I found this absolutely fascinating. Thanks to Dr Light for the presentation and to
@Kati for putting the slides up.
A few points
1. If in fact mitochondrial genetic mutations
are the ultimate upstream source of our problems, then it is definitely good news that the Crispr gene editing technology is believed to work on mitochondrial DNA.
Source:
https://www.hindawi.com/journals/bmri/2015/305716/
2. However this is a pilot study, not the sort of study on which you base treatment decisions. It's designed to guide future research, (And happily it seems Light has funding, and is proceeding with that future research.
)
3. I was initially underwhelmed by the statement that there was (almost) no overlap in the genetic mutations in patients vs controls. As I understand it, mutations are random (especially when they are environmental, i.e. not inherited) and while mitochondrial DNA is limited compared to nucleic DNA there's still a lot of it and I'm not sure you'd expect much overlap. Once you dive into the detail it's a bit more suggestive, however. I'm interested in this but not utterly convinced.
3.1 That said the graph showing decreased mitochondrial proteins in FM patients is impressive.
4. Like
@Rossy191276 I don't understand how this fits with the recent findings that the problem is in the serum and our cells are okay.
5. His is a complicated theory of the disease, requiring a particular combination of genetic problems followed by certain pathogens and an auto-immune response, and subsequent problems too. Fans of Occam's razor may be unimpressed. (I think sometimes you have to let Occam's beard grow long.)
6. I like his idea for a clinical trial of propranolol to test its effect on beta-receptor autoimmunity. I recently went off the drug for about ten days and then back on it and my sense is it really helps in my case, even though the heart rate effect is not massive.