In talking to the MitoSwab test people they've told me that the typical pattern for ME/CFS patients they've tested, is impaired complex I and hyperactive complex IV.
Working with repeated tests and interventions over time, I've been able to improve my complexes one through three but my complex IV is still around 400% of normal activity. I read the article, and then there's some suggestion, but I'm afraid it's a bit over my head to be able to pinpoint what could be causing the hyperactive complex IV. The explanation I got from MitoSwab was that complex for was compensating for the underactive complex I, but as that is no longer the case for me, I'm still looking for an explanation.
The other things I'm looking for answers to are why my pyruvate and lactate keep dropping, and why my mitochondria prefer to burn glucose rather than fat even though my carnitine is sufficient and I'm on a lower carb/ higher fat diet.
Unfortunately, none of the doctors I run into even a conferences could answer these questions, so I think this article is a very good investigation that should be looked into further. However, there are also the topics of mitochondrial fission and fusion, recycling of mitochondria and apoptosis, that all are factors to consider.
Very interesting. I'm reading a book (The Vital Question, by Nick Lane) which is about a theory for how life started and developed the way it has. Mitochondria are a critical part of that. What I've read so far has raised a few questions for me regarding ME. I was planning to start a new thread about it, but I'm still working my way through the book.
One thing to point out: it's not just defective mito DNA genes that cause problems with metabolism; mito function also depends on proteins made by cellular DNA. The mitochondria are extremely stripped-down engines, with lots of support functions handed over to the cell nucleus. If there's a mismatch between those DNA functions, the mitochondria don't work properly. So, if you are looking at DNA scans for problems, you have to look at both types of DNA and be able to know which specific gene variations are optimal matches, which I doubt is known at present. It's quite possible to have genes that are known to be 'good', but they just don't work well together.