• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Coverage from IACFS/ME Florida conference, 27-30 Oct 2016

Kati

Patient in training
Messages
5,497
All this talk about lactate, does anyone else remember the study that showed we have higher levels of lactate in our brain? I remember a webinar Suzanne Vernon did explaining it. Seemed like a good discovery at the time (She was with CFIDS Association at the time).
Wasn't it Jarred Yonger that suggested that?
 
Last edited:

dreampop

Senior Member
Messages
296
I seem to be understanding that the anti-mitochondrial antibodies are problem in autoimmune disease, suggesting we have an autoimmune problem, rather than the mitochondrial antibodies being a problem themselves. Of course having an autoimmune disease seems to make sense, but also kinda are contradictory to people like J Goldstein's practice/results. Of course, some autoimmunity in the brain or the nerve cords would make a ton of sense and fit in with that too. Still seems like a couple major findings off from getting a grasp on this thing or things.

There was a discussion about Collins not attending. I know he has a busy schedule, and only attends high profile conferences. Yet, clearly if he intends to make this a priority, he needs to break a pattern that inhibits misunderstood disease. Yes, it would be unusual him to go to this conference, but imagine the signal that would send out to the research community and to the media. He/the NIH often complain about things they have the power to quite easily fix. They complain about no new young researchers - but then spurn the opportunity to draw media attention to this conference and signal to young researchers this is an area of emerging research opportunities. To me Collins has shown far less than his position requires. Sure he's starting to ramp up the bare minimum but that shouldn't impress 1 million of the sickest Americans.
 

Hip

Senior Member
Messages
17,824
I seem to be understanding that the anti-mitochondrial antibodies are problem in autoimmune disease, suggesting we have an autoimmune problem, rather than the mitochondrial antibodies being a problem themselves.

Fluge said studies suggest that the immune system is producing anti-mitochondrial antibodies that are whacking the mitochondria. So the autoantibodies are likely a problem in themselves.
 

ash0787

Senior Member
Messages
308
You could probably liken the antibodies to bullets or perhaps paintball rounds, but the overall problem could be described as friendly fire, with other parts of the immune system taking the incorrect decision to shoot.

There seems to be a lack of clear evidence that this is actually the case though, but its still early days on that front I suppose.

I had a thought the other day, it might be completely irrelevant but didn't the mitochondria originally come from bacteria ? could that by a clue as to why the immune system might be disposed to attack them were that the case ?
 
Last edited:

Tuha

Senior Member
Messages
638
I read all Cort´s tweets and PR thread about this ME conference in Florida - it looks very interesting from my unscientific point of view. But what can we make all of it - i know that probably it´s too premature to ask but anyway what do we need now?

For example we have those metabolic findings but we still need to understand it better and to confirm it? If it will be confirmed, can there be already some treatement options or we still need to find the cause? There were some other topic like PEM, inflamation, exercise testings,... - did these things confirmed the previous findings and did it move us further or it´s still the same and we need confirmation? (btw. I have impression that we always need confirmation of confirmations of previous confirmations...). Did we for example moved somewhere from the last IiME conference in 2016?
Was anything said about Davis big data study - i think they said to release the data in few weeks - I am wondering if there are already some informations behind the scene what we can expect of it.

Sorry, too many questions - it´s always difficult to read about exciting findings and movements if you dont understand the science but on the end you would just like a treatement but it´s still not there. I know, I know we have to be patient. Just I hope that those metabolic findings will offer us in a short time a treatement option which could at least improve our health but maybe it´s not that easy.
 

Seven7

Seven
Messages
3,444
Location
USA
I seem to be understanding that the anti-mitochondrial antibodies are problem in autoimmune disease, suggesting we have an autoimmune problem, rather than the mitochondrial antibodies being a problem themselves. Of course having an autoimmune disease seems to make sense, but also kinda are contradictory to people like J Goldstein's practice/results. Of course, some autoimmunity in the brain or the nerve cords would make a ton of sense and fit in with that too. Still seems like a couple major findings off from getting a grasp on this thing or things.

There was a discussion about Collins not attending. I know he has a busy schedule, and only attends high profile conferences. Yet, clearly if he intends to make this a priority, he needs to break a pattern that inhibits misunderstood disease. Yes, it would be unusual him to go to this conference, but imagine the signal that would send out to the research community and to the media. He/the NIH often complain about things they have the power to quite easily fix. They complain about no new young researchers - but then spurn the opportunity to draw media attention to this conference and signal to young researchers this is an area of emerging research opportunities. To me Collins has shown far less than his position requires. Sure he's starting to ramp up the bare minimum but that shouldn't impress 1 million of the sickest Americans.
Next year play the game, invent some award that will make him go. Best year support from NIH whatever and we both get we get that important apperience.
 

waiting

Senior Member
Messages
463
Messages
2,158
My conclusion is that the real value of conferences like this is for researchers to learn about each others research projects and findings and discuss them amongst themselves so they can make steps forward with their research and hopefully form collaborations.

Many of the studies done so far are preliminary and based on small samples, so they provide promising pointers towards things to home in on in future research, rather than any definite answers.

For us patients it's a case of getting a bit excited and pleased that research is happening, but trying to be patient. I guess we'll need to wait a year or 2 for papers to be published about the findings discussed here. And then further years before diagnostic tests and treatments are available.

I don't see how we can draw any conclusions yet about possible treatments. Most of us don't have the depth of knowledge required to see whether a study of, say, antibodies or metabolites has any immediate treatment implications.

It's so hard when we've been sick for so long to be patient, but I, for one, am going to go on as before, keeping on hoping, but not making any assumptions. I don't think I have the strength to cope with excitement and raised hopes being dashed over and over as I read each scientific paper that adds a bit to knowledge, but is in reality only a tiny step forward in a very long journey.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
I think it depends on how high the titers are of these anticardiolipin antibodies.

This study, which found 95% of ME/CFS patients have anticardiolipin antibodies, says:

CL = cardiolipin.

ACA = anticardiolipin antibodies.

Yes, to be fair although I would be sceptical about claims of 95% having ACA there are studies going back years that suggest that PWME do have more ACA. One was done by Patrick Venables and I think it likely valid because he was never expecting to get that result.
 

snowathlete

Senior Member
Messages
5,374
Location
UK
I'm sorry for the misinterpretation of my comment about "angst."

I was contrasting the involvement and collaboration and discussion from the past, where instead of working with us, they were the target of our angst. I was pointing out that even though Collins isn't there, we have seen a change. I was not saying your comment reflected angst. I was saying that used to be the only way we dealt eith them because they weren't "our team."

Thanks @usedtobeperkytina I worry that some might wrongly have interpreted my question about Collins as angst because although things have moved on, there is still more progress needed, and some members of the community do still, rightly or wrongly, come across as a bit angsty about Collins and the NIH and some of those comments can come across as a bit unreasonable as a result.

For my part, I am happy there has been some progress and the NIH are involved more than they were before, but I do think they have some responsibility for the problems we face presently and I'd like to see Collins turn up to help increase the profile of the disease and do whatever he can to stimulate more interest so that the disease is seen as worth getting involved in.

This is probably the most common severely debilitating disease out there with such an unmet need so it really ought to be a priority above diseases with established support. I certainly don't expect Collins to turn up to every conference or to devote all his time to it, but it sure would be appropriate if he turned up for one day of one of these conferences at some point soon. Maybe he can give that apology someone at the conference suggested to VW that the NIH should give, praise those who have dedicated their careers to this even thought they were unsupported, give some legitimizing statements about the disease and talk about the research opportunities he sees. And if he wants to announce an RFA at the same time then we might start to see some tangible progress.

Also if he wants to get out his guitar he could adapt his CF song for CFS (I think we'd forgive him using the CFS label to fit with the lyrics!) and show some of that passion he has for making people better through research:
 

Denise

Senior Member
Messages
1,095
I agree that high profile recognition of, and support for ME (by NIH, others) would be helpful for us.

It might be worth keeping in mind that the position of head of NIH is a political appointment.
Collins has been in the position since 2009 and is currently 66 years old.
No matter what the results of the upcoming US election, it is unlikely that Collins will continue as head of NIH beyond FY2017.

While it is useful to have allies at agencies and in Congress, I believe that rather than support by an individual (for instance Collins) what we need is written policy that mandates support and recognition.
(We also need appropriate education of healthcare professionals and much more.)
 

CFS_for_19_years

Hoarder of biscuits
Messages
2,396
Location
USA
Thanks @usedtobeperkytina I certainly don't expect Collins to turn up to every conference or to devote all his time to it, but it sure would be appropriate if he turned up for one day of one of these conferences at some point soon. Maybe he can give that apology someone at the conference suggested to VW that the NIH should give, praise those who have dedicated their careers to this even thought they were unsupported, give some legitimizing statements about the disease and talk about the research opportunities he sees. And if he wants to announce an RFA at the same time then we might start to see some tangible progress.

Also if he wants to get out his guitar he could adapt his CF song for CFS (I think we'd forgive him using the CFS label to fit with the lyrics!) and show some of that passion he has for making people better through research:

Not sure about his singing, but he definitely has some guitar skills!
 

mfairma

Senior Member
Messages
205
I've increasingly checked out over the last few years from this stuff, in part because I think too much of this community has normalized stagnation and accept glacial change too readily. I agree with Denise and would also add that Collins could have signaled real commitment through hard and soft measures.

We've yet to see real money and, more importantly to my eyes, he hasn't engaged in a PR offensive that would lock his and other agencies into a real forward path. His showing up at this conference could have been part of such an offensive, but the real problem is the broader issue of his apparent unwillingness to stake out a position publicly and fight for it. Given that he will be gone soon anyways, it's hard to see this as anything other than us being a low priority. I find the whole thing -- their low-level behind the scenes moves and us debating the merits and demerits of those tiny moves -- depressing and farcical.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
If 95% of ME/CFS patients demonstrated ACA and HC's did not, wouldn't it be diagnostic
It would also require that no other condition had high ACA for it to be potentially diagnostic. That would be the specificity requirement, whereas the high ACA in ME would be the sensitivity requirement. However an ideal marker would be one that is linked to the physiology somehow, and its not clear that ACA has any causal role. Its also possible its more important in a patient subset but not other patient subsets.
 

Hip

Senior Member
Messages
17,824
It would also require that no other condition had high ACA for it to be potentially diagnostic.

Anti-cardiolipin autoantibodies still could be a useful tool in helping to confirm an ME/CFS diagnosis.

But if the ME/CFS mitochondrial dysfunction research of Myhill, Booth and McLaren-Howard is anything to go by, it appears there's more than one type of mitochondrial dysfunction in ME/CFS patients, and even a single patient might have several mitochondrial dysfunctions going on, all contributing to their overall mitochondrial defects.

Some of the mitochondrial dysfunctions might correspond to an autoantibody cause, or the same dysfunction might alternatively be due to some toxins or compounds that affect mitochondria. I believe one of John McLaren-Howard's interests in the laboratory is looking at what compounds appear to be blocking the mitochondrial translocator proteins of ME/CFS patients. In the Myhill et al 2012 paper they say:
One of us (JMH) is making further studies of TL [mitochondrial translocator protein] function and has found chemical blocking [in ME/CFS patients].

Possible sources of blocking agents are byproducts of viral or bacterial pathogens, cellular debris due to oxidative damage, and some environmental chemicals.

Results from molecular level fluorescence microscopy, and the identification of the blocking agents by Micro Raman Spectroscopy and Fourier Transform Infrared Spectroscopy, will be the subject of a further paper.
 

usedtobeperkytina

Senior Member
Messages
1,479
Location
Clay, Alabama
Wasn't it Jarred Yonger that suggested that?
No, before him. It was when Suzanne Vernon was with CFIDS Association. He found leptin levels (in body) go up and down with symptoms severity. And I can see he might have mentioned higher lactate in the brain based on the study I' referring to. But I'm thinking about a study before he got involved.