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

He says the IDO2 mutation appears necessary to develop ME.

 

I can only speak for myself, but if the video was designed to boost my morale, it has had the opposite effect.

On hearing that a mutation had been identified that ALL ME/CFS patients must carry--my hopes soared. I even shared the news with family--something I never do, out of caution.

To then hear how tenuous this evidence is (at best) is positively deflationary.

I do not wish to the fed false hopes. Bums me out.

Bill

 

Well, I would like to see the nanoneedle test Bravo probiotic. In our case, it helps with neurological pain, mcs, sleep. It is not a definite answer but it provides help. It is the only thing we have stuck with when everything else stopped, including vitamins except vitamin c and magnesium. Don[t take too much when you start. I notice that although it has been around for a few years that people dont talk about it. But my cfs family member does not miss a single day taking it because she goes downhill the next day even.
Since she is particularly sensitive and she is able to take it I think it will agree with most people.

 

Probiotics are intended to work in a specific place, namely the gut and the large intestine. I'd say if you tested how a white blood cell responded to a probiotic in the nanoneedle, it would be a bit similar as injecting probiotics directly into the bloodstream and seeing what the reaction is, which would likely be a septic shock. I reckon the nanoneedle will mainly be a useful screening for drugs that are bioavailable and systemic. For probiotics you need to do tests with the patients unless you can somehow simulate an artificial intestine (which I read is actually work in progress).

 

@Kitty - oh my, ill for nearly 45 years. I'm closing in on 35 years. I'm just a newbie in comparison. How awful for you to deal with this scourge so long!

I hope we get some more good news soon!

 

@Mij

Thanks for your comment about chelation therapy. It's certainly not the answer to ME, but it may help some a bit. I emphasize may help. No guarantees at all. Not much is guaranteed with this whole ME thing is there, except to feel ghastly for an indeterminate time.

And, pwME have to be very careful because of drug and chemical sensitivities - chelation drugs are not always easy to deal with.

Medical supervision a must with these treatments.

 

Me too! Even if it turns out that we could never have unpicked ME without current or future technology (which is entirely possible), it would have been nice to be supported instead of gaslighted by the medical profession. However long we've been ill, all our lives would have been so much easier!

 

@Kitty

Yes, because the medical profession disdains and denigrates pwME, our friends, family and the press do too. Awful. This shatters families, and individual's lives.

 

Finding out the mutation is present in 90% controls is a little bit perturbing, agreed. However, if we phrase it differently and say people without the IDO2 mutation can not get ME/CFS, they’re somehow inherently protected against the possibility of ever contracting it, then you can see why it becomes an intriguing data point. To announce this with any degree of confidence beyond random chance, I’d want a very big data set. I hope they have that.

 

If this mutation is present in most people, then given the rest of the ingredients in the ME mix, (ie. triggers, and perhaps other gene mutations), then almost anyone can develop ME. Which is something I recall Carol Head emphasizing in one of her presentations.

Odd, but not really surprising, because that's their MO, how complacent governments have been about this threat to public health.

"ME could happen to YOU!"

 

That's a reasonable point.

As is wanting a very big data set to back up the claim.

Bill

 

Dr. Phair has said that when he first started looking into ME/CFS he realized that if a genetic mutation were involved it would have to be relatively common. Why? Because only a common genetic factor could explain the outbreaks where the attack rates could be as high as 25%.

He was also looking for a mutation that could create a "bi-stable" state - i.e. one which alters a stable normal state into an equally stable abnormal state.

Dr. Phair's talk from September 2018

https://www.youtube.com/watch?v=uej1LXzRbnY

ETA: I think Dr. Davis' emphasis on the fact that they've found an IDO2 mutation in all of the ME patients they've tested so far is precisely because the hypothesis is falsifiable. If they find a patient that they feel certain has ME and that patient DOES NOT have an IDO2 mutation, that would really bring the hypothesis into question. Even if just 10% of the population is free of IDO2 mutation, this would still allow the hypothesis to be falsified if you tested enough patients. The more patients that test positive for an IDO2 mutation without a mutation free patient showing up, the greater the odds that the hypothesis (that "broken" IDO2 is necessary) is true.

 

The problem is there are hundreds if not thousands of possibilities that fit that criteria.

 

No suggestion it could be a biomarker, it obviously couldn't. It's about predisposition.

Many cars have internal combustion engines (piston engines so far as cars are concerned), so they have a predisposition to the many failure modes that can afflict piston engines - ignition problems, fuel problems, worn pistons, piston rings, cylinders, etc, etc. But if your car is 100% electric, with no piston engine, then it will not be predisposed to these faults that piston engines get but electric motors do not.

If your car does have a piston engine, then of course it might get all manner of the issues they can suffer from, but by no means for certain. Pick any one 'ailment', and some will go down with it and others will not.

But of course with human biology the scenario is vastly more complex than my trivial example above. There are presumably millions of potential predisposing factors for people to get ME, and when the truth is finally known there may be several of them in combination needed before a person can then actually get ME. So if Dr. Ron Davis and his team manage to show that the IDO2 mutation is one of them, then to me that would be a massive advance.

I find the video very heartening, so long as it it taken in the context of what I believe it is - a simple layman's presentation of where their science currently is, and what the possibilities might be.

 

But presumably that's what science is often about? Once you identify a potential illness mechanism, but with a great many possible causes, there may be no choice but to do the grunt work and keep trying them until you find the right one ... assuming your theory was right in the beginning. It's presumably also possible - maybe even likely? - that as you do this you may turn up a few more clues along the way.

 

Yep

 

@RDP we would be very grateful if you could please tell us how many patients and how many controls have been tested for IDO2 mutations.
And, since Ron has now said that all patients tested have the mutation - does this mean that the one patient previously said to not have the mutation, has been excluded from the dataset for some reason? Thanks.

 

I've done a chi-squared calculation based on the following assumption:

- Helmfrid on Twitter said he thinks they tested at least 70 patients. I am assuming 70 for this calculation. But if it was more than 70, then that would make our p-value even lower.

So, we get a p-value of 0.0168. This is the probability of finding just by coincidence that only 1 out of 70 tested has a mutation (compared to 90% of controls having mutation).

This is quite a good p-value, many would consider it "significant".

If the 1 patient who didn't have a mutation has been excluded from the dataset for some reason (E.g. if their diagnosis of Me/cfs had been replaced with something else?), then we re-calculate the test, the probability of 0 out of 69 having a mutation is 0.0056, which is an even better p-value.

(In essence, the lower the p-value, the more likely that a result is to be significant.)

Sorry no energy to explain more about p-values for those who don't know.

HOWEVER - my brain is quite foggy, and it's quite possible that this might not have been the right situation to use a chi-squared calculation. Or I may have made some other mistake. Please correct me if so.

But if I've done this right, and if the assumptions that I based the calculation on are accurate, then this would be pretty encouraging regarding the IDO2 hypothesis.

(My old statistics teacher would probably have a fit at some of the clumsy language that ive used here to explain statistics. Oh well. Brain fog.)

 

Do we know if the patients they've tested have come from a variety of severity levels? I'm just thinking that severe patients might be more likely to be a homogeneous group, even though I'm sure that Stanford screens all patients to the extent possible.

 

@RDP