New developments in understanding chronic illness, Nov. 8-10 Washington DC Davis/Hanson

[Trish]

These are quite the statements by Nath, if true, especially if a pathogen is the antigen in question, I wonder how the patient commentators on this forum will react after bashing such ideas (and researchers pursuing them) for many years. Interesting to note that this comment by Nath is not already discussed more.

I don't bash any researcher or idea. I do however wait for evidence to be strong before accepting any hypothesis to be likely to be true, and criticise politely those scientists who claim to know the answer when they don't have evidence to back it up.

All I know right now is I'm sick and nobody knows why. I don't care which hypothesis turns out to be backed by evidence, or which scientists establishes that evidence.

Commentators on this forum are free to share any ideas they have so long as they do so within the rules. Our purpose is to allow free discussion of scientific ideas, including challenging those ideas that aren't backed by evidence, whoever those ideas come from. It's not about bashing anything or anyone, it's about seeking scientific understanding of what's going on in ME/CFS.

 

[Andy]

Not so much about point scoring but gatekeeping and bias in the name of 'the real science'.

Gatekeeping and bias how? All members are free to start a thread about anything that fits within the forum's remit and the rules that all members agree to abide by when they join. Equally all members are free to express their opinions, again so long as what they post abides by the forum's rules. One reason for this forum is to question the evidence for every theory, and long may that continue - that is how we will encourage the science to advance.

Edit: crossposted with Trish.

 

[Sean]

I have no idea what is causing ME, and neither does anybody else, at this stage.

But I would not be surprised if it was enteroviruses. That would tie a lot together in one bow.

 

[duncan]

Nath:
(Conclusion) we think all our findings suggest persistent antigen leads to immune dysfunction and microbial dysbiosi in GI tract. Neuroimmune axis gets dysregulation, contributing to metabolic abnormalities. Leads to abnormalties in function (in brain) Autonomic dysfunction
Autonomic dysfunction leads to (shortness of breath).
(Our) hypothesis of persistent antigen as (cause of ME) is based on immune markers. That made us wonder if persistent antigen--whether host or foreign--that's what made us make that hypothesis.
The journal has accepted our data, but is waiting on a number of things that must be uploaded to journal. My guess is it will be soon. Nature Communications is the name of the journal.

Hansen:
Which viruses have been implicated in pre-2020 ME. Herpes viruses, Ross River, influenza, enteroviruses...if we are to judge these viruses, EVs are convicted by preponderance of evidence. EBV may be accomplices, but influenza and Ross River virus don't pay a large role.

If this proves to be their finding, it may be important to remember this is the US. There likely will be major institutional resistance. Strike that. There will be depending on which pathogens they invite to the party.

I don't want to get ahead of the results, though. But, yeah, politics and science. Strike that. Politics vs science.

 

[Hoopoe]

(Our) hypothesis of persistent antigen as (cause of ME) is based on immune markers. That made us wonder if persistent antigen--whether host or foreign--that's what made us make that hypothesis.

Nath talks about a host or foreign persistent antigen. If I understand correctly that means he is not sure whether it's autoimmunity or a persistent infection.

PS: also my negative attitude towards the persistent infection hypothesis had more to do with the advocacy surrounding it. That advocacy behaved in a way that contributed to the status of ME/CFS as fringe topic, engaged in gatekeeping ("true ME"), fueled conspiracy theories about authorities not wanting to admit an ongoing epidemic, and other things that are counterproductive. Even if the hypothesis turns out to be right, I will have no regrets, and maybe even feel more frustration towards the way this topic has been handled by the patient community.

 

[duncan]

Even if the hypothesis turns out to be right, I will have no regrets, and maybe even feel more frustration towards the way this topic has been handled by the patient community.

Bad lot, patients.

 

[Trish]

I will have no regrets, and maybe even feel more frustration towards the way this topic has been handled by the patient community.

I'm OK with that so long as it's clear the criticism is of some patients, and not about what they believe, which they are entitled to do about their own health, but about how they treat other patients who have a different perspective, experience and understanding of the lack of evidence for any causal factor for the disease defined by current diagnostic criteria.

Bad lot, patients.

Sadly that attitude among the BPS cabal is too true to be funny.

 

[duncan]

Sadly that attitude among the BPS cabal is too true to be funny.

Were it only limited to that crew.

 

[Ash]

I know in every cell of my body that pathogens are driving the pathological processes of my illness. I don’t know if this happens in addition to other processes that would have caused permanent damage regardless, in combination or separately causing accumulated impairments. So I agree with these researchers line of inquiry at that base stage. But not because I have to or I am in some way obliged to. I could be wrong and that’s fine I have no obligation to be right. Nor does any other patient. It is the research scientists doing work who are obligated to prove their hypothesis, scientifically. That’s what they signed up for.

As patients we get to decide whether to be grateful for the work and to faithful to one avenue of research, if we want to. Or not. At our whim. That’s a matter of individual choice. We can argue our side, others can argue we’re wrong. But to argue that there is an obligation to put faith in one person one organisation or one hypothesis, I think wouldn’t the best approach.

Everyone has bias whatever we’re into or averse to. The people on here tend not to rate the active infection hypothesis for various reasons including certain scientific observations and a lack of scientific findings upon which this could rest, in theory. This is a forum about formal scientific research. That’s just how it is. This infection idea doesn’t seem convincing to everyone.

There are plenty of sources of information out there who will not criticise the infection hypothesis or its proponents. However I’d prefer to see harsh opinion based criticism and judgements made after comparisons with known biology and scientific methodology.

Infection based treatments for ME have been pushed upon patients by fewer sources than BPS but sometimes with the same zeal and intensity. It isn’t harmless. Its expensive. It’s not surprising patients, clinicians and other researchers are particularly suspicious of this avenue starting as it does from a conclusion and working backwards. It’s not scientifically promising looking at it from this angle. I still see potential but others see it as skipping ahead, failure to build foundations of knowledge on the ground. It’s a history of promising more than is delivered in this area. It’s okay to want evidence not another promise evidence is coming. It’s okay to resent the empty promises. Or to think resources could be spent better elsewhere from a scientific standpoint point.

 

[LarsSG]

FWIW, Nath's hypothesis seems to be:

"(Our) hypothesis of persistent antigen as (cause of ME) is based on immune markers. That made us wonder if persistent antigen--whether host or foreign--that's what made us make that hypothesis."
"We hypothesize--one possibility that there is persistent antigen...no virus. No evidence that they're transmitting anything to anybody."

So it sounds like they found some difference in immune markers between patients and controls, but they don't think it is due to an active virus (presumably in an absence of evidence kind of way, i.e. they looked and didn't find anything). He also seemed quite negative about herpesviruses:

"EBV cannot be causing every disease known to man. HHV6 + EBV are reactivated very easily. All this other stuff is just reactivation."

and similarly about LC:

"Studies show pwLC have reactivation of EBV. If you find it, does that mean it's the cause? No. Association is not causation--people make that mistake all the time. Everyone's infected with EBV. In totally unrelated diseases, you'll find reactivated EBV."

Also:

"Gut microbiome. Just because it's abnormal, doesn't mean it's the cause of the disease. Unless you alter the microbiome in clinical setting, you'll never know if that's contributing to the disease. There's no unique microbiome signature in this disease"

 

[duncan]

So it sounds like they found some difference in immune markers between patients and controls, but they don't think it is due to an active virus (presumably in an absence of evidence kind of way, i.e. they looked and didn't find anything).

You may be right. I was mildly taken aback at the thought the NIH at any meaningful level would suggest persistence. Could you help my brain reconcile your take with this other tweet that seems to suggest something different?

Nath:
(Conclusion) we think all our findings suggest persistent antigen leads to immune dysfunction and microbial dysbiosi in GI tract. Neuroimmune axis gets dysregulation, contributing to metabolic abnormalities. Leads to abnormalties in function (in brain) Autonomic dysfunction
Autonomic dysfunction leads to (shortness of breath).

I appreciate the handicap that trying to interpret tweets (vs the study or article) presents.

 

[LarsSG]

You may be right. I was mildly taken aback at the thought the NIH at any meaningful level would suggest persistence. Could you help my brain reconcile your take with this other tweet that seems to suggest something different?

Just going off the content of these tweets, I think the idea is that there is antigen (could be persistent antigen from past infection or could be some kind of autoimmune situation), but not active infection. But it doesn't sound like they've found any particular antigen, so it's all just a hypothesis. Maybe whatever immune markers they are measuring are downstream of something else, who knows.

 

[Hoopoe]

It sounds as if the findings are at best an incremental step. We've been at the "is it an abnormal immune response or an infection?" stage for decades with no clarity.

But maybe Nath is not revealing everything.

 

[duncan]

I think the idea is that there is antigen (could be persistent antigen from past infection or could be some kind of autoimmune situation), but not active infection. But it doesn't sound like they've found any particular antigen, so it's all just a hypothesis. Maybe whatever immune markers they are measuring are downstream of something else, who knows.

Curious they used "persistent" as a qualifier in this context, perhaps even more so with Dr. Kim Lewis there. I'd gladly pay way too much to be seated at the same table as Nath, Hanson and Lewis. Persistence - or at least persisters -would likely have come up at some point.

It's been my experience that half the value of these events resides in sidebar conversations.

Edited to add "gladly." I realized the sentence could be interpreted another way without it.

 

[anniekim]

In Hilary’s Johnson’s tweets of Nath’s presentation she says ‘“Kaplan thanks him for "long overdue" work. Kaplan: only 40 % noted worsening of energy after cardiovascular exercise, 20% reported mental fatigue, etc. Talk more about PEM."

Anyone find it strange that he said only 40 % noted worsening of energy after cardiovascular exercise?

 

[Sean]

"Studies show pwLC have reactivation of EBV. If you find it, does that mean it's the cause? No. Association is not causation--people make that mistake all the time. Everyone's infected with EBV. In totally unrelated diseases, you'll find reactivated EBV."

Also:

"Gut microbiome. Just because it's abnormal, doesn't mean it's the cause of the disease. Unless you alter the microbiome in clinical setting, you'll never know if that's contributing to the disease. There's no unique microbiome signature in this disease"

I think it is pretty clear that just about every finding and symptom so far in The Great ME Saga are the downstream consequences of the primary pathology, often a long way downstream.

Which is why there are still no consistent findings, it cannot be well defined, and there are no clear answers nor effective treatments.

 

[Milo]

But I would not be surprised if it was enteroviruses. That would tie a lot together in one bow

I have a positive lab test for EBV and an exposure. That’s what triggered it. 15 years ago this month.

However at this point, I’d suggest they did something, like if their life depends on it. Many of us don’t have another 20 years.

Instead of LDN, how about trying an EBV vaccine? how about a large N# studies of stomach biopsies patients vs control?

Why are we so unworthy.

 

[Ash]

I have a positive lab test for EBV and an exposure. That’s what triggered it. 15 years ago this month.

However at this point, I’d suggest they did something, like if their life depends on it. Many of us don’t have another 20 years.

Instead of LDN, how about trying an EBV vaccine? how about a large N# studies of stomach biopsies patients vs control?

Why are we so unworthy.

Yes…

 

[Ash]

I think it is pretty clear that just about every finding and symptom so far in The Great ME Saga are the downstream consequences of the primary pathology, often a long way downstream.

Which is why there are still no consistent findings, it cannot be well defined, and there are no clear answers nor effective treatments.