented studies are needed.

Web | DOI | PDF | Forum der Psychoanalyse | Paywall
 
Honestly I read more robust scientific stuff than this when I borrow my partner's Fortean Times.

In all seriousness though, the FT often publishes articles about psychosomatic illness, which shows you how seriously the field deserves to be taken. At least ghost hunters never hurt anybody...
 
Dr. Zipper seems to wear a lot of different hats.

From Bluesky:




Mirja Nicolas @privilegienschreck.bsky.social

Completely normal in medicine for those who set and oversee the assessment standards for insurers and the Medical Service to also determine the scientific discourse. Structural conflicts of interest? Never heard of them.
​



Dr. Zipper's Institute website:
Google Translate link.




Insurance Medicine Assessment and Consulting in Frankfurt am Main

The role of a medical expert is to provide an impartial assessment of medical facts within a given legal context. Expert assessments are conducted, in particular, in the following areas:

  • Neurological consequences of accidents(private accident and liability insurers;statutory accident insurance institutions)
  • Occupational diseases (occupationaldisease codes BK 1317, BK 2113, BK 2106,and BK 3102, e.g., neuroborreliosis)
  • Occupational disability
  • Inability to work (social compensation law)
  • Medical malpractice matters (medicalnegligence)
Your Medical Expert

Dr. med. Stephan G. Zipper
Specialist in Neurology · Emergency Medicine · Intensive Care Medicine · Clinical Neurophysiology

​

 
Zipper said:
From a phenomenological and hermeneutic perspective, the condition can be viewed as a disturbance of bodily resonance and of the relationship between the self and the world.
You know it’s bad when you can’t tell the difference between a scientific publication and a leaflet you’d find on the counter of a healing crystals shop.
 
High hopes for Germany?
Yep, see the list of reasons I mentioned the other day here.
I explicitly mentioned the German neurologist and their psychosomatic tendencies as a problem.
But maybe there's hope even in that regard:
I have reason to believe that we are making some progress. I have been in touch with half a dozen relevant people and there is interest. I won't say more for the time being. I wouldn't be surprised if Germany got there first with some competent neurologists who understand the implications of the genetics.
 
There is therefore a call for a form of medicine that takes subjective experience seriously and communicates scientific uncertainties transparently
This form of medicine exists. It's called medicine. It's explicitly because we are excluded from it that things are so disastrous. It only works at taking subjective experience seriously when it's related to a known pathology, and there is nothing forcing anyone to do that.

The only thing that's never been tried is precisely to practice real medicine seriously. This "predictive processing" horseshit is just the same old Freudian hallucinations with a different hat.
 
Honestly I read more robust scientific stuff than this when I borrow my partner's Fortean Times.

In all seriousness though, the FT often publishes articles about psychosomatic illness, which shows you how seriously the field deserves to be taken. At least ghost hunters never hurt anybody...
I read lots of more robustly scientific stuff than this from political science classes. Political science is not a science, and yet it might be quantum mechanics compared to this trash nonsense.
 
From NichtGenesen via Twitter,
It cannot be the responsibility of patient organizations to keep having to demand these minimum scientific standards retroactively every time another publication appears.

Machine Translation:
We have only just formally raised a substantive objection with Springer Nature over the portrayal of ME/CFS in Verhaltenstherapiemanual Erwachsene (Behavior Therapy Manual for Adults). Now comes a second objection.

Again, this is not about differences of opinion, but about minimum scientific standards: an inaccurate presentation of the ICD, the reframing of PEM as a theoretical perceptual model, a lack of disease-specific evidence, implications for patient safety—and the question of how the conflict-of-interest declaration was reviewed in light of decades of work as an expert assessor.

Today, the objection was sent to Springer Nature, Research Integrity, the editorial team, the publisher, the author, and relevant professional and expert-assessor associations.

Scientific debate may be controversial. It must not be methodologically arbitrary.

It cannot be the responsibility of patient organizations to keep having to demand these minimum scientific standards retroactively every time another publication appears.

Read the full objection here:


@bmftr_bund @BMG_Bund @SilkeLaunert @MatthiasHauer


Full objection, page 1, machine translated:
NichtGenesen

Patient Organization for Long COVID, ME/CFSand Post-Vac
www.nichtgenesen.org | info@nichtgenesen.org

25 September 2026

To the Editorial Office of Die Psychotherapie, Springer Nature, and Dr. med. Stephan Zipper

Subject: Formal substantive objection to the article “ME/CFS: das Enigma einer Störung leiblicher Resonanz und predictive processing” [“ME/CFS: The Enigma of a Disorder of Embodied Resonance and Predictive Processing”]—inaccurate ICD representation, insufficiently substantiated interpretation of the illness, reframing of PEM, implications for patient safety, and review of the conflict-of-interest declaration

Dear Sir or Madam,

We are contacting you regarding the article by Dr. med. Stephan Zipper, “ME/CFS: das Enigma einer Störung leiblicher Resonanz und predictive processing” (“ME/CFS: The Enigma of a Disorder of Embodied Resonance and Predictive Processing”), published online on 22 September 2026 (Die Psychotherapie; DOI: 10.1007/s00278-026-00874-w).

As a patient organization for people with Long COVID, ME/CFS and Post-Vac, we object to significant aspects of the article’s scientific presentation.

Our criticism is not directed at research into possible neurocognitive mechanisms or at psychotherapeutic support for people with chronic illnesses. It is directed at applying a theoretical model that has not been validated as specific to the illness to ME/CFS, and at drawing conclusions that go beyond the evidence presented in support of that application.

Of particular concern is that this is not an isolated incident. In our formal substantive objection of 2 September 2026 concerning Chapter 91, “Chronic Fatigue Syndrome,” in Verhaltenstherapiemanual – Erwachsene (Behavior Therapy Manual for Adults), we had already alerted Springer Nature to scientific misclassifications, problematic interpretations of the illness and statements with implications for patient safety.

The article now published is a separate text, by a different author and based on a different theoretical approach. However, it again raises fundamental issues whose accurate presentation we have already called upon your publishing house to ensure.

1. Factually inaccurate presentation of ICD coding

In the very first paragraph, the author claims that ME/CFS has not been included in the ICD with a distinct code (p. 1).

This statement is factually incorrect with respect to the classification applicable in Germany.

ME/CFS was already listed in ICD-10-GM 2025 under G93.3. Since 1 January 2026, the classification has also explicitly distinguished between post-infectious ME/CFS (G93.30), non-post-infectious ME/CFS (G93.31) and unspecified ME/CFS (G93.39). The new system also distinguishes chronic fatigue with PEM under R53.0 from chronic fatigue syndrome under G93.3-.

A publication from September 2026 must not present an existing official disease code—one that has only recently been further differentiated—as if it did not exist.

We request that this statement be corrected and that the editorial process be reviewed to establish why this fundamental fact was not identified.

Sources: BfArM: ICD-10-GM 2026, G93.3- | BfArM: ICD-10-GM 2026, R53.-

2. The absence of a single diagnostic marker does not imply misperception

The author states that, at present, no single biomarker meets the sensitivity, specificity and reproducibility required for clinical diagnosis (p. 2).

However, this does not support an inference either of a psychological cause of the illness or of miscalibrated bodily perception.

The absence of a single confirmatory laboratory test does not mean that ME/CFS cannot be diagnosed. NICE recognizes the illness on clinical grounds; the US Centers for Disease Control and Prevention (CDC) describe diagnosis based on medical history, the pattern of symptoms, physical examination and targeted testing to rule out other conditions.

A symptom can be subjectively experienced and still be clinically valid. This is also true, for example, of migraine and other conditions for which diagnosis relies substantially on a characteristic pattern of clinical symptoms.
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Subjectively reported symptoms are not evidence of a perceptual disorder simply because they cannot be confirmed by a single laboratory value.

The article must therefore clearly distinguish between the absence of a single diagnostic marker, the biological and functional findings that do exist, and the theoretical interpretation proposed by the author.

This very shift—from diagnostic uncertainty to an interpretation of illness compatible with a psychosomatic framework—was among the fundamental problems we addressed in our objection of 2 September.

This distinction has also been documented in a directly relevant recent specialist publication that Springer Nature itself published on 27 July 2026: Kathryn Hoffmann, “Von der Ausschlussdiagnose zur Multisystemdiagnostik – Aktuelle diagnostische Ansätze bei ME/CFS” (“From Diagnosis by Exclusion to Multisystem Diagnostics—Current Diagnostic Approaches to ME/CFS”). The article describes ME/CFS as a clinically defined multisystem disease, with PEM as a central diagnostic feature. Its diagnostic approach includes the structured assessment of autonomic, immunological, neurocognitive, neuroendocrine-metabolic and pain-related manifestations.

The timing is significant: the Zipper article was revised on 24 August 2026 and accepted on 26 August 2026. By then, the Hoffmann article had already been publicly available for nearly four weeks. Thus, before the editorial process was complete, a current, disease-specific account was available demonstrating precisely that the absence of a single diagnostic biomarker does not preclude structured clinical assessment of multiple systems, supplemented by objectively measurable findings.

Additional source: Hoffmann K. “Von der Ausschlussdiagnose zur Multisystemdiagnostik” (“From Diagnosis by Exclusion to Multisystem Diagnostics”), Schmerz Nachrichten 26, 150–155 (2026), DOI: 10.1007/s44180-026-00309-7

Sources: NICE NG206: Diagnosis and management | CDC: Diagnosing ME/CFS

3. PEM is interpreted as the misprocessing of bodily signals without disease-specific evidence

On page 3, the author links PEM to a possible overreaction to “prediction errors.” Bodily signals, such as an increased heart rate or sweating, are said to be interpreted as threats, irrespective of their objective severity. On page 4, PEM is then presented in the context of a disrupted resonance system.

This is the central scientific objection: What empirical data demonstrate that such misprocessing of bodily signals causes PEM in ME/CFS?

PEM is not merely an exertion experienced as subjectively unpleasant. The NICE guideline describes a worsening of symptoms that often begins after a delay, is disproportionate to the preceding activity and frequently involves a substantially prolonged recovery time.

Studies have also documented objectively measurable functional and biological changes following exertion. Appelman et al. (Nature Communications, 2024) report such changes in Long COVID with PEM; for ME/CFS, Hoffmann’s recent article describes disease-specific exertion testing, including the 2-day CPET. Findings from individual testing methods are not entirely consistent, and such tests do not replace clinical assessment of PEM. However, they contradict an account that reduces the bodily response from the outset to the interpretation of sensory signals.

The example of an elevated heart rate is particularly problematic. In the presence of orthostatic intolerance or postural orthostatic tachycardia syndrome (POTS), corresponding cardiovascular changes can be objectively measured and may be diagnostically relevant. The German ICD-10-GM 2026 explicitly codes POTS under G90.80.

On what scientific basis does the author distinguish between an allegedly exaggerated interpretation of threat and a response that is genuinely relevant to the underlying pathophysiology?

Without this distinction, there is a risk that an appropriate perception of, and response to, physical exertion will be interpreted as faulty processing.

This directly parallels the concern raised in our previous objection: there, we criticized the problematic reframing of protective behavior necessitated by illness and the inadequate distinction between pacing and activation.

PEM must not be redefined—through different theoretical terminology—as a problem of perception, appraisal or behavioral regulation without the evidence required to support that interpretation.
Page 3:
The contrast with the Hoffmann article, published by the same publisher just a few weeks earlier, is particularly striking: PEM is described there not as merely a subjective perception of fatigue or threat, but as a pathological worsening that often begins after a delay and follows physical, cognitive, orthostatic, sensory or emotional exertion. The article explicitly identifies “drive and motivation remain unchanged” as a characteristic diagnostic feature.

The article also identifies autonomic dysfunctions as frequently objectively measurable manifestations of ME/CFS and lists the Schellong test or NASA Lean Test, long-term ECG monitoring and tilt-table testing as methods for objectively assessing orthostatic symptoms. It describes the 2-day CPET as the best-studied objectively measurable exertion test, while explicitly cautioning that it is not suitable for routine clinical use because of the risk of a severe and prolonged crash.

Against this background, the passage in the Zipper article stating that signals perceived during exertion, such as an increased heart rate or sweating, are interpreted as threats “not on the basis of their objective severity” takes on added scientific significance. Anyone applying such an interpretation to ME/CFS must demonstrate, specifically for this disease, which validated criteria can distinguish a pathophysiologically relevant autonomic or exertion-induced response from an alleged misweighting of interoceptive signals. The article provides no disease-specific validation data demonstrating this kind of discriminative precision.

It is not scientifically sufficient to first downplay clinically characteristic or objectively measurable manifestations as nonspecific, and then fill the resulting explanatory gap with an unvalidated perceptual model.

Additional source: Hoffmann K. 2026—PEM, objectively measurable autonomic manifestations and 2-day CPET

Sources: NICE NG206: PEM and energy management | Appelman et al., Nature Communications, 2024 | BfArM: G90.80 POTS

4. A theoretical model is not evidence of a disease mechanism

The article links general concepts from predictive processing with philosophical and phenomenological considerations concerning embodied resonance.

Such models may inspire scientific hypotheses. However, they do not demonstrate that ME/CFS is caused by the alleged regulatory or resonance disturbances.

At a minimum, it would need to be established which disease-specific predictions the model makes, which findings would favor it over competing explanations, and under what conditions it could be considered falsified.

An explanatory model that can interpret almost any symptom after the fact as an expression of miscalibrated predictions, without specifying clear criteria by which it could be falsified, does not, in itself, provide an adequate basis for causal claims about the disease.

We expect a precise distinction between empirically supported findings, theoretical analogies, philosophical interpretations and the clinical hypotheses derived from them.

5. Biopsychosocial factors are not evidence of a psychosomatic etiology

On page 2, the author calls into question the notion that ME/CFS could be a disease whose severity and persistence are not influenced by psychological and social factors.

This argument misses the central scientific issue.

The fact that psychological and social factors can influence how a person copes with an illness, their quality of life and, potentially, the course of individual symptoms is entirely compatible with a disease grounded in biological pathology.

The possibility of psychosocial influences does not in any way demonstrate that these factors cause or perpetuate the underlying disease.

Conflating these levels substitutes a general reference to interactions between body, mind and environment for an etiological explanation.

This conflation warrants objection in its own right. Recasting it in the language of predictive processing does not make it scientifically more convincing.
 
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6. Therapeutic conclusions without adequate assessment of efficacy and safety

On page 4, the author proposes an integrative biopsychosocial approach to treatment. He explicitly defines the therapeutic aim as “disidentification from the EGO identified exclusively with the biological perspective”; the “subject speaking from the unconscious” is to enter the discourse and “ideally bring about healing in a second step.”

A clear boundary is necessary here.

Psychotherapeutic support can be helpful, for example, in coming to terms with illness or coping with additional psychological burdens. However, it does not follow that changing how the illness is interpreted affects the underlying disease process.

In ME/CFS, neither the alleged miscalibration of interoceptive predictions as a disease mechanism nor the efficacy and safety of a treatment targeting that mechanism has been established.

Any practical application that downplays physical warning signals, calls necessary limits on activity into question or encourages patients to increase their exertion would be particularly concerning.

The NICE guideline expressly cautions against blanket advice to exercise and against programmes that prescribe fixed increases in activity; management must be guided by each individual’s energy limits.

We are not objecting to the author explicitly recommending a particular harmful exercise therapy—that is not what the text before us says. We object that the patient-safety limits on the therapeutic application of his model are not adequately addressed.

On 2 September, we had already alerted Springer Nature to the risks of insufficiently accounting for PEM and conflating pacing with activation.

Sources: NICE NG206: physical activity, GET and CBT

7. Scientific weighting and editorial responsibility

The article appears in the “Reviews” section, while the author himself describes his approach in the text as an essay.

A theoretical essay has a legitimate place in a scientific journal. However, its epistemic status must be clear to readers.

A theoretical interpretation must not acquire the appearance of an empirically substantiated explanation of ME/CFS simply by being presented as part of a scholarly review publication.

This is all the more important when the article is behind a paywall and readers cannot initially verify substantial parts of its argument. In such circumstances, precise wording in the title, abstract and introduction is particularly important.

Springer Nature’s publication of another ME/CFS article that is problematic in significant respects also raises the question of how disease-specific evidence, existing clinical guidelines and patient safety are taken into account during editorial review.

We see a clear parallel with our previous objection: once again, the scientific basis for an interpretation of illness compatible with a psychosomatic framework has to be challenged after publication, rather than its evidentiary basis being adequately clarified beforehand.

7.1. Springer Nature had already published directly relevant disease-specific literature presenting a contrasting perspective

This case makes the question of editorial weighting considerably more pressing. On 27 July 2026—before the Zipper article was revised and accepted—Springer Nature published a recent, open-access specialist paper that explicitly describes ME/CFS as a multisystem disease with structured diagnostic assessment, PEM as a central core feature, and autonomic and exertion-related manifestations that are, in some cases, objectively measurable.

Scientific journals are, of course, entitled to publish different hypotheses. Scientific pluralism does not, however, mean treating claims with differing levels of empirical support as epistemically equivalent.

When a publisher publishes, within a matter of weeks, both a recent account of disease-specific multisystem diagnostics and, in a specialist publication designated as “Reviews,” a claim that a miscalibration …
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…interoceptive predictions as a possible explanatory framework for ME/CFS, the difference in evidentiary status must be made unmistakably clear, and the relevant literature presenting a contrasting perspective must be discussed substantively.

This is precisely the central editorial question: How could a far-reaching psychophysiological explanatory model be published without incorporating the current ME/CFS diagnostic literature already available from the same publisher in a way that enables readers to make a well-founded distinction between hypothesis, clinical findings and objectively measurable manifestations?

Repeated appeals to scientific uncertainty must not become a one-way street in which biomedical evidence is viewed with the utmost skepticism, while a speculative psychophysiological model is introduced into the clinical interpretive framework subject to a substantially lower burden of proof. Such an asymmetrical assessment of evidence is scientifically unacceptable.

Source: Hoffmann K. 2026, Springer Nature Link, published 27 July 2026 | Zipper S. 2026, revised 24 August 2026, accepted 26 August 2026

8. The author’s expert-assessment work and review of the conflict-of-interest declaration

The author’s professional activities raise an additional consideration.

On his practice website, Dr. Zipper describes more than 25 years of work as an expert assessor for courts, employers’ liability insurance associations, private accident and liability insurers, conciliation bodies and the Medical Service of the Health Insurance Funds (MDK). The areas in which he conducts assessments include, among others, neurological consequences of accidents, occupational diseases, occupational disability, incapacity to work and medical liability.

The article, by contrast, declares that there is no conflict of interest.

We do not allege that the author has already used the model presented in the article in specific assessments concerning ME/CFS, that a commissioning party influenced the article, or that his expert-assessment work in itself establishes a financial conflict of interest that should have been disclosed.

However, given the potential implications of his statements for insurance and social medicine, we request a transparent review of the conflict-of-interest declaration.

An interpretation suggesting that ME/CFS symptoms may be substantially attributable to miscalibrated bodily predictions or disrupted resonance could be relevant to assessments of functional limitations, occupational disability or capacity to work.

We therefore request an explicit statement as to whether any relevant commissioned work, remuneration, institutional relationships or other interests requiring disclosure under the publisher’s policies existed in connection with the article or its subject matter, and what criteria were used to review the declaration.

In addition, we expect a clear scientific qualification:

A theoretical explanation that has not yet been validated must not be treated in medical assessments as established knowledge about the cause, objectifiability or potential reversibility of limitations resulting from ME/CFS.

Source: Dr. Zipper’s practice website: Insurance-medical assessments

9. Renewed objection—recurring fundamental issues

In our letter of 2 September 2026, we had already alerted Springer Nature to fundamental shortcomings in the portrayal of ME/CFS.

The article now published must be assessed independently of the chapter challenged at that time. However, it once again raises issues that go beyond individual formulations: the distinction between fatigue and ME/CFS; the treatment of PEM; the significance of objective and clinical findings; the distinction between hypothesis and evidence of causation; and the safety of therapeutic approaches derived from such claims.

It cannot be the responsibility of patient organizations to keep having to demand these minimum scientific standards retroactively every time another publication appears.

Anyone addressing ME/CFS in a scholarly context must take into account the existing disease classification, diagnostic criteria, current state of the evidence and guidelines relevant to patient safety.

The development of theoretical models does not exempt authors from these requirements.
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Our demands
  1. Correct the inaccurate presentation of the ICD coding;
  2. review the statements concerning the miscalibration of bodily predictions and the interpretation of PEM to determine whether the asserted level of certainty is supported by disease-specific evidence;
  3. reassess the article on expert grounds with respect to the distinction between established findings, hypotheses and therapeutic conclusions;
  4. review the implications for patient safety, explicitly taking the NICE guideline into account;
  5. transparently review the conflict-of-interest declaration in light of the author’s publicly described expert-assessment work;
  6. determine whether an editorial correction, additional expert clarification or further action is required, and provide us with a written response; and
  7. explain whether and how Hoffmann’s article, published on 27 July 2026 (“Von der Ausschlussdiagnose zur Multisystemdiagnostik” [“From Diagnosis by Exclusion to Multisystem Diagnostics”]), was taken into account during the revision, peer review and editorial assessment of the Zipper article, and why its disease-specific account of PEM, multisystem diagnostics and objectively measurable autonomic manifestations was not explicitly distinguished from the proposed predictive-processing model.
We also request information on how the editorial team conducted its expert review of the article before publication, particularly with regard to ME/CFS-specific expertise and the distinction between theoretical interpretation and clinically substantiated claims.

We are not seeking a generic appeal to the openness of scientific debate, but a point-by-point expert response to the objections set out above. In particular, we ask you to address the following questions: What disease-specific data support the alleged miscalibration of interoceptive predictions in ME/CFS? How is such miscalibration to be distinguished from objectively measurable autonomic or exertion-induced manifestations? And how have the publisher and editorial team assessed the author’s publicly disclosed expert-assessment work under their rules on the disclosure of potential conflicts of interest?

A general statement about the controversial nature of the field does not answer these questions.

We ask that our objection of 2 September 2026 be considered in this review as a separate but thematically relevant matter.

Scientific debate about ME/CFS may be controversial. It must not be methodologically arbitrary.

Yours sincerely,

NichtGenesen
Patient Organization for People with LongCOVID, ME/CFS and Post-Vac

Article challenged: https://doi.org/10.1007/s00278-026-00874-w

Additional recent specialist source: Hoffmann K. “Von der Ausschlussdiagnose zur Multisystemdiagnostik – Aktuelle diagnostische Ansätze bei ME/CFS” (“From Diagnosis by Exclusion to Multisystem Diagnostics—Current Diagnostic Approaches to ME/CFS”)
 
They go a bit beyond the evidence with regards to pathophysiology, but overall it’s a well argued criticism of most of the things that are wrong with academia in general and BPS specifically.

This bears repeating:
An explanatory model that can interpret almost any symptom after the fact as an expression of miscalibrated predictions, without specifying clear criteria by which it could be falsified, does not, in itself, provide an adequate basis for causal claims about the disease.
I hope they are arguing that everything should be viewed with utmost skepticism:
Repeated appeals to scientific uncertainty must not become a one-way street in which biomedical evidence is viewed with the utmost skepticism, while a speculative psychophysiological model is introduced into the clinical interpretive framework subject to a substantially lower burden of proof. Such an asymmetrical assessment of evidence is scientifically unacceptable.
I doubt this will change anytime soon, but it’s worth pointing it out every time:
It cannot be the responsibility of patient organizations to keep having to demand these minimum scientific standards retroactively every time another publication appears.
 
An explanatory model that can interpret almost any symptom after the fact as an expression of miscalibrated predictions, without specifying clear criteria by which it could be falsified, does not, in itself, provide an adequate basis for causal claims about the disease.​

An hypothesis/narrative cannot be used as a proof of itself, which is the claim a lot of the BPS club make, whether they realise it or admit it, or not.
 
I definitely agree that doing a more general complaint about lack of standards is probably a better approach than doing it piecemeal for every bad paper published. It's hard to argue against that, and it's clear that there is a special exemption status happening here, where the lack of standards is clearly intentional, and massively abused to promote pet theories.

I have no idea how to go ahead with that, though. But there is clearly a case here, accusing major journals and publications of failing to uphold basic standards. And it could be the go-to response every time it happens, instead of doing the basic review that journals fail to bother doing, the general case could be argued.

Of course this applies to all of psychosomatic papers, so it's a major battle in itself. The special exemption exists for a reason: without it, none of this would get published. Or at best it could get published as opinion, which it is.
An hypothesis/narrative cannot be used as a proof of itself, which is the claim a lot of the BPS club make, whether they realise it or admit it, or not.
Unfortunately too hard to accept for a community built entire out of self-citation. As far as they are concerned, they are the evidence.
 
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