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

hixxy

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Just copy pasted these tweets of Cort's from The Microbe Discovery Project on Facebook:

Levine - Allergic subgroup - not IgE mediated more associated w/ non-allerginic rhinitus, Mast Cell activation, autonomic

Levine - Big study! @200 patients in 5 sites- 80% - "any allergy, Sinusitis and hives best distinguished ME/CFS and HC's

Levine - ME/CFS patients with sinusitis or hives experience greater pain than patients without sinusitis/hives

Levine - Plus these patients had much, much higher prevalence of migraine and fibromyalgia..suggests histamine/mast cell

Levine - mast cell may contribute plus GI symptoms also occur - and could be due to histamine, next step - immune testing

Levine - both mast cells and neurons secrete nerve growth factor and substance P plus there's tryptase
 

Kati

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I had my AT measured without bb and it was 115bpm.
On bb I get PEM even if I don't reach to 115bpm. The doctor told me once you are on Bb you have to adjust for AT but the relation is not linear ( if without bb rhr was 101 but AT is 115, when on bb RHR is 64 your AT will not be 78( the 14bpm gap I had without the bb).

So I was " ok doctor if is not linear then what is the formula?" " he said don't worry about that" of course the doctor was a POTs doctor which they think as you excercise the AT will increase. I which is not the case w CFS found the hard way after trying to increase for 5 years.

So now I am stuck w the question. It was easy to avoid PEM before bb. Now not so easy for me.
Personally, i don't wear a heart rate monitor. I go with what my body is telling me. I pace lots. (Everything I do vertically is spaced with horizontal time) at the first sign of exertion (heavy feeling in my head, pain in my muscle) i go lay down. You can understand your limits by listening to the cues your body is giving you.

The tricky thing is that from one day to the next, the amount of energy available varies and what seemed acceptable one day may not be the next.

You may want to lower your threshold to 80 and see how it goes.
 
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Lucinda Bateman - Jason was someone she looked up to and was mentored by when she came into ME/CFS.

They were astounded by the CDC Reeves study. The CFS-like people were astounding and indicating a public health issue that needed to be addressed.

The IOM report is to improve CLINICAL DIAGNOSIS of ME/CFS in primary care.

- Core criteria based on Jason's research - mostly
- Emphasis on objectively identifiable issues
- Worked to a core criteria

Core Criteria:
- Put impaired function in there to distinguish from fatigue in other diseases
- PEM
- Unrefreshing sleep
- Either Cognitive impairment or orthostatic intolerance. She felt the cognitive was being overlooked and that it was easy to measure and can be done at bedside.

Exclusionary Criteria
- Not there because it can occur in other illnesses
- allows diagnosis to be made in those with comorbid illneses

Canadian Criteria
- there is a lot of overlap with the CCC

SEID or ME/CFS?
Chose SEID so that core criteria is included in the name

Confusion
- in academic SEID is being used
- at federal ME/CFS is being used
- There is significant confusion occurring now.

I'm glad she was there to explain and make the case for the IOM report.

Five things I like about the IOM committee recommendations:
1. Does not require excluding other illnesses to be diagnosed in a clinical setting. If I have anxiety disorders, I can also have this disease. If I have a heart murmur, I could also have this disease. If I have fibromyalgia, I could also have this disease. If I have depression, I could also have this disease. It's a positive diagnosis based on having the combination of symptoms that is unique to this disease, particularly PEM. It's not helpful to patients and messes up statistics if you say you can't be diagnosed with this disease if you also have depression. Now for research, absolutely get a pure cohort that excludes those with many other conditions that could skew the results.

2. It requires PEM, which is somewhat unique to this disease and is the most life altering part of the disease. The problem is that the spectrum of severity and exact symptoms that come during PEM vary with each individual. And, for the newly sick, it can be hard to notice the association of symptoms with the activity because PEM can be delayed by as much as 3 days and the activity may not be strenuous, so it just seems episodes come without any provocation, more at random. It may take time or particular circumstances (as in a mild case of someone generally sedentary who only occasionally exerts) to catch the association. But, if it is a requirement, then some questions can be used by the clinician to identify PEM if it is suspected as a cause for the patient's symptom complaints. These could include questions about timing of symptoms relative to days of the week or time of day, questions about if there are times of no symptoms or times they are more severe. For many, we have some "good days." This is part of the PEM that when you aren't in PEM, you may feel almost healthy.

3. It requires diminished function instead of 6 months of fatigue. Every person I know with this disease is forced to do less, give up something. But in many other diseases, fatigue is a symptom, and may be even more constant, but their function is not reduced, they can push through (not all other fatiguing diseases, obviously, but true of many others). This makes it clear to the doctor that this is life altering, not just chronic fatigue.

4. While not perfect, the name communicates more accurately about the disease than any of the other names and even can prevent misguided and harmful treatment recommendations, such as "join a gym and start exercising more." The person has a systemic intolerance to exertion so exercise is not the treatment. "ME," while medical sounding, supposes a biology not yet proven to the standards that doctors would consider conclusive. And many don't have myalgias, as I did not have for three years and largely don't have now. And we don't want doctors to be ordering spinal taps looking for inflammation in the brain before giving a diagnosis. While 68% is a majority, it was not a scientific survey in that patients were not randomly chosen and that means that even of those highly engaged patients, 30% don't think "ME" is the best name. I won't go into the problems with "CFS," we all know them. Also, the name communicates that we will likely have good days where we can temporarily function without debilitating symptoms because the primary trigger for symptoms is exertion. So a doctor will not look at the perky and alert and well-dressed person in their office and dismiss them as being a complainer or just having symptoms from stress because this disease is an up and down, good days and bad days situation. The name emphasizes that the symptoms do not have to be constant.

5. The name says it is a disease. The advantage of that is self-evident.
 
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John Kaiser

- Pateint
- CEO of Company doing Pharmaceutical
- Researcher

BIG PHARMA
- feels that they need to be involved
- Funding will go up by 50 to 100 times if they become involved
- the lack of name and criteria is holding them back
- they are risk averse and don't like uncertainty
- In AIDS, $30Billion came in once it was identified and named

WAY FORWARD
- must set name and diagnostic criteria
- Pharma accept it is there

CRITERIA
- Agrees with Lenny
- Fukuda is not specific enough. Lets too many with ME/CFS into the cohort;
- The CCC has not been taken up in the US by primary care doctors. This is an issue. Feels it is overly complex. Good for an ME/CFS specialist, but not a family practice doctor. Needs something simple to enable diagnosis in one or two visits.
- More comfortable with the IOM process doing a thorough and deep analysis
- SEID is not confusing and can be applied by primary care doctors.
- comfortable that it is scientifically derived
- believes it identifies ME/CFS patients
- comfortable in using it BUT the name is not good.
- Name is not key issue - just identify the criteria well
- A word map of the conference would see that ME/CFS has been the most used term here at this conference.
- he is comfortable with ME/CFS
- more important to develop a consensus about it.
- Comorbid illnesses allow for more than one disease and he likes that - he cited a case of a stabilised AIDS patient who developed ME/CFS.
- In clinical practice - allowing for the codiagnosis of comorbid illness is an important step forward

CLINICAL v RESARCH
- believes that comorbid illnesses would muddy the research studies
- should be allowed for clinical practice, but use pure ME/CFS without comorbid to avoid confounding in research
- Would give clean research data
I agree with all he said here, except I think the "SEID" name is an improvement. Glad he spoke up.

One of the reasons this disease has not had credibility and considered "the wastebasket diagnosis" or not a disease entity is because it's what the doc is supposed to diagnose you with when all the other tests for other real diseases come up negative. It's like "other" on the racial questions on the census. Saying it can occur with other conditions and that the combination of symptoms is particular to it means it's a distinguishable disease entity.
 
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Bit confused about the comments on ICD-10 - regardless of differences of professional opinion over sufficient inflammation to justify the name, ME and PVFS are coded in ICD-10 at G93.3 and WHO added CFS to the alphabetical index of ICD-10 with a reference to G93.3 so according to WHO, ME, PVFS, CFS are all ICD-10 G93.3.
US has decided to code CFS differently in their clinical modification to ICD-10 w/e Oct. 2015 so that was an unnecessary muddying of the waters. It may well transpire that what they are currently researching as ME/CFS is better classified elsewhere than as neurological, but that is how US should code CFS for the time being.
This is true, except putting CFS elsewhere in US clinical coding happened before ICD-10.
 
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Why wasn't Francis Collins there? If he is serious as he tells us he is, why doesn't he show up to get educated about the disease and see where things are firsthand?
I would imagine that his attending any conference of researchers would be awkward because all would be buddying up to him or asking him to fund this or that. I think it's great that Whittemore from NIH is there and that we now have NIH and CDC people coming to these conferences, participating and giving presentations. It's a step forward in making them our team members instead of those we complain to. They can join our efforts and interests instead 8f being targets of our angst.

This is much progress from the days of Strauss and Reeves.
 
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One of the potentially most important tweets from the conference in my opinion:
Yes, this seems like a pretty big deal, repeating what they said in Norwegian earlier this month (as reported in that Cort blog, previously linked), but now presented directly in English.

Sounds like a pretty compelling justification to (re)examine Dr Myhill et al claims of finding translocator protein autoantibodies blocking ATP out of and/or ADP into mitochondria, in a subset of her tested patients reviewed. As @Hip calls for in his thread summarizing those 3 papers. I've no idea if Fluge/Mella, Davis, etc, can already rule such things out? Or what percentage of Myhill's subjects were supposed to have significant problem with these auto-antibodies, if that could match up with the number of Rituximab responders...? (Without B cells making these anti-bodies anymore.)

The depth, breadth and consequence of Øystein Fluge and Olav Mella's work is huge. Like they say, if it had been achieved in a well known US academic location there would have been bigger waves by now. Interesting to know they have been working on @ChrisArmstrong's metabolomics insights for a year:

Digging back through Cort's one man Tweet deluge from the last few days, we're inundated with so many different instances of great, direct observations of organic malfunctions going on. But what's most encouraging is the sound of collaboration between researchers, with more open publications and powerful new (commercially available) medical tools (plus the space-tech level stuff Ron Davis is spearheading). Reference to the trajectory of the human genome project sounds excitingly fitting - that got only 1% of the way done after 7 years of the 15 year project, but then busted out it's first complete draft 4 years after that! (Following exponential gains in sequencing and international collaborations.)

I think this Tweet about Hanson finding *increased* (gut) viral diversity is tantalizing.
Although, studying such things is so cutting edge (even compared to now seemingly accepted decreased bacterial gut diversity), I've no idea if anyone will have a clue what to make of it...? If there's something big and unsubtle going wrong, maybe that'll be something. Maybe gut is a promising site for 'latent' viral problems? Anti-virals helping here?


I think it's cool that Michael VanElzakker is in the mix. His hypothesis that viral infection of the vagus nerve itself, which normally detects systemic inflammation to get the brain and body to throttle activity appropriately, makes it massively sensitive to an amount of cytokines that can not be found in the blood. Hopefully he's progressing towards some actual studies...

Of course, there was the first direct sighting of the brain's lymphatic system, earlier this year (I think), which was presumably good material for Dr Raymond Perrin. (Personally, I've felt my lymph nodes weren't quite right since going to the doctor about them as a teenager, but never enlarged/sore, just firm and ever pressent.) Personally expect this is more just a part of the body wide fall-out from more fundamental problems.
Then some kind of disheartening insights, of seemingly permanent, long term degeneration:
But sorry, I've gotten carried away up there... Really hoping that Cort (and others) will be able to write up a whole bunch of these talks and information in more detail. :)
 

aimossy

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Here is a compilation of Fluge and Mella tweets from Cort on their talk about amino acid metabolism and the TCA cycle. I've pulled this from Microbe Discovery Project FB. Do we have any biochemistry, metabolism or TCA cycle guru's around? There must be model images of these processes.

"Fluge - 200 Biobank samples - autoantibody screening, peptides, immunophenotyping, immunogenetic, exome sequencing...
Fluge - with researchers from across the world - from Canada to US to Germany

Fluge - publication under review - finding where obstruction in mitochondria is located......

Fluge - analyzed 20 standard amino acids and derivatives in 200 paitents and 100 controls

Fluge - Amino acids catabolized to either pyruvate, acetyl-- CoA or to anaplerotic AA's

Fluge - Pyruvate - no difference in amino acids catabolized in first part of cycle

Fluge - catabolize to acetyl-COa reduced in women but not in men, same in anaplerotic AA's

Fluge - supplying CoA and TCA cycle and TCA capacity = impaired pyruvate dehyrogenase complex

Fluge - men - increased 3 - methylhistidine - = increased enodogenous protein catabolism - taking AA's from muscles

Fluge - PDH kinases inhibit PDH and Sirtuin - PH inhibition could explain findings, increased pyruvate - lactate

Fluge - Gene expression indicated taht PDK enzymes increase in both male and females

Fluge - same system disturbed in men and women but different compensation in both

Fluge - highlights metabolic obstruction in central energetic pathway at PDH complex level causes profound lack energy

Fluge - believes functional obstruction is caused by immune response - perhaps autoreactive B cell subset (?)

Fluge -exposed muscle cells in culture to serum from severe ME/CFS suggests something in serum is responsible

Fluge - perhaps autoantibodies....Fluge told me "We are just scratching the surface" - in a year we will know much more

Fluge - studies suggest that immune system is producing anti-mitochondrial antibodies that are whacking the mitochondria

Fluge - nothing structurally wrong with mitochondria but are affected by disease process (similar to Naviaux)

Fluge - the room is completely filled up! First time in conference

Fluge - Q&A - Rituximab side effects - no major life-threatening side effects - otherwise just temporary effects mosty

Fluge -really remarkable how wide the variety of work done by Fluge and Mella is - they are looking everywhere they can"
 
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Hip

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Fluge - studies suggest that immune system is producing anti-mitochondrial antibodies that are whacking the mitochondria
Sounds like a pretty compelling justification to (re)examine Dr Myhill et al claims of finding translocator protein autoantibodies blocking ATP out of and/or ADP into mitochondria, in a subset of her tested patients reviewed. As @Hip calls for in his thread summarizing those 3 papers.
Wow, that possibility if it pans out might neatly tie in with the mitochondrial dysfunction findings of the Myhill, Booth and McLaren-Howard studies.

And it would also tie in with the studies on chronic coxsackievirus B infection of the heart muscle (similar to the chronic CVB infections in ME/CFS patients' skeletal muscles), in which they found autoantibodies which target and disable mitochondrial translocator protein (see this post).
 

Hip

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Fluge - exposed muscle cells in culture to serum from severe ME/CFS suggests something in serum is responsible
That sounds like a fascinating experimental procedure: I wonder what the serum from severe ME/CFS patients did to the muscle cells in culture? Serum has the blood cells removed, but still contains hormones, cytokines and antibodies.
 
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Never Give Up

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Yes I get the impression Ron Davis is about 2 years ahead the game if not more.
It's great that he is pushing the limits but because publishing is the least of his worries we may not hear of all his work for a good while after it is done.
Hopefully we will just wake up some day and Ron will have found a cure !
During the pre-conference he expressed a great deal of disgust with the publication process and what is and isn't being published. I think he's stepping away from that game, building a collaborative network, sharing data, and focusing on the end goal. Go Ron!
 

aimossy

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That sounds like a fascinating experimental procedure: I wonder what the serum from severe ME/CFS patients did to the muscle cells in culture? Serum has the blood cells removed, but still contains hormones, cytokines and antibodies.
Thanks Hip, that made me look up good old wiki:

"In blood, the serum (/ˈsɪərəm/ or /ˈsɪrəm/) is the component that is neither a blood cell (serum does not contain white or red blood cells) nor a clotting factor; it is the blood plasma not including the fibrinogens. Serum includes all proteins not used in blood clotting (coagulation) and all the electrolytes, antibodies, antigens, hormones, and any exogenous substances (e.g., drugs and microorganisms)."
 

Jill

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Thanks Hip, that made me look up good old wiki:

"In blood, the serum (/ˈsɪərəm/ or /ˈsɪrəm/) is the component that is neither a blood cell (serum does not contain white or red blood cells) nor a clotting factor; it is the blood plasma not including the fibrinogens. Serum includes all proteins not used in blood clotting (coagulation) and all the electrolytes, antibodies, antigens, hormones, and any exogenous substances (e.g., drugs and microorganisms)."
Heck so if theres something in the serum - what is it likely to be? Kinda gotta make you think that would be easy to find if it was a microorganism. So are there any other other obvious things - antibody? autoantibody. Way out of my league - but thinkits seriously cool that after all this friggin time something is different in simple serum!!!!
 

ash0787

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Autoantibodies attaching to metabolic critical components inside the cell or on the surface rather than destroying the cell outright is my new favourite theory, its the only one that explains how the immune system and energy system can be equally important but neither is instrumental which is something I always felt.
 

NL93

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Heck so if theres something in the serum - what is it likely to be? Kinda gotta make you think that would be easy to find if it was a microorganism. So are there any other other obvious things - antibody? autoantibody. Way out of my league - but thinkits seriously cool that after all this friggin time something is different in simple serum!!!!
I might not be one thing. We know that in severe ME a lot of things are out of whack at the same time (hormones, cytokines etc.). I wouldn't be surprised if it's a lot of things together that cause the mitochondria to behave differently.
But it would be awesome if they could actually find something kind of simple in the serum that is the main cause of mitochondria shutting down. If that could be found, finding a treatment might not be that hard?

But oh well, what do I know. It's good to see some competent researchers working on this! All very exciting:)
 

snowathlete

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I would imagine that his attending any conference of researchers would be awkward because all would be buddying up to him or asking him to fund this or that. I think it's great that Whittemore from NIH is there and that we now have NIH and CDC people coming to these conferences, participating and giving presentations. It's a step forward in making them our team members instead of those we complain to. They can join our efforts and interests instead 8f being targets of our angst.

This is much progress from the days of Strauss and Reeves.
Might it be awkward? Yeah, possibly, but I still don't see that as a reason not to attend. I expect he is well used to handling researchers chasing him for funding. Does he not attend any research conferences then? I'd be surprised if that was the case. I agree things have improved and we all welcome that, but I think it's important not to interpret a question such as mine as angst. The NIH say they've had not one application from a young researcher. This really isn't surprising as there has been no money available, not even much seed funding from non-profits. The message has always been that it isn't a field that it is possible to work in, that the NIH aren't interested. It's also true of drug companies, who still don't see this as an opportunity. One of the key reasons he should be there is to increase the profile of the disease. He can help change these perceptions. While I am confident the attendees from the NIH were there for a genuine purpose and represent true progress, others, including potential young researchers, and drug companies, may assume this is a superficial display (if they even hear about it). I think the director of the NIH attending would convince more outsiders, and create more publicity, that the NIH's interest in this disease was serious and this was a field worth looking at.