ME/CFS

First, what the words mean. Not a diagnosis.

• Fatigue

  Not ordinary tiredness. Rest does not take it away. It is out of proportion to what was done.

• Post-exertional malaise

  Called PEM. Not tired muscles after sport. After a small effort, a conversation, a shower, a short walk, the whole state gets worse: body, thinking, sleep, sometimes a flu-like feeling. Often hours later or the next day. It lasts more than a day, often several days. After that the threshold is even lower.

• Brain fog

  Thinking, finding words, staying with a task.

• Memory

  Holding something and recalling it.

• Unrefreshing sleep

  One sleeps and still wakes wrecked.

• Shortness of breath

  The feeling of not getting enough air. More often after COVID.

• Chest pain

  Pain in the chest. More often after COVID.

• Taste or smell

  Changed or gone. More a mark of Long COVID.

Then the comparison. The common symptoms sit close together. Shortness of breath, chest pain and disturbed smell sit higher in Long COVID. Shares from a survey, not a diagnosis.

How many with Long COVID meet ME/CFS. Three sums, three different denominators. Do not add them together.

• 4.5 percent after the infection

  Vernon and others, RECOVER, Journal of General Internal Medicine 2025. 531 of 11,785 adults, at least six months after COVID, met the ME/CFS criteria. Without infection, 9 of 1,439, which is 0.6 percent. Of the 531, 471, that is 88.7 percent, also met the Long COVID criteria. This is the share among all infected people, not among Long COVID.

• 45 percent in the fatigue clinic

  Kedor and others, Charité, Nature Communications 2022. 19 of 42 with lasting fatigue and exertion intolerance six months after COVID met the Canadian criteria. Most of the other 23 did not, because the worsening lasted under 14 hours. Selected patients, not the population.

• 15.6 percent in the billing codes

  Central Research Institute of Ambulatory Health Care, fourth quarter of 2025. Of 208,361 with a post-COVID code, 32,595 also had an ME/CFS code. 32,595 divided by 208,361 is 15.6 percent. Of 189,252 with an ME/CFS code, 32,595 also had post-COVID. 48 percent of the ME/CFS codes had no documented COVID infection. Codes are often missing. Not a severity scale.

At the end of 2025 a model for Germany estimates about 757,000 with Long COVID and 657,000 with ME/CFS. Those are two stocks. They must not be divided into each other.

Vernon and others, 2025 · Kedor and others, 2022 · Billing codes, fourth quarter 2025

Eckey and others, survey, 2025

New on 30 September 2026. The Charité study is published: a year of integrated care did not improve physical function. In 45 percent the state was worse afterwards. Michael Stingl: if PEM is present, rehabilitation is not the basis. On the chest: a US paper finds, in some people with ME/CFS, poorer oxygen uptake in the tissue even though the heart delivers it. One clinic, not a test.

On 2 October 2026 Carmen Scheibenbogen wrote on X: the day before, the Leopoldina told the Federal Press Conference about serious gaps in care for Long COVID and ME/CFS. The statement calls for a better data base and for research on mechanisms, treatments and prevention. The speakers of the working group are Regina T. Riphahn and Norbert Suttorp. Carmen Scheibenbogen reviewed the paper as one of 16 reviewers. A citation. No treatment from this app.

The Leopoldina is the source behind that post. It is the German National Academy of Sciences. Its full name is the German Academy of Natural Scientists Leopoldina. Founded in 1652, based in Halle. A scientific academy: it advises politics and the public, and it does not treat patients. Membership is by election.

Andreas Meyer-Lindenberg has been a member since 2009, section neurosciences. He is a psychiatrist and director of the Central Institute of Mental Health in Mannheim. He did not write this statement.

Carmen Scheibenbogen, 2 October 2026 · Statement, October 2026 · Meyer-Lindenberg, member entry

In ME/CFS there are changes in the brain. A routine clinical MRI usually does not show them and does not diagnose the illness. Research measures them, with specialised methods. Not a test.

A routine clinical brain MRI is usually unremarkable in ME/CFS. The illness is not diagnosed from it. NICE: there is no test, it is recognised clinically. A standard MRI is used to rule out other neurological diseases, for example multiple sclerosis or a tumour.

The coloured slices below are not those clinical pictures. They come from research, with a special diffusion analysis, not from Mannheim. Yu and others, Scientific Reports, July 2025. Red-yellow: after an infection, higher axial diffusivity than in healthy people in several tracts. Blue: with a gradual onset, lower in the corpus callosum. Two patterns. Research reports the same direction, measurable differences with specialised imaging, in some people after COVID. Not a test from this app.

It is also on record that other areas join in during a task. Shan and others, review of 2020: extra brain areas during thinking tasks are a frequent finding, in 11 papers from different groups. The brainstem was abnormal in 9 papers. Schönberg and others, 2024, 34 people with ME/CFS and 34 healthy people: on the second pass the signal gets quieter in healthy people. In ME/CFS it stays loud, including the right postcentral gyrus, the inferior parietal lobule on both sides and the right superior temporal gyrus. The extra work in the left primary motor cortex tracked how severe the fatigue was. Not a test.

Weber-Fahr, Dommke, Ende, Schilling and others, Central Institute Mannheim, Biological Psychiatry, online 10 January 2026. The NEULOCO study. 27 people with post-COVID, 23 who had recovered. Measured with phosphorus spectroscopy, 31P-MRS, not a clinical MRI. The ratio of ATP to phosphocreatine was lower in the cingulate cortex, at the front, in the middle and at the back. ATP is the cell's energy carrier, phosphocreatine a short store for it. In the front part, a lower ratio went with worse scores on cognitive tests. About half also met the criteria for ME/CFS. That subgroup showed a similar pattern. Not a test.

The institute writes that MRI uses no X-rays and that people in studies can be scanned as often as the question needs.

NICE NG206 · Yu and others, Scientific Reports 2025 · Shan and others, 2020 · Schönberg and others, 2024 · Weber-Fahr and others, 2026 · HITKIP · MRI at the ZI

Charité, Carmen Scheibenbogen and PD Dr Grabowski, patient sheet of February 2020. The four marked lines are that note. Four weeks as a trial. Not a treatment, and no new dose.

• B vitaminsCharité

  Four weeks.

• Coenzyme Q10Charité

  At most 100 mg. Passes electrons along the respiratory chain. Fat-soluble, like vitamin D3. Take it with some fat.

• D-riboseCharité

  3 × 5 g.

• NACCharité

  2–3 × 600 mg.

• B12, NADH, carnitine, arginine

  Named. Not a Charité dose.

Pacing comes first. This app sets no drug. Q10 can shift the INR on phenprocoumon or warfarin.

Almost everyone knows the word. Less known is what it acts on: the mitochondria. Not a treatment.

• Mitochondria

  The power stations. They make ATP, the cell's fuel.

• Superoxide

  The first exhaust. Electrons that leak from the respiratory chain turn oxygen into superoxide.

• Hydrogen peroxide

  Superoxide dismutase turns superoxide into hydrogen peroxide.

• Lipid peroxides

  Peroxides in the fats of the membrane. GPX4 takes them down with glutathione.

• SOD2

  Superoxide dismutase inside the mitochondria. It catches superoxide. It does not repair the chain.

• Glutathione

  The body's own antioxidant. Catalase splits hydrogen peroxide into water and oxygen. Catching more is not automatically better.

• Q10 and NAC

  Q10 sits in the chain and also catches exhaust in the membrane. NAC supplies the building block for glutathione. The dose is the Charité one above.

• A few names

  Coenzyme Q10, glutathione, NAC, vitamin C, vitamin E, alpha-lipoic acid. The Charité names only B-complex, Q10, D-ribose and NAC. This app sets no dose for the others.

Lymphocytes, Mark M. Davis and others, PNAS 8 July 2025: 27 people with ME/CFS, 20 with Long COVID, 25 healthy people. More oxidative stress, especially in memory cells. Less protein of the mitochondrial superoxide dismutase, damage to membrane fats via GPX4. In some, glutathione was higher, not lower. Not a test, not a treatment.

Davis et al., PNAS 2025

This was not in the app yet. Left, cancer: the cell does not die because cell death is switched off. Right, Long COVID: viral proteins, Nsp, block the repair. Below: cells block renewal. An illustration, not a measurement in ME/CFS and not a scientific paper.

Birgitta, @NeherBirgitta, 25 August 2026

DecodeME: 29 genes in the first tier and three in the second. The study set histone genes aside. Not the same genes in every person, and not equally strong in each. Each line says what the gene is for, and then a possible effect. That effect is not a must. Added, the readout of mitochondrial genes, which is not an inherited change, and CLYBL, BICD1, GRIN2A, CSMD1 and RORA from the Edinburgh preprint. Not a test, not a diagnosis, not a treatment.

• RABGAP1L

  Tier 1

  Switches Rab proteins off. They decide where vesicles in the cell stop. The cell also uses this to clear viruses inside it. Can disturb vesicle traffic and the clearing of viruses inside the cell.

• DARS2

  Tier 1 · mitochondria

  Loads the amino acid aspartate onto mitochondrial tRNA. Without that step the mitochondria cannot build their own proteins. Can slow the building of the mitochondria's own proteins.

• RC3H1

  Tier 1

  Also called Roquin. Binds RNA of immune genes and sends it to be broken down, so T cells do not stay switched on. Can leave T cells switched on for longer.

• GPR52

  Tier 1

  A receptor on nerve cells, mostly in the striatum. It is somewhat active on its own and shifts the dopamine signal. Can shift the dopamine signal in the striatum.

• ZBTB37

  Tier 1

  A zinc finger with a BTB clamp. Proteins of this kind switch genes on or off. The exact target genes are still thinly described. Can switch genes on or off. Which ones is open.

• TNFSF4

  Tier 1

  Also OX40L. Sits on cells that show an antigen and keeps the matching T cell alive. Can keep the matching T cells alive for longer.

• ANKRD45

  Tier 1

  Two ankyrin repeats, a clamp for other proteins. During cell division it sits on the midbody. More than that is not settled. An effect on cell division is possible. It is not settled.

• KLHL20

  Tier 1

  Hands selected proteins to a ubiquitin ligase, which marks them for breakdown. This also touches autophagy and interferon. Can shift protein breakdown and the interferon response.

• PRDX6

  Tier 1

  Neutralises peroxides in the membrane and can cut oxidised membrane fats. Can leave oxidised membrane fats in place.

• SERPINC1

  Tier 1

  Antithrombin. Inhibits thrombin and factor Xa, and so stops clotting. Can brake clotting less.

• SLC9C2

  Tier 1

  Exchanges sodium for protons. That holds the acidity of the cell. It is described mainly in sperm. Can shift the acidity of the cell. In people this is barely described.

• BTN2A2

  Tier 1

  A butyrophilin on the cell surface. It brakes the activation of T cells. Can loosen the brake on T cells.

• TRIM38

  Tier 1

  Adds ubiquitin to signalling proteins of innate immunity and thereby dampens NF-κB and interferon. Can dampen NF-κB and interferon less.

• ZNF322

  Tier 1 · zinc finger

  A zinc finger that binds DNA and starts the reading of some genes. No single known target system. Can shift the reading of some genes. No target is known.

• ABT1

  Tier 1

  Helps RNA polymerase start reading a gene at all. Can disturb the start of reading a gene.

• HFE

  Tier 1

  Sits on the transferrin receptor and lowers iron uptake into the cell. A broken form lets too much iron in. Can let too much iron into the cell.

• BTN3A3

  Tier 1

  A butyrophilin. Helps certain T cells recognise unusual molecules inside the cell, and can slow some viruses. Can weaken the recognition of unusual molecules and the slowing of some viruses.

• HMGN4

  Tier 1

  Binds nucleosomes and loosens chromatin so the genes underneath can be read. Can make genes harder to read.

• SUDS3

  Tier 1

  Part of the Sin3 complex. It takes acetyl groups off histones and makes the genes underneath quieter. Can leave genes loud that should be quieter.

• PEBP1

  Tier 1

  Also RKIP. Inhibits the kinase chain Raf–MEK–ERK. Also the precursor of a small peptide in the hippocampus. Can brake the Raf–MEK–ERK chain less.

• VSIG10

  Tier 1

  A surface protein with an immunoglobulin fold. What it does exactly is not settled. An effect is not settled.

• CA10

  Tier 1

  Related to carbonic anhydrase, but it does not run that reaction. It binds neurexin and sits at synapses. Can shift the synapse through neurexin.

• CSE1L

  Tier 1

  Also exportin-2. Returns importin-alpha from the nucleus to the cytosol, so import into the nucleus can continue. Can stall transport into the nucleus.

• ARFGEF2

  Tier 1

  Also BIG2. Switches ARF proteins on. They send vesicles off from the Golgi and from endosomes. Can disturb the sending of vesicles from the Golgi.

• DDX27

  Tier 1

  An RNA helicase in the nucleolus. It unwinds RNA that is needed to build ribosomes. Can slow the building of ribosomes.

• STAU1

  Tier 1

  Binds double-stranded RNA, moves it along the cell's fibres, and can send some RNA to be broken down. Can shift the transport and breakdown of RNA.

• ZNFX1

  Tier 1 · zinc finger

  A different zinc finger from ZNF322. It recognises viral RNA and starts the interferon response. Can weaken the interferon response to viral RNA.

• B4GALT5

  Tier 1

  Adds galactose to sugar-fats of the membrane and makes lactosylceramide. Can change the sugar-fats of the membrane.

• PTGIS

  Tier 1

  Prostacyclin synthase. Makes prostacyclin from prostaglandin H2. That widens vessels and stops platelets sticking. Can widen vessels less and let platelets stick more easily.

• FBXL4

  Tier 2 · mitochondria

  Brakes mitophagy, the clearing of mitochondria. If it is missing, too many are cleared. Can let too many mitochondria be cleared.

• OLFM4

  Tier 2

  Olfactomedin-4. Lies in neutrophil granules and marks one subset. Also in stem cells of the gut. Can shift one subset of neutrophils.

• CCPG1

  Tier 2

  A receptor for ER-phagy. It sends stressed pieces of the endoplasmic reticulum to autophagy. Can clear stressed endoplasmic reticulum less well.

• MT-RNR1 · MT-RNR2

  Mitochondrial RNA

  The 12S and 16S RNAs. They are the frame of the mitochondrial ribosome. Without them the proteins of the mitochondria are not made. Can slow the building of mitochondrial proteins. Here this is a readout, not an inherited change.

• MT-ATP6 · MT-CO1 · MT-CO2 · MT-CO3

  Respiratory chain

  MT-ATP6 is part of ATP synthase, which makes ATP. MT-CO1 to MT-CO3 are the core of cytochrome c oxidase, which passes electrons to oxygen. Can mean less ATP and a weaker last step of respiration.

• MT-CYB · MT-ND3 · MT-ND5

  Respiratory chain

  MT-CYB is cytochrome b in complex III. MT-ND3 and MT-ND5 are parts of complex I, which takes the electrons from NADH. Can disturb the handover of electrons in complexes I and III.

• CLYBL

  Enzyme

  Citramalyl-CoA lyase in the mitochondria. It splits citramalyl-CoA, an intermediate in metabolism that also touches vitamin B12. Can leave a metabolic piece in the mitochondria that also touches vitamin B12.

• BICD1

  Transport

  Hooks cargo to dynein. That motor protein pulls vesicles along microtubules toward the centre of the cell. Can stall transport toward the centre of the cell.

• GRIN2A

  Nerve cell

  The GluN2A subunit of the NMDA receptor. It lets calcium into the nerve cell when glutamate binds. Can shift the calcium inflow at the synapse.

• CSMD1

  Complement

  Brakes complement at the cell surface, so innate immunity does not punch the cell's own membrane. Can brake complement less.

• RORA

  Switch

  A nuclear receptor. It steers the body clock, development of the cerebellum, and parts of inflammation. Can shift the body clock, cerebellar programmes and parts of inflammation.

DecodeME, medRxiv 2025 · Mitochondrial genes, Int. J. Mol. Sci. 2026 · CLYBL, medRxiv 14 September 2026

• WASF3

  Protein

  Higher in muscle in some people with ME/CFS. Can disturb mitochondrial supercomplexes. Endoplasmic stress can raise it.

• PDH

  Enzyme complex

  Pyruvate dehydrogenase. This is where carbohydrate enters the mitochondria. Fluge describes a brake here.

• Komplex I

  Respiratory chain

  Protein machines in the mitochondrial membrane. Muscle biopsies show less oxidative output. Inactivity alone does not explain it.

• Komplex IV

  Respiratory chain

  Cytochrome c oxidase. Lower in muscle together with higher WASF3. Hwang 2023.

• GDF15

  Protein in blood

  A stress signal from mitochondria. Rises after exertion with fatigue and PEM. A marker, not a treatment.

• Komplement

  Immune proteins

  Proteins of innate immunity. More active after exertion in ME/CFS.

• ADRB2 · CHRM

  Receptors

  The β2-adrenergic receptor and muscarinic receptors. Autoantibodies in some people. One ELISA separates poorly.

• ATP1A

  Ion pump

  Na+/K+-ATPase in the muscle membrane. Wirth: a hypothesis, no proven mutation. No drug from this app.

• IDO1

  Enzyme

  First step from tryptophan to kynurenine. DecodeME does not name it. Newer measures see an active IDO, not a simple block.

• IDO2

  Enzyme

  Sister of IDO1. Phair and Davis 2019: the hypothetical trap sits here. Not a DecodeME signal.

• MAPK9 · NLGN1 · PTPRD

  Overlap

  Three genes that appear together in one ME analysis and in fatigue-dominant Long COVID. Candidates.

• LAG3

  Gene, candidate

  A 2026 network paper. Sits on T-cell exhaustion. Not confirmed as a cause.

New on 1 October 2026. Serum from Bergen: August and Fredrik Hoel, with Øystein Fluge, Olav Mella and Karl Johan Tronstad. 50 people with ME/CFS, 29 healthy people. 7,326 protein targets in the blood. After correction, 845 still differed. More secreted proteins, fewer from inside the cell, including muscle. Fewer proteins from activated neutrophils. A selection was checked with antibodies, not all of them. Not a test, not a treatment.

WASF3, PNAS 2023 · Muscle, Scheibenbogen and Wirth 2025 · IDO trap, Phair and Davis 2019 · Serum, Hoel, Fluge, Tronstad 2026

MicroRNAs are short pieces of RNA. They do not build a protein. They turn other genes down. In ME/CFS they are not a Long COVID finding alone. A 2024 review of ME/CFS and fibromyalgia names microRNAs on the immune response, the mitochondria and oxidative stress, including miR-146a, miR-21, miR-150 and miR-29. A 2023 computation finds that the circulating microRNAs differ from person to person, yet point at the same gene cluster. Eight of the ten most central ones are raised by herpesviruses, including Epstein-Barr, even while the virus is latent. Epstein-Barr also makes its own microRNAs, from the BART and BHRF1 clusters, that help it evade immune defense. That is shown for the virus in general, not yet as a blood test in ME/CFS. A 2026 vesicle paper measures less let-7b in ME/CFS after COVID, together with fatigue and immune activation. The group measured is post-COVID. The same paper names Epstein-Barr as another trigger, and did not measure that group. Not a test, not a treatment.

For each paper, the X post that carries it, and the authors. The work stays theirs. No voice is presented as ours.

1. 1

   Maria Tsamou

   Paper, not X

   Where: microRNA

   Maria Tsamou, Fabiënne A. C. Kremers, Keano A. Samaritakis, Erwin L. Roggen.

   A 2024 review of ME/CFS and fibromyalgia, not only Long COVID. MicroRNAs named more than once sit on the immune response, mitochondria and oxidative stress, including miR-146a, miR-21, miR-150 and miR-29. Not a test.

   Tsamou et al., Int. J. Mol. Sci. 2024

2. 2

   Mateusz Piotr Kaczmarek

   Paper, not X

   Where: microRNA · EBV

   Mateusz Piotr Kaczmarek.

   A 2023 computation: circulating microRNAs in ME/CFS differ from person to person, but hit the same gene cluster. Eight of the ten most central ones are raised by herpesviruses, including Epstein-Barr, also in latency. Not proof of an active infection. No X post with this file.

   Kaczmarek, PLOS One 2023

3. 3

   Anthony Sunseri

   Paper, not X

   Where: Mitochondria

   Anthony Sunseri, Roger Gaudreault, Frédérique Retornaz.

   Review of 27 October 2026. mTORC1 as a possible switch when energy stress should start autophagy and recovery. Direct measurements in people are thin. The mitochondria can still look passable at rest and fail to find the way back under load. Rapamycin is not advice from this app. Not a test. No X post with this file.

   Sunseri et al., J. Transl. Med. 2026
4. 

   4

   Carmen Scheibenbogen

   @C_Scheibenbogen · post

   Where: Reading

   Nature news desk. Shared by Carmen Scheibenbogen.

   Post of 8 September 2026. A survey of the research on Long COVID and ME/CFS. A citation. No treatment from this app.

   Nature, News Feature 2026
5. 

   5

   Carmen Scheibenbogen

   @C_Scheibenbogen · post

   Where: Reading

   Carmen Scheibenbogen, Jonas Bergquist and others.

   Post of 17 October 2025. ME/CFS is not a result of avoiding activity. PEM remains the leading symptom. A citation.

   Nature Communications 2025
6. 

   6

   Michael Stingl

   @neurostingl · post

   Where: Vienna

   Kathryn Hoffmann, Astrid Hainzl, Michael Stingl and others. Carmen Scheibenbogen is a co-author.

   Neurologist in Vienna, one of the few in Austria whose work centres on ME/CFS. Post of 9 January 2025. He links the 2024 D-A-CH consensus: PEM is the leading symptom, no activation. A citation, no treatment from this app.

   Hoffmann, Stingl et al., Wien. Klin. Wochenschr. 2024
7. 

   7

   Michael Stingl

   @neurostingl · post

   Where: Vienna

   City of Vienna, WWTF and the WE&ME Foundation. ME-RESET: Lukas Haider, Martin Krššák, Kathrin Kollndorfer. Second project: Matthias Wielscher, Kathryn Hoffmann.

   Post of 13 October 2026. He thanks Vienna for taking the lead on ME/CFS. The city awards two consolidation grants of about one million euro each. ME-RESET tests whether energy failure in brain and muscle sits in blood flow or in the mitochondria. The second project uses whole-genome sequencing to look for rare genetic diseases that look like ME/CFS. A PAIS clinic is planned from summer 2027. A citation, no treatment from this app.

   Rathauskorrespondenz Wien, 13. Oktober 2026
8. 

   8

   Solve ME/CFS Initiative

   @PlzSolveCFS · post

   Where: Reading

   Carmen Scheibenbogen, Jonas Bergquist and others.

   Post of 23 October 2025. The same paper, shared by Solve. A citation, not our voice.

   Nature Communications 2025
9. 

   9

   Carmen Scheibenbogen

   @C_Scheibenbogen · post

   Where: Pacing

   Charité, CFS_CARE. Shared by Carmen Scheibenbogen.

   Post of 27 June 2026, on the preprint. Published 22 September 2026 in the American Journal of Medicine: after twelve months, physical function was not better. On the Bell score, 45 percent were worse afterwards. A citation, not a recommendation.

   Kedor et al., Am. J. Med. 2026
10. 

    10

    Carmen Scheibenbogen

    @C_Scheibenbogen · post

    Where: Pacing

    Claudia Kedor, Carmen Scheibenbogen, Kirsten Wittke and others. Charité, CFS_CARE.

    Post of 30 September 2026, in the evening. Her CFS_CARE study is in the American Journal of Medicine. No improvement after twelve months. After rehabilitation the Bell score was lower in 45 percent, even though patients rated the specialised rehab in Kreischa positively. Fitness for rehab must be judged very carefully in ME/CFS. A citation, not a recommendation.

    Kedor et al., Am. J. Med. 2026
11. 

    11

    Michael Stingl

    @neurostingl · post

    Where: Pacing

    Claudia Kedor, Carmen Scheibenbogen, Kirsten Wittke and others. Charité.

    Post of 30 September 2026. The same Charité study, now published. If PEM is present, rehabilitation is not the basis of treatment. Many get worse. A citation, not a recommendation.

    Kedor et al., Am. J. Med. 2026
12. 

    12

    Tom Kindlon

    @TomKindlon · post

    Where: Pacing

    The same Charité study: Kedor, Scheibenbogen, Wittke and others.

    Post of 30 September 2026. He shares the published paper. A citation, not our voice.

    Kedor et al., Am. J. Med. 2026
13. 

    13

    Tom Kindlon

    @TomKindlon · post

    Where: Genes

    Joshua Slaughter, Sjoerd V. Beentjes, Ava Khamseh, Chris P. Ponting and others. University of Edinburgh.

    Post of 21 September 2026. Preprint: seven genetic places that show up again in a second cohort, including CLYBL. DecodeME does not see them. None of the places in all three cohorts. A citation. Not a test.

    Slaughter et al., medRxiv 2026
14. 

    14

    Tom Kindlon

    @TomKindlon · post

    Where: Chest pain

    Zoë Mackay, Samit Shah, Inderjit Singh and others.

    Post of 29 September 2026. Among people with chest pain and no blocked coronary arteries, 18 percent also had ME/CFS. In a small, selected group the heart delivered oxygen and the tissue took less of it up. One clinic. A citation. Not a test.

    Mackay et al., AJP Heart 2026
15. 

    15

    Tom Kindlon

    @TomKindlon · post

    Where: Serum

    August Hoel, Fredrik Hoel, Sissel Dyrstad and others. Bergen, including Øystein Fluge, Olav Mella and Karl Johan Tronstad.

    Post of 10 March 2026, with a graphic. Serum from 50 people with ME/CFS and 29 healthy people. 7,326 protein targets. After correction, 845 differed: more secreted proteins, fewer from inside the cell, including muscle, and fewer from activated neutrophils. A selection was checked with antibodies. A citation. Not a test.

    Hoel et al., Cell Reports Medicine 2026
16. 

    16

    Jon Douglas

    @atranscendedman · post

    Where: Triangle

    Braeden T. Charlton, Anouk Slaghekke, Brent Appelman, Moritz Eggelbusch, Rob C. I. Wüst and others. Vrije Universiteit Amsterdam.

    Post of 28 July 2026. Muscle and mitochondria in Long COVID and ME/CFS differ from 60 days of bed rest. Inactivity does not explain it. A citation.

    Charlton et al., Nature Communications 2026
17. 

    17

    Thailand Medical News

    @ThailandMedicaX · post

    Where: Triangle

    The same muscle paper: Charlton, Wüst and others.

    Post of 29 July 2026. A news piece on the same finding. A citation, not our voice.

    Charlton et al., Nature Communications 2026
18. 

    18

    AMMES

    @AmmesAdmin · post

    Where: Triangle

    Sergio Abanades, Irene Fernández, Nuria Capdevila, Francisco Cardona.

    Post of 28 August 2026. A review of micronutrients and mitochondria in ME/CFS, including B-complex, Q10, GlyNAC and L-carnitine. No dose from this app.

    Abanades et al., Nutrients 2026
19. 

    19

    Tom Kindlon

    @TomKindlon · post

    Where: Reading

    Named in the post as a US paper, without an author line.

    Post of 10 June 2026. Vesicles and mitochondrial membrane potential in Long COVID and ME/CFS. A citation.

    Open Forum Infectious Diseases 2026
20. 

    20

    Carmen Scheibenbogen

    @C_Scheibenbogen · post

    Where: Reading

    Sonya Marshall-Gradisnik and others. Shared by Carmen Scheibenbogen.

    Post of 21 May 2025. LDN and the ion channel TRPM3, with a link to mitochondria. A citation. This app sets no drug dose.

    Frontiers in Molecular Biosciences 2025
21. 

    21

    Carmen Scheibenbogen

    @C_Scheibenbogen

    Where: Triangle · reading

    Claudia Kedor, Carmen Scheibenbogen and others.

    Nature Communications 2022: SARS-CoV-2 can trigger ME/CFS. Patient sheet of February 2020 with Grabowski: four weeks of B-complex, Q10 at most 100 mg, D-ribose 3×5 g, NAC 2–3×600 mg. No single X post carries this file. A citation. Not a treatment.

    Kedor et al., Nature Communications 2022
22. 

    22

    Jesús Castro-Marrero

    @JCastro_Marrero

    Where: Q10

    Jesús Castro-Marrero, Maria José Segundo, Marcos Lacasa, Alba Martinez-Martinez, Ramon Sanmartin Sentañes, José Alegre-Martin.

    Nutrients 2021: 200 mg Q10 plus 20 mg NADH. A small effect on cognitive fatigue. The app stays at most 100 mg Q10. The post for this exact file was not at hand.

    Castro-Marrero et al., Nutrients 2021

23. 23

    Jacob Teitelbaum

    Paper, not X

    Where: Ribose

    Jacob Teitelbaum, C. Johnson, J. St. Cyr.

    Open pilot study 2006, no placebo: D-ribose 3×5 g. Weak evidence. No X post with this file.

    Teitelbaum, Johnson, St. Cyr, 2006

24. 24

    Dikoma C. Shungu

    Paper, not X

    Where: NAC

    Dikoma C. Shungu and others.

    IACFS/ME 2016 and an MRS abstract 2020: four weeks of NAC, glutathione in the brain. No proof that fatigue falls in a clinically relevant way. No X post with this file.

    Shungu et al., ISMRM 2020
25. 

    25

    Carmen Scheibenbogen

    @C_Scheibenbogen · post

    Where: Leopoldina

    Leopoldina working group, speakers Regina T. Riphahn and Norbert Suttorp. Carmen Scheibenbogen reviewed it as one of 16 reviewers. Andreas Meyer-Lindenberg has been a Leopoldina member since 2009, section neurosciences. He is not an author of this statement.

    Post of 2 October 2026. On 1 October the Leopoldina told the Federal Press Conference about gaps in care for Long COVID and ME/CFS. The statement calls for a better data base and for research on mechanisms, treatments and prevention. The Leopoldina is the German National Academy of Sciences, founded in 1652, based in Halle. It advises. It does not treat. A citation. Not a treatment.

    Leopoldina, Stellungnahme Oktober 2026

26. 26

    Qiang Yu

    Paper, not X

    Where: MRI

    Qiang Yu, Richard A. Kwiatek, Peter Del Fante, Anya Bonner, Vince D. Calhoun, Grant A. Bateman, Takashi Yamamura, Zack Y. Shan.

    Scientific Reports, 7 July 2025. Diffusion MRI in ME/CFS. After an infection, higher axial diffusivity than in healthy people in several tracts. With a gradual onset, lower axial diffusivity in the corpus callosum. Two patterns. The figures in the app are unchanged from this paper, not from Mannheim. No X post with this file. Not a test.

    Yu et al., Scientific Reports 2025

27. 27

    Emanuel Schwarz

    Paper, not X

    Where: MRI

    Emanuel Schwarz leads the Hector Institute for Artificial Intelligence in Psychiatry at the ZI Mannheim. Andreas Meyer-Lindenberg directs the ZI.

    HITKIP has existed since April 2023. It analyses large data sets, including imaging, on mental illness. The ZI has 3-tesla scanners and one 7-tesla scanner. MRI uses no X-rays. This app only puts questions to an AI. Not a test.

28. 28

    Zack Y. Shan

    Paper, not X

    Where: MRI

    Zack Y. Shan, Leighton R. Barnden, Richard A. Kwiatek, Sandeep Bhuta, Daniel F. Hermens, Jim Lagopoulos.

    Journal of Translational Medicine, 1 September 2020. A review of 63 papers. Extra brain areas during thinking tasks are a frequent finding, in 11 papers from different groups. The brainstem was abnormal in 9 papers. No X post with this file. Not a test.

    Shan et al., Journal of Translational Medicine 2020

29. 29

    Laura Schönberg

    Paper, not X

    Where: MRI

    Laura Schönberg, Abdalla Z. Mohamed, Qiang Yu, Richard A. Kwiatek, Peter Del Fante, Vince D. Calhoun, Zack Y. Shan.

    Journal of Cerebral Blood Flow and Metabolism, online 7 August 2024. 34 people with ME/CFS, 34 healthy people. On the second pass the signal gets quieter in healthy people. In ME/CFS it stays loud, including the right postcentral gyrus, the inferior parietal lobule on both sides and the right superior temporal gyrus. The extra work in the left primary motor cortex tracked how severe the fatigue was. No X post with this file. Not a test.

    Schönberg et al., JCBFM 2024

30. 30

    Wolfgang Weber-Fahr

    Paper, not X

    Where: MRI

    Wolfgang Weber-Fahr, Sandra Dommke, Markus Sack, Nabil Alzein, Robert Becker, Traute Demirakca, Gabriele Ende, Claudia Schilling. Central Institute of Mental Health, Mannheim.

    Biological Psychiatry, online 10 January 2026. The NEULOCO study. 27 people with post-COVID, 23 who had recovered. 31P-MRS, not a clinical MRI. ATP to phosphocreatine was lower in the cingulate cortex, at the front, in the middle and at the back. In the front part this went with worse cognitive test scores. About half also met ME/CFS criteria and showed a similar pattern. No X post with this file. Not a test.

    Weber-Fahr et al., Biological Psychiatry 2026

31. 31

    Mark M. Davis

    Paper, not X

    Where: Antioxidants

    Mark M. Davis and others. Stanford.

    PNAS, 8 July 2025. Lymphocytes from 27 people with ME/CFS, 20 with Long COVID and 25 healthy people. More oxidative stress, especially in memory cells. Less mitochondrial SOD protein, membrane fats damaged via GPX4. Glutathione higher in some. No X post with this file. A citation. Not a test, not a treatment.

    Davis et al., PNAS 2025

32. 32

    Suzanne D. Vernon

    Paper, not X

    Where: Share

    Suzanne D. Vernon and others. RECOVER-Adult.

    Journal of General Internal Medicine 2025. 531 of 11,785 after COVID met ME/CFS criteria, 4.5 percent. Without infection, 9 of 1,439, 0.6 percent. 471 of 531, 88.7 percent, also met Long COVID. A share among infected people, not among Long COVID. Not a test.

    Vernon et al., JGIM 2025

33. 33

    Kassenärztliche Versorgung

    Paper, not X

    Where: Share

    Central Research Institute of Ambulatory Health Care in Germany.

    Billing data, fourth quarter of 2025, report of 24 July 2026. 32,595 of 208,361 with a post-COVID code also had ME/CFS, 15.6 percent. 32,595 of 189,252 with an ME/CFS code also had post-COVID. 48 percent of the ME/CFS codes had no documented COVID infection. Codes, not severity. Not a test.

    Zi, ME/CFS-Auswertung Q4 2025
34. 

    34

    Birgitta

    @NeherBirgitta · post

    Where: Picture

    Birgitta. An illustration, not the authors of a study.

    Post of 25 August 2026, with a video. Left, cancer: the cell does not die because cell death is switched off. Right, Long COVID: viral proteins block the repair. Under it: cells block renewal. Not a measurement in ME/CFS. Not a scientific paper.

• Charité Fatigue Centrum
• Fatigatio e.V.
• German Association for ME/CFS

From notes that have been published. Not a diagnosis, not a treatment, not a substitute for the doctor who treats you. If you get suddenly worse, use emergency medical care, not this app.