The overviews of the 2021 IACFS/ME Conference continue with a focus on exercise studies.
- “A Huge Problem and Major Crisis”: Avindra Nath on Long COVID at the IACFS/ME 2021 Conference
- “Emerging Options for Autoimmune ME/CFS”: Scheibenbogen at the 2021 IACFS/ME Conference
The Big Test: Is Long COVID Really Like ME/CFS?
Cardiopulmonary Exercise Test Findings in Post-acute Sequelae of COVID-19
An exercise study suggests that long COVID causes similar energy production problems as ME/CFS
Donna Mancini’s presentation may have been the most consequential of the conference. If long COVID impacts one’s ability to produce energy and exercise, we have a direct tie-in to the defining feature of ME/CFS. If it doesn’t, then long COVID may, despite its many similarities to ME/CFS, be, at its heart, something very different.
Given how drastically COVID-19 can affect lung and heart functioning, it was important to determine how they were doing. The long-COVID patients’ normal chest x-rays, pulmonary and cardiac functioning indicated that nothing structural was impeding their ability to exercise. Something else was causing their exercise problems.
Her use of a 1-day vs a 2-day cardiopulmonary exercise test (CPET) handicapped her a bit, as we know that some people with ME/CFS with normal readings on a 1-day CPET can see their readings fall dramatically on the second exercise day of a 2-day CPET.
As the CPET maximal exercise test slowly ramps up over the 8-10 or so minutes of the test, it’s able to determine how much energy a person can put out, at what point they blow through their aerobic energy production capacity and enter into anaerobic function, if their heart rate is able to keep up the pace, and what’s going on with their breathing, etc.
CPET studies have shown that people with ME/CFS tend to rely on their less productive (and more symptom-producing) anaerobic energy production systems more quickly, aren’t able to produce as much energy, have trouble increasing their heart rates to the levels expected, can display hyperventilation and others. As noted above, these problems are usually much more obvious on the 2nd day of a 2-day exercise test than on the 1st day.
Despite doing only one exercise test, Dr. Mancini found evidence that people with long COVID, like people with ME/CFS, are having trouble with exercise. Peak VO2 dropped about 25%, and 50% of long-COVID patients entered into their anaerobic threshold – the point at which anaerobic energy production becomes dominant – early.
Ninety-two percent had a reduced O2 pulse and 96% had an excessive ventilatory response. That appeared to go hand in hand with the hypocapnia (low CO2 levels) found – which suggested that the long-COVID patients were having trouble removing that toxic compound.
Those long-COVID patients with more normal peak energy production levels tended to have odd patterns of ventilation; i.e. they had problems in other areas.
In short, once they were put on the bike, most of the long-COVID patients looked very much like people with ME/CFS – which, given the extraordinary amount of funding going into long COVID, is good news for the ME/CFS community. It suggests that long-COVID researchers would do well to take deep dives into energy production, and trying to understand what’s going on during exercise in their studies.
This is a field that ME/CFS researchers, in particular, have, despite much pushback, led in. Exercise stressors are often used in ME/CFS provocation studies because they’re so revealing, and that fact alone tells us much. Instead of beneficial boosts that exercise usually brings, exercise has been used time and again to reveal and uncover derangements in ME/CFS patients’ (and probably long-COVID patients) systems.
This study surely wouldn’t have happened without a large amount of work put into assessing energy production and exercise from ME/CFS researchers. It’s very good to see a long-COVID exercise study popping up so quickly. Hopefully, it’s the first of many to come.
The Natelson and Mancini study underway tests out the idea that low blood volume play a major role in the exertion problems found in ME/CFS
Interlude: Opportunity Knocks! The Natelson – Mancini ME/CFS Exercise Study Is Open
A fascinating exercise study led by longtime ME/CFS researcher Ben Natelson and long-COVID researcher Donna Mancini recently got underway. An NIH-funded 2-day exercise study – called “A Cardiovascular Analysis of Post-exertional Malaise” – aims to dig deeper into the exercise problems found in ME/CFS than has been done before.
The question they’re trying to answer is a central one: why do people with ME/CFS tend to blow through their aerobic energy production systems so quickly during exercise – leaving them trying to squeeze little bits of energy out of their anaerobic energy production system?
They believe reduced blood volume – which leads to reduced blood being pumped by the heart (stroke volume) – may have something to do with it. The deep, rapid breathing occurring in people with ME/CFS during exercise results in even greater losses of blood volume – and causes further drops in energy production during the second day.
It’s an intriguing idea given that Visser-Van Campen-Rowe found reduced blood flows to the brain in virtually every person with ME/CFS tested.
They’re going to determine blood volume levels before each exercise test and assess cardiac output, and then they’re going to replenish blood volume in a group of patients and see if their ability to exercise improves. That too is intriguing given that oral rehydration saline was recently found to be pretty darn effective at relieving orthostatic intolerance.
This several million-dollar, 120-person study is going to have severe and non-severe ME/CFS patients, and healthy controls. It’s taking place at the Icahn School of Medicine at Mount Sinai University In New York City. They have funds to help participants with travel expenses and time spent (but not airfare). To find out more, call the Pain & Fatigue Study Center research staff at 212-844-6665.
Plus……Natelson’s Rocking Bed Study Reopens
After a pandemic initiated break Natelson’s unique study to see if a rocking bed can improve sleep is back open. If you live in New York City and want to see if this unique kind of nap can improve your symptoms check out this study.
Gender Matters and Metabolomic Weirdness in ME/CFS
Progression of Post-exertional Malaise in ME/CFS Patients from a Plasma Metabolomics Perspective – Arnaud Germain, PhD
Maureen Hanson’s Big Data metabolomic study uncovered the kind of intriguing findings that only large, complex studies can.
Arnaud Germain from Maureen Hanson’s team at Cornell University presented on what is almost certainly the biggest exercise/metabolomic ME/CFS study ever done. With over 1,000 metabolites being picked up, the study produced what Gernain called an unprecedented dataset containing almost 500K data points. The 105-person two-day CPET study compared the metabolites showing up before and after each exercise bout in people with ME/CFS and healthy controls.
Since metabolomic studies assess what’s going on right now in the body, they’re a particularly good match for uncovering what happens when something like an exercise stressor is included in an ME/CFS study.
We’ll surely learn much more when the study is published, but the initial findings are intriguing. The gender difference that Nancy Klimas’s modeling study has suggested is present showed up in spades. The study suggested that exercise affects many more metabolites in women than men – about 3x’s more. Plus, as the second exercise test was done, the levels of even more metabolites were altered in the ME/CFS women.
The second exercise test in the men, on the other hand, didn’t appear to affect the levels of the men’s metabolites much. Only during the recovery period did the number of altered metabolites jump up in the ME/CFS men.
This doesn’t necessarily mean that exercise affects men less but does appear to suggest that the metabolic hit from exercise is broader in women with ME/CFS than men.
Past metabolomic research has suggested that some form of hypometabolism exists in ME/CFS and this study bore that out. Most of the metabolites that popped up in ME/CFS were found in lower concentrations. While the cause of this is unclear, it would seem to jive with the energy production problems found thus far in ME/CFS: since it takes energy to metabolize or break down substances, less energy production could – at least to this layman – very well result in lower levels of metabolites.
The Gist
- The first cardiopulmonary exercise test done in long COVID produced results much like those found in ME/CFS. That was very good news given the extraordinary funding given long COVID and the potential it provides for a REALLY deep dive into energy production in long COVID (and ME/CFS).
- The biggest exercise/metabolomic study ever done in ME/CFS found that a 2-day exercise study altered the levels of many more metabolites in women than in men, that new and different kinds of metabolites were altered during the recovery periods, that many of the metabolites that appeared to play a significant role in ME/CFS had unknown functions, that some metabolites that increased or decreased in the healthy controls did the opposite in some ME/CFS patients, and that the metabolites that popped up the ME/CFS patients were associated with energy production, metabolic processes, and the immune system.
- Benjamin Natelson’s NIH-funded New York study is seeking to determine whether low blood volume plays a major role in the exercise problems in ME/CFS. It will also attempt to repair some of the exercise problems in ME/CFS by increasing blood volume. His “rocking bed” study which seeks to determine if a rocking bed could improve sleep is now open again after a pandemic associated shutdown as well. See the blog for enrollment information.
- Two symptoms were all a Workwell study needed to differentiate ME/CFS patients from healthy controls after exercise. The two symptoms (reduced functioning/lack of positive affect or mood) demonstrated how different ME/CFS is from most diseases as exercise usually produces the opposite result. More work is needed but ultimately Workwell hopes that these two symptoms will help doctors quickly determine when they’re treating a person with ME/CFS.
- Another Workwell study did not find that ventilation (lung functioning) problems were affecting energy production. Instead, the study validated past findings of energy production issues and pointed a finger at the autonomic nervous system.
It wasn’t just that the metabolite levels were often low in the ME/CFS patients and increased in the healthy controls (HCs) – they were often altered in weird ways. Arnaud showed graphs of one unknown metabolite which increased during exercise in the healthy controls but decreased in about 30% of the ME/CFS patients. Another which decreased in the healthy controls, as one would expect, during the recovery period, actually increased in about half the ME/CFS patients. (So much for recovery).
As the participants went into the recovery period, the clusters of metabolites that popped up in the study shifted as well. The fact that many new clusters of altered metabolites showed up during the recovery phase in the ME/CFS patients suggested that both the exertion part of exercise and the all-important recovery phase were damaged – and in different ways. While the metabolite levels tended to be lower before and during the exercise period in ME/CFS patients, they were higher than normal in the recovery period.
It was encouraging to see that the kinds of metabolites that popped up in the big exercise/metabolomic study were as expected: many were involved in the regulation of metabolism, the immune system, and energy production.
This study is going to unpack much and should, one would hope, lead to even larger, more comprehensive studies that allow researchers to start teasing out which metabolites are being altered in which patients – thus providing a personalized approach to the metabolic problems found in ME/CFS.
This is the kind of big, complex study that the NIH typically funds and was part of Maureen Hanson’s NIH-funded ME/CFS Research Center grant. Hanson’s decision to use exercise stressors to dig into ME/CFS pathophysiology appears to have been a good one.
Two Symptoms to Rule Them All?
Two Symptoms Accurately Identify Post-Exertional Malaise in Myalgic Encephalomyelitis/ Chronic Fatigue – Todd Davenport, DPT, MPH – Workwell
ME/CFS breaks a lot of rules… It’s not just that physicians don’t know about ME/CFS – they don’t even know the right questions to ask. The questions they would need to ask to uncover ME/CFS’s signature symptom – PEM – didn’t come with their training.
Reduced functioning after exercise was one of the two symptoms that differentiated people with ME/CFS from healthy controls
Hence the need to develop something that our overworked doctors can easily “grok”. (Grok – to understand profoundly and intuitively.“) Something that will stick in their minds. Something like a single question that could identify if someone was in a PEM-like state after exercise. Workwell knew that symptoms tend to increase dramatically after exercise in people with ME/CFS. The big question was which symptoms were able to accurately differentiate people with ME/CFS from healthy controls.
They used open-ended symptom questionnaires to assess symptoms up to a week after two-day CPET exercise tests, and then they used binary logistic regression to identify symptoms that best identified people with ME/CFS compared to sedentary controls.
Fatigue, not surprisingly, was first; then came cognitive dysfunction and brain fog, and others. They found that even a single report of one symptom a week after exercise was enough to identify someone with ME/CFS.
What they wanted, though, was simplicity. They wanted to find a few symptoms that differentiated people with ME/CFS from people without ME/CFS. In order to pull that feat off, the symptoms had to be overwhelmingly present in ME/CFS and mostly absent from the healthy controls. That restriction would clearly knock off a really common symptom like fatigue.
The findings were simplicity themselves – and very telling. Just two symptoms – reduced functioning and the lack of positive feelings/mood – correctly classified almost 90% of people with ME/CFS and 72% of the sedentary healthy controls.
Not only did they fit ME/CFS like a glove, but they demonstrated how very different exercise experience and its aftermath is for ME/CFS compared to the vast majority of diseases. Exercise almost always leaves people more functional and feeling better, but it did neither in ME/CFS and actually left them less functional. This finding should produce quite a “tell” for doctors used to prescribing exercise for their anxiety/depressed patients. If exercise has the opposite effect, they have an ME/CFS patient before them – not someone who’s depressed.
The next steps are validating the findings in a larger study; integrate step counts, assess ability to do activities of daily living, and integrate CPET findings.
Do the Lungs Have It?
Todd Davenport: Ventilatory Functioning During Serial Cardiopulmonary Exercise Testing in People With and Without Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
We know a bunch of things go wrong during exercise in ME/CFS. The anaerobic energy production system kicks in too early, lactic acid builds up, reduced glycolysis, problems, and problems with redox. We’re seeing evidence of impaired energy production at both the systemic and cellular levels, but we don’t know much about a crucial part of the energy production system – lung functioning.
Ventilation did not appear to be a problem in ME/CFS. Instead, Davenport pointed to the autonomic nervous system. (Image from Wikimedia Commons).
The lungs don’t just deliver oxygen to the tissues; they also play a crucial role in getting rid of the CO2 gases produced during exercise. CO2 certainly has its place in a well-functioning body, but if you can’t get rid of it when its levels are too high, then the body acidifies.
In this study, Davenport and the Workwell Foundation used their two-day maximal CPET test to assess both the energy production and ventilatory function on 75 ME/CFS patients and sedentary healthy controls.
The study validated once again the abnormal (and thus far) unique energy production findings in ME/CFS. Particularly during the second exercise test, VO2, workload, heart rate, respiratory rate, and amount of air moved were blunted enough compared to the healthy controls to be functionally disabling.
The one abnormal pulmonary finding – hypoventilation – could, by its inability to “breathe off” CO2 – exacerbate acidosis. Measures of lung functioning (tidal volume, end-tidal oxygen, end-tidal CO2), on the other hand, were normal. After finding no problems in lung functioning that could be causing problems with oxygen delivery, Davenport turned to a common theme. He proposed that a dysfunctional autonomic nervous system (ANS) that is simply not up to the demands that exercise places on it was the cause.
More overviews from the IACFS/ME 2021 Conference
- “A Huge Problem and Major Crisis”: Avindra Nath on Long COVID at the IACFS/ME 2021 Conference
- “Emerging Options for Autoimmune ME/CFS”: Scheibenbogen at the 2021 IACFS/ME Conference
No vaccine side effects – just a sore
Arm for a day
Thank you as always, Cort, for a fascinating summary that’s easy to understand.
I have been meaning to write a comment about the oral rehydration solution you referred to. We tried making it up for our son who has ME/CFS. Shortly thereafter he developed slow gastric emptying & started needing to bring up indigested food before being able to sleep at night. This has continued for a year & is ongoing. We think it MIGHT have been triggered by the glucose in the rehydration solution. He now has a marked intolerance for any of the sugars.
That is interesting Di. I tried to help my POTS symptoms with a homemade rehydration drink (just water with added sea salt and sugar, and later just with salt) but it made my gastric emptying and gasteroparesis much worse. I believe that because my slow digestion is caused by autonomic dysfunction, a large volume of water is only making the problem worse. Constant drinking also dilutes the stomach acid and enzymes, which impairs digestion even further. My digestion works much better when I don’t drink very much at all! And when my digestion works better, I also feel a bit better overal. But I’m struggling to eat enough and I am massively underweight. I am now finally going to take the jump and try Huperzine. Huperzine is said to increase acetylcholine by blocking the enzyme that breaks it down, and this should improve gastric function. I’ve been afraid to try it, because I usually don’t do well with supplements. I hope you find a solution for your son.
I wonder how many gut problems in ME/CFS are due to autonomic nervous system issues. They can, as you note, impair gut motility which, I was surprised to learn, can then result in bad gut flora. Apparently, simply having the food sit longer than usual in the gut creates an environment in which certain kinds of bacteria exist. On the other hand, I read somewhere that replenishing the gut flora can help with gut motility problems as well – so it’s not clear what is causing what.
Morning Di. May I suggest you look up Rumination Syndrome? I have had it since I was a teenager-and it sounds like your son has the same issue . It is to do with gastric volume and oesophageal tone and learning to breathe with my diaphragm more has made a huge difference to my symptoms. I am now 52 and have developed CFS in the past 3 years. Taking saltwater has been the single thing that truly helps me. You may just need to play about with the volume or timing of the fluids so your son’s rumination is less provoked. I suspect it isn’t the sugar as I don’t add sugar but I only take the saltwater after meals- sugar is needed to help with the absorption of the salt but the sugar can come from food. Sugar is added to help absorption for those who cannot eat e.g. someone with vomiting and diarrhoea. Saltwater without sugar or food is not well absorbed and can trigger a laxative effect… I hope this helps
Darn Sorry to hear that. The Trioral salts have been one of the few things that have actually worked for me but the body is a mysterious and complex thing and we are a heterogeneous bunch. I hope you can find a way around this.
Late to this conversation, but along with my Fibromyalgia and Chronic Fatigue, I have terrible esophageal motility. A bit like acid reflux, but more that pills and even water often does not go down at all. But I have large muscle cramping problems too (electrolyte imbalance). SO, I bite off a little piece of a “nuun” electrolyte tablet (not the vitamin ones), and put it on, or under, my tongue with a tiny sip of water. It burns a bit, but I have grown accustomed to that and it resolves ALL of these issues much better than trying to put it in water (that may not go down) …then have a fizzy, burning substance caught part way down my throat. If it gets too strong I can just spit it out, lol!
I’ve done about 6 CPET’s throughout the last 20yrs. A few were mandatory (insurance & ‘Cfs’ clinic), 1 was bc of oesophageal spasms (ruling out a heart attack which resembles the symptoms), and one was by choice: a double CPET done by a cardiologist.
The strangest thing? My Vo2max remains the same. 20yrs and it stays the same. 5,1Mets.
The CPETx2 mainly lowered my AT at day 2. Reached AT at 50Watts day 2. And max HR dropped further.
The cardiologist concluded (knowing nothing about ME): “severe nervous system dysfunction”.
Based on CPET data plus very low HRV (always), “conduction problems”, “right bundle tack block”, and sth with my heart waves always pops up (“flattened waves”).
As for exerting oneself & after?
I don’t know if I’m the only one but there’s a difference between physical & social exertion.
If it’s sth purely physical I’m flattened out right away. Practically in a crash state all the time tbh.
Getting up, going downstairs, sitting and reading a bit online … back to bed.
If it’s a rare ‘social occasion’ where I interact w/ people? However short? Could be seeing a friend but also having to go to the doctors’.
I stay in a wired (adrenaline?) state for a while afterwards.
I’m bubbly by nature and can’t help myself from engaging in conversations or laughing.
I know health wise I should stay quiet.
I also know I’m “driving on adrenaline rather than energy” when “outside my cage”.
But I’m human and nice occasions have become oh so rare. So I try to enjoy as much as I can. Build a few precious memories to hold on too later on.
When the adrenaline goes away?
That’s when symptoms flare with a vengeance.
Mood? Yes. It lowers.
As soon as the adrenaline that kept me upright & interacting drops, symptoms flare, so my mood drops below zero of course.
How to be cheerful when feeling very very ill and being yet again bed or coach bound, with pain going through the rooftops?
Punished so harshly again for “daring to taste” a few hours from “normal life”.
How to be cheerful when 10 times a few hours outside the house in one year means 355 days of being able to do next to nothing? Not even wash yourself.
Plus i feel like it’s something physical too these mood changes after exertion.
Perhaps cytokines going up & other metabolites? immune system kicking in?
Ps: I notice the difference w/ my brother in law. He’s an IT guy. So he has a sedentary job and isn’t sportive at all.
His job is mentally very very straining.
He recently ended up having a burn-out. Never been ill in 58yrs, but his job caught up with him.
He followed doctor’s advice and recently started to cycle every day.
1 hour a day. And yes, he says it feels good. He can clear his head and his body doesn’t react badly at all. On the contrary.
So here’s me. Before getting ill I was physically pretty active. Liked sports, going for long walks in the weekends, didn’t get my driver’s licence until age 28. Everything on foot or by bike.
And there is him: never been active, never did sports, never took long walks, cycled, …
I react disproportionately bad to a minor exertion (can’t even handle an electric bike … tried 2 … had to sell them both) and he reacts very good to 1 hour normal cycling a day.
Physically and mentally.
While never ever having been active in his life.
Could it get any clearer?
Elise,
This is sure a disease that makes no sense.
I soo get the wired tired too, and the bad thing is when I have to use Adrenalin in a conversation, just to have a conversation, it makes me more reactive and louder than I am normally.
If wishes were horses, I would be sending you a whole herd of beautiful horses.
sunie
I get so excited when I read of the findings in the studies
That enthusiasm
just dives of a cliff
when I read the hypothesis
as to why X is happening…
The ANS system 🤦 🤦 🤦
To that end,
I wish to revive Dr Chenney’s heart studies
So that we can all understand that this is a problem of an energy production deficiency at the level of the cell. The heart can’t function like it should.
https://paradigmchange.me/wp/cheney/
Correct the energy production problem, and then the ANS should fall in place.
[ hint, thyroid is involved. So is glucose and the liver. Chenney mentions how he saw liver function impairment in the presentation ]
.
.
Oooh, imagine if more layers were added to these exercise studies – if they looked at glucose, catecholamines, free fatty acids, and brain function (EEG). I think Hansen’s team does measure lipids.
I was reading research into how attuned certain brain cells are to the levels of glucose in the body, and how they may be participating in glucose homeostasis. So that when there is hypoglycemia, the brain is perhaps activating all these responses.
As I remember Cheney believed the diastolic dysfunction he found was due to energy problems in the heart muscle. If I ‘m reading this correctly Systrom found reduced preload which resulted in the heart not getting enough blood – which could be responsible for what Cheney found.
Nobody has found evidence of damage to the heart which should over time lead to heart failure, an enlarged heart, etc. That just doesn’t happen in ME/CFS. I know Cheney had an explanation for why people with ME/CFS have heart failure but don’t have heart failure but for me, at least, too many strange things had to happen for that to be likely.
While energy production may be at the heart of ME/CFS I don’t know that Cheney’s explanation holds up. Natelson’s study may help, though, as it’s assessing stroke volume albeit from a different angle.
Hi Meirav,
Your comment about energy was interesting. I also agree about the Liver.
I am an integrated practitioner of Chinese Medicine with a specialist interest in CFS/ME/FMS after recovering myself 7 years ago. From my experience thus far, the Liver, Spleen, Kidneys and Heart are the organs most implicated but the Liver ALWAYS needs treatment.
My end of degree research paper was about the incidence of stress, shock or trauma preceding the onset of the physical symptoms and this is huge. From a CM perspective this effects the Heart/Kidney connection which is really important but I also see how the Heart, which is so much more than just a pump has been affected.
It frustrates me how western medicine focuses on just one thing and gets obsessed with it. I am having great results with my patients…albeit early days as I am newly graduated but I see widespread organ involvement producing the wide range of symptoms and in addition lingering pathogenic factors in the Chinese equivalent of the immune system.
Nicola, Do you blog about CFS/ME from a Chinese medicine approach? If you have a website or blog, would you mind sharing it here? It would also be nice if Cort could interview you and post that on this blog or his website.
I remember a story of someone presenting the results of his double exercise test to a sports doctor. without talking about ME/CFS. He didn’t understand and said that the equipment must have been broken. Which was not the case. Such a low vo2, AT, and oxygen pulse is bizarre. These findings are still inexplicable. As far as the heart is concerned, there are indications that ME patients die on average 20 years earlier from heart failure – and also cancer – suicide also scores high. The left ventricle is often hardened.
The ANS
Just look at this Review by Adam J O’Neal ,Maureen R Hanson
The Enterovirus Therory of Disease in ME/CFS A Critical Review
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8253308/
The intro covers much about ME/CFS
The section
Enterovirus Cell and Tissue Tropism covers the CNS ANS and effects
Each enterovirus has a distinct cell and tissue tropism that is governed by both host and viral factors…….
including cellular virus receptor availability, tissue-specific activity of IRES on viral RNAs, and innate immune antiviral activities such as interferon (IFN) response. Given these conditions, EVs as a whole display a wide spectrum of cell and tissue tropism leading to a wide array of disease outcomes. The diseases may appear as short-duration sicknesses such as the common cold and acute hemorrhagic conjunctivitis or may cause more serious diseases through infiltration into secondary infection sites such as organs, muscle or central nervous system (CNS), causing myocarditis, pericarditis, encephalitis, meningitis, pancreatitis, paralysis, and death (75).
CNS regulation of autonomic nervous system output occurs through multi-synaptic connections descending from the hypothalamus and midbrain to preganglionic neurons in the brainstem and spinal cord. The central autonomic system is further comprised of connections between a multitude of limbic system structures, such as the amygdala and hippocampus, to collectively regulate autonomic nervous system (ANS) outflow (76). The ANS is subdivided into the sympathetic, parasympathetic and enteric nervous systems, which act to control internal body processes such as blood pressure, heart and breathing rates, body temperature, digestion, metabolism, fluid retention, production of bodily fluids, urination, defecation, and sexual response (77).
ME/CFS patients have a number of pathophysiological traits that point to abnormalities in the ANS, including impaired blood pressure variability, orthostatic intolerance, high prevalence and severity of posturalorthostatic tachycardia syndrome (POTS), delayed gastric emptying, impaired thermoregulation in adolescent patients, loss of capacity to recover from acidosis on repeat exercise, abnormal cardiac output and altered brain characteristics in a wide variety of brain regions including the limbic system structures that govern the ANS (1, 78–81). These altered brain characteristics include reduced cerebral, brainstem, and cerebral cortex blood flow; impaired reciprocal connectivity between the vasomotor center, midbrain, and hypothalamus regions; increased neuroinflammation across widely distributed brain areas including but not limited to the hippocampus, thalamus, midbrain and pons; reduced cerebral glucose metabolism, and lower brain glutathione (1, 82–86). Many of the altered brain characteristics seen in ME/CFS patients are similarly reported in clinical cases associated with neurotropic enteroviruses. For instance, focal enterovirus encephalitis caused by coxsackievirus A3 is associated with focal hypoperfusion in the right frontal lobe that cleared upon patient recovery from the neurotropic enteroviral infection. This example case is largely similar to multiple SPECT studies indicating ME/CFS patients have significant hypo-perfusion in regions of the brain consistent with their patient-specific symptoms (87–92).
Sound like our symptoms/problems?
Just read a report that Francis Collins will be stepping down as the director of the NIH. In the article there are several paragraphs about criticisms of his (lack of) dealings with ME/CFS. One of his comments is telling, calling it a ‘blurry diagnosis’ and I will paraphrase here, that ME/CFS could actually be accounted for, say something like depression.
https://www.medpagetoday.com/publichealthpolicy/washington-watch/94861?xid=nl_covidupdate_2021-10-06&eun=g1240599d0r&utm_source=Sailthru&utm_medium=email&utm_campaign=DailyUpdate_100621&utm_term=NL_Gen_Int_Daily_News_Update_active
I think this shows how he really has been thinking about us… Do hope the new director thinks differently!
how can we support the direction of a new NIH director?
These terms:
PEM
exercise intolerance
exertion fatigue
How are they different?
– Are they?
The last two, are mentioned in relation to quite a number of different diseases/conditions/syndromes.
(hypothyroidism, mitochondrial myopathies, aphasia, stroke, etc etc)
I wonder if they did that two-day Cpet in those other diseases/conditions/syndromes
– would the findings be similar?
would there be differences?
How did you all find Dr. to believe you and treat you? I’ve been years with issues and I believe I’ve developed white coat PTSD from the treatment I’ve received from the medical community. I’d like to find ANYONE who can help me. I’m in the US on the northern west coast.
Help is coming- stay tuned.