IACFSME 2022 Virtual Medical Conference: Day 4 Presentations: 30 July (9 am to 3.30 pm EDT)

[Science For ME]

We have four threads, one for each day of the conference. Please add the following to these threads:
* reports from forum members attending the conference
* tweets and reports from other social media
* your thoughts about the information presented.
* any questions you would like asked of presenters

IACFSME 2022 Virtual Medical Conference: Day 1 Workshops: 27 July (9 am to 5 pm EDT)
IACFSME 2022 Virtual Medical Conference: Day 2 Presentations: 28 July (9 am to 5 pm EDT)
IACFSME 2022 Virtual Medical Conference: Day 3 Presentations: 29 July (9 am to 4.40 pm EDT)
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9.15 am - 9.45 am
POTS Research Update & Review of Autonomic Dysfunction in ME/CFS
Lauren Stiles, Dysautonomia International/ Stony Brook University, USA


9.45 am - 10. 45 am
IMMUNOLOGY/INFECTIOUS DISEASES 2

Immune-related profiles of long COVID patients in the Japanese population
Wakiro Sato, National Institute of Neuroscience, National Center of Neurology & Psych, Japan

Spoiler: S4ME threads on Wakiro Sato's recent work

Patients with ... (ME/CFS) Who Have Already Visited Some Medical Institutions: Diagnosis, Treatment and Research, 2022, Sato
Skewing of the B cell receptor repertoire in myalgic encephalomyelitis/chronic fatigue syndrome, 2021, Sato et al

Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE)
Gunnar Gottschalk, Simmaron Research Inc., USA

Spoiler: S4ME thread on this research

Elevated ATG13 in serum of pwME stimulates oxidative stress response in microglial cells , 2022, Gottschalk et al

EBV and HHV-6A dUTPases Contribute to ME/CFS Syndrome by Exacerbating TFH Cell Differentiation and Extrafollicular Antibody Responses
Brandon Cox, The Ohio State University, USA

Spoiler: S4ME thread on this work

EBV/HHV-6A dUTPases contribute to ME/CFS pathophysiology by enhancing TFH cell differentiation and extrafollicular activities, 2022, Cox et al

 

[Science For ME]

11.00 - 12.15 am
TREATMENT

An international survey of experiences and attitudes towards pacing using a heart rate monitor for people with ME/CFS
Nicola Clague-Baker, University of Liverpool, England

Spoiler: S4ME thread on related work by Nicola Clague-Baker

* UK Planned study: Feasibility of investigating VO2, HR, BP, lactic acid and activity of pwME during normal daily activity, 2020/21, Clague-Baker et al

Stellate ganglion block (SGB) improves symptoms of ME/CFS: a case series
Luke Liu, Neuroversion, Inc., USA

Spoiler: S4ME threads on Stellate Ganglion Block treatment

* Stellate ganglion block reduces symptoms of Long COVID: A case series (2021) Liu et al
* Stellate Ganglion Block treatment

BREATHE: A mixed-methods evaluation of a virtual self-management program for people living with long COVID
Rosie Twomey, University of Calgary, Canada

Spoiler: S4ME threads on Rosie Twomey's papers

* Chronic Fatigue and Postexertional Malaise in People Living with Long COVID: An Observational Study, 2022, Twomey et al
Other papers: https://www.s4me.info/tags/twomey/

Oxaloacetate improves physical and mental fatigue in ME/CFS and long-COVID
David Kaufman, Center for Complex Diseases, USA

Spoiler: S4ME threads on this work and oxaloacetate as a treatment

* Oxaloacetate Treatment For Mental And Physical Fatigue In (ME/CFS) and Long-COVID fatigue patients, 2022, Cash and Kaufman
* Oxaloacetate

12.15 pm - 1.30 pm
AWARDS CEREMONY

 

[Science For ME]

1.30 pm - 2.30 pm
PUBLIC HEALTH 2

Engaging patients and caregivers in teaching health professional students about ME/CFS: A workshop model
Cathy Kline, Gloria Gray, University of British Columbia, Canada

Chronic Absenteeism and ME/CFS: A Nurse-Led Approach to Establish the School-Based Active Surveillance Process
Erin D. Maughan, George Mason University School of Nursing, USA

Spoiler: S4ME thread on the School-based Active Surveillance

USA: CDC: School-Based Active Surveillance (SBAS) of ME/CFS Among Schoolchildren, comments invited until 20th Sept 2022.

COVID-19: Understanding recruitment strategies in a community-based assessment of fatigue, cognitive and functional impairments among those after SARS-CoV-2 infection
Nancy Klimas, Nova Southeastern University, USA

Spoiler: S4ME threads related to Nancy Klimas

https://www.s4me.info/tags/klimas/

 

[Science For ME]

2.30 pm - 3.30 pm
COVID-19 2

Covid-19 infection in patients with ME/CFS– an update
John Chia, EV Med Research, USA

Spoiler: S4ME thread on a recent interview of John Chia

John Chia Interview by Amy Proal and Enteroviruses in ME (Blogpost)

A classification system for post-acute sequelae of SARS CoV-2 infection
Leonard Jason, DePaul University, USA

Prevalence, clinical correlations and predictors of fatigue and severe fatigue 3 and 6 months following confirmed infection by SARS-CoV-2 in The BC Respiratory Cohort
Luis Nacul, University of British Columbia/ BC Womens Hospital, Canada

Spoiler: S4ME thread on a recent post-Covid epidemiology paper co-authored by Luis Nacul

Preprint: Post-viral fatigue following SARS-CoV-2 infection during pregnancy: a longitudinal comparative study, 2022, Oliveira, Nacul et al

 

[Hutan]

9.15 am - 9.45 am
POTS Research Update & Review of Autonomic Dysfunction in ME/CFS
Lauren Stiles, Dysautonomia International/ Stony Brook University, USA

Notes - Part 1

Lauren said there is a lot of overlap between ME/CFS and POTS, and sometimes she thinks they are the same things, but just different flavours. She also noted the underfunding of research is something that the two conditions share: the annual NIH funding for POTS research is only about $1 million per year, which is extraordinary given the number of people affected, and the severity with which they can be affected, and the overlap with many other conditions.

She noted that POTS now has its own code in the US ICD-10: G90A.

2019 NIH Consensus Meeting resulted in a list of top research priorities which included basic things like defining the role of genetics and clarifying the natural history of the disease, as well as considering the role of autoimmunity among other things that I did not have time to write down.

Lauren and Dysautonomia International are clearly major advocacy forces for POTS research. DI have funded 40 studies and have supported 57 other studies. They have an 'expert patient' service that can help with studies, providing knowledgeable patients to advise on study design and recruitment - this was an interesting idea, one that would be very good to see other patient charities take up. I think every study on an illness population should have a patient expert involved in much the same way that any study on an ethnic group should have at least one person from that ethnic group as part of the research team. DI has research funds for Dysautonomia; POTS; and now Long Covid. I wasn't able to write down the areas that are being researched, but there is a wide scope including quite a lot of possible treatments (e.g. the ubiquitous LDN; ivabradine; fulvic acid; enhanced external counter pulsation).

Autoimmunity and Immune Dysfunction in POTS
The Universities of Oklahoma and Karolinska have done studies, and have found autoantibodies in over 90% of POTS using functional cell receptor based assays.

Dr Kem was an innovator in the field. He died as a result of Covid-19; Lauren was clearly very sad that that had happened. He was working on (autoimmunity in) Graves disease and noticed that lots of people with Graves disease had POTS in their medical histories and wondered 'what's going on here?'. He tested POTS patients for autoantibodies and found adrenergic and angiotensin autoantibodies in nearly all POTS patients. The autoantibodies appear to have a sympathetic activating role.

Lauren isn't yet ready to write it in stone that the autoantibodies are the cause of POTS - they might be the result of the disease process rather than the cause.

Celltrend
This is one of the major bits of news I took away from the part of the conference I watched. I think this is the first we have heard of this? Celltrend offers testing for autoantibodies with a panel for POTS and ones for ME/CFS and for Long Covid too. S4ME and Phoenix Rising have had lots of members get excited about the number of autoantibodies they have tested positive for, from the Celltrend analysis. I think this following study was supported by Dysautonomia International, and is exactly the sort of thing national and international patient charities should do, to protect their constituency.

So, 116 POTS patients and 81 healthy controls. Their blood samples were sent off to Celltrend for testing against the POTS panel. 98.3% of the POTS patients had an adrenergic receptor autoantibody. BUT 100% of the controls did too! (Yes, I think this warrants an exclamation mark.). This suggests that the Celltrend analysis doesn't tell us anything about the pathology of POTS, and probably doesn't tell us anything about ME/CFS and Long Covid either.

Lauren strongly encourages the use of healthy controls and careful blinding when testing for autoantibodies. She said that it doesn't mean that autoantibodies aren't relevant in the pathology of POTS; it might be just that the Celltrend test doesn't really work. Lauren mentioned that the Celltrend assays might be two dimensional, whereas the assessment needs to be of the 3D structure.

Edit - Unlike me, this forum rarely fails . I see we already have a thread on this study and I am behind on the news, thanks to @Milo for posting and for the other posters on the thread: Detection of G Protein-Coupled Receptor Autoantibodies in Postural Orthostatic Tachycardia Syndrome Using Standard Methodology (2022) Hall et al

 

[Hutan]

9.15 am - 9.45 am
POTS Research Update & Review of Autonomic Dysfunction in ME/CFS
Lauren Stiles, Dysautonomia International/ Stony Brook University, USA

Notes - Part 2

University of Toledo - Platelet storage pool deficiency
34 people with POTS. 85% were found to have a platelet storage pool deficiency (immune mediated).
Also IL-1B, IL-21, TNFa, INFy and CD30 were elevated [interesting about the IL-21 given the recent Cox study that found the same in ME/CFS)
Decreased CD40L and RANTES
Platelet storage pool deficiency can cause problems in blood clotting, easy bruising. Lauren said that she had put these researchers in touch with Pretorius re the microclotting in Long Covid - but, I would have thought these are opposite problems?

Here's the forum thread on this study, thanks to @Ryan31337 for posting it:
Platelet Storage Pool Deficiency and Elevated Inflammatory Biomarkers Are Prevalent in POTS, 2022, Gunning, Grubb et al





Glucose dysregulation in POTS [relevant to low carb diets]
12 people with POTS, 13 age-matched controls
Lauren said that most people with POTS are hyperadrenergic to some degree [i.e. have high levels of adrenalin (epinephrine, nor-epinephrine) in their blood].
It was found the POTS patients were more insulin resistant. Lauren felt this was not surprising as increased sympathetic activity is known to contribute to insulin resistance.

GIP is a potent vasodilator especially of the splanchnic vasculature (ie around the abdomen where is where a lot of blood pooling occurs in POTS). Levels correlated with POTS symptoms including heart rate increase upon standing (I didn't catch if GOP levels were found to be elevated compared to controls - I think they were.). Lauren said that someone (the authors, a POTS authority? - sorry I didn't record who) were suggesting that this was sufficient evidence to support clinicians suggesting to POTS patients to try a low carb diet. Lauren said that many POTS patients naturally gravitated to a low carb diet, or avoiding large meals and just having small ones throughout the day, because they feel bad when they eat a lot of carbs.

Here's the forum thread on the study, thanks to @Mij for posting it:
Worsening Postural Tachycardia Syndrome Is Associated With Increased Glucose-Dependent Insulinotropic Polypeptide Secretion, 2022, Nicholas C Breier

Vagus nerve stimulation
There have been 5 trials in POTS to date. Lauren uses vagus nerve stimulation and she thinks vagus nerve stimulation helps her a lot - she has POTS that seems to be part of her Sjogrens.

Diedrich et al 2021 review paper
Transdermal auricular vagus stimulation for the treatment of postural tachycardia syndrome
Lauren recommended reading this paper. Again, I'll make a thread if we don't have one yet, and link it.
It reported that right hand side Vagal nerve stimulation works better than left hand side stimulation.
It suggested that there is evidence that vagal nerve stimulation reduces orthostatic symptoms, orthostatic tachycardia and inflammation.

The review also points out that there is more autonomic modulation achieved by attaching to the concha part of the ear, as opposed to the tragus part of the ear. I've previously pointed out that it isn't at all clear that putting an electrical current on the tragus does anything at all to the vagal nerve, as it hasn't been certain that the vagal nerve goes to the tragus. So, I think, the finding of a benefit in open label studies that have applied the stimulation to the tragus is looking quite shaky. And, therefore, any open label study of vagal nerve stimulation with just subjective outcomes is probably also suffering from bias.

First Vanderbilt study - a pilot study
14 POTS patients. They all had sham and vagal nerve stimulation in a random order. The treatment was reported to be safe and tolerable. The VNS applied during a tilt table test was found to reduce tachycardia in this study. But it didn't answer the question 'does VNS provide any benefits when it's not clipped to your ear?'

Second Vanderbilt study
Transcutaneous VNS + placebo + transcutaneous VNS with mestinon. The study is ongoing. It uses TENS.

Humanitas study
11 hyperadrenergic POTS patients and a NEMIS device providing vagal nerve stimulation. 14 days of VNS, 4 hours a day. This study is open-label. Improvements were reported, including a particularly dramatic reduction in gastrointestinal scores.

Lauren felt that 4 hours a day was way too long. She says that US studies and most VNS experts think that two to six minutes a day should be enough. She also commented that theoretically it is possible to over-stimulate the nerve and put oneself into an immune suppression state.


Lauren then is very positive about vagal nerve stimulation. She says that it is very well tolerated and therefore is a more attractive option than some of the drug treatments for POTS. She would like to see more studies in ME/CFS and LC. I remain skeptical for now.

 

[Hutan]

9.45 am - 10. 45 am
IMMUNOLOGY/INFECTIOUS DISEASES 2

Immune-related profiles of long COVID patients in the Japanese population
Wakiro Sato, National Institute of Neuroscience, National Center of Neurology & Psych, Japan
Patients with ... (ME/CFS) Who Have Already Visited Some Medical Institutions: Diagnosis, Treatment and Research, 2022, Sato
Skewing of the B cell receptor repertoire in myalgic encephalomyelitis/chronic fatigue syndrome, 2021, Sato et al

Dr Sato moved very quickly through a lot of papers. I didn't manage to record much that was useful; my notes below are subject to confirmation when the recording is available. I missed things.

He mentioned his 2021 paper on B cell receptors (link above), noting "deviated functional B cell subsets; differentiation defect in B cell development"' clonal expansion; skewing of the B cell receptor repertoire".

He mentioned this paper which he coauthored.
Altered Structural Brain Networks Related to Adrenergic/Muscarinic Receptor Autoantibodies in CFS, 2020, Fujii, Sato, Yamamura et al
You'll see on the link, I was a bit skeptical about the paper back in 2020. Unfortunately, that paper is behind a paywall and the Scihub link no longer works, so it's hard to review its conclusions. Dr Sato noted that the Loebel paper found that 30-40% of patients have elevated antibodies to these autoantibodies [but the subsequent issues with the Celltrend autoantibody test that that paper used surely makes that finding very questionable. I don't know what testing was done by Fujii et al to support their findings regarding adrenergic and muscarinic receptor autoantibodies.]

Dr Sato noted that, in the Japanese ME/CFS clinic he is involved with, they see patients with decreased blood flow in parts of the brain.

Dr Sato agrees with the hypothesis set out by Mehandru and Merad in their paper "Pathological sequelae of long haul Covid". This seems to involve some or all of viral persistence, inflammation and autoimmunity. He notes that GPCR antibodies can disturb normal circulation.

Treatments for Long Covid patients are ATP, Vitamin B12, Vitamin C and neurotropin.

 

[Hutan]

Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE)
Gunnar Gottschalk, Simmaron Research Inc., USA
Elevated ATG13 in serum of pwME stimulates oxidative stress response in microglial cells , 2022, Gottschalk et al

These heavy duty immunology presentations only had 15 minutes each, with 15 minutes for combined questions. Rather than two presentations on the questionable Stellate Ganglion Block treatment for example, I think in future it would be better for presenters with detailed biochemistry content to have 30 minutes to present their work and up to 10 minutes for dedicated questions. Otherwise, you just end up with a rushed, once over lightly sort of presentation. People coming to the study cold probably mostly go away confused. People who do have some understanding of the study don't learn anything new.

If you are interested Dr Gottschalk's work - and I do think it is an interesting and detailed set of preliminary findings - I suggest you read the paper and the thread we have on the paper (link above).

Below is what I jotted down from Dr Gottschalk's presentation:

Autophagy removes depolarised mitochondria and inactive proteins [and invading organisms] from the cell
ATG-13 is a protein that initiates the formation of the autophagosome [a membrane around the rubbish being cleared]. The autophagosome fuses with the lysosome [which contains the digestive enzymes].

Elevated serum levels of proteins related to autophagy and lysosomal degradation are associated with many diseases. Recent studies find these issues in ME/CFS.

Dr Gottschalk (with blinded analysis) found that ME/CFS serum had more ATG13 than controls, suggesting issues in the functioning of autophagy. He did not find differences in lysosomal proteins (cathepsin) and concluded that there are no disruptions in lysosomal function.

What are the consequences of microglia being exposed to increased levels of ATG13 in serum?
ME/CFS serum increases the production of reactive oxygen species (ROS), iNOS and nitrite by microglia; control serum doesn't.
ME/CFS serum that is depleted of ATG13 doesn't increase the production of ROS, iNOS and nitrite by microglia.
Phosphorylated (activated) ATG13 induces microglia to produce ROS etc

How is the ATG13 affecting the microglia? It appears to be via the Receptor for Advanced Glycation End Products (RAGE). If RAGE is inactivated, iNOS isn't increased.

Dr Gottschalk will be continuing to work on this. He's working with Daniel Peterson and Avik Roy. It will be very interesting to see how this work develops.

 

[Hutan]

EBV and HHV-6A dUTPases Contribute to ME/CFS Syndrome by Exacerbating TFH Cell Differentiation and Extrafollicular Antibody Responses
Brandon Cox, The Ohio State University, USA
EBV/HHV-6A dUTPases contribute to ME/CFS pathophysiology by enhancing TFH cell differentiation and extrafollicular activities, 2022, Cox et al

Another interesting biochemistry study, with a lot of analyses. Again, check out the paper itself, and our thread on it if you are interested.

Viruses can produce dUTPase during lysis [when the cell membrane is ruptured (lysed) to allow all the replicated virions to burst out and go about their business infecting new cells). They can also produce dUTPase during abortive lysis, when they just release viral particles into the cell rather than the whole virions. [These viral particles seem to be able to bend the host cell to the virus's will - EBV for example seems to persist in human B cells, undergoing abortive lysis which modulates the immune response to the infection.]

EBV and HHV dUTPases in human cells induce the secretion of Activin And IL-21.
Activin A causes naive CD4+ T-cells to differentiate abnormally into impaired TFH cells. The impaired TFH cells may not be able to properly help B cells mount a good response to the infection.

In ME/CFS serum, levels of Activin A and IL-21 are increased. ME/CFS serum causes that same abnormal T-cell differentiation while control serum does not.

Mice injected with EBV dUTPase were found to produce those impaired TFH cells, among other things.

Brandon Cox was asked about whether anti-virals might be effective treatment for ME/CFS. He said that the drugs block viral enzymes associated with some of the proteins that are produced later in lytic reproduction e.g. they might act on the capsid of the virion. The dUTPases are produced early in lysis (hence they are produced in abortive lysis as well as full-on lytic reproduction). So, the anti-viral wouldn't have an effect. Brandon did make a disclaimer about this, and I saw his written response to the question was that he wasn't qualified to answer the question. But, I thought it was interesting. It isn't just a matter of 'a virus is the problem, anti-virals will fix it'.

He was asked about the potential mechanism for viral dUTPase-dysfunction to cause the symptoms of ME/CFS including PEM. He said that Activin A is known to cause muscle fatigue and muscle atrophy; that it might be stimulating the catabolic muscle degradation pathway. This is what he will be working on next.

As with Gunnar Gottschalk, it's great to see good young scientists working on ME/CFS with supportive teams and funding. I hope Brandon's work will be replicated in larger samples - even if we aren't exactly sure what is going on, just knowing that Activin A really is higher in people with ME/CFS would be a great step forward.

 

[ahimsa]

During the conference volunteers live-tweeted during several of the conference sessions using the forum's twitter account, s4me_info.

This post is a copy of notes made the morning of July 30.

There's a brief announcement made by Irina Rozenfeld on changes to ICD coding followed by notes on the 9:15 AM session, Postural Orthostatic Tachycardia Syndrome Research Update & Review of Autonomic Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, presented by Lauren Stiles.

All notes were taken from this twitter thread (link in quoted section):

=== start of comments ===
Today is the 4th and last day of the IACFS/ME Conference.

Irina Rozenfeld (IACFS/ME) starts the day by highlighting upcoming changes in the ICD-CM where ME and CFS will be listed under code G93.3 "Postviral and related fatigue syndromes" starting on 1 October 2022.

The first presenter of today, Lauren Stiles (Dysautonomia International) adds that Postural Orthostatic Tachycardia Syndrome (POTS) will have its own ICD-10 code in the US.

It will have code G90.A and will be listed under disorders of the autonomic nervous system.
Stiles hopes that this code will improve epidemiological data on POTS.

Before the COVID-19 pandemic, it was estimated that 1-3 million Americans suffered from POTS.

But the condition only receives $1 million NIH funding per year, which is less than ME/CFS.
Stiles is discussing studies that found adrenergic, muscarinic and angiotensin receptor antibodies in over 90% of POTS patients.

A pioneer of this research, Dr. David Kem, unfortunately, passed away recently due to COVID-19.

In Memoriam:
http://dysautonomiainternational.org/blog/wordpress/in-memoriam-dr-david-kem/

Stiles is critical of CellTrend assays, which have been used in ME/CFS research, because one blinded study showed that it could not distinguish between POTS and healthy controls.

All controls had abnormal levels (7 units/mL) of a1 adrenergic receptor autoantibodies.

This is the paper on CellTrend assays that Stiles referred to:
https://pubmed.ncbi.nlm.nih.gov/35766055/

Stiles is summarising research on glucose dysregulation which she thinks might explain why some POTS patients feel better on low carb diet.

There are 5 studies ongoing into vagus nerve stimulation for POTS patients (at Vanderbilt University, Humanitas University, University of Oklahoma, and Children's Wisconsin)

Stiles thinks this is going to be a “really big deal” in POTS and ME/CFS research.

=== end of comments ===

 

[ahimsa]

Continuation of notes from the @s4me_info twitter thread.

This post is a copy of notes made during the July 30 session at 9:45 AM, Immunology/ Infectious Diseases 2. There were three presenters, Wakiro Sato, Gunnar Gottschalk, and Brandon Cox.

=== start of comments ===

The next presentation is by Wakiro Sato (National Institute of Neuroscience, Japan).

He starts by discussing his previous findings on skewing of B cell receptor repertoire in ME/CFS.

Sato has since extended his study to patients with Long Covid.

Much like in ME/CFS, they found increased antibody-producing B cells and increased autoantibodies (as measured with CellTrend assays) in a subgroup of patients.

The next speaker is Gunnar Gottschalk (Simmaron Research)

He found the protein ATG13 to be increased in the serum of ME/CFS patients suggesting an impairment in autophagy.

There was no difference in lysosomal proteins between patients and controls.

Gottschalk also found that serum ATG13 induced an oxidative stress response (ROS and iNOS) in microglia.

The next speaker is Brandon Cox (Ohio State University)

His research focuses on human Herpesvirus dUTPase proteins which can stimulate the production of pro-inflammatory cytokines.

In ME/CFS patients they found increased levels of antibodies against herpesvirus dUTPase.

Their main hypothesis is that these viral dUTPase are increasing the levels of Activin A and that these on their turn cause abnormal differentiation of T follicular helper cells in a subgroup of ME/CFS patients.

Activin A is a cytokine that is involved in the muscle degradation pathway therefore Cox wants to study if this is related to muscle fatigue in ME/CFS.

There is a short 15 minute break now but afterwards we will have 4 talks on the topic of Treatment.

=== end of comments ===

 

[ahimsa]

Continuation of notes from the @s4me_info twitter thread.

This post is a copy of notes made during the July 30 session at 11:00 AM on Treatment. There were four presenters, Luke Liu, Nicola Clague-Baker, Rosie Twomey, and David Kaufman.

=== start of comments ===

The first speaker is Luke Liu (Neuroversion, Alaska) who provides more information on 'Stellate Ganglion Block' as means to improve ME/CFS symptoms.

Seems similar to the presentation by Deborah Duricka yesterday.

Liu and Duricka co-authored a case series on Stellate ganglion block reducing symptoms of Long COVID: https://pubmed.ncbi.nlm.nih.gov/34922127/

Now, Liu reports similar improvements in 5 ME/CFS patients.

The second speaker is Nicola Clague-Baker (University of Liverpool). She is one of four members of Physios for ME.

They want to improve physical therapy for ME/CFS and have become more and more involved in scientific research.

They found that many ME/CFS patients pace themselves with a heart rate monitor.

The idea behind this is that, if ME/CFS patients keep their heart rate below their anaerobic threshold, it would lead to less post-exertional malaise.

Clague-Baker and colleagues set up an online survey on the experiences of ME/CFS patients with this type of heart-rate monitoring.

Patients said that the it helped them to understand their PEM triggers better.

The next speaker is Rosie Twomey (University of Calgary, Canada). She and her colleagues created the BREATHE-program a virtual self-management program for Long Covid patients.

The program includes pacing to minimize post-exertional malaise (PEM) because Twomey found that post-exertional malaise is also common in Long Covid.

A preliminary trial of the program will be published soon.

According to Twomey the BREATHE program helps patients to manage a chronic illness and to reduces social isolation. It is patient-centered and group-based.

The next presentation is by David Kaufman on his pilot study of Oxaloacetate Treatment as a treatment for ME/CFS and Long COVID.

Kaufman cautions that this was a small pilot study, not randomized and without a placebo control.

This trial is published here:
https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-022-03488-3

Kaufman was encouraged by the results so is now setting up a proper randomized controlled trial of Anhydrous Enol-Oxaloacetate (AEO) on 80 patients in collaboration with the Bateman Horne Center.

Kaufman stresses that his pilot trial could not provide strong evidence but it did not cost much money (almost all ME/CFS patients came from his clinic, long covid patients were recruited online). It helped to quickly query a new compound for a signal of efficacy.

Side note: On S4ME, forum members have provided a critical analysis of the Oxaloacetate trial, including potential financial conflicts of interest of the first author.
https://www.s4me.info/threads/oxalo...fatigue-patients-2022-cash-and-kaufman.28316/

Staci Stevens of the Workwell Foundation wins the First IACFS/ME Innovator Award for developing and applying two-day cardiopulmonary exercise testing in ME/CFS.

There is a 1 hour 15 minutes lunch break now.

=== end of comments ===

 

[ahimsa]

Continuation of notes from the @s4me_info twitter thread.

This post is a copy of notes made during the July 30 session at 1:30 PM on Public Health. There were four presenters, Cathy Kline, Gloria Gray, Erin D. Maughan, and Nancy Klimas.

=== start of comments ===

The next presentation is by Cathy Kline and Gloria Gray of the University of British Columbia, Canada.

They have developed a patient-led interprofessional workshop for medical students on poorly understood chronic diseases, such as ME/CFS and Lyme disease.

Students found the workshop useful because they could ask questions and interact with patients in a context where they weren’t directly responsible for their care.

The next presentation is by Erin Maughan (George Mason University School of Nursing) on chronic absenteeism and undiagnosed ME/CFS.

The goal was to come up with tool that could help school nurses identify medical reasons for long-term school absenteeism, in particular ME/CFS.

They did a feasibility study with 6 pilot sites in 4 states. They helped nurses to reach out to students and their family to determine the reasons for their absenteeism and ask about ME/CFS symptoms.

Among hundreds of absent students, however, they could not find students that were undiagnosed with ME/CFS.

4 were suspected of having ME/CFS but turned out to have something else when referred to a physician.

One caveat is that the corona pandemic made this pilot study rather difficult to conduct.

Many of the school nurses and medical providers had also not heard of ME/CFS.

The authors will expand the study to include up to 50 districts over a period of 3 years.

The next presentation is by Nancy Klimas (Nova Southeastern University).

She reports on a study, contracted by the CDC, that will apply the extensive testing of the Multi-Site Clinical Assessment study of ME/CFS (MCAM) to persons with a SARS-CoV-2 infection.

The presentation is mostly about recruitment difficulties of the study.

A mass email strategy, for example, did not work well.

Of 13.000 emails sent out, only 2.4% clicked to open the email and only 0.5% signed the consent form.

That's the end of our live-tweeting.

=== end of comments ===

 

[Kalliope]

Medscape Treatments Explored to Ease Post-Viral Symptoms of ME/CFS and Long COVID by Miriam Tucker

Quote:
"At the virtual annual meeting of the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (IACFS/ME), speakers presented data for a variety of approaches to ease symptoms common across post-viral conditions, such as extreme fatigue, post-exertional malaise ("crash"), cognitive dysfunction ("brain fog"), orthostatic intolerance including postural orthostatic tachycardia syndrome (POTS), and chronic pain."

Treatments mentioned in the article are:

• Pyridostigmine (Mestinon, Others)
• Oxaloacetate (benaGene)
• Inspiritol
• Stellate Ganglion Block
• Transcutaneous Auricular Vagus Nerve Stimulation

 

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Medscape Increasing Data Link ME/CFS, Long COVID, and Dysautonomia by Miriam Tucker

quotes:

At the virtual annual meeting of the International Association for Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (IACFSME), speakers presented data showing similar pathophysiologic abnormalities in people with systemic symptoms associated with ME/CFS who had a prior SARS-CoV-2 infection and those who did not, including individuals whose illness preceded the COVID-19 pandemic.

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"My way of understanding these illnesses is that they're not just multisystem illnesses, but all these interactive systems that lean on each other are dysregulated…I would say that a very common underlying mediator of both ME/CFS and long COVID is autonomic dysfunction, and it presents as POTS," Nancy Klimas, MD, director of the Institute for Neuro-Immune Medicine at Nova Southeastern University, Fort Lauderdale, Florida, told Medscape Medical News.

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Lucinda Bateman, MD, founder and director of the Bateman Horne Center, Salt Lake City, Utah, advises using all applicable codes for a given patient. "If a patient came into my office with long COVID and met criteria for ME/CFS, we would code both, and also any other syndrome criteria that they may meet, such as POTS or fibromyalgia.

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In a keynote address during the conference, Akiko Iwasaki, PhD, of Yale University, New Haven, Connecticut, pointed out that long COVID and ME/CFS are among many unexplained post-acute infection syndromes associated with a long list of viral pathogens, including Ebola, the prior SARS viruses, Epstein-Barr virus, and Dengue, as well as non-viral pathogens such as Coxiella burnetii (Q fever syndrome) and Borrelia (post-treatment Lyme diseasesyndrome).

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The long COVID patients also showed greater ventilatory inefficiency, which "is entirely related to hyperventilation, not intrinsic lung disease," Systrom said, adding that while there may be subsets of patients with interstitial lung disease after acute respiratory distress syndrome, these patients didn't have that. "This for all the world looks like ME/CFS. We think they are frighteningly similar, if not identical," Systrom said.

 

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Medscape Clinicians Can Help People With Severe ME/CFS, Even Unseen by Miriam Tucker

Quotes:
Speaking at the recent virtual meeting of the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (IACFS/ME), patient advocate Helen Baxter, of the UK charity 25% ME Group, presented a case series of five patients bedbound with ME/CFS who became severely malnourished because of delays in the placement of feeding tubes. The delays occurred because it was not recognized that the patients were unable to eat.

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Asked to comment, Lucinda Bateman, MD, founder and director of the Bateman Horne Center, Salt Lake City, Utah, told Medscape Medical News, "It's a big gap, even in the knowledgeable community. The research is totally skewed towards people who can get up and go participate in research.... I don't think most clinicians have any idea how sick people can get with ME/CFS."

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Importantly, Speight stressed, "avoid referral to psychiatrists unless specifically indicated for additional psychiatric morbidity, in which case, make clear that the psychiatrist accepts [that the] basic illness is medical."


He also advised that clinicians stop using the term "chronic fatigue syndrome" because it suggests the illness is mild and/or psychosomatic. "Maybe the US should embrace the term ME once and for all," he said.