I've been reading Dr Sarah Myhill's theory that ME/CFS is all about mitochondrial dysfunction. I'm wondering whether this is the view of major figures in the research field - I'm thinking Klimas, Montoya, Bell, people of that kind of stature. I don't recall seeing much about mitochondria in conference summaries.
I'd like to discuss her stuff with my GP but don't want to if he will consider it left-field - I need to keep him on my side and don't want to freak him out with weird stuff.
Dr Myhill is offering a mito function profile based on a blood test and says that results correlate with patients' energy levels - I wonder if that is recognised by mainstream doctors, particularly in the UK. It seems to be a fairly new thing, done by a Dr John McLaren-Howard.
Hi, Sasha.
I think I would have to say that most of the "major figures" in ME/CFS research and treatment have yet to take on board the existence and importance of mitochondrial dysfunction in this disorder. I would say that the appreciation of this is coming along much faster in the autism community (as you may know, I believe that autism and ME/CFS are essentially the same disorder from the biochemical perspective, though the symptoms and epidemiology differ strikingly, I believe due to the different ages at onset, in relation to brain development and puberty, but this also is not a view shared by the "mainstream" medical community).
At the most recent IACFS/ME confererence in early 2009, mito dysfunction came up a few times in the course of the talks there, but the only one who really focussed on it was Norman Booth, who presented the paper by himself, Myhill and McLaren-Howard. At least the conference committee allowed this to be presented orally, rather than being relegated to the poster session.
Dr. Myhill and I wrote a draft review paper on this topic and submitted it to two journals about 3 years ago. It was rejected by both. One of them was the journal Mitochondrion. Of course, we can have different views about why it was rejected, but my impression was that the reviewers either didn't accept the existence of ME/CFS as a physiological disorder, or didn't accept the connection between ME/CFS and mito dysfunction. We may try again in the future.
I would say that Dr. Bell does take it seriously, and in fact he recently wrote a piece in his "Lyndonville News" newsletter about the Myhill et al. work and the more recent Vermeulen et al. paper, which argued against it. Dr. Cheney also takes the mitochondria seriously, and understands that the diastolic dysfunction he observes in the heart is associated with mito dysfunction. Prof. Martin Pall recognizes mito dysfunction as part of his NO-ONOO model for ME/CFS and other disorders.
Dr. Klimas and Dr. Montoya have certainly heard about it, but I don't believe it's a major part of their thinking. Most of the ME/CFS researchers are specialists in one aspect or another, but I don't think any of them focus on the mitochondria or the energy metabolism (also called the intermediary metabolism) in general. Dr. Klimas focuses on the immune system. Dr. Montoya is an infectious diseases specialist, and is currently focussing on viruses.
In my view, mito dysfunction in ME/CFS is real and significant, and accounts for problems in the skeletal muscles, the heart, the immune system, the nervous system, and part of the endocrine system. I believe it can be traced back to a vicious circle mechanism that includes glutathione depletion, a functional B12 deficiency that results from glutathione depletion, a partial block in the enzyme methionine synthase that results from the B12 functional deficiency, draining of folate from the cells as a result of this partial block, and disruption of the sulfur metabolism, also as a result of this partial block, which causes the glutathione depletion to continue, completing the vicious circle and therefore making ME/CFS a chronic condition.
Putting known biochemistry together with the detailed results of Dr. McLaren-Howard's testing, I believe that it is straightforward to explain the mito dysfunction as a direct result of this vicious circle mechanism. I believe the validity of this argument is supported by reports of increased energy level in people who are able to lift their partial methylation cycle block, as found in the clinical study conducted by Neil Nathan, M.D. and myself.
I don't think I've ever seen a result of mito testing in a person who has ME/CFS that did not show mito dysfunction. Likewise, the methylation pathways panel seems always to show glutathione depletion or partial methylation cycle block, and most commonly, both, in ME/CFS patients. I have a pretty good collection of both by now, which people have sent me, in addition to the methylation panels we ran in the clinical study.
I wish I could tell you that the entire ME/CFS research and clinical community has been totally turned on to this, but unfortunately this has yet to occur, and it will likely take considerably longer for it to trickle down to the mainstream GPs. If a pharmaceutical company figures out some way to make a buck or two from it, things could go much faster, but my view is that working with the biochemistry using orthomolecular treatments, rather than blocking part of it, as most patented drugs do, is more likely to help the function of the mitochondria.
Best regards,
Rich
