The third in a series of studies on mitochondrial function in ME/CFS has been published. Having established in the first two papers that mitochondrial dysfunction is a central pathophysiological lesion in ME/CFS, the aim of the third study was to see how well patients respond to a tailored package of treatments and what impact, if any, those treatment packages have on both the ATP profile test results and also on the patient fatigue scores.
Abstract:
We report on an audit of 138 ME/CFS patients who attended a private practice and took the ATP Profile biomedical test. The results revealed that all of these patients had measureable mitochondrial dysfunction. A basic treatment regime, based on 1) eating the evolutionary correct stone-age diet, 2) ensuring optimum hours of good quality sleep, 3) taking a standard package of nutritional supplements, and 4) getting the right balance between work and rest, was recommended for all patients. Additions to the basic regime were tailored for each patient according to the results of the ATP Profile and additional nutritional tests and clues from the clinical history.
Mitochondrial function is typically impaired in two ways: substrate or co-factor deficiency, and inhibition by chemicals, exogenous or endogenous. For the former, additional nutrients are recommended where there is a deficiency, and for the latter, improvement of anti-oxidant status and selective chelation therapy or far-infrared saunas are appropriate.
We show case histories of nine patients who have taken the ATP Profile on three or four occasions, and a before-and-after treatment summary of the 34 patients who have had at least two ATP Profile tests separated by some months. Finally, we summarize the results for the 30 patients who followed all aspects of the treatment regime and compare them with the 4 patients who were lax on two or more aspects of the treatment regime. All patients who followed the treatment regime improved in mitochondrial function by on average a factor of 4.
From the press release:
The nature of this study was an audit – that is to say clinical decisions were made for the benefit of the patient, not for the doctor or researchers. However, the information that this audit yields is very encouraging. Essentially what is shown is that those patients who are able stick to the demanding treatment packages, involving a ‘’stone age’’ low carbohydrate diet, discipline about sleep and pacing, together with a package of nutritional supplements, do indeed improve biochemically reliably well. That is to say their ATP Profile test results improve consequentially with their treatment package compliance. Moreover, most of these biochemical improvements were accompanied by clinical improvements, as measured by patient fatigue scores.
It was also notable that four patients who did not adhere to the treatment packages either saw no improvement or indeed worsened. In a clinical setting, therefore, it is incumbent upon the physician both to understand the difficulties that patients face with such a wide ranging treatment package and also to support fully the patient with the challenges they face.
It is clear from these studies that mitochondrial function is not the only factor in ME/CFS, but it is an important one and correcting mitochondrial function is an essential part of improving functionality and therefore of recovery. Indeed it is my personal view that to put a patient on a graded exercise programme without first checking these essential biochemical parameters is not good medicine. One risks making the patient much more ill because the underlying cause of their disease has not been addressed.
Conversely if the improvement in mitochondrial function, consequent upon compliance with the treatment package, is not paralleled by clinical improvement then there must be a further reason for fatigue.
Targeting mitochondrial dysfunction in the treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) – a clinical audit. Dr Sarah Myhill, Norman E Booth, John McLaren-Howard
First two papers: Chronic fatigue syndrome and mitochondrial dysfunction Mitochondrial dysfunction and the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
