At the Berlin event, researchers presented initial results of new clinical trials. All of the controlled trials presented for the first time at the conference failed to meet goals.
Key points you should know:
- More than 50 experts from around the world presented the latest findings in basic and therapeutic research on myalgic encephalomyelitis (ME) and Long COVID at a conference in Berlin.
- Researchers unveiled first preliminary results from several highly anticipated clinical trials, including studies on low-dose naltrexone (LDN) and immunoadsorption.
- While the randomized controlled trial treatments presented failed to meet their primary endpoints over placebos, smaller studies pointed to potentially promising therapies.
- One study found that even under optimized conditions, physical rehabilitation can worsen ME.
At a major myalgic encephalomyelitis (ME) conference in Berlin, Germany, international researchers met to exchange new insights. Scientists presented the first, mostly preliminary findings from several clinical trials. The results were largely sobering, though some smaller studies and advances in basic research pointed to more promising approaches.
The meeting, held on May 7 and 8, was the fourth International ME/CFS Conference organized by the Fatigue Center at Charité, Berlin’s university hospital, in cooperation with the ME/CFS Research Foundation. The foundation was established in 2022 by management consultant Joerg Heydecke and lawyer Martin Hippe, who has ME, to support biomedical research into the disease.
More than 270 researchers, physicians, and other participants attended the conference in person, while more than 6,000 people from 55 countries registered for online livestreams of the event, according to the event organizers.
However, according to preliminary data, all of the randomized, placebo-controlled trials (RCTs) presented failed to meet their primary endpoints:
- Cardiologist Valentina Puntmann, associate professor at Goethe University in Frankfurt, presented results from the “Myoflame-19” study. Conducted at four centers in Germany and Austria, the trial enrolled 280 people with cardiac symptoms following a SARS-CoV-2 infection. Researchers investigated whether early combined treatment with heart medications and anti-inflammatory drugs (Prednisolon and Losartan) could prevent long-term heart damage. But after 16 weeks, the treatment showed no benefit over placebo on the study’s primary cardiac outcome measure.
- The “PoCoVIT trial” at Charité, which investigated the anti-inflammatory drug methylprednisolone — a potent corticosteroid that suppresses the immune system — was stopped early after 96 of the planned 418 participants with cognitive impairments from Long COVID received treatment. Five participants experienced serious adverse events such as deep vein thrombosis and pulmonary embolism, which neurologist and study co-author Lucas Adam described as “really shocking.” Data analysis also found that after eight weeks, the drug was no more effective than placebo at improving participants’ self-reported memory satisfaction.
- Epidemiologist Luis Nacul of the University of British Columbia presented early data from a randomized controlled trial of low-dose naltrexone (LDN). The Canadian study enrolled 66 people with ME following COVID-19 who received the opioid antagonist, which is thought to have immunomodulatory effects. Participants took the drug over 16 weeks, with the dose increased from an initial 1 milligram per day to up to 4.5 milligrams per day. Another 71 participants received a placebo. The trial primarily examined whether LDN could reduce fatigue, which it failed to demonstrate. “Is it still useful?” Nacul asked. “We don’t have the answers yet.” Analyses of subgroups were still pending as was the question of whether LDN can reduce pain. Many people with ME and Long COVID already use the drug off-label and report such an effect. Another trial testing the drug in children is currently being planned in the U.S.’s RECOVER program.
- At Charité, 44 people with ME received five sessions of immunoadsorption, an apheresis procedure designed to filter potentially harmful autoantibodies from the blood. Another 21 participants in the “IA-PACS-CFS trial” underwent a sham version of the treatment. After 60 days, researchers compared the treatment’s effect on fatigue using the Chalder Fatigue Scale. While some improvements were observed, there were “no statistically or clinically significant differences” between the intervention and placebo groups, as Charité neurologist Hannah Pressler summarized the underwhelming findings.
However, some researchers were quick to critique the methodology of the immunoadsorption trial. Charité biochemist Birgit Sawitzki, addressing her colleagues on stage during a Q&A session, pointed out that the study did not select for participants who tested positive for autoantibodies, thus weakening the study. “Some of the patients were benefiting tremendously,” she said, urging the team to conduct a subgroup analysis.
Immunologist Carmen Scheibenbogen, head of the Charité Fatigue Center and chair of the conference, agreed with the criticism. In fact, internist Elisa Stein from Scheibenbogen’s research group had presented related data earlier at the conference: In a case series, 7 of 15 people with ME — all of them positive for autoantibodies — responded to the treatment. That study, however, did not include a control group.
Warning against overinterpreting observational studies
Luis Nacul’s LDN trial underscored the importance of a control group. In it, the placebo effect was substantial: More than 40% of participants who received placebo instead of LDN later reported subjective improvements. In any case, placebo responses of such magnitude pose a major challenge for research.
According to Nacul, the findings should serve as a warning that studies without a control group have limited generalizability. “We have to interpret observational studies with caution,” he said.
We have to interpret observational studies with caution.
luis nacal, researcher
Still, some of the smaller studies presented at the conference appeared to offer more reason for optimism than the RCTs.
Here are some of those observational studies:
- Long COVID researcher David Putrino, professor of rehabilitation at Mount Sinai, presented data suggesting that a wearable neurotech device that uses Microtesla Magnetic Therapy could improve cognitive symptoms and emotional wellbeing in people with Long COVID. A multisite RCT is now underway.
- In a pilot study, Gunnar Gottschalk of Simmaron Research reported symptom improvements in some people with ME treated with the immunosuppressive drug Rapamycin. This drug is intended to stimulate cellular cleanup processes, a process that is disrupted in some people with ME.
- Øystein Fluge, an oncologist at Haukeland University Hospital in Bergen, Norway, is investigating the cancer drug Daratumumab as a means to reduce autoantibodies through plasma cell depletion. In a pilot study, the drug showed responses in six of 10 participants with ME. According to Fluge, five of those patients remained in remission two to three years after treatment. A randomized controlled trial is now expected to examine whether those effects can be confirmed. Charité is pursuing a similar approach using the drug Inebilizumab, which removes autoantibody-producing immune cells called B-cells.
- Another Charité study presented by rheumatology specialist Claudia Kedor assessed hyperbaric oxygen therapy (HBOT), in which patients breathe pure oxygen inside specialized chambers. Participants reported reduced inflammation and improved muscle cell regeneration in the trial after undergoing HBOT, as well as improvements in endothelial and mitochondrial function. Previous RCTs of HBOT have produced conflicting results, with studies using different numbers of treatment sessions. The Charité study compared 20 versus 40 sessions, administered three to five times per week over three months. According to the findings, significant improvements were observed only in the group receiving 40 sessions.
Study clarifies that even specialized rehab can worsen for ME
By contrast, an effort to develop a specialized rehabilitation program for ME ended unsuccessfully. Clinics have traditionally relied on exercise, an approach that can cause harm in ME. A defining feature of the illness is that exceeding physical limits does not produce a training effect, but instead can trigger prolonged worsening of symptoms, known as post-exertional malaise (PEM).
In the CFS Care study led by Carmen Scheibenbogen, even specialized rehabilitation focusing on pacing strategies and taking into account personal limits proved harmful to some participants. Participants were rated on the Bell fatigue scale at the start and end of the study. “There is a large number of patients who came home with a lower Bell score and only a few with a better Bell score,” study author Kirsten Wittke said. All in all, the intervention showed no meaningful benefit and in fact it worsened the condition of 42 of the 97 participants.
Wittke argued that it is problematic that people with ME are still being “forced” into rehab programs in order to qualify for disability benefits. “That must be changed,” she said.
New clues from mechanistic research
Mechanistic research also featured in several notable presentations. Chris Ponting, chair of medical bioinformatics at the University of Edinburgh, is convinced that ME has a genetic component. As part of the large-scale “DecodeME” project, researchers led by Ponting identified genetic differences associated with ME by comparing more than 15,000 DNA samples from people with the illness with 260,000 DNA samples from the general population. In a second phase, the team now plans to fully sequence 6,600 genomes to investigate whether something akin to “ME genes” may exist. The disease is known to cluster in some families, although the reasons remain unclear.
In addition, Michelle James, associate professor of radiology and neurology at Stanford University, presented images from whole-body positron emission tomography (PET) scans. Using PET, an advanced imaging technique, she compared 15 people with ME with 15 healthy controls. Participants received a radioactive tracer that binds to the translocator (TSPO) protein, a marker associated with inflammation. Areas with elevated signals appeared as brightly highlighted regions on the scans.
James had set out to test the hypothesis that neuroinflammation — processes driven by immune cells in the brain — plays a central role in the development of Long COVID and ME. But to her surprise, the PET scans revealed no unusual findings in the brain. Instead, she observed “strong signals” in muscles, including the thighs and shoulders, signals that correlated with the severity of fatigue in the patients. “These results are striking,” James said. “There is something significant going on.”
What exactly is driving these signals remains unclear. The TSPO protein can indicate not only areas with highly active immune cells, but also changes in cellular energy metabolism and in the mitochondria, the cell’s energy-producing structures. The glowing PET scans therefore lend support to a line of research suggesting that ME could result from impaired blood flow and self-reinforcing mitochondrial damage.
Note: Recordings of the presentations are expected to be available on the ME/CFS Research Foundation website in late May.
Martin Rücker is an investigative science reporter based in Berlin, Germany. For several years, the freelancer has been reporting on the gaps in care for people with Long COVID and ME. You can follow Rücker on X, Bluesky, LinkedIn, and Instagram.
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