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Readers' comments on UK research trio’s ME/CFS mitochondrial dysfunction paper

  [ 6 votes ]   [ Discuss This Article ] • July 31, 2012

ProHealth readers have posted comments that may add to our understanding of the findings published June 30 by Drs. Norman E Booth, Sarah Myhill and John McLaren-Howard (“Mitochondrial dysfunction and the pathophysiology of ME/CFS”). Importantly, the researchers state their study “clearly established ME/CFS as a physical condition with physical causes,” and “gave backing to certain treatment interventions.”


Poster “Sandy10m” writes:

What This Means in English -

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:  - S


Poster "IanH" writes to comment on Sandy10m’s Question

ME and Mitochondria (In a Nutshell) -

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. - I

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