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Breaking news: ME/CFS & severity definitively linked to mitochondrial dysfunction, cellular damage

  [ 80 votes ]   [ 5 Comments ] • July 1, 2012

CFS Mitochondrial DysfunctionArticle:
Mitochondrial dysfunction and the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
– Source: International Journal of Clinical and Experimental Medicine, June 30, 2012

By Norman E Booth, Sarah Myhill, John McLaren-Howard

[Note: The full text of this article is available free at To read the authors' press release summarizing their crucial findings, click here. The concluding paragraph of their clearly written paper reads:

“Implications for the treatment of ME/CFS. Here we have emphasized the use of biomedical tests to aid in the diagnosis and to vastly improve our knowledge of the pathophysiology involved in this illness. In addition, these biomedical tests can act as a valuable guide for medical and therapeutic interventions. These will be discussed in a paper which is in preparation.” They also note that "no mildly ill patients were tested" and the findings may not be specific just to ME/CFS because certain other illnesses/syndromes are associated with mitochondrial dysfunction.]

The objectives of this study are to:

• Test the hypothesis that the fatigue and accompanying symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome are in part due to defects in energy provision at the cellular level,

• And to understand the pathophysiology of the defects so that effective medical intervention can be implemented.

We performed an audit of 138 patients (ages 18-65) diagnosed with ME/CFS and attending a private practice.

The patients and 53 normal, healthy controls had the ATP Profile test carried out on neutrophils from a 3-ml venous blood sample. [Ed note: Neutrophils are the most common kind of white blood cell.]

This test yields 6 numerical factors that describe the availability of ATP and the efficiency of oxidative phosphorylation in mitochondria. [Oxidative phosphorylation is the metabolic pathway that uses energy released by oxidation of nutrients to produce energy-supplying ATP.]

Other biomedical measurements, including the concentration of cell-free DNA in plasma, were made.

The results of the audit are compared with the controls and a previous cohort of 61 patients.

We find that:

• All patients tested have measureable mitochondrial dysfunction which correlates with the severity of the illness.

• The patients divide into two main groups differentiated by how cellular metabolism attempts to compensate for the dysfunction.

• Comparisons with exercise studies suggest that the dysfunction in neutrophils also occurs in other cells. This is confirmed by the cell-free DNA measurements which indicate levels of tissue damage up to 3.5 times the normal reference range.

• The major immediate causes of the dysfunction are lack of essential substrates and partial blocking of the translocator protein sites in mitochondria.

• The ATP Profile is a valuable diagnostic tool for the clinical management of ME/CFS.

Source: International Journal of Clinical and Experimental Medicine, June 30, 2012;5(3):208-220. /ISSN:1940-5901/IJCEM1204005, by Booth NE, Myhill S, McLaren-Howard J. Department of Physics and Mansfield College, University of Oxford, Oxford UK; Sarah Myhill Ltd, Llangunllo, Powys UK; Acumen, Tiverton, Devon UK. Address all correspondence to: Dr. Norman E Booth, PhD FInstP, Emeritus Professorial Fellow in Physics, Mansfield College, University of Oxford, UK. [E-mail:]

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Article Comments Post a Comment

Mitrochondrial Dysfunction
Posted by: KathyCFS1989
Jul 4, 2012
I remember in 1989, a year before I was diagnosed with CFIDS, I had High Anti-Mitochondrial anitibodies.
Not sure at that time what that meant. So long ago ,guess it doesn't matter any more.
By the time they figure out what causes CFS I will be dead of old age :-(
Reply Reply

Posted by: IanH
Jul 13, 2012
Do you have gluten sensitivity or coeliacs disease? Both of these are associated with a rise in mito-antibodies. There are are some genetic polymorphisms eg in the PDHA1 gene which is responsible for pyruvate dehydrogenase and which result in mito-antibodies.


What this means, in English
Posted by: Sandy10m
Jul 5, 2012
I am a physicist, not a medical researcher. I had to teach myself the basics of biochemistry to treat my ME/CFS since the doctors were clueless. I read the full paper trying to glean the essential things, and here is what I came up with, in English we can understand.
- The fuel for our cells is ATP, or adenosine TRI-phosphate. The ATP is made of ADP, which is DI-phosphate. The mitochondria take ADP and make ATP for our cells to use. The mechanism that does this is the Krebs Cycle, which starts with pyruvic acid.
- About 70-90% of the ME/CFS group were very low in ATP before the study.
- Intracellar Magnesium is also low in 90% of the ME/CFS patients. Magnesium is one of the natural resources needed for the Krebs Cycle.
- Blood samples from the patients were taken for this study. The samples were checked for mitochondrial function. Then the samples were mixed with a substance (azide) that blocks ATP production by the mitochondria. Then the azide was washed off, and the cells were allowed to recover. The recovery time was recorded and compared to the severity of ME/CFS symptoms.
- They found that ME/CFS blood does not recover as well as the normal blood. But, the ME/CFS blood is not as affected by the blocking of ATP as the normal blood. The conclusion is that ME/CFS patients already are using an alternative ATP cycle to compensate for the dysfunctional Krebs Cycle in their bodies, so they don't make enough ATP overall.
- The alternative ATP cycles are much less efficient than the primary one, and they create more waste products that make their bodies more acidic and create more damage in their tissues. So, we get tired because we don't make enough ATP and we make too many waste products. And the negative effects can be delayed, so that we feel worse the next day.
- Waste products include lactate (lactic acid), which is transported to the liver to be recycled into glucose. But, if the liver isn't functioning properly (such as the mitochondria in the liver are dysfunctional), then the lactate isn't processed fast enough, and it accumulates.
- Two ways that ATP is blocked are: (a) the sites on the mitochondria are blocked by something so the ADP can't get in, and (b) there aren't enough natural resources for the Krebs Cycle.
- The study found that ME/CFS patients also have a problem with a Krebs Cycle key player called translocator protein TL, which has not been studied before but is important for getting the ADP in and ATP out of the mitochondria.
- Natural resources that are needed for the full ATP cycle: pyruvic acid, ADP, CoQ10, reduced niacinamide (NADH), Magnesium (Mg), inorganic phosphate.
- ATP is also essential as a neurotransmitter for our brains and neurons, which might explain why we have such terrible brain fog. We don't make enough for all the requirements.

**Possible solutions:
- supplement with Magnesium in a bioavailable form, such as Magnesium Citrate or Magnesium Threonate.
- supplement with CoQ10, niacinamide (Vit B3), pyruvate
- do not supplement with inorganic phosphate, since high levels are shown to cause serious health problems

**My question: is it possible that ME/CFS is caused by an environmental source of azide at a very low dose, or perhaps it's created by a virus or bacteria inside our bodies?

**Excellent website to learn more about mitochondria, ATP, ADP and all their friends.
Reply Reply

ME and mitochondria
Posted by: IanH
Jul 13, 2012
**Possible solutions:
- supplement with Magnesium in a bioavailable form, such as Magnesium Citrate or Magnesium Threonate.
- supplement with CoQ10, niacinamide (Vit B3), pyruvate
- do not supplement with inorganic phosphate, since high levels are shown to cause serious health problems

**My question: is it possible that ME/CFS is caused by an environmental source of azide at a very low dose, or perhaps it's created by a virus or bacteria inside our bodies?

Environmental sources of azides are rare but there are many similar compounds in the environment such as the quaternary ammonium salts such as the agricultural chemical "Paraquat" and those found in disinfectants and antimicrobials. These substances are known endocrine disruptors, particularly of mitochondrial function/health. In addition they react with other endogenous results of oxidative phosphorylation (energy production) to form worse ROS's and also to interfere with our mitochondrial enzymes and the membranes of mitochondrion. When you consider that the concentrations of our enzymes and substrates are in the picograms it doesn't take much environmental toxin to start disrupting normal mitochondrial function.

Also consider that people with ME were not normal (in the strictest sense) in the first place. That is their genes probably contain "polymorphisms" or variations of "normal" genes. That is, one or more of their genes is a "risky" one so that when an environmental threat such as paraquat or rotenone comes along then that person will have a mitochondrial stressor impeding its function and ROS will build up faster than it can be removed. In addition glutathione becomes depleted, which is the main ROS remover. If this is in the neurons of the brain (which don't have as much glutathione then the neuronal function is impaired = brain fog).

If this happens in a baby then you have the pre-conditions for autism spectrum disorder. (there are many who think that the main increase in ASD is actually ME in the child. I have a grandson who is in this category, his mother has ME).

When these pre-conditions happen and a viral infection occurs the mitochondria are further affected by the increase of IFN (Interferon) which is important for ridding us of the virus but which also causes further mitochondrial stress. At this point the ME symptoms become very severe and many people crash.

There is more to it such as dietary health, but that is it in a nutshell


Conflicts of Interest not declared
Posted by: beanier
Jul 8, 2012
One of the authors either works for or owns the company doing these tests, and therefore stands to make money off these tests should ME/CFS patients decide to purchase them, yet this was not declared in a Conflicts of Interest statement in the paper. If an author has a potential Conflict of Interest then this is not inherently a problem, but CoI's should at least be declared in the paper somewhere and the fact that this major CoI was not mentioned in the paper gives me pause when considering the claims made therein.
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