Mitochondrial malfunction?


The mitochondria are small organelles (or subunits) found in most animal and plant cells. They are often described as the power plants of the cell because their main job is to generate chemical energy, although they also have other roles in signalling and cell growth.

Mitochondrial dysfunction seems to be implicated in a number of diseases, including mental disorders and heart problems, as well as being involved in the ageing process. Since ME/CFS is characterised by a profound, generalised post-exertional loss of muscle power, it seems reasonable to suggest that mitochondrial dysfunction may be involved. Indeed, over the years, there have been diverse smaller investigations exploring this aspect, ranging from the first study by Byrne et al (1987) to the following two recent investigations.

A Spanish study (Dolor, 2008) explored mitochondrial function in 15 patients, from the CIMA clinic in Barcelona, diagnosed with idiopathic chronic fatigue (but not with the full ME/ CFS symptom complex). The researchers took medical and family histories to look for signs of mitochondrial impairment, conducted an exercise stress test, and performed an open muscle biopsy from which a sample was obtained for electron microscopy. The number of mitochondria was increased in 60% of patients, and mitochondrial function was abnormal in a similar number. In one third of patients, these abnormalities correlated with hearing loss, and with headache in their mothers (mitochondrial genes are passed on from mother to child).

While this study was relatively small (and had no matched control group for comparison), it does provide a glimpse of the kind of intriguing findings that could be uncovered from a battery of validated mitochondrial tests from a larger sample of patients and their extended families. In another study from the UK (Myhill et al, 2009), 71 CDC defined CFS patients provided blood samples from which mitochondrial function was assessed using an ATP profile test on white blood cells.

The major finding was a correlation between the degree of mitochondrial dysfunction and the severity of illness as assessed by a simple 10-step ability scale. However, we cannot say whether this correlation is meaningful clinically since simple correlations are notoriously open to confounder bias (in which other unidentified factors might be behind the relationship). Nor do we know if the results are specific to ME/CFS, since comparison mitochondrial function data from other chronic illnesses (such as neuromuscular disorders and frank mitochondrial myopathies) is not presented.

A further complication is that the study used neutrophils, phagocytic cells of short life-span, which do not synthesise much ATP and are rarely used for mitochondrial research (which tends to use cells from high energy tissues such as muscle). Nevertheless, the results are intriguing and provide grounds for investigation of mitochondria in ME/CFS.

It is now almost 25 years since the first study of the modern ME/CFS era reported some aspect of mitochondrial physiology or function. Since then, a patchy and sometimes contradictory picture has emerged from the relatively small number of scientific investigations conducted. Yet, there remains a sense that not all is well with mitochondria in ME/CFS patients, and that the time is ripe for well-planned hypothesis-driven mitochondrial studies on well-characterised patients, using properly validated techniques and outcome measures.

References: a) Implicación de la mitochondria en la fatiga crónica. Poca-Dias V. Dolor 2008; 23. b) Chronic fatigue syndrome and mitochondrial dysfunction. Myhill S et al. Int J Clin Exp Med 2009; 2(1): 1-16.

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