1) 🇧🇪 A small Belgian study reports that patients with ME/CFS and FM might have abnormalities in the opioid system.

They found that the opioid receptor genes were more often methylated, suggesting that these patients might be less sensitive to this type of pain relief. 2) This paper focuses on epigenetics: how our genes are switched on or off. This is done by adding methyl groups to specific pieces of DNA, making it less likely that a gene will be expressed.

The genetic code remains exactly the same but it becomes harder to acces and read.

1) Reminder: the Horizon Europe work program for 2026-2027 includes a call on post-infection long-term conditions. It has a budget of 6-8 million per project and seems ideally suited for ME/CFS and Long Covid research.

The opening date is 10 February 2026. 2) The full name of the call is: HORIZON-HLTH-2026-01-DISEASE-03: Advancing research on the prevention, diagnosis, and management of post-infection long-term conditions.

More info can be found here:
ec.europa.eu/info/funding-t…

1) ME/CFS patients often reported problems with their working memory. This review examined 34 studies that used cognitive tests to investigate this.

The effect was quite large for verbal working memory, while no clear effect was found for visual memory. 2) One of the most used tests is the Digit Span Backwards, where you have to remember and repeat a series of digits in reverse order (e.g., hearing "3-8-9" and saying "9-8-3").

Several studies showed a clear deficit in ME/CFS patients using this test.

1) This hypothesis paper argues that herpesviruses aren't either active (lytic replication) or passive (latency) but that there's a third state called 'abortive lytic replication' where the virus is active but doesn't replicate itself.

They suspect this plays a role in ME/CFS. 2) During this partially active state, the virus activates some genes and proteins but doesn't fully complete its replication. So there's no increase in viral load, which would explain why no such difference has been found between ME/CFS patients and controls.

1) 🇨🇳 A Chinese study looked at the mycobiome, the fungi living in the human body, in 59 ME/CFS patients and 59 controls.

Patients had, for example, more Aspergillus and less Candida. 2) Overall, ME/CFS patients seemed to have less fungal diversity than controls, but because of heterogeneity (large variation within the ME/CFS group), some of the difference were not statistically significant.

1) 🇸🇪 A Swedish study of 111 ME/CFS patients found reduced levels of vasopressin, a hormone that regulates water retention.

Low vasopressin could lead to low blood volume and some of the orthostatic symptoms that ME/CFS patients report. 2) The authors looked into this as ME/CFS patients often suffer from polyuria, similar to diabetes patients.
They write: "Patients with ME/CFS often describe excessive thirst and high urine volumes, symptoms that are regularly dismissed if not specifically asked about."

1) We’ve just published our review of the most interesting ME/CFS studies of 2025.

It feels like this year, we’ve made a significant step towards understanding the pathophysiology of ME/CFS.

A brief overview of the studies that caught our eye 👇 2) The biggest piece of the puzzle comes from DecodeME and the genetics study by Mark Snyder’s team at Stanford.

Both pointed to the brain and neuronal communication as being key to ME/CFS pathology.

1) Elizabeth Worthey's group published their findings on rare gene mutations in ME/CFS patients. Unfortunately, the evidence seems a bit underwhelming.

Only 31 individuals were screened and it's unclear if the mutations found are truly pathogenic. 2) Take the mutations for the KCNJ18 gene which codes for a potassium channel. A 2016 study showed that mutations for this gene are "seldom pathogenic". This includes the Q407X mutation which Worthey et al. describe as "pathogenic: definitive".
pubmed.ncbi.nlm.nih.gov/25882930/

1) Moving paper by young ME/CFS researcher Katherine Cheston. She was aware of the great disability it causes but "encountering the reality of this suffering first-hand was still shocking and deeply saddening."

She gives examples of patients who do not get appropriate care. 2) One patient had been ill for 3 decades and "had all her teeth removed as the severity of her illness meant that she had been unable to care for them."

"Multiple interviewees spoke of their distress at only being able to take a shower once every couple of months."

1) New blog post: NIH funding for ME/CFS keeps falling.

Last year, we calculated that the NIH funded 23 ME/CFS projects, totalling an investment of $10.1 million. In 2025, however, this amount decreased to $7.4 million for 18 projects. 2) Even if we include funding for Ian Lipkin’s team at Columbia University (which did not appear in the database), the funding still decreased by 7% to $ 9.4 million.

1) 🇦🇺 This new study tested the kynurenine pathway in the plasma of 61 ME/CFS patients and 61 controls.

There were no differences in tryptophan or kynurenine, but further downstream, patients had increased levels of 3HK and lower levels of picolinic acid and quinolinic acid. 2) In the white blood cells of patients, the researchers found increased AMP and a lower ATP/ADP ratio, which both hint at an issue with sufficient energy production in immune cells.

1) Interesting new hypothesis paper by the team of Ron Davis.

They suspect that the recently discovered glymphatic system (the 'lymph nodes' of the brain) plays a role in ME/CFS pathology. 2) The glymphatic system helps to clear waste products from the brain, similar to the lymphatic system elsewhere in the body. It assists with various clean-up processes, especially during sleep.

So ME/CFS could be due to a failed clean-up/reset problem in the brain.

1) This study from Cornell University tested more than 6000 proteins before and after two exercise tests.

It found altered patterns in ME/CFS patients compared to controls, particularly in proteins involved in the immune system, signal transduction, and muscle contraction. 2) The study included 79 ME/CFS patients (selected using the Canadian criteria) and 53 controls. Participants underwent 2 exercise tests, and samples were collected at 5 different time points before and between these tests.

1) Dr. Vanessa Velasco gave preliminary results on OMF's new neutrophil study.

She found that neutrophils of ME/CFS patients died quicker and more often than those of healthy controls, under inflammatory conditions. 2) Neutrophils are immune cells that form the first line of defence when there is an infection. The researchers were able to isolate the neutrophils from whole blood, without changing them, and then mimic inflammatory conditions in the lab.

1) Impressive study from Johns Hopkins researchers.

They infected mice with SARS-CoV-2, found that female mice had a stronger immune response and more cognitive problems after 84 days than males, and that this was due to over-expression of genes such as Tlr7 on the X chromosome. 2) The study tries to answer the paradox of why males are more likely to be severely ill during infection, while females are more likely to develop Long Covid.

They confirmed this in mice: males had more severe acute illness while females had more lingering cognitive problems.

1) The most interesting presentation during the 2025 Stanford symposium was on PET scans of the entire body.

Dr. Michelle James explained that they found a striking pattern with more TSPO signal in various muscle groups of ME/CFS patients, such as the thigh and shoulders. 2) PET scans work by injecting a radioactive molecule into the veins. The scan records annihilation events where a positron leaves the cell and collides with an electron, creating two photons. That signal tells us where in the body the radioactive molecule is binding.

1) We’ve just published our second instalment on the DecodeME results, this timing zooming in on the genes associated with ME/CFS. 2) In our view, the clearest signals point to genes such as CA10, SHISA6, SOX6, LRRC7, and DCC, which are involved in neuronal development and communication in the brain.

1) We’ve written an article about the DecodeME results: what the study measured, what the results show, and why its findings are important. 2) DecodeME is by far the biggest study on ME/CFS ever done. It may not have caused a big breakthrough, but it adds an important piece to understanding the puzzle of ME/CFS.

1) This lecture by Prof dr Vivienne Matthies-Boon is a good introduction to the problems with the biopsychosocial (BPS) model and the harms it has caused in the ME/CFS community. 2) In brief: BPS proponents think there is no objectionable pathology in ME/CFS, so they see the disorder as mainly caused by the belief one is ill and the inappropriate resting behavior that follows (sleeping too much, exercising too little, focusing on symptoms, etc.).

1) During his presentation at the 2025 Fatigatio conference, Prof. Bhupesh Prusty argued that physiologically, ME/CFS patients look similar to healthy individuals until they are put under stress. 2) He thinks there is something in ME/CFS patients that keeps the sickness response alive. And to study the illness and make it visible, one has to put the cells under different types of stress.

1) Prof. Carmen Scheibenbogen's talk at the 2025 Fatigatio conference was mostly about off-label therapies in Germany.

But at the end she also talked about new treatment trials they have planned to pursue the hypothesis that ME/CFS is caused by antibodies. 2) She claimed that immunoadsorption led to an improvement in about 75% of treated ME/CFS patients but that this improvement is unfortunately not sustained. It's not a curative treatment.

Therefore, they are looking at a more targeted treatment.