Dr Ron Davis - Updates on ME/CFS research - September 2019 onwards

I find it interesting that parkinsonian-like syndrome is referred to as manganism. I would humbly advise not to take Mn, or at least not a high dosage. Mn toxicity seems to accelerate neurotoxicity from what I've read.

I had parkinsonian-like-syndrome back in 2000 and took mg/taurine injections for over 2 years.

 

Any use of metals as supplements will first be titrated in research and then, if shown useful, in individual patients. The safe range for most metals is very small. Its very easy to overdose. However if supplementation includes ongoing testing it should be possible to figure out the optimum dosage for an individual patient, and then keep monitoring it. Just taking these kinds of supplements from off the shelves at a static dose runs a much higher risk than with most other supplements.

 

I would like to know what is causing the underlying deficiencies. It can't all be caused from malabsorption?

My test panels indicated countless deficiencies.

 

Without investigating much I can think of four broad issues, and it could even be a mixture of all four.

Malabsorption could be one. This is about how much is absorbed.

Malutilization could be another. We could need more and so run out. Or it could be used up inappropriately.

Malexcretion means we might be losing more of that substance.

The other one is trickier to look for: sequestration. We might have increased amounts somewhere, leading to deficiencies elsewhere. Blood levels might be low, for example, if certain tissues are absorbing or using too much.

These are not simple issues. Measuring simple deficiency is easy. Figuring out all the mechanisms is mondo difficult.

Clinical trials offer us an empirical way to find out a practical solution. If we correct the problem with a supplement, and don't have major side effects, and benefits are long term, then we have a solution even if we do not fully understand what is happening.

This investigation problem used to be the case with the common cold, though I am way out of date on the research so cannot speak to current understanding especially for corona viruses. We knew enough about causation and common pathology that we almost ceased looking. We lack knowledge of the fine details of the disease. Yet much of this is due to historical technological limitations, and I think that with current and future generation technology we will slowly fill in much of the missing picture.

I think this is currently a major issue with type 2 diabetes, with potential for major paradigm shift that seems to be happening right now. The notion that we need to optimize to blood glucose is under challenge as its better than nothing but quite suboptimal. People are being cured of type 2 diabetes, but a focus on blood glucose actually impedes a cure as many strategies to limit blood glucose spikes also drive diabetes progression in the long term.

 

I think it might help but definitely wont solve everything. I have tried almost every supplement I thought promising, and countless thousands of patients have done the same. Some improve, some don't, and some attribute recovery to a supplement. Nothing is reliable in this kind of evidence. Heck, every now and again I found a supplement that some assured me would help but it made me worse.

What supplements are more likely to do, if we can advance the science enough, is tweak around the edges. It might set us up for a better response to treatments that we don't even know about yet. It might help prevent relapse. It might improve quality of life. All of this has yet to be demonstrated however. I really hope we can figure out what objective outcome measures to use, as I am very suspicious of quality of life questionnaires. Returning blood concentrations of something to the normal range might not be what we want at all. So much still needs to be figured out.

If they can figure out why something is deficient or in excess it might point to mechanisms, extra things that can be tested. This is where such data on nutrients outside the normal range might be best used, and will feed into the metabolic and systems models that are being developed.

 

Hi, around 14.00 - 14.15 minutes Ron mentions something which sounds like "bimer campations" --- OK I often misspell things (!) but anyone got a clue what he said/what he's referring to?

Thanks

 

You mean where he says “..five or ten patients..”?

 

Thanks laughing - just noticed the text [on the video] and yes it's 5 or ten patients!

 

Thank you so much for summarising the video. What incredibly interesting and exciting research. Very curious about what the enzyme results will be.

 

Another update.

https://www.youtube.com/watch?v=8drZ5eF7FI4

 

Has anyone confirmed the IDO2 genetic mutations in any other cohort or are they still basing this on the 20 severely ill patients alone?

It's confusing to me why we've heard so much about yeast experiments and little about confirming the genetic basis for the hypothesis, which seems like it would be cheaper and faster — though I assume DecodeME will answer this as well.

 

I have said before that this might only be a marker for severity risk. It might not apply to the general ME population. Any finding in the severe group has to be confirmed in a larger and more typical patient group. Its just easier to find things in severe patients.

 

New update

https://www.youtube.com/watch?v=MwypF_KoRDM

 

This jumped out at me as well. Perhaps these results suggest EBV re-activation is common in the early months or years of Long Covid and ME, but not later. It would be interesting to know how long the patients had been sick for, especially the ME patients. This would suggest that maybe EBV re-activation is a consequence of some kind of immune dysregulation and not a cause of ME or LC (or it's a hit and run cause). That also tracks with the fact that some healthy people have EBV re-activations and it doesn't seem to be a problem.

 

I'm thankful for the people doing the write-ups here as it's hard for me to follow the video's. With regards to EBV, the doctor at the hospital that diagnosed me with M.E. said I had traces of inactive EBV or something along those lines. It was apparently still in the blood, but not active.

 

I'm completely unqualified - but from what I understand - this is quite common for ME/CFS patients - IGMs found in the blood indicate a current infection, and IGGs found in the blood indicate a previous infection..

 

https://twitter.com/user/status/1565572813695492096


https://twitter.com/user/status/1565807748532486144


Unfortunately, it's not going to be recorded for us to be able to watch.

Edited to add:
Later in the video Janet said that an individual researcher may request that their presentation be recorded and that the recording will be given to that researcher to do what they want with.

Edited to add another tweet:

https://twitter.com/user/status/1565700028982853632