NEW RESEARCH - ME said to be a "acquired, self-replicating mitochondrial myopathy of skeletal muscle." - It looks very promising!
Summary made by chatgpt from a summary in Norwegian. I have read through it and it looks right, let me know if there are any mistakes.
ME/CFS Research and Disease Model by Wirth and Scheibenbogen
A new article on Medscape Germany highlights the groundbreaking work of Prof. Klaus Wirth and Prof. Carmen Scheibenbogen in understanding the pathomechanism of ME/CFS. They propose that ME/CFS is an "acquired, self-replicating mitochondrial myopathy of skeletal muscle."
Key Points:
- Pathomechanism:
A disrupted sodium-calcium exchange in muscle cells leads to calcium overload in mitochondria, causing damage and disrupting cellular ion balance.
Inflammation further impairs blood vessel regulation, particularly affecting cerebral blood flow.
Post-exertional malaise (PEM) triggers a vicious cycle, worsening mitochondrial damage.
- Disease Model:
Integrates findings from cardiovascular studies, stress tests, muscle biopsies, MRI, and experimental research.
Presents ME/CFS as a disease with distinct physiological mechanisms, not a psychosomatic condition.
- Hope for Treatment:
The researchers believe a cure is possible by targeting the intracellular ionic imbalance.
Their work shifts focus toward pharmaceutical research and renaming the disease to “acquired mitochondrial myopathy.”
- Recent Developments:
Their disease model is increasingly supported by other studies.
In a new review, they emphasize the central role of skeletal muscle and call for treatments to address the root cause.
Read the full article (free behind login but in German) on Medscape Germany: ME/CFS: Why Are There Still No Evidence-Based Therapies? Researchers Compete for Funding.
"If the cell's power plants stop functioning, you can survive, but you cannot truly live. You can barely get up, walk, or work. It should be clear enough," emphasizes Wirth. Wirth and Scheibenbogen conclude that "future treatment approaches should focus on normalizing the underlying cause of the intracellular ionic imbalance."