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

[Tuha]

I can't remember saying that specifically, but that means very little... My brain isn't working well this morning so I hope the following addresses your point.

There are a number of high profile Australian sports people who got something like ME and have attributed it to over-training. Also, there was something about ME being more prevalent in professional cyclists, the inference being that they push their bodies with extreme levels of physical activity and this either triggered ME or made them more vulnerable to it.

I do wonder though if it is just that very active people and particularly professional athletes are more likely to notice say a 20% decrease in energy, be worried by it and seek medical treatment. Whereas a couch potato with the same decrease in energy may not notice that on their amble to the fridge or may just attribute it to getting older/less fit/fatter/having kids. So, the threshold for being diagnosed with mild ME may be different in active vs inactive people.

It was very interesting though about that twin study mentioned above where the more active twin was the one who got ME.

It is very difficult to address this question (whether people who do a lot of physical or mental activity are more at risk of developing ME) until there are good biomarkers.

I am former professional footballer and had to stop my career because of ME. I am not sure if it´s for everyone but even if ME didnt hit me so bad on the beginning I had to stop immediately after getting ME. I can imagine to follow the trainings for a time but after each heavier exercise I felt very bad and had collapsing states (fast heart beating, muscle weakness, diziness,...). I think if you are overtrained you feel differently.

 

[snowathlete]

It'd be very unusual for Collins to hang out at a science conference unless he's a headline speaker. He's running a $30 billion agency.

Here are some recent conferences he attended as keynote/headline speaker - these are all meetings with 1,000's of attendees:

http://www.asbmb.org/asbmbtoday/201510/2016Meeting/Collins/
http://www.tedmed.com/speakers/show?id=6584
http://www.lupusresearchinstitute.o...upus-conference-highlights-precision-medicine
http://www.ashg.org/2015meeting/

It's not like he carries that $30 billion around in his wallet and has to worry about getting mugged. I don't see what the size of the budget he heads has anything to do with it. He's the head of an agency which has overall responsibility for ME/CFS research. I think it'd be great if he turned up to one of these conferences for a day. It work help. I'm sure everyone would be happy for him to give a keynote speech.

 

[Sushi]

Do you know what these specific autoantibodies are called or how they are tested for (or is this still in the experimental stage)?

See below:

An anti-mitochondrial antibody has already been described...and some of us (including me) test positive for it. It's the anti-cardiolipin antibody. Cardiolipin is part of the inner membrane of mitochondria.

From a 2009 publication: "Examination of anticardiolipin antibodies (ACAs) in the sera of patients clinically diagnosed with chronic fatigue syndrome (CFS) using an enzyme-linked immunoassay procedure demonstrated the presence of immunoglobulin M isotypes in 95% of CFS serum samples tested."

http://www.ncbi.nlm.nih.gov/pubmed/19623655

 

[Hip]

An anti-mitochondrial antibody has already been described...and some of us (including me) test positive for it. It's the anti-cardiolipin antibody. Cardiolipin is part of the inner membrane of mitochondria.

Indeed. I was recently referring to this anti-cardiolipin autoantibody in this post. From what I can make out, it may have the potential to disrupt mitochondrial oxidative phosphorylation, which produces around 90% of our ATP, but I have not seen any studies which demonstrate cardiolipin autoantibodies can cause mitochondrial dysfunction. These anti-cardiolipin autoantibodies are found in other diseases, including lupus.


Also of note is the adenine nucleotide translocator (ANT) autoantibodies found in chronic coxsackievirus B (CVB) infections of the heart muscle (myocarditis), which have been shown to impair cellular energy production in myocarditis (see the bottom half of this post). Such chronic CVB heart muscle infections are likely very similar to the chronic CVB skeletal muscle infections found in many ME/CFS patients.

ANT plays a vital role in ferrying the ATP made in the mitochondria into the cell where its energy is needed. The Myhill, Booth and McLaren-Howard studies on mitochondrial dysfunction in ME/CFS found that the ANT protein is dysfunctional in approximately half of ME/CFS patients (see this post).

If you ignore the effects of purinergic signalling you can find yourself looking for a kind of biochemical ghost when the data you have already shows changes you have ascribed to metabolism without considering them as signals.

Would you have any hunches about how purinergic signaling (via molecules such as ATP) might lead to some of the symptoms of ME/CFS?

 

[anciendaze]

...Would have any hunches about how purinergic signaling (via molecules such as ATP) might lead to some of the symptoms of ME/CFS?

The one I've mentioned before is ATP dumped by RBCs entering a region of local hypoxia caused by exercise resulting in vasodilation similar to that seen in Systrom's patients with low pressure on venous return. Several of the characteristics of this response would make it hard to notice with standard medical assumptions. It is transient, localized and episodic, and scarcely anyone is measuring pressure on venous return to the heart. But this is only one hunch. Purinergic signalling often serves as confirmation that a process signaled by other chemicals is taking place in cells nearby. This is not trivially simple signalling, which people often assume. Nothing in nature limits cellular signalling to one chemical for one purpose.

 

[BurnA]

Everybody has anticardiolipin antibodies if you do the test a certain way.

 

[Never Give Up]

The #MEAction Network
7 hrs ·
Watch Dr. Lucinda Bateman's livestream update this November 2nd, as she recaps her experiences participating in several important ME conferences. She will discuss what happened at the IACFS/ME Conference, the ME/CFS Conference in Sweden, and the SMCI Scientfic Advisory Council Meeting.


Watch Dr. Bateman's Livestream | #MEAction
If you couldn't make it to some of the biggest conferences this month, you can get the recap from Dr. Bateman this November 2nd.
MEACTION.NET

 

[Hip]

Everybody has anticardiolipin antibodies if you do the test a certain way.

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:

This study demonstrates that a large percentage of patients clinically diagnosed with CFS have elevated levels of the IgM isotype to CL (95%), suggesting that CFS may be an autoimmune condition.

CL = cardiolipin.

For comparison, in clinically "normal" individuals, ... one study showed that 77.3% of assayed individuals had negative ACA titers, 15.0% were considered low positives, and 7.7% had moderately high titers.

ACA = anticardiolipin antibodies.

 

[duncan]

If 95% of ME/CFS patients demonstrated ACA and HC's did not, wouldn't it be diagnostic - assuming the results were replicated? I cannot access the study, so don't know sample size etc.

Sorry for the sidebar question. Don't mean to derail the thread.

 

[Denise]

If 95% of ME/CFS patients demonstrated ACA and HC's did not, wouldn't it be diagnostic - assuming the results were replicated? I cannot access the study, so don't know sample size etc.

Sorry for the sidebar question. Don't mean to derail the thread.

ACA apparently occurs in several diseases so findings in patients with ME wouldn't be and indication of ME.
This is from Wikipedia (fwiw) -
"Anti-cardiolipin antibodies (ACA) are antibodies often directed against cardiolipin and found in several diseases, including syphilis,[1] antiphospholipid syndrome, livedoid vasculitis, vertebrobasilar insufficiency, Behçet's syndrome,[2] idiopathic spontaneous abortion,[3] and systemic lupus erythematosus (SLE).[4] They are a form of anti-mitochondrial antibody. In SLE, anti-DNA antibodies and anti-cardiolipin antibodies may be present individually or together; the two types of antibodies act independently.[5] This is in contrast to rheumatoid arthritis[6] with systemic sclerosis (scleroderma)[7] because anti-cardiolipin antibodies are present in both conditions, and therefore may tie the two conditions together."

 

[AndyPR]

Found this using my google-fu, I think it's the same study? http://www.ncf-net.org/pdf/AnticardiolipinAntibodies.pdf
If it is the same, sample size = 40

 

[alex3619]

I think it depends on how high the titers are of these anticardiolipin antibodies.

An important point is being overlooked here. There are most likely many kinds of anticardiolipin antibodies. They are likely to have different binding affinities and impact, in part because they may bind in different ways. So the quantity of antibodies is only one factor, what they are doing is the other.

PS I thought I should elaborate. While cardiolipin is a relatively simple molecule it does have alternative forms and is important in the mitochondrial membrane. I wonder if an antibody binding to it might have an impact if its close enough to another molecule such as a transporter protein etc. This is all speculation, but my point is we just don't know enough to rule things out, not just not knowing enough to say its certainly a problem.

 

[anciendaze]

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.

Hip, I have to warn you that the ACA test used in that study is not the same as those offered by clinical labs. They started out looking for biomarkers to indicate ciguatera poisoning. This turned out to be responding to cardiolipin antibodies.

When I looked into the history of standards for ACA, I found that there was a time when many M.D.s felt too many patients were being diagnosed with autoimmune disorders. The result was that the thresholds for clinical laboratory tests were adjusted to match diagnoses by clinical signs like the rash in lupus. CFS has no such obvious sign, so clinical tests were implicitly adjusted to exclude CFS patients.

 

[Sing]

@usedtobeperkytina

Simple question: Does the label SEID receive the same diagnostic code as CFS has? or PVFS? or ME?

 

[Kati]

Please join me in thanking journalist Miriam Tucker for attending IACFSME this week.

https://twitter.com/i/web/status/792862776272171008

(Click the box above, like and retweet on twitter)

 

[Denise]

@usedtobeperkytina

Simple question: Does the label SEID receive the same diagnostic code as CFS has? or PVFS? or ME?

@Sing - I hope it's okay for me to answer this (you tagged @usedtobeperkytina) - there is currently no ICD code for SEID.

 

[Denise]

Please join me in thanking journalist Miriam Tucker for attending IACFSME this week.

https://twitter.com/i/web/status/792862776272171008

And thank you to everyone who attended!

 

[usedtobeperkytina]

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.

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."

 

[usedtobeperkytina]

@usedtobeperkytina

Simple question: Does the label SEID receive the same diagnostic code as CFS has? or PVFS? or ME?

The recommendation included creating a "SEID" code. Yet, to my knowledge, no one has started that process.

 

[usedtobeperkytina]

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).