Not just tired: further research suggests cell energy production impaired in M.E.

There’s a big difference between us feeling like we have zero energy and that actually being the problem within our cells but the link between our symptoms and the underlying processes in M.E. is becoming clearer.

New research published in JCI Insight by Fluge and Mella’s Norwegian research team, also trialling rituximab to treat M.E. as an autoimmune condition, suggests the way cells generate energy is also at fault in people with the illness. This study builds upon research earlier this year by Naviaux’s team, finding potentially twenty abnormal metabolic processes in people with M.E., summarised for Action for M.E.

In this latest research, the biochemistry of 200 M.E./CFS patients and 102 healthy individuals was studied, revealing markedly lower levels of amino acids that are used in our cells in the production of energy, called mitochondrial respiration, particularly in the female patients. In the male patients, a marker of energy production from protein was higher than in controls, possibly because protein is being broken down as an alternate energy source.

These results may indicate that one of the processes affected by M.E. is the tricarboxylic acid (TCA) cycle, sometimes known as the citric acid cycle, or the Krebs cycle . This is a series of chemical reactions which occur in the mitochondria, the powerhouses of our cells, to convert the sugars from broken down carbohydrates, fats and proteins we eat into chemical energy in the form of adenosine triphosphate (ATP).

The pattern of reduced amino acids found in the patients suggests impairment of pyruvate dehydrogenase (PDH), an enzyme that converts pyruvate to acetyl-CoA at the start of the TCA cycle. The authors state that the amino acid changes found could not be otherwise explained by symptom severity, disease duration, age, BMI, or physical activity level of the patients.

In addition to the amino acid changes, when cells called myoblasts, which give rise to muscle cells, were grown in serum from the blood of patients with severe M.E., both mitochondrial respiration and lactate production were increased, possibly because the cells try to compensate for the impaired part of the energy metabolism process.

This research is promising, as it could reveal potential targets for new or existing drugs. Recent drug research has demonstrated a connection between autoimmunity, energy metabolism problems, and inflammation, which could be the direction M.E. research needs to take. It also bodes well for the much larger scale MEGA research project examining the biochemistry of 12,000 people with M.E.

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