Oslo Chronic Fatigue Consortium får flengende kritikk av fagfolk for sitt nylig publiserte manifest; “Chronic fatigue syndromes: real illnesses that people can recover from”
Bakgrunn
I fjor høst samlet 50 personer seg til et hemmelig seminar om virusutløste sykdommer i Oslo, under ledelse av prof. Silje Reme (UiO) – ME-krigens nye hærfører.
Like etter seminaret (13/10/22) startet Reme en stygg svertekampanje av ME-syke i både media (21/10/22) og en podcast (21/10/22), der hun bl.a. fremstilte pasientene som en farlig trussel mot fagfolk. I mangel på faglige argument, blir propaganda deres våpen. Jo flere som tror på fiendebildet de skaper, jo færre vil tro på pasientene.
Få dager senere hevder Reme, Flottorp (FHI) og Wyller (Ahus) at psykologiske behandlinger mot ME er “grundig dokumentert” (25/10/22), før Remes svertekampanje fortsatte på nyåret (7/2/23).
Da grunnlaget var lagt, ble et ideologisk opprop sendt til et skandinavisk tidsskrift (17/2/23) – signert av de fleste deltagerne på det hemmelige seminaret, som nå kaller seg “Oslo Chronic Fatigue Consortium” (OCFC).
Oslo-manifestet ble publisert 23. september 2023. Pressemeldingens 10 bud handler om deres tro, håp og maktgriskhet for å definere ME og Long Covid i sitt bilde.
Reaksjoner fra fagfolk
Under finner du skjermdumper fra kritikk delt på X/Twitter. Etter navneendringen til X får jeg ikke delt «embedded links.» Linker deles derfor under de ulike bildene.
1
Jonas R. Kunst, psykologiprofessor UiO
2
David Tuller, PhD i folkehelsejournalistikk, og prof. Jonas Kunst:
3
Prof. Resia Pretorius, Physiological Science, og David Tuller:
4
Herberto Dhanis, PhD i neuroscience
5
Prof. Todd Davenport, Physical Therapy
6
Lou Corsius, Msc Health Sciences, til en psykiater som deler manifestet:
7
Prof. David Putrino, Physio, PhD Neuroscience
8
Dr. Deepti Gurdasani, epidemiolog, til Paul Garner (OCFC)
9
Sten Helmfrid, Sr. Scientist, PhD i fysikk
10
Dr. Claire Taylor, MBChB, BSc Neuroscience (Hons)
11
Lisa Norén, legespesialist allmennmedisin, LC-pasient
12
Physios for ME svarer Paul Garners deling av Bud 3:
Vedlegg: “Pathological Mechanisms Underlying ME/CFS”
13
Legespesialist Ottar Gadeholt til Signe Flottorp (FHI)
Dr. Gadeholt om Paul Garners deling av Bud 2:
14
Janet Dafoe, PhD i psykologi, pårørende
15
Siri Ann Mauseth, lege, PhD epidemiologi, til Signe Flottorp (FHI, OCFC)
Vedlegg: Videointervju av Prof. Iwasaki og studie fra Prof. Altmann
16
Kunngjøring fra Dr. Charles Shepherd, medisinsk rådgiver til ME Association:
“This latest effort from Norway appears to confirm that a concerted effort is underway from a handful of professionals – some of whom have clear conflicts of interest – that are once again trying to self-aggrandise at the expense of people who have been maligned and stigmatised.”
17
Frøydis Lilledalen, psykologspesialist, ME-pasient
Debattinnlegg i Dagens Medisin; “Håpspredikantene”
Flaut, OCFC
Dagen etter David Putrino kritiserer manifestet (nr. 7), publiserer Nature en ny studie som viser at Long Covid er en biologisk sykdom (25/9/23). Putrino er hovedforsker, sammen med velrenommerte prof. Akiko Iwasaki (Yale, ref. nr. 15).
Studien har siden skapt overskrifter over hele verden, inkl. i TV2, VG, og Nettavisen. Samt har amerikanske helsemyndigheter (NIH) oppsummert resultatet på sin nettside.
Pressemelding: “Research conducted at Mount Sinai and Yale confirms long COVID is a biological disease by showing blood biomarkers that can predict who has it”
31. august 2023 publiserte også britiske forskere en studie på en nyutviklet blodprøve som kunne skille mellom ME, MS og friske kontroller med 91% nøyaktighet.
Mens i Norge forsker fagfolk i OCFC på Lightning Process og Silje Remes tilsvarende selvhjelpskurs – der Long Covid-pasienter skal starte dagen med å spørre;
«Hva feiler det meg?» Pålagt svar: «Ingenting.»
Flaut, FHI
Mens amerikanske helsemyndigheter sprer ny kunnskap og forskning, sprer ansatte ved Folkehelseinstituttet et skadelig manifest. Forskningssjef Signe Flottorp og avdelingsdirektør Kjetil Brurberg står også som medforfattere, mens fagdirektør Preben Aavitsland bidrar med likes og deling i sosiale medier.
Aavitsland mener oppropet er en «policy statement» og «call to action» – for deretter å innrømme at det er basert på personlige meninger – ikke på forskning. Mens Flottorp deler grandiose påstander om at OCFC består av «Top people in the field…»
Tiden der Oslo-konsortiet og Folk & Røverinstituttet avsløres som falske profeter nærmer seg med stormskritt.
Tilgi dem ikke. For de vet godt hva de gjør.
Hilsen Sissel
Aavitsland (tråd) | Garner/Flottorp
“Top people in the field” sin behandling av en biologisk sykdom:
Life with ME by Sissel 
(As a lot of the blog post is in English, I’ll write this comment in English as well, in case there are some international readers who might be interested.)
The theory espoused by the members of the Oslo-consortium is that ME/CFS (and also Long Covid evidently) are a consequence, not of any distinct biological pathology, but rather what they call a “sustained arousal” (otherwise known as sympathetic nervous system activation or just sympathetic activation).
There are numerous observations that seem to suggest the sympathetic activation is not responsible for the symptoms, at least not on it’s own, which is what this group proposes. I don’t have time to go through them all, and it would be difficult to do so in the context of a blog comment, but I will discuss two interesting observations.
The first one is that an abnormal sympathetic activation is a common factor in many different diseases:
“An overactive sympathetic nervous system has become an identified characteristic of several cardiovascular diseases including, ischemic heart disease (Graham et al., 2004), chronic heart failure (Leimbach et al., 1986), and hypertension (Grassi, 1998). However, elevated SNA is not isolated to diseases of the cardiovascular system and has also been reported in a plethora of other conditions including: kidney disease (Converse et al., 1992), type II diabetes mellitus (Huggett et al., 2003), obesity (Grassi et al., 2007), metabolic syndrome (Grassi et al., 2005), obstructive sleep apnea (Narkiewicz and Somers, 1997), pre-eclampsia (Greenwood et al., 2003), depression (Barton et al., 2007), and ulcerative colitis (Furlan et al., 2006).”
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2679852/
How can something that is present in so many diseases be behind symptoms that aren’t present in any of them, except ME/CFS? If sympathetic activation was indeed the only thing behind the symptoms of ME/CFS and LC, one would expect other diseases with sympathetic activation to share the same symptomology as ME/CFS, but they don’t. Hence it’s highly unlikely that it is what’s behind them, at least on it’s own, although it could possibly be a contributing/mediating factor. But this is not what they are saying – they are saying this stress response, which is present in so many wildly different diseases, is what’s behind it.
Also many patients with ME/CFS don’t show a primarily sympathetic activation, at least not all the time, as you can see from this study which tries to group ME/CFS-patients into different groups based on the unique characteristics of their ANS dysregulation:
“Using cluster analyses, these factors were grouped in four autonomic profiles: 34% of patients had sympathetic symptoms with dysautonomia, 5% sympathetic alone, 21% parasympathetic and 40% had issues with sympathovagal balance.”
Source: https://www.mdpi.com/2077-0383/9/8/2531
As you can see here, it seems that sympathetic activation does not occur in all patients with this disease. How can it be that sympathetic activation alone is behind the symptoms when it’s not consistently observed, at least not in all patients? If sympathetic activation is behind the symptoms, it would be very strange indeed that it’s not necessarily present while the disease is active?
Don’t get me wrong, I definitely think dysregulation of the ANS is present in ME/CFS and LC, as in many other immunological diseases. I think a lot of evidence points to that. However, this dysregulation is most certainly not described satisfactorily through the “sustained arousal”-framework championed by this particular group of researchers. It’s much too simplistic and doesn’t square well with numerous empirical observations. I think dysautonomia is a better, and more open concept, that fits more neatly to the data than the “sustained arousal”-framework. And I think it’s fairly surprising to see that they continue to cling to this framework in 2023, as the most likely explanation, despite the many studies that strongly suggest otherwise.
If any of the supporters of the “sustained arousal”-framework sees this post and would oblige me by providing me with their reasoning behind supporting it, I would be very interested to hear how you’re thinking to arrive at this conclusion.
LikeLiked by 2 people