Despite the current lack of consensus as to the underlying biological basis of CFS, there is considerable evidence … to highlight an abnormality of the autonomic nervous system as a unifying pathological factor. Newton et. al. 2013
A fascinating case of research confluence took place a couple of years ago which suggested that hyperadrenergic POTS and chronic fatigue syndrome (ME/CFS) patients may not be as far apart as they seem.
The two diseases share similar symptoms and some findings. Problems with blood pooling and/or the brain have sent norepinephrine levels soaring in hyperadrenergic POTS patients. Norepinephrine levels have not been well studied in ME/CFS but one larger study found increased levels.
POTS, however, is not present in all or probably most ME/CFS patients. Grubb warned about placing too much importance on POTS criteria, but a large Australian study (n=306) nevertheless found POTS present in just 11% of ME/CFS patients. Those POTS-positive ME/CFS patients, interestingly, tended to be younger than the non-POTS patients. Newton’s large (n=179) U.K. study produced similar findings. POTS was present in about the same percentage of patients (13%), who tended to be younger than non-POTS patients.
The overlap between POTS and ME/CFS appears to be much greater than the overlap between ME/CFS and POTS; that is, far more people with POTS appear to meet the criteria for ME/CFS than vice versa. (Compare the 64% of POTS patients which met the criteria for ME/CFS with the 10-15% of ME/CFS patients who met the criteria for POTS in Biaggioni’s 2012 study.)
That discrepancy makes sense given the more rigorous biological criteria for POTS and less rigorous, symptom-based criteria for chronic fatigue syndrome. POTS may be a syndrome – a biological state which can be caused in a variety of ways – but ME/CFS is still something of a waste-basket disease. God knows how many subsets are present in it.
Upon being tilted up, the POTS patients had an immediate thirty percent reduction in cerebral blood flow. Struggling to make up the deficiency, their hearts exploded into action – almost doubling from a normal 78 bpm to 130 bpm. That compensation appeared to have at least partially worked as their cardiac output (pumped blood volume) remained stable.
Yet thirty percent less blood was reaching their brains. As noted above, at the same time their hearts were pounding away, chemoreceptors – picking up signs of reduced blood pressure – triggered their breathing pattern to change resulting in hyperventilation. (Some studies suggest the chemoreceptors in POTS may not be operating properly). The hyperventilation sent their CO2 levels lower, which in turn caused the blood vessels in their brains to constrict, possibly reducing blood flows – and oxygen delivery (whoops!) – to the brain.
A condition called ischemic or “stagnant” hypoxia resulted. Stagnant hypoxia occurs when the blood oxygen content is normal but the blood is flowing too slowly to deliver normal amounts of oxygen. (That condition sounds tailor made for ME/CFS patients, who typically have normal blood oxygen levels but appear to utilize that oxygen properly).
Remarkably, the researchers were able to resolve these hyperadrenergic POTS patients’ mounting problems in the simplest way possible – by giving them CO2. CO2 normalized the blood flow to their brain and stopped their tachycardia (rapid heart beats).
One group of POTS patients called “cerebral blood flow driven POTS” takes a slightly different pathway, but ends up in the same place. This group, which experiences shortness of breath when they stand, is characterized by large initial drops in cerebral blood flows when they stand up. The immediate large drop in blood flows to the brain causes stagnant hypoxia to occur, which activates the chemoreflex, which produces hyperventilation, which results in reduced CO2 levels, sympathetic nervous system activation and rapid heart beats (tachycardia).
A Chronic Fatigue Syndrome (ME/CFS) Connection?
“Although conventionally CFS has been considered to be a disease with primary CNS pathologies and secondary peripheral consequences, our results point to possible alternative disease mechanisms. It is possible that CFS is driven by a primary peripheral abnormality … where a compromised skeletal muscle cellular membrane function underpins the observed abnormalities. “ He et al. 2013
Those results were eerily similar to Dr. Newton’s 2013 findings in a small group of ME/CFS patients. Newton used the Valsalva maneuver instead of the tilt table test to stress her patients, but also found reduced cerebral blood flows she believed were likely associated with hyperventilation and reduced CO2 levels. To make matters worse, dropping blood pH levels triggered the “Bohr effect”, which reduced CO2 levels further.
The kicker was that Newton was able to link the constricted brain blood flows – not to a primary brain problem or blood pooling – but to increased acidity in the blood (decreased blood pH) caused by energy production problems in the muscles.
Vermeulen also concluded that the reduced aerobic metabolism he found was probably caused by problems with oxygen delivery and its result – stagnant hypoxia. Natelson similarly concluded that low blood flows were responsible for the twenty percent drop in aerobic capacity he found in people with ME/CFS.
Both suggest that energy production problems in ME/CFS are more likely caused by delivery issues; e.g. blood vessel problems, than due to problems with producing energy at the cellular level.
The same may be true in fibromyalgia, where studies suggest that hypoxia – produced by low blood flows – is causing pain and fatigue and even allodynia.
Are Oxygen Starved Tissues Causing Pain and Fatigue in Fibromyalgia and Chronic Fatigue Syndrome (ME/CFS)?
When Touch Hurts and Blood Matters: Getting at the Pain in Fibromyalgia and Chronic Fatigue Sydnrome (ME/CFS)
Different Paths – Similar Results?
Newton’s study suggested that ME/CFS and hyperadrenergic POTS patients may take different paths which end up in the same end result – constricted blood vessels which reduce blood flows to the brain. In hyperadrenergic POTS, blood pooling problems in the lower body are a main cause, while in ME/CFS, problems with energy production and reduced blood flows to the muscles may be. Both result in hyperventilation, reduced CO2 levels and reduced blood delivery to the brain. (Reduced blood flows to the brain have been documented in both conditions.)
Damage to the nerves lining the blood vessels in the lower body plays a major role in POTS. Newton’s study and others suggest problems with the small blood vessels may be impeding oxygen delivery to the muscles in ME/CFS.
Unfortunately, we don’t know much about energy production in POTS. It’s possible similar energy production problems exist in POTS – just not to the same extent.
It’s tempting to think of POTS as ‘ME/CFS-plus-orthostatic intolerance’ except for the more severe exercise issues in ME/CFS. Moderate exercise, in general, appears to be much better tolerated in POTS and fibromyalgia. Given what we know about the history of these diseases, that makes sense.
It was ME/CFS experts, after all, not POTS or fibromyalgia specialists, who coined the term post-exertional malaise (PEM) decades ago. PEM is considered to be the core symptom in ME/CFS, while dizziness/fainting and widespread pain are core symptoms for POTS and fibromyalgia. Very carefully fine-tuned, heart rate-based “exercise” programs have been produced for ME/CFS but not, to my knowledge, for POTS or FM. Energy production has become a major research topic in ME/CFS, but not yet in these other diseases.
Exercise appears to be a more dicey proposition in ME/CFS, possibly because energy production problems in the periphery (the muscles) are a more fundamental issue. Severe fatigue, however, is very common in POTS and FM as well; post-exertional malaise is present in all three diseases, and few, if any, patients are running marathons. Energy production problems may be more severe in ME/CFS while problems with cardiovascular control (racing heart upon standing) play a more significant role in POTS.
All these diseases, though, probably share autonomic nervous system problems, issues with orthostatic intolerance, reduced blood volume, autoimmunity issues, and probably problems with energy production. Large studies which probe these diseases in tandem in an attempt to find core abnormalities and differentiating factors would be fascinating, and might end up creating a new set of disease entities.
Boston pulmonologist David Systrom and neurologist Anne Oaklander may be able to provide some answers to these complex questions. Systrom has invasive exercise data on a large set of ME/CFS, POTS and FM patients. Anne Oaklander uncovered the small nerve fiber problems in FM. Both believe autoimmune processes which affect the autonomic nerves across the body probably play a large role in these diseases. I don’t know if Systrom and Oaklander are working with dysautonomia specialists, but combining Systrom’s CPET data with Oaklander’s small fiber data and tilt table data could begin teasing out who has what.
This kind of analysis is underway, on a smaller scale, in ME/CFS in the NIH’s intramural study which is combining exercise, tilt table tests, energy production testing, small nerve fiber testing and much more. A blog on that study is coming up.
Articles From the 2018 Dysautonomia Conference
- 2018 Dysautonomia International Conference I: Small Fiber Neuropathy, POTS, MCAS and Vagus Nerve Stimulation
- The 2018 Dysautonomia Conference Pt. II: Could You Have a Spinal Fluid Leak? An ME/CFS, POTS, FM Perspective
- Dysautonomia International Conference Pt III: The Autoimmunity Revolution in POTS
- “Sticky Blood” – Antiphospholipid Syndrome, POTS, Chronic Fatigue Syndrome and Fibromyalgia – The Dysautonomia Conference #4
Might be interesting for those suffering from low CO2 and associated symptoms to check out “The Oxygen Advantage ” breathing techniques (or similar)? If I remember right, these techniques seemingly and paradoxically increase Co2 in the blood, which causes the body to be able to use oxygen more efficiently, and increases oxygenation of working muscles and organs, including the heart and brain- leading to increased energy and improved aerobic performance, among other reported benefits. It’s very possible my limited knowledge of physiology is in play here(!), but there may be some connection and/or some benefit? (I’ve been using the exercises just a little bit over time, and have seen an increase in my energy level and improvement in my heart’s response to a little bit of aerobic demand.) (These exercises seem related to some basic pranayama techniques, but I don’t know enough about either to fully compare the effects.)
Ha! That makes me think of Wim Hof’s breathing techniques which are supposed to assist autonomic nervous system functioning.
Check out Health Rising’s Breathing Techniques Resource Page for ME/CFS and Fibromyalgia.
Also refer to Buteyko breathing techniques
What a fascinating article. I have ME/CFS,FM and POTS.I was also diagnosed with Ehlers Danlos Syndrome this past year. My doctor believes as much as 85% of POTS sufferers have EDS as the underlying cause.
Additionally, I’ve also been on supplemental oxygen for the past 7 years due to hypoxia. We know the hypoxia is happening but can’t prove why exactly. It is not something my EDS specialist has seen before. Genetically my mutation doesn’t fall into a known EDS subtype. It’s believed to be either a gene not yet linked to the myopathic subtype or possibly a new subtype altogether.
We’ve been trying to look at how the ME/CFS and EDS impact each other. The next time I’m due for a stress test, the plan is to do it on 2 consecutive days to try and collect data on the severe post exertional malaise I exhibit as well as to try to figure out how it might be linked to the EDS and hypoxia.
I would love to see Systrom and Oaklander combine
their data with the extensive autonomic, small fiber neuropathy, and exercise data my EDS specialist has collected on his patients.
One note, there are heart rate guided exercise programs in existence for POTS. In fact, it’s one of the main treatments recommended by all the POTS specialists I’ve seen over the years.
Thank you for all you do on keeping us up to date on the latest research!
Dr. Rodney Grahame has said as much as 95% of so-called ME/CFS Lyme/Fibro patients have undiagnosed Ehlers Danlos Syndrome & the other 5% have other connective tissue disorders…I have always questioned
the silly term ME/CFS or even Fibro these are all the same illness with rather stupid label Names…Research seriously needs to get their Acts together it is killing patients across the globe. Another thing now
arising is how many now have undiagnosed ALOHA GAL MEAT ALLERGIES I have seen it now in all of the conditions above & it could also be causal in the majority. Dr. Grahame also said that he no doubts he felt
Michael Jackson had undiagnosed EDS 3 Hypermobility & had he been properly diagnosed he would be Alive today & not have died from an overdose…He was also reported to be dealing with some quack Woman
giving him all kinds of herbal remedies for so-called Lyme & pain he was suffering 24/7 & nothing was helping him either, look around at all the celebrities Sick now all told Mold Lyme Fibro etc all B.S. Label
illness is sickening…If this is ALPHA GAL it explains why all react so badly to foods medicines vitamins additives etc even environmental issues…I also think Mold is a croquet stupid diagnosis
total madness…Let’s give all these patients Mammalian content medicines these total Quack Doctors…
‘typo’ above ‘ALPHA GAL MEAT ALLERGY’
With having EDS, one cause of hypoxia can be visceroptosis where lax ligaments allow the abdominal organs to compress either the celiac artery or left renal vein (Median Arcuate Ligament Syndorme or Nutcracker Syndrome).
Autonomic dysfunction that occurs as a consequence of these abdominal vascular compression disorders results in a fairly significant number of patients having POTS (about 20%) and I know of several cases who were first diagnosed with ME/CFS before these vascular issues were found.
Hypoxia is generally more of a bowel related thing (chronic mesenteric ischemia) but many do complain of chest pain and breathing difficulties although I don’t know of anyone requiring oxygen supplementation.
ME/CFS is just another name for EDS & those nutcracker & MALS conditions do not improve the majority of patients…I have seen one patient with MALS Surgery her IGE Total blood panel
is over 700+ Normal is under a 100 & to me, it looks like she has Alpha Gal all along…Obvious if someone continues to take Doctor infester mammal products buys every vitamin on
the internet or eats these foods from mammal products they will never get well…Patients mention HERX it likely is ALLERGIC responses to these products
Hi! I am also on supplemental oxygen. I’m 28 with severe POTS and dysautonomia. I use an electric wheelchair pretty much full time. I also get infusions and have a port. It hasn’t done much for my symptoms. I am believed to have EDS as well and more than one genetic condition since I have a lot of problems (prolactinoma, unspecified brain lesion similar to demyelination, low cortisol but oddly not related to adrenal insufficiency at all- they said could be congenital). I recently did genetic testing at Georgetown with a geneticist. I won’t have results for 4 months. My doctors have also said they’ve never seen this happen (the hypoxia) or such a severe case of dysautonomia like this. I don’t use supplemental oxygen full time, but I use it numerous times a week as needed. I have a portable oxygen machine and a home oxygen machine.
Good luck Syanne!
Have you checked out craniocervical instability?
I have the same symptoms and diagnosis, on oxygen for only a year though. Do you have any neck issues?
I hope this reaches you…it’s been a year since you wrote this. I too have EDS, POTS, MCAS along with supplemental O2. I also have Vascular Eagle syndrome and 3 CSF leaks. I’ve been on the oxygen now for 18 months and they cannot determine what is happening. I’ve not come across anyone with the same problem until now. Are you still on O2?
Can you please tell me what kind of oxygen machine you are using and on what specific level and setting? Also how much it has improved your oxygen saturation levels? This is very important to me i am going through very similar experience.
Reach for a paper bag to breath into for a while when have rapid heart rate? Will try – I don’t like that feeling of not being able to slow the HR down by resting and meditating, but those things won’t help if what I need is CO2. Thanks!
I would give it a try. It would be particularly interesting to try it which standing and during “exercise” and see if anything happens. However I hasten to point out how complicated these things are and how impacting one thing may not impact others that need to be resolved. Good luck, though. I will try the same thing.
I was wondering if extra magnesium might help? It relaxes blood vessels.
Of course, it would need to be taken with calcium (esp. if you don’t regularly eat 3 servings/day dairy due to lactose intolerance or the desire to reduce mucus and inflammation), Vit D3, and Vit K2 so as to not create a mineral imbalance.
One side effect is reversing osteoarthritis, cataracts, and any other calcium deposits in soft tissues. Too much Magnesium can result in loose stools; just back off a little if that happens.
Extra magnesium is also part of the late virologist Dr. Martin Lerner’s supplement protocol for CFS (so as to support ATP production).
‘CALM’ powder in your water bottle is an easy way to add magnesium (and they have one with calcium, too).
Another is ‘Dr’s Best Bone Maker Complex’ from Amazon.
Try either (or both?) for a month and see if it helps!
“…found reduced cerebral blood flows she believed were likely associated with hyperventilation and reduced CO2 levels. To make matters worse, dropping blood pH levels triggered the “Bohr effect”, which reduced CO2 levels further.
The kicker was that Newton was able to link the constricted brain blood flows – not to a primary brain problem or blood pooling – but to increased acidity in the blood (decreased blood pH) caused by energy production problems in the muscles.”
I found it a bit confusing to me. Normally increased acidity leads to vasodilation IMO. The last paragraph lead me to believe increased blood acidity leads to vasoconstriction which is not true IMO.
I believe that (after diagonally reading the paper):
…found reduced cerebral blood flows she believed were likely associated with hyperventilation and reduced CO2 levels trough following mechanism:
* increased blood acidity from muscle problems makes blood acidity get problematically
* this provokes a hyperventilation reflex
* hyperventilation is helpful for reducing too high blood acidity as it expels CO2 out of the blood and thus lowers blood CO2 concentrations
* lower blood CO2 concentrations lead to lower H2CO3 content in blood, and H2C03 is carbonic acid. Lowering carbonic acid in blood makes it less acidic
* downside to having low CO2 content in blood is that A) CO2 is a vasodilator; having less of it will constrict blood vessels B) O2 release is dependent on CO2 levels through the Bohr effect; too low blood CO2 does decrease oxygen release (rate) at tissue; this makes less of the carried oxygen available for aerobic energy production
=> thus increased blood acidity from muscle problems is proposed to cause indirectly reduced cerebral blood
And: thanks Cort for all the great work you do, you’re ME hero ;-).
Thanks. This is one of the most complicated subjects in ME/CFS/POTS to me. 🙂
You are wright that “dropping blood pH levels… …reduced CO2 levels further.”
Higher blood acidity means the blood has slightly reduced C02 carrying capacity. This is not commonly referred to as the Bohr effect IMO.
The main confusion I had was “to link the constricted brain blood flows… …to increased acidity in the blood (decreased blood pH) caused by energy production problems in the muscles.”
It suggest that increased blood acidity leads to constricted blood vessels. The opposite is true. If for example very locally I build up lactic acid in my index finger, the acid will trigger local blood vessels to dilate. If however global acidity is high it may trigger hyperventilation reducing global blood CO2 levels. Lower blood CO2 levels constrict blood vessels.
Too further complicate matters, it’s well possible that, at equal blood pH, increased (lactic) acid levels with lower CO2 levels (due to pH stabilizing hyperventilation) could yield net vasodilation as both acids have dilating properties. It’ll depend on relative dilation strength (data is not easy to find quick).
At least for the Bohr effect https://en.wikipedia.org/wiki/Bohr_effect: “If muscle cells aren’t receiving enough oxygen for cellular respiration, they resort to lactic acid fermentation, which releases lactic acid as a byproduct. This increases the acidity of the blood far more than CO2 alone, which reflects the cells’ even greater need for oxygen. In fact, under anaerobic conditions, muscles generate lactic acid so quickly that pH of the blood passing through the muscles will drop to around 7.2, which causes haemoglobin to begin releasing roughly 10% more oxygen.”
Roughly translated: if lactic acid buildup is the driving factor, it has good chances to increase O2 delivery to tissues (Bohr effect) more then CO2 loss through hyperventilation would reduce it.
If however blood pH could not be stabilized by lack of hyperventilating for example then biochemistry could be impeded. Even if the net Bohr effect could increase oxygen release, the cells would be unable to make good use of it. Complicated indeed ;-).
I was communicating with a Woman last night online I asked her if anyone did the IGE Total blood Panel on her she said yes my immunologist ran that test but could not understand
why it was so high a Normal is 100 or under she said hers was 700+ extremely high I then asked her to test for the Alpha-Gal blood Panel telling her about the Meat Allergy she is now
getting back in touch with this Doctor to ask him to run the blood test now. Shortness of breath & drops in blood pressure tachycardia are all hallmarks of ALPHA GAL & delayed
reactions…It is even in sugar & added to countless products. Most are Allergic/Intolerant to all Dairy. She also has MALS surgery with no success she even shows high antibody
to the SPS GAD-65 at 250 but some do not show this antibody at all…
I read your comment below my comment but there wasn’t a reply button for some reason. So there was an incidental finding during a scan at the dentist (checking my TMJ) where she told me that my head is not sitting fully straight on my body. She said it is slightly crooked. Her daughter has EDS as well so she knew what it looked like. It is ever so slight. The strange thing is that extreme emotions will make my oxygen levels drop into the 80s and 70s. Whenever I get my period (I also have severe endometriosis) I get the worst of my oxygen issues. One time I was almost hospitalized because my levels wouldn’t even go up while I was in the ER with oxygen. After a few hours it did and they couldn’t explain it. And I happened to be on my period during that time as well. Other things that trigger it are the heat and very cold weather. Activity that lasts more than 3-4 minutes, even when seated. My Hopkins doctors have no explanation for it. I want to help them find a theory.
Here’s a link with some of us POTS people exploring this about CO2. https://www.dinet.org/forums/topic/18979-standing-co2-clue-to-why-we-get-lightheaded/
I figured out that I was having a build up of CO2 when I snorkel and was rebreathing from my snorkel tube, CO2. With the pressure of the water on my body and being in salt water – end result was POTS and uncontrollable hyperventilating that made me even sicker. I think I was trying to expel the CO2 and increase O2, is my guess. But breathing in a bag made everything worse. I feel I do better to dilate (to a certain level) rather than constrict. Many of us POTS people hold our breath, especially with exertion.
I was thinking about your snorkel story when I wrote this first post. I wanted to make it clearer that, if the body started hyperventilating because of too high blood acidity, reducing hyperventilation by breathing in extra CO2 could be betting against ones own body.
Even if it worked in the short run, I’d look out for any long term effects. The body seems to do sometimes things that makes us feel bad in the short run (having racing hart and weakness upon standing for example) in order to get less problems in the long run (getting worse over time). That is probably one of the causes for thing initially being great to quickly backfire.
@dejurgen – exactly. And the water pressure constricted my body even more. Then there is massive amounts of salt causing other issues. Since I tend to have higher blood pressures with hyperPOTS – I’m certain all this together compounded my issues.
I’m about to repeat this experiment. I’m on a vacation and the ocean is calling me. We will see how it goes. ….
There is also the Buteyko method that is said to help with asthma. It teaches you to breath less and thus raise CO2 levels.
Yes. Thanks for the reminder. The Buteyko method has been suggested for ME/CFS. Dr. Cheney also recommends the Weil 4-7-8 breathing technique. Both increase the exhalation phase of the breathing.
Check out Health Rising’s Breathing Techniques Resource Page for ME/CFS and Fibromyalgia.
A higher level of CO2 contributes to a greater unloading of oxygen in the form of oxyhaemoglobin to the tissues. This mode of action is known as the Bohr effect referring to the observation that increases in the carbon dioxide partial pressure of blood or decreases in blood pH result in a lower affinity of hemoglobin for oxygen. Thus more oxygen is made available to body organs and tissues, in this instance, the brain.
Interesting article. What are your thoughts on how these processes tie into the overproduction of serotonin / receptor theory that Cortene drug trial is exploring?
Hi Liz, I’ll give it a go.
From https://www.healthrising.org/blog/2018/02/17/cortene-chronic-fatigue-syndrome-hypothesis/ I’ve got:
“Cells don’t just respond to their environment, however. By altering the kind and number of receptors on their surface they determine the kinds of response that are possible.
As we’ll see, cells often prime themselves for one type of action by loading their surface with one type of receptor.”
On https://www.healthrising.org/blog/2018/08/15/sticky-blood-antiphospholipid-syndrome-pots-chronic-fatigue-syndrome-and-fibromyalgia/ I wrote a piece on the relation between blood flow and receptors. It’s the “August 16, 2018 at 3:54 pm” at the bottom (@Cort: numbering comments would be a nice addition if easy to do).
Here is part of it; the full comment also has ideas on links to auto-immunity:
“Coagulation and other sources of poor (capillary) blood flow may cause a strong increase in receptors of all kind in capillaries and nearby tissue.
With crippled blood flow, the flow of many messenger molecules per second to a certain location may be strongly reduced. In order to achieve a proportionate/sufficient reaction to these messenger molecules it would be natural to increase the amount of local receptors.
If so, this could create potential problems:
* With increased receptors one introduces a certain “amplification” of signals. In technical systems stronger “amplification” increases risk of instability and erratic behavior considerably.
* Blood flow through these capillaries varies, for example while exercising (increased local supply), digesting meals (diverting supply) or by day/night rhythms. With increased amount of receptors this would make the local reaction to messenger molecules/stimuli continuously oscillating between underreacting and overreacting. This is both wasteful (energy and bio molecules) and a potential explanation to being oversensitive to stimuli, pain, food, chemicals, visual and auditory stimuli, caffeine, adrenaline… and relates to calcium ion channels regulation and similar. It could also explain how our bodies “seem to have lost their ability to regulate processes well”.”
Very impressive! 🙂 I don’t know about the serotonin connection Cortene connection. It’s such a complicated area.
I haven’t learned yet where many key “energy” enzymes are produced like pyruvate dehydrogenase or the many enzymes used in the Krebbs cycle. But if key enzymes have to be delivered by the blood stream as well, then cellular energy production is hurt deeply by this same mechanism as well.
It is worth reviewing this material in the light of some of the work of Leon Chaitow. He comments on the high rate of neck injury in Fibromyalgia cases:
Now Chaitow comments specifically on the role of a small muscle at the back of the neck in preventing kinking of the dural membranes between the neck and the skull. He also comments that brain scans have shown ischaemia in the brainstem in an area that is consistent with impaired vertebral artery flow.
Now this area is the area where blood pressure is regulated, and it is an area that is also under investigation in the causation of essential hypertension. (Baker Institute Melbourne Australia).
It is also the area in which chiropractors focus most of their attention, and due to the availability of upright MRI is now being comprehensively studied by a number of neurosurgeons, chiropractors and radiologists.
One of the doctors involved has advanced the idea of a new syndrome (crevice- medullary syndrome) as an effect of the upper neck issue.
Its symptoms include most of the symptoms of chronic fatigue and fibromyalgia:
Symptoms are variable but can include any of:
Blue hands in the cold weather
Irritable bowel syndrome
Gastro oesophageal reflux
I have issues with my neck and one of the problems I have been having is wild blood pressure fluctuations between hypotensive and significantly hypertensive.
I had not considered the chemoreceptor role, but clearly it is likely to be important. However it may be that the hypoxic area is much more narrowly circumscribed than is being proposed in this model.
It is of note that the parts of the brainstem involved are essential for the generation of our conscious experience- so it is entirely possible that a small, localised area of ischaemia could generate all the symptoms being proposed in this model.
Ive been looking at this area for some time given the health problems I have (almost indistinguishable from fibromyalgia) and have recently encountereda good del of material looking at this problem from the point of view of MRI.
I have a blog that covers it– though the new material is so substantial that it is somewhat overwhelming.
I attach the link to the relevant page. I hope this is ok.
Another abnormality of Ehlers Danlos Syndrome & these surgeries actually makes people worse…
Yes, sadly I know an EDS, POTS girl who the surgery proved, in the end, to be fatal for. It created more problems for her and she has since passed. (I have issues with my neck and spine too.)
Thanks Mind/Body. At least in my case I believe my neck is involved. This seems to fit in with Ray Perrin’s belief of thwarted cerebral spinal flows in ME/CFS/FM and I think cerebral spinal fluid leaks could fit in here too.
Thanks for providing the link – the more information the better 🙂
Very interesting. I have wondered about the diffusion of gases across the dura meningeal system to the CNS. Especially if this connective tissue differs from ‘normal.’
I am remembering the comment made to me ( via interpreter) from a QiGong Grandmaster ( the Jewel of China) when I asked him what Incould do to get well and stay well. His response, “Try to breathe.” Hmmmm.
I am currently (0-10) Level 3 CFS and can bicycle 2x/wk. It is about the only time I leave the house.
I used to compete in powerlifting.
With bicycling, after going just to the nearby park at first, and after 5 or 6 months I could go 30+ miles on the flat. After 3 years of regular bicycle riding (with a few months off here and there when my CFS or tendonitis got worse), I have not improved much at all. Per my books, a Normal novice cyclist improves 10% a week, not per year!
Even the mildest hills still put my heart rate in the 180’s and leave me gasping for more oxygen. My breathing can not keep up like it should. I am now accustomed to it, but it scares my riding companions.
My riding partners are a dozen other older retirees in their mid 70’s (on average), and they have no issues like I do in my 50’s. Some even have had triple bypasses or heart attacks, and on hills, I am worse off!
My legs otherwise feel fine and have no burning/lactate build up, which IMHO shows good circulation. I do not get light-headed, which shows adequate electolytes, BP, and glycogen.
My blood tests show high EPO, Ferratin, and iron, which shows higher than normal oxygen carrying capacity, and are identical to training in thin air at high altitude (7000’+), even though I bike at near sea level (200′) elevation.
EKG treadmill test is normal.
I know recent studies Cort has posted (and by Dr. Montoya at Stanford, the late Dr. Martin Lerner, Dr. Sarah Myhill, and several others) have pretty much confirmed EBV is one of the main viruses behind CFS, and other researchers show (like many microbes) it does NOT like oxygen.
I assume EBV makes epigenetic changes to reduce oxygen in it’s surrounding environment.
One previous article here mentioned something weird going on with the pyruvate hydrogenase enzyme reaction.
So I am curious to find out exactly why the oxygen is not getting into my cells, and how to best fix it!
Please reply with helpful links.
FWIW My goal is to compete in Powerlifting again sometime after I turn 60, and to ride a (hilly) ‘Century’ bike ride. (Also to declutter my small house, filled with projects I never started or finished, but that isnt as fun).
And yes, it does still take me about 3 or 4 days at home to recover from a 2 or 3 hour ‘easy’ (12 mph) group bike ride, and 2-3 days from an easy gym work out, but I am retired and can afford the recovery time; my adult kids moved back home & do the shopping, cooking, etc. for me.
Cort’s article states how not exercising made the Exercise Intolerance worse, and that is so true! The body adapts to whatever we subject it to, including inflammatory viruses, or a lot of lounging about, like an old cat. My tabby has trained me well: bed-food-couch repeat.
What is it like exercising with CFS?
These days, after a ‘easy’ 25 mile bike ride I feel OK, but the next day it feels like I have prickly fiberglass particles in my blood, and I am achy like when getting over the flu; everything hurts BUT my leg muscles! It is weird.
If I push myself too hard, it sets me back for weeks or months. Exercising just once a week prevents me from progressing.
UK Doctors talk about Graded Exercise for CFS people, but I doubt they allow the needed recovery time for aerobic exercise, nor tried short (20 second?) weightlifting sets of 6-10 reps with 3 minutes inbetween. Add weight if you can do more than 10.
I have noticed nobody here who is/was an athlete and has recovered somewhat from fairly severe CFS talks very much about what they did or ate to improve it.
I assume almost everyone here is on some version of the late virologist Dr. Martin Lerner’s supplement protocol, since almost every top CFS specialist in the US & UK recommends it. It has helped me, and also Iodine (Iodoral) & Selenium (+200mcg) for the heart per Dr. David Brownstein, MD.(along with Lerner’s CoQ10). It no longer aches like a sore muscle after a ride.
After the first year of bicycling, my heart rate now recovers from a small hill in about 1 minute instead of 20 minutes, and after 2 years my low Heart Rate Variability (HRV) has increased, showing better Vagus nerve responsiveness.
After 2 years, FM pain-points also suddenly went away over 2 days.
So anyone else figure out how to get the oxygen from the veins and directly into the clams
Consider this……we sometimes take anti-oxidents. Maybe we need less of concentrated supplements. Using foods in their whole forms with assisters gives us less chance of imbalancing our ratio. Oxygen can cause more free radicals. So there has to be a balance.
How interesting. I am have a similar response to exercise – which for me is walking – everything hurts BUT MY LEGS! In particular my upper body hurst. How weird.
Actually I just realized how that could make sense. If our blood is pooling in our legs we might have enough blood down there but we don’t have enough in our upper body. The most exercise we do with our legs the more we pull from the upper body
If the capillaries re being clogged with fibrin – see the Sticky blood post – or are shut down or are otherwise impaired, I don’t know how to get more blood to the muscles. I guess you have to fix that problem. If inflammation is the problem you have to get the inflammation down.
Thanks for the interesting comment.
Really enjoyed reading your reply Susan, are you based in the UK? May I ask for a link or mention of who the athlete is that you discussed? Did Dr Lerner’s protocol help you that much?
I do not suffer with these issues but unfortunately my wife does, hence my search for answers
Susan, I used to be a power lifter as well. Was your onset sudden? For me, I can pinpoint the exact day my symptoms started.
You write “Severe fatigue, however, is very common in POTS and FM as well; post-exertional malaise is present in all three diseases” but the study you link to describes only post-exertional FATIGUE in POTS, NOT post-exertional MALAISE (although PEM is listed as a diagnostic criteria for CFS but again, not for POTS), and FM is not mentioned at all.
Are you aware of any studies that find “true” PEM in conditions other than ME/CFS?
Anecdotally I’ve heard some POTS-diagnosed patients describe PEM-like symptoms but in each case it was unclear if those particular patients weren’t simply misdiagnosed and actually had ME.
Or if the case that the POTS-with-ME and the ME-with-POTS subgroups should should be viewed together as a separate and distinct disease entity.
I do consider post-exercise fatigue as PEM but you’re right we don’t know about the other symptoms – for me the muscle burning, the cognitive issues, the sleep problems, etc.
The fact that no studies that I know of have assessed PEM in POTS, fibromyalgia and other diseases does suggest, altho it doesn’t prove, that PEM – a dramatic exacerbation of symptoms after exertion which generally lasts several days – if it occurs, is not as central for those diseases.
The only study that I know of which compares PEM in another was I believe a fascinating Allan Light study. From the blog
“The MS patients were indeed fatigued. In fact their self-report fatigue scores prior to the exercise test were twice those of the people with ME/CFS (72-35). The pain scores at baseline, on the other hand, were significantly higher for ME/CFS patients than for the MS patients.
Fatigue is present in both disorders – but only the ME/CFS patients got whacked by exercise
Despite their enormous fatigue, the MS patients mostly sailed through the exercise period. Their physical and mental fatigue did rise 8 hours after exercise, but both was back to baseline at 24 and 48 hours. At no point did exercise increase their pain levels.
The Chronic Fatigue Syndrome patients, on the other hand, immediately experienced increased levels of physical and mental fatigue and pain after exercise – which were still present 8, 24 and even 48 hours later.
Simply looking at the symptoms indicated that MS is primarily a fatiguing disorder, and that MS patients may, in fact, experience more fatigue than ME/CFS patients. They do experience some PEM, but nothing like what shows up in ME/CFS.
Fatigue is obviously present in Chronic Fatigue Syndrome, but it’s more of a post-exertional malaise disorder. This study suggests Post-Exertional Relapse Syndrome would have been a better name for ME/CFS than Chronic Fatigue Syndrome.”
I think Lenny Jason would agree with you. He believes that ME/cFS patients with FM should probably not participate in ME/CFS research studies.
So the easy (and cheap)solution then would be to drink sodium bicarbonate to a)increase CO2 level, b)reduce blood acidity and c) boost nitric oxide production to increase blood flow through vasodilation.
An added benefit is that it also activates the cholinergic anti-inflammatory pathway from the spleen end of things in the event that vagus nerve signalling is dysfunctional and contributing to causing POTS in the first place.
Cool find. I’ve been working on my pH levels of recent. Somehow went very acidic and trying to get back alkaline. Apple cider vinegar is supposed to help too.https://www.longevitylive.com/live-healthier/drink-apple-cider-vinegar-daily/
Hi Sue and Issie,
In the link I read: “Our data indicate that oral NaHCO3 activates a splenic anti-inflammatory pathway”
After thinking uric acid might be problematic (by reducing blood flow by forming uric acid crystals) I decided to have two times a day a tiny bit of NaHC03 as I believed it would be good to reduce uric acid levels. A study confirmed that it is helpful in people with kidney stones and those consist largely of crystallized uric acid.
Results: even the small amounts, significantly smaller then used in the study, did let me feel a bit better. I however abandoned the experiment after I realized that sufficiently high uric acid levels are important in preventing cancer development. So please take note of that and keep an eye on uric acid levels. Too high ain’t good, but significantly low is just as bad for other reasons… :-(.
There *may* be a tiny margin to play with by maxing out vitamin C supplementing, but oral it’s limited due to causing diarrhea and limited uptake. Vitamine C is, for some functions, the closest replacement/supplement to uric acid.
Yes, it’s possible. Check out Hip’s Crash and Flare Buster’s resource on Health Rising – some people have used baking soda to reduce flares and crashes. I have found apple cider vinegar does help out a bit as well.
On Baking Soda/Citrulline – One person reported
I needed to report this to you all because it worked so well. Today I went to the gym. I actually did 30 minutes of exercise and lifted weights afterwords. Usually the weights at the end would kill me for about a week and I would be recovering from the cardio for at least 2 days. And, usually after exercise, I get a sore throat, headache, swollen lymph nodes, bad muscle and nerve pain, chills, and the cold sweats. When I go to bed the night I exercise, I wake up the next morning drenched in sweat. I have had very little to none of that recently.
I take a lot of supplements, but I find the ones I mentioned above work the best to reduce PEM after exercise. Most effective is two baking soda pills before exercise and lots of catalase immediately after. I take 600 mg of Catalase after the exercise.
Hip noted that
Studies have shown (see here and here) that both bicarbonate and catalase (via its scavenging of hydrogen peroxide) improve muscle recovery after exercise.
Q10 and creatine monohydrate have been shown to improve muscle endurance, and increase muscle recovery after injury respectively (see hereand here), so that makes sense.
One study found creatine monohydrate reduced blood lactate, so would further augment sodium bicarbonate’s lactate-reducing activities. The study detailed here found that by inhibiting the L-system transporter, BCAA suppressed the uptake of tryptophan, thereby alleviating fatigue….. This study found citrulline reduces lactate levels produced by exercise. This study and this study found the drug dichloroacetate lowers lactate levels produced by exercise.
On CoQ10 – From Hip
Breathing techniques and such aside, I was amazed how helpful it was to buy a cheap finger O2 monitor on Amazon
for less than 25 bucks. I have to spend
many hours each day in my recliner. When I’m just sitting and breathing normally my O2 levels will measure 92-93. When I become cognizant of my breathing and pop the meter on my finger I can bring it up to 97-99.
Nice biofeedback idea :). Thanks. I will include it in our resource section
It does make for a good feedback tool. But consider this:
At a certain point in my disease I learned that I could “erase” part of the exhaustion by breathing in very deep for some prolonged time after exercising. It felt like magic!
The first two weeks I improved at a very nice rate, the third week improvement rate went down. Then my health levels went erratic. As it was summer I attributed that to the hot weather and went on using my “magic tool”. But for the remainder of the year I kept losing health towards significantly lower abilities by the end of the year. No matter how hard I tried to turn this around I failed.
A lot later I started recovering, but recovering only went in a steady upward spiral as I realized there is something as “the breathing envelope”.
Just like we ME patients have an energy envelope, we have a breathing envelope. In fact, for the more ill of us 24 hours a day of breathing is the largest and single most exhausting “exercise” we do over 24 hours.
So by using extra deep (exhausting) breathing to recover better from exercise, I used a larger portion of my breathing envelope. Already before I did do that, breathing at night was often problematic (breathing deep and still lacking oxygen). Having a lesser remainder of “breathing envelope” for the night, breathing problems became even more problematic and with it associated “unrefreshing sleep” became significantly worse.
Learning to breath more efficiently, by getting good breathing exercises from my superb physical therapist, I learned to breathe more efficient. I decided this time around to not use the gains to increase activities until gains grew *a lot*.
That yielded two benefits:
* Learning to breathe more efficient spills over to when you don’t take note of it. That’s during all of the day including the night. So with the same breathing “resources” I got less into trouble at night.
* By not “consuming” the gains I got during the day by breathing more efficient, I got a larger portion of my breathing envelope left for the bad nights.
That is when in fact I looked at Buteyko Breathing differently. It (the having more energy by breathing less part) didn’t make sense to me, but it did seem to help some patients. Now I understand part of it is likely to “pace” on breathing during the day / when resting in order to have a larger part of the breathing envelope available for when in exhaustion, sleeping and have spare for slow health improvements.
It actually reminds me of my problem with energy and treatments – when I find something that produces energy and makes me feel good (and relaxed)I tend to fall apart. Not because I’m doing too much – something else happens. It’s like the energy gets funneled into the wrong pathway or something builds up in my system.
My body seems to want to be in the state it’s in.
One of my primary (and worst) symptoms is shortness of breath. For many years I chalked up my fatigue and bad PEM to my marathon training (yes, I was still doing it somehow, but not well)! The CO2 supplementation idea is interesting. Another thing I’ve read about is supplementing with NACO2 (sodium bicarbonate, or baking soda). It helps me some when I take it before exercise.