The research group around Karl Johan Tronstad at the Department of Biomedicine has been granted 9.5 million to investigate the causes of Chronic Fatigue Syndrome, or Myalgic Encephalomyelitis CFS/ME.
The project “Defective Energy Metabolism in ME / CFS” is one of four projects towards user-identified research on CFS/ME, that have been granted funding from the Norwegian Research Council. The announcement has been a new approach by the Research Council, which uses input from patients, relatives, and therapists to identify research needs.
Researchers in Bergen will respond to these needs by investigating whether metabolic disorders are involved in the disease mechanism for this serious and relatively common condition. The project is building upon close cooperation with Professor Olav Mella and Øystein Fluge at the Department of Oncology and Medical Physics at Haukeland University Hospital, and has received support from The Kavli foundation for several years.
The research group of Mella and Fluge has coordinated the collection of samples from over 200 ME / CFS patients and 100 healthy control subjects in a research biobank. This biobank will now be used to study molecular mechanisms in the laboratory. Among other things, changes in the patient’s energy metabolism will be mapped by measuring biochemical changes in the patient’s blood (called metabolomics). At the same time, it will be investigated whether hereditary changes in genes can explain increased disease risk. This is done by means of exome sequencing, comparing genes of sick and healthy family members. This will identify key factors, which will be the starting point for further mechanistic laboratory studies.
The researchers have previously been successful in finding that the function of a metabolic enzyme, pyruvate dehydrogenase, is inhibited in ME patients. This inhibition probably means that the patient’s cells have less energy available, and it leads to exaustion and fatigue. The study was published in the Journal of Clinical Investigation Insight last December. Based on this finding, the hypothesis is that ME patients have limitations in the ability to generate energy (ATP), as well as increased effort-induced production of lactate. Additionally, there are several indications that ME / CFS may be due to a malfunctioning immune response.
The main objective of this project is to acquire new knowledge of ME / CFS mechanisms to promote the development of new treatment methods and biomarkers. The project will receive support for 3.5 years and will start in July 2017.