Ronald W. Davis, PhD's presentation at the IIMEC13

Alvin said:
I'm so sorry to hear this :(

That is interesting, was it a mild return or sudden?
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You see she hemorrhaged, and her hemoglobin would drop very low, 6 or 7, and when she received the blood day after day, she would improve. Then this better state remained, and she would come home with it, but then after two or three weeks, various symptoms started returning day after day, one after the next, until she was back to the ME misery. Usually after 3 or 4 weeks out of hospital the ME was there again.
 
Perrier said:
You see she hemorrhaged, and her hemoglobin would drop very low, 6 or 7, and when she received the blood day after day, she would improve. Then this better state remained, and she would come home with it, but then after two or three weeks, various symptoms started returning day after day, one after the next, until she was back to the ME misery. Usually after 3 or 4 weeks out of hospital the ME was there again.
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Aye carumba :emoji_face_palm:
I'm so sorry to hear about this, its just awful

Is she ok?
 
alex3619 said:
There is some data about blood transfusion transmission, but we still cannot be sure why or what might be transmitted. I asked the question earlier because this large molecule in the blood that triggers our cellular dysfunction would trigger it in others. The issue though is whether or not it would be just temporary, or if it could trigger the full disease.
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A random citation :)

Don't know much about how these things work, but been wondering about this molecule. Could it be some of the reason for why salt water infusions give some patients some symptom relief - by diluting the blood and lessen it's impact....?
 
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Judee said:
I'm just wondering how we know the genes are similar if no one has a bio-marker for ME/CFS? (At least that has been my understanding so far.)

Sorry, it may be a dumb question but I just wondered. :oops:
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This is both correct and false. The problem is the multiple meanings of biomarkers.

We have hundreds of validated biomarkers, and thousands of less validated markers. We have no proven diagnostic biomarkers. We have detailed genetic and epigenetic maps of quite a few patients now. This similarity is based on the expressed genes from what I can gather. So the patients so far examined by Ron Davis have an expressed gene pattern that matches African Sleeping sickness. I presume this is in his severely ill study.

In other words we know a heck of a lot about what is wrong now, we just don't know what is wrong and unique to ME. This requires studying a great many control diseases with candidate diagnostic biomarkers in mind.

The oldest test that finds a biomarker, and not common enough to be diagnostic by itself, is the tilt table test. It was invented in 1940 or prior, but the knowledge of how to use it might not have been public till after 1955 and the Royal Free cluster. It was validated in 1995.

The CPET test was first shown to be useful in us in 2007, but its a 1949 test.

There are of course additional issues with TTT and CPET.

There is a long way to go, requiring time, resources and funding, from a first biomarker to knowing if its useful, and a way to go after that to showing its diagnostic.

When Ron and his team publishes these findings we will have more to scrutinise, and to rationally criticise.
 
alex3619 said:
The oldest test that finds a biomarker, and not common enough to be diagnostic by itself, is the tilt table test.
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Edit: I've just realised I misread your point. I think we are agreeing.

I thought the tilt table test was a test designed to find the cause of fainting or lightheadedness on standing, usually either abnormal drops in blood pressure, or abnormal rises in pulse rate or both. So it's used to diagnose POTS, dysautonomia etc.

I had assumed that not everyone with ME has orthostatic intolerance, and note everyone of those who do have POTS or dysautonomia as the cause. For example the inability to stand upright for long could be caused by muscle weakness in the legs due to ME rapid muscle fatiguability.

I therefore don't think the TTT is a biomarker distinctly for ME, though it is a biomarker for symptoms common in ME, ie POTS and fainting.
 
Trish said:
I've just realised I misread your point. I think we are agreeing.
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Yes, its a biomarker but nowhere near good enough to be diagnostic. That is the case with most of the markers we have now, though a subset are being investigated further to see if they are diagnostic.

Biomarkers are just things that show something is measurably wrong.

We know many things that are wrong. We just don't know any single test, nor currently any combination, that is proven to be reliable and unique to ME.

PS I personally do not have POTS, I have NMH, neurally mediated hypotension, and bad enough I have passed out many many times, and even gone into cardiac arrest once.
 
inox said:
Don't know much about how these things work, but been wondering about this molecule. Could it be some of the reason for why salt water infusions give some patients some symptom relief - by diluting the blood and lessen it's impact....?
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Speculation ahead:

Fluge and Mella thought that it was the concentration of some unknown factor in the blood ("X") that produced symptoms. Below a certain concentration of "X" in the blood, symptoms abated. They reasoned that the patients who responded most quickly to Rituximab were those whose levels of "X" were not much above the response threshold to begin with. Maybe they were right about "X," but wrong about Rituximab's ability to influence it.

As you say, one way to reduce the concentration of "X" in the blood without reducing the amount of "X" in the blood is to increase the blood volume, thereby diluting "X."

So, might an infusion, any infusion, into the bloodstream be enough to temporarily reduce the concentration of "X" and ease symptoms? The answer might vary from patient to patient depending on their initial concentration of "X." If it's already quite high, an infusion might not reduce the concentration enough to make any difference.

Dr. Bell has reported temporary improvement in some patients who simply got saline or a blood transfusion. I'm also reminded of Dr. Stephen Straus' acyclovir trial in which subjects and controls not only received infusions of the drug, but also received substantial infusions of saline to ward off drug induced kidney damage. Both subjects and controls reported similar numbers and degrees of improvement, showing that acyclovir was not the cause of that improvement. Then what was? It was written off as a placebo effect - but both patients and controls would have had their blood volume expanded equally. The "responders" might have simply had lower concentrations of "X" to begin with.

I'm not sure how long the blood volume remains expanded after an infusion. Normally, I'd assume it would be eliminated through the kidneys pretty quickly. The situation might be different if patients actually already had low blood volume, as has sometimes been reported. It might take longer to go from normal back to subnormal than it takes to go from above-normal back to normal.

Which raises another question. Could some patients have a "normal" amount of "X" for a healthy person, but yet are symptomatic because their low blood volume increases their concentration of "X?"
 
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not able to follow this sufficiently for health reasons. also this post might not make sense.

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if rd is saying a first goal is to show that the disease exists, then can he publish the serum swap experiment?

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what /would/ convince people who think a disease that has killed many people and attacks many body symptoms severely does not exist? who is rd's audience? funders? biologists? general public? politicians?

what is the fundamental thing that is blocking the particular audience from believing that the disease exists?

do they think whitney is faking? do they believe in magic? which is it? which is it? seriously. which is it? if the audience is biologists, why are we training them to believe that whitney is not sick?

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is it truly convincing that is necessary, rather than political power? are we really talking logical reasoning here?

i'm not sure empirical approaches are always called for when it comes to persuading. we make so few a priori arguments, when we should be shouting them from the rooftops. but rd probably knows what he is doing. so what am i missing?

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maybe i am the only person who thinks this:

it was never a legitimate debate /in the first place/.

a priori.

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is he saying that [well-poisoning and similar tactics + literal claims of magic + claims of deconditioning that do not match the population] are blocking biologists from believing it exists?

why is it not enough that rd says there's this disease and here are some facts?

one guy dies in africa from an unknown viral-type disease and the world panics. they don't question whether the disease exists for a hundred years. they send a team out.

but no, a serious chronic disease with a huge population ... meh. because bodies get sick for no reason. why are we training biologists to believe this?

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if the audience is biologists, what is their iq level? do they understand the concept of prior probability?
 
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I am not sure if this is relevant to what you mean, but for many years I felt that all we needed was proof that the disease was physical. It gradually dawned on me that this was not the case. The people who "do not believe" in ME have an agenda, either political or personal which depends on it not being a physical disease so there will never be enough evidence in the world to sway them.

If they had been interested in helping patients with ME, or preventing it spreading there have been lots of clues over the years that could have been followed up. At the very least, there have been studies for decades that show deconditioning is not important and we could have been treated as having a physical disease that was not well understood. Supportive and palliative care may not have cured us, but it would have improved our lives immensely. It does not even have to be beyond what is given to people with better understood diseases but the same level of disability as us.

Our only hope is that they will lose their influence and the evidence is so overwhelming or obvious that people outwith the BPS agenda will become involved. I think that is happening.
 
Mithriel said:
I am not sure if this is relevant to what you mean, but for many years I felt that all we needed was proof that the disease was physical. It gradually dawned on me that this was not the case. The people who "do not believe" in ME have an agenda, either political or personal which depends on it not being a physical disease so there will never be enough evidence in the world to sway them.

If they had been interested in helping patients with ME, or preventing it spreading there have been lots of clues over the years that could have been followed up. At the very least, there have been studies for decades that show deconditioning is not important and we could have been treated as having a physical disease that was not well understood. Supportive and palliative care may not have cured us, but it would have improved our lives immensely. It does not even have to be beyond what is given to people with better understood diseases but the same level of disability as us.

Our only hope is that they will lose their influence and the evidence is so overwhelming or obvious that people outwith the BPS agenda will become involved. I think that is happening.
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They think their house of cards is real and believe the rest of us are enemies because we don't agree and have in fact disproven it.
I'll bet money they actually see themselves as heroes or martyrs to their righteous cause.

I used to think we needed a disease mechanism but from watching the OMF conference i changed my mind, that would be a good bludgeon but all we really need is an effective treatment. For example in Parkinsons the best spect scan or MRI imaging does not often show abnormalities but having a drug that improves symptoms was more then enough to make it real. The discovery of Levodopa made it hard to prove that its not a dopamine deficiency condition.

Though a diagnostic test should do the trick but these shysters are like a dog with a bone and they have powerful allies, they will stop at nothing and nobody to keep their lies in power. No matter how much harm or torture they have to inflict
 
If a treatment helps 20 people in a trial, they will argue that the trial was too small to be relevant. If it helps 200 in a trial they will say that it was a placebo effect. If it helps 2000 they will say it is because they were specific patients who are a subgroup but what about all those poor people who have a psychological cause, are they just going to be neglected now?
 
I think the purpose of research is to get the silent majority of doctors, especially the younger generation, to accept that this is real, people who may not have strongly held BPS views or may not even know what ME/CFS is. Obviously the BPS lobby will never accept any amount or quality of evidence because their salary and reputation depends on not accepting it. All we can do is wait for those people to retire and go away. The chances of them recanting are zero.
 
Mithriel said:
If a treatment helps 20 people in a trial, they will argue that the trial was too small to be relevant. If it helps 200 in a trial they will say that it was a placebo effect. If it helps 2000 they will say it is because they were specific patients who are a subgroup but what about all those poor people who have a psychological cause, are they just going to be neglected now?
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Let them try this.
If we had a medication that worked it would be end up in medical journals with many positive trials, in medical textbooks, taught in medical school, recommended by the CDC, governments would be demanding patients use it and if not denying them disability benefits and so on.
They will be laughed at and shunned if they keep claiming a proven drug that becomes the standard of treatment is fake. At that point i would move for their medical licenses to be revoked and criminal charges pursued.
 
Samuel said:
not able to follow this sufficiently for health reasons. also this post might not make sense.

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if rd is saying a first goal is to show that the disease exists, then can he publish the serum swap experiment?
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I'm afraid it's necessary to go one step further than that. Even a proof of a disease existing is still a big step away from having an approved treatment. As long as no approved treatments are available, I think ME/CFS is always going to be a target of biopsychosocial treatment approaches.

As long as there is no approved treatment available, I think it's sadly human nature for some doctors to think "well, there's gotta be something we can do to help you, exercise, psycological treatments, or otherwise". That's a lot more appealing than just saying "your disease is real, but I don't know how to help you".
 
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