We hear from Cara Tomas about her recent study on cellular bioenergetic deficiencies in ME/CFS | 13 November 2017

 


This relates to new research from Newcastle University, published in the open-access journal, Plos One.

Cara Tomas is a PhD student working with Professor Julia Newton at the Institute of Cellular Medicine, and her research was featured in the New Scientist last week, in an article which received much acclaim from the ME/CFS patient community:

“For many years, arguments have raged over whether CFS — also known as myalgic encephalomyelitis, or ME — has a physiological or psychological basis.

 

“But the latest research comparing samples of peripheral blood mononuclear cells (PBMCs) from 52 people with the condition and 35 without has reinforced the case for a biological explanation.”

Cara has personal and ongoing experience of M.E. and was bedbound by the disease. We asked if she would provide a summary explanation of her research so that more people might be able to appreciate what it involved, and she kindly obliged.

 


Cellular bioenergetics is impaired in chronic fatigue syndrome: A summary

“Mitochondria are the part within the cell tasked with energy production, because of this they are often called the ‘powerhouse’ of the cell. They produce energy in the form of a molecule called ATP, often referred to as the energy currency of the cell. This is what powers all of the processes carried out by the cell.

“In our recent publication ‘Cellular bioenergetics is impaired in chronic fatigue syndrome’ we used peripheral blood mononuclear cells (PBMCs) taken from the blood of ME/CFS patients and healthy controls to investigate energy production.

“PBMCs are a group of cells that help make up the immune system which protects the body against disease and foreign invaders. This research utilised a technique known as ‘extracellular flux analysis’ to assess mitochondrial function. The technique involves using probes to detect oxygen levels around the cells.

“The output of the experiments showed the oxygen consumption rate (OCR) of cells which represents the amount of oxygen that is being taken up by cells and used in the production of ATP. We used inhibitors of different components of the process to allow us to calculate different phases of energy production.

“Results from our experiments showed energy production to be consistently lower in cells taken from ME/CFS patients compared to controls.

 

“Both the basal rate and the maximal rate of energy production of the control cohort was shown to be double that of the ME/CFS cohort.

“These results show that both under normal conditions (basal respiration) and when maximally stimulated, the ME/CFS cells are less able to produce energy to meet the energetic requirements of the cell and fulfil cellular energy demands.

“We also showed production of ATP via the glycolysis pathway, which is a minor ATP production pathway, was not different in the PBMCs of ME/CFS patients when compared to healthy controls.

“It is important to state that, while we showed clear differences in the ability of ME/CFS PBMCs to produce energy, these results do not establish whether differences in PBMC energy pathways are a cause or a consequence of ME/CFS.

 

“However, this data clearly implies that these cells may play a role in the disease pathway, therefore, the use of PBMCs may present a new and valuable model for the subsequent design of novel therapeutic approaches to the treatment of ME/CFS.

“Replication of these results from other research groups, as well as increasing the sample sizes of the study presented in the manuscript, would aid in strengthening the validity of the observations.

“Additionally, these abnormalities have only been identified in one cell type, therefore, replication in other cell types, such as skeletal muscle cells, will be sought to see if these abnormalities are confined only to the PBMCs or are also present in other cells.

“This research is a great step in the right direction in terms of identifying physiological abnormalities in ME/CFS and directing the future of research in ME/CFS, however, we still need more research into the mechanisms that underpin ME/CFS.”

Cara Tomas.

 


Funding for this study came from the Medical Research Council, the ME Association, ME Research UK, Action for M.E., and the Newcastle Molecular Pathology Node (jointly sponsored by the Medical Research Council and the Engineering and Physical Sciences Research Council).