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Dr. Myhill Explains ME/CFS Mitochondrial Support Protocol & Results

  [ 13 votes ]   [ Discuss This Article ] • November 28, 2012

Source: press release from Dr. Sarah Myhill, Nov 28, 2012
Upper Weston Llangunllo Knighton Powys Wales LD7 1SL
01547 550 331

Subject: Discussion of the release of the paper:
"Targeting mitochondrial dysfunction in the treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) – a clinical audit" Int J Clin Exp Med 2013;6 (1):1-15. Sarah Myhill, Norman E Booth, John McLaren-Howard.


We are pleased to announce our third publication which looks at targeting mitochondrial dysfunction in the treatment of ME/CFS.

Our first two papers established that mitochondrial dysfunction is a central pathophysiological lesion [pathological change] in ME/CFS: and

Those papers demonstrated that:

• The patients with the worst levels of fatigue had the worst levels of mitochondrial (energy) function and vice versa.

• There was a very strong relationship between mitochondrial energy scores and patient fatigue scores,

• And these studies clearly place ME/CFS as a physical disorder.

Mitochondrial (energy) function scores are calculated from the ATP profile test. This is a test that measures:

• How efficiently mitochondria can make ATP,

• How well they move ATP from the mitochondria into the cell where it is needed and recycled back,

• And also how efficiently energy can be released from ATP once in the cell.

These are important measurements because from them one can further deduce whether the mitochondria are "going slow’’ either:

• Because they are lacking the “raw materials’’ to “do the job’’,

• Or because they are “blocked’’ from doing their ‘’job’’. This ‘’blockage’’ could result either from an external source [a toxin] or from an internal source, notably the fermenting gut.

Knowing and understanding what the biochemical lesions [problems] are, and whether they derive from “internal’’ or “external’’ sources, means that treatment packages can be tailored to individual patients.

The aim of this third study was, therefore, to see:

• How well patients respond to this tailored package of treatments

• And what impact, if any, did those treatment packages have on both the ATP profile test results and also on the patient fatigue scores.

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 program [aka graded exercise therapy or GET] 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.

Discussion of reasons why correcting the mitochondrial function is not paralleled by clinical improvement and treatment options in this case.

The symptom of fatigue arises when energy demand exceeds energy delivery. The way I think about CFS/ME is that we all have a certain ‘’bucketful’’ of energy available to us every day. Fatigue is the symptom we all experience at the end of every day which prevents us from FULLY emptying that bucket of energy.

Of course part of my job is to make that bucket of energy as full as possible through addressing mitochondrial function, sleep, thyroid function, diet and so on. This third study demonstrates that patient compliance with the tailored treatment packages will help to achieve this “filling” of the bucket.

However, we - myself and the patient - also have to look at how that energy is spent (i.e., how the bucket is emptied) and essentially it can be spent in four different ways: mentally, physically, emotionally, or immunologically.

Patients quickly work this out for themselves (it’s called “survival’’) and the careful spending of mental and physical energy is what we call pacing. The spending of emotional energy can be helped by a variety of means, and again patients often work this out for themselves via methods such as meditation, deep relaxation methods or perhaps talking therapies.

However, the most difficult problem to address is the immunological hole in our energy bucket.

We all know this exists - take a “normal’’ person and give them a dose of ‘flu and they will develop a very acute fatigue. This is because the immune system is enormously demanding of energy. Please see the following link for further discussion of this issue [see “Dr. Myhill’s Notes on Fatigue, the Immune System’s Energy Demands, and Rituximab”]. 

Therefore there is a two pronged approach - firstly to look at energy delivery systems and secondly to look at how energy is being spent.

A very useful analogy is to think of the body as a car which means that the mitochondria constitute the engine of the car, the diet the fuel, the antioxidants the cooling system, the thyroid gland the accelerator pedal, the adrenal gland the gear box, and so on.

Once the expenditure on physical, mental and emotional energy has been addressed, along with putting in place the treatment packages as tailored via the ATP Profile test results, the most common reason therefore for a failure to improve is an immunological hole in the energy bucket.

A common cause of failure to respond within this bracket of “immunological hole issues’’ is a problem with the upper fermenting gut. For further details of how to treat the fermenting gut, please see: “Fermentation in the Gut & CFS as a Protective Adaptive Response.” 

In addition, I have seen success using pure T3 where there is evidence of hypothyroidism. [T3 is the 'active' form of thyroid hormone.]

The idea here is that there is thyroid hormone resistance - there are clear parallels here with type II diabetes in which we have essentially the same problem. In type II diabetes there are high levels of insulin, but insulin hormone receptor resistance. There is now good evidence to suggest that this resistance results from toxic stress.

Indeed this issue was flagged up in a paper published in the Lancet which looked at the levels of persistent organic pollutants [POPS] in the general population. What was found is that those with the highest levels of POPS, compared with those with the lowest level, were 38 times more likely to be diabetic. For further details of how to treat this issue of thyroid hormone receptor resistance please see “Thyroid – the Correct Prescribing of Thyroid Hormones.” 

The abstract of the new paper is HERE.

The full text is available free at:

The details of the regimes necessary to recover are available for free download as part of Dr. Myhill's book, Diagnosing and Treating Chronic Fatigue Syndrome (CFS) - at
[See especially Part III, pp 31-44]


Note: This information has not been reviewed by the FDA. It is general information based on the research and opinions of Dr. Myhill and colleagues; it is not intended to prevent, diagnose, treat or cure any disease; and is not a substitute for the personal attention of a physician.

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