Video: Professor Warren Tate's Update on His Research into ME/CFS - 11th November 2017

Andy

Andy

Retired committee member
Watching at the moment but I think it should be an interesting watch.
Professor Warren Tate spoke at the ANZMES Annual General Meeting, which was held on 11th of November 2017. Professor Tate updated everyone on his current research that he is undertaking into ME/CFS which show some very promising results linking his research very closely with other research that is being carried out internationally! Professor Tate is recognised internationally for his work into ME/CFS and was a guest speaker at the 12th Invest in ME Research International ME Conference in London earlier this year.
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Code: 
https://youtu.be/ZZGlVJYyAO4
 
Just watched this. I should have taken notes! A really interesting talk in which he focuses on the studies being done in New Zealand while referring as well to how they connect with studies elsewhere, particularly Stanford, Japan and Norway.

Includes 2day CPET, cytokines, epigenetics, metabolomics, proteomics etc.
His data support the work elsewhere that shows reduced energy capacity.
They are getting the Seahorse technology next year and excited about that because it can measure energy metabolism in fresh blood cells.
He thinks the effects on cytokines after exercise might be a useful biomarker.
 
Yes, but after watching it all, we were no further on...same questions. I was hoping for a little more but realise they are doing what they can with the resources they have. I agree about the brain needing to be looked at bigtime.
 
Just watched it. I thought MitoQ sounded interesting until I read a thread on Phoenix Rising where several people had tried it to no longstanding avail, including the original poster who concluded that apparent initial improvement was due to something else (though that's a collection of anecdotes rather than a trial, of course).
 
Sasha said:
Just watched it. I thought MitoQ sounded interesting until I read a thread on Phoenix Rising where several people had tried it to no longstanding avail, including the original poster who concluded that apparent initial improvement was due to something else (though that's a collection of anecdotes rather than a trial, of course).
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After diagnosis, MitoQ was one of the first things I tried. 9 months with no discernible benefit, as I posted on PR.

My wife loves the MitoQ skin cream product, however. :rolleyes:
 
Andy said:
@Woolie any comment on what Professor Tate talks about here in regard to lack of brain studies in ME research? Please copy and paste the URL to start at the relevant point
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Can I just say I LOVE this guy! He's so adorably down to earth and unpolished, eh?

Okay, now to answer your question. First, he makes the comment that there are a lot of cognitive symptoms in ME and they might be a consequence of inflammation within the brain. We need to study that more. Fair enough, agreed. good so far.

But then he kind of does a switcheroo and starts suggesting that the brain is doing ME. "Maybe the key control centre is actually in the brain" he says, because it can explain so many things. He suggests maybe the energy and immune system dysfunctions might be the "outer shell" of the Russian doll, but the brain cold turn out to be "inner doll", driving all that other stuff. He then mentions there's a correlation of microglial activation* with severity of MECFS... Then he discusses "stress centres" in the brain (most notably the paravenrtricular nucleus of the hypothalamus) that may directly modulate the HPA axis, etc.

I am not that impressed with this kind of thinking for a number of reasons.

First, its kind of like the brain is being used as a fallback here (just like the psyche has been in the past). Its like, "after all, its powerful, and we don't quite understand what's going on, so why not put it all on the brain? We know its capable of all sorts of complex things!" No - the brain isn't there to be your explanatory fallback when all else fails - you need a really good hypothesis as to how the brain dysfunctions in a specific way that could lead to the other symptoms. Without that, you're just waving your arms in the air and chanting the stress/HPA mantra.

Second, Tate makes the usual correlation/causation confusion. Sure neuroinflammation is worse in more severe ME cases - you would never expect the opposite, would you? Doesn't mean the neuroinflammation causes the ME at all. Until you know the causal direction of this relationship, its not really that helpful.

Third, I want a reason to believe a brain explanation would be a plausible account. I want specific mechanisms, how they are impaired, and how they lead to the specific symptoms of ME. Sorry, "the brain's just so complex, anything's possible", that's just not good enough for me. And it smells of an easy cop out.

And fourth. Treatments. If the brain is the culprit, we might as well all pack up our bags and go home, cos the only place this will lead is psychoactive drugs. Even the neuro ones (L dopa, ritalin), I'm not up for. You can count me out of that. Modify the peripheral stuff, now you're talking, I'm up for that!

* The cells within the brain that respond to inflammation.
 
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PS. I've already banged on way to long about the brain (and there's lots of other good stuff in the talk aside from the brain stuff). But why do researchers act so astonished when a systemic illness like ME affects cognitive functioning? Given that the brain is probably the most finely tuned organ in the body, and therefore likely to be most vulnerable to systemic impairment, why would you not expect that? It doesn't mean the problem originates in the brain at all.

I suspect the brain inflammation they all talk about (which is this activation of brain microglia) is a consequence of systemic inflammation. That is logical, simple, and fits all the facts.
 
Woolie said:
Second, Tate makes the usual correlation/causation confusion. Sure neuroinflammation is worse in more severe ME cases - you would never expect the opposite, would you? Doesn't mean the neuroinflammation causes the ME at all. Until you know the causal direction of this relationship, its not really that helpful.
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I am pretty sure neuroinflammation is a consequence.

I think the meninges work very hard to keep the agent out and that alarms the microglia.
 
Woolie said:
Can I just say I LOVE this guy! He's so adorably down to earth and unpolished, eh?

Okay, now to answer your question. First, he makes the comment that there are a lot of cognitive symptoms in ME and they might be a consequence of inflammation within the brain. We need to study that more. Fair enough, agreed. good so far.

But then he kind of does a switcheroo and starts suggesting that the brain is doing ME. "Maybe the key control centre is actually in the brain" he says, because it can explain so many things. He suggests maybe the energy and immune system dysfunctions might be the "outer shell" of the Russian doll, but the brain cold turn out to be "inner doll", driving all that other stuff. He then mentions there's a correlation of microglial activation* with severity of MECFS... Then he discusses "stress centres" in the brain (most notably the paravenrtricular nucleus of the hypothalamus) that may directly modulate the HPA axis, etc.

I am not that impressed with this kind of thinking for a number of reasons.

First, its kind of like the brain is being used as a fallback here (just like the psyche has been in the past). Its like, "after all, its powerful, and we don't quite understand what's going on, so why not put it all on the brain? We know its capable to all sorts of complex things!" No - the brain isn't there to be your explanatory fallback when all else fails - you need a really good hypothesis as to how the brain dysfunctions in a specific way that could lead to the other symptoms. Without that, you're just waving your arms in the air and chanting the stress/HPA mantra.

Second, Tate makes the usual correlation/causation confusion. Sure neuroinflammation is worse in more severe ME cases - you would never expect the opposite, would you? Doesn't mean the neuroinflammation causes the ME at all. Until you know the causal direction of this relationship, its not really that helpful.

Third, I want a reason to believe a brain explanation would be a plausible account. I want specific mechanisms, how they are impaired, and how they lead to the specific symptoms of ME. Sorry, "the brain's just so complex, anything's possible", that's just not good enough for me. And it smells of an easy cop out.

And fourth. Treatments. If the brain is the culprit, we might as well all pack up our bags and go home, cos the only place this will lead is psychoactive drugs. Even the neuro ones (L dopa, ritalin), I'm not up for. You can count me out of that. Modify the peripheral stuff, now you're talking, I'm up for that!

* The cells within the brain that respond to inflammation.
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I agree with the comments of not using the brain as a dumping ground for poor theories.

Problem is there are plenty of brain diseases that are not understood, so I'm not sure what you mean by a good explanation ...do these really exist yet?

They haven't explained over half the cases of epilepsy in all these years so what explanations could they come up with?

A big part of this is due to poor research and social stigma. A lot of neurologists from the papers I've read have more leanings towards the "easy option" outlook on life ( similar to psychiatrists) and default to "its complex, don't worry if it's confusing, I'll make some shit up" as an excuse for sloppy practice.

I just wonder what hope we have if it really is a brain problem?

I also think we should not be too scared of exploring the function of the brain just because some bunch of crackpot social scientists that think they are proper doctors have given it a bad name. It is a logical area to explore. I just wish we had better people to do it and there was less social stigma around this area.
 
arewenearlythereyet said:
They haven't explained over half the cases of epilepsy in all these years so what explanations could they come up with?
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I think there's a pretty coherent explanation for epilepsy: an abnormality in neural firing patterns within a region of brain tissue. Covers pretty much every facet of the phenomenology of epilepsy. Its the distal cause of that abnormality (why it occurs in a particular person) that is not well understood.
 
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arewenearlythereyet said:
I also think we should not be too scared of exploring the function of the brain just because some bunch of crackpot social scientists that think they are proper doctors have given it a bad name. It is a logical area to explore. I just wish we had better people to do it and there was less social stigma around this area
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I think the way to go is to characterise the peripheral features first (cytokines, energy production). Then if you want to go into the brain, you are armed with a set of phenomena that you need to explain. Because the symptoms of ME are so variable and most are so peripheral, it would be a tough task coming up with a single brain dysfunction that can generate them all, and that can also capture their variability (and having to propose multiple brain dysfunctions, one for each - that would be a sign you're explanation is not working).
 
Woolie said:
I think the way to go is to characterise the peripheral features first (cytokines, energy production). Then if you want to go into the brain, you are armed with a set of phenomena that you need to explain.
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Yes, pretty much every "central" or brain-based hypothesis completely fails to account for most ME symptoms. They only make it look plausible by focusing on pain, fatigue, etc.
 
This is where I am ...if there is brain dysfunction then it does need to be directly relatable back to the symptoms /symptom profile...which appears to be quite variable. I doubt there are many capable of doing this well. In the case of epilepsy they can identify signatures and sub types, but they still don't know why this happens for most cases (once you remove physical brain injury cases). This makes treatment a mix of extremely blunt medications with a load of side effects and management/living with it and hopes it goes away. Unsatisfactory in other words and this is because they don't really understand it.

I think if we do end up back at the brain then it doesn't bode well for any treatment.
 
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