New MRI technique reveals the oxygen from the lungs is having trouble getting through to the small blood vessels in long COVID. It could explain shortness of breath and exercise problems in long COVID and possibly ME/CFS.
The Breathing-Oxygen series continues on Health Rising with an intriguing new long-COVID study that could have ramifications for chronic fatigue syndrome (ME/CFS) as well.
- A Gas Exchange Disease? Huge CDC Exercise Study Puts New Slant on ME/CFS
- Uneasy Breaths: Strange Breathing Patterns in Long COVID May Contribute to Exercise Intolerance
Health Rising recently produced a review of an exercise study that found that “gas-exchange” problems were preventing people with ME/CFS from producing normal amounts of energy during exercise. The study found alterations in ventilation during exercise which suggested that people with ME/CFS may be breathing more deeply and slowly in an attempt to shove more oxygen from their lungs into the blood.
This new Canadian long-COVID study found problems with “gas exchange” as well – but this time on the cellular level.
Lung function tests are usually normal in long COVID, but many people experience shortness of breath and exercise intolerance. This study may have revealed a cause.
Many people with long COVID experiencing shortness of breath, fatigue, dizziness, and other symptoms are being met with normal lung function test results. In the past, a result like that would have led researchers to conclude their symptoms are psychological in nature and to ignore them. Many doctors now are probably telling their long-COVID patients that their lungs are fine and they should go home and exercise.
We can dig deeper now, though – and that makes all the difference. On the ME/CFS side, we’ve always thought that new technology would make the difference – the problem has been getting to it. The low funding and interest in the ME/CFS field means it takes longer to get access to the new technologies that can really dig deep.
But then came long COVID – a virtual stand-in for ME/CFS – which does have funding – and here we have a small Canadian study (n=40) from the LIVEFREECOVID project which used a new imaging technique to dig much deeper into the “gas-exchange” issue than has ever been done in ME/CFS.
A CT study of hospitalized patients provided one clue, though: microclots and/or blood vessel changes were causing the blood to be shunted away from the smaller blood vessels, where the majority of gas exchange takes place, to the larger blood vessels. Another study found evidence of small airways disease in long-COVID patients whether they’d been hospitalized or not.
The Technique
That led a Canadian group to try what is apparently a fairly new imaging technique that employs radiolabeled xenon gas to assess the functioning of the tiniest blood vessels in the lungs. Two years ago, Grace Parraga, one of the co-authors of this study, lauded the new technique, stating:
“Xe MRI provides rapid, sensitive, non-invasive, and simultaneous measurements of pulmonary ventilation, lung tissue microstructure as well as diffusion within the alveolus and into the alveolar tissue and red blood cells, providing new opportunities to more deeply investigate lung diseases and unravel enigmas in respiratory medicine.”
This technique enables researchers to actually watch the oxygen moving through the membrane of the lung cells into the blood. The microvascular blood vessels and the microcirculation in general, are, of course, of great interest in ME/CFS and fibromyalgia (FM) as well. This study also used CT scans.
The Study
The study “Persistent 129Xe MRI Pulmonary and CT Vascular Abnormalities in Symptomatic Individuals with Post-Acute COVID-19 Syndrome” findings were stark.
The CT scans found that many of the very smallest blood vessels – the ones that allow the oxygen from the lungs to diffuse into blood – were simply gone in previously hospitalized in long -COVID patients. This was not true in people with long COVID who had not been hospitalized.
They did, however, find problems with oxygen diffusion into the small blood vessels even in people with long COVID who had not been hospitalized. The Canadian study was quickly followed by a small Oxford xenon study, “Lung Abnormalities Depicted with Hyperpolarized Xenon MRI in Patients with Long COVID“, which produced similar results.
In an editorial “Step on the 129 Xe Gas: The MRI Race to Uncover Drivers of Post-COVID-19 Symptoms” published alongside the Oxford study, Parraga and Matheson (two co-authors of the Canadian study) emphasized how important the findings were for the vast majority of long-COVID patients who experienced an initial mild illness and were never hospitalized.
“…the take-home message is clear: you don’t need to have been hospitalized with a severe COVID-19 infection to suffer long-term symptoms and abnormal MRI gas-exchange measurements. Moreover, even if spirometry, DLco, and chest CT are normal, symptoms and 129Xe MRI gas-exchange abnormalities persist for long periods of time post-infection.”
These findings seem to jive with a recent long-COVID study – produced by ME/CFS researchers, by the way – which found bizarre breathing patterns during exercise in almost 90% of long-COVID patients.
Causes
The Canadian study author’s first guess as to the cause involved microclots blocking oxygen from freely flowing into the capillaries. Other possibilities included damage to the blood vessels, the blood being shunted past the small blood vessels, and “vascular remodeling” which can produce narrowed blood vessels.
The Gist
- Despite the shortness of breath and problems exercising, lung functioning studies are usually normal in long COVID. In the past, a finding like that has led the medical profession to go down the psychological rabbit hole.
- Technology has improved, however. Two studies employing a new MRI imaging technique that’s able to measure the gas exchange between the lung cells and smallest blood vessels may have found an answer.
- Even in the long-COVID patients who had not been hospitalized, the Canadian and Oxford studies both found reduced rates of oxygen diffusion from the lungs into the small blood vessels where gas exchange occurred.
- Many small blood vessels appeared to have been pruned away entirely in formerly hospitalized long-COVID patients.
- The problems long-COVID patients have moving oxygen into the small blood vessels exercises may mirror what we recently saw in ME/CFS. People with ME/CFS have developed a strange breathing pattern apparently in order to shove more oxygen into their lungs, and ultimately, their blood as well.
- A recent blog reviewed a long-COVID study – produced by ME/CFS researchers – which found that bizarre breathing patterns appeared during exercise as well.
- The Canadian authors proposed four possible mechanisms for the poor gas exchange between the lungs and the blood. (Note that gas or oxygen = energy, so poor gas exchange equals poor energy production).
- All four – a shunt that propels blood away from the lung cells, micro blood clots, narrowed blood vessels, and damaged blood vessels have all been hypothesized to happen in ME/CFS. The Ron Davis/Open Medicine Foundation findings of poorly deformable red blood cells could also contribute to problems with gas (e.g. energy) exchange.
- The Canadian authors are continuing their studies.
The narrowed blood vessel idea was intriguing because narrowed blood vessels could help explain the low blood volume found in ME/CFS. Because blood volume is a function of blood vessel volume, abnormally narrowed blood vessels could result in reduced blood volume.
The central theme was “increased vascular resistance”; i.e. more difficulty getting the blood to flow through the blood vessels. Besides the shortness of breath sometimes seen in long COVID, they noted that their findings could also explain the exercise problems commonly found.
The leader of the million-dollar study, Grace Parraga, seemed confident they’d found a key problem in long COVID and was looking forward to figuring out exactly why this is happening.
“Now that we have the what’s happening, where it’s happening and when it’s happening, we can figure out the why and the who,”
A one-year follow-up study is underway.
Two Gas Exchange Diseases? The ME/CFS / Long-COVID Connection
You might say – well, since COVID-19 often affects the lungs – you might expect there would be lung problems in long COVID – but what about ME/CFS? It’s never been associated with lung problems. No one has ever dreamed of doing a xenon gas study in a disease like ME/CFS, which has never been thought to be respiratory in nature.
The authors of the Canadian study noted, though, that they didn’t find lung or respiratory problems in long COVID – they found vascular or blood vessel problems. To this layman, at least, that suggests their findings could potentially apply wherever the small blood vessels are found.
One of the main avenues of attack by the coronavirus, after all, is the endothelial cells lining the blood vessels. All four of the possible causes put forth by the Canadian researchers to explain the gas exchange problems they found in long COVID have been proposed at one time or the other in ME/CFS. They include microclots, damaged blood vessels, a shunt, and “vascular remodeling”, which produces narrowed blood vessels.
Clotting was, for a short time, a pretty hot topic in ME/CFS and could result from damaged endothelial cells. Systrom has suggested that small nerve fiber damage could be shunting blood away from the muscles in ME/CFS. Wirth and Scheibenbogen proposed that narrowed blood vessels in ME/CFS are triggering an explosion of vasodilators which, in turn, are producing a wide array of symptoms. Those narrowed blood vessels could be reducing blood volumes. (I haven’t found a blood volume long-COVID study yet.)
Plus, we have our own ringer – the Ron Davis/Open Medicine Foundation work on red blood cell deformation – that could be impairing blood flows as well. As noted at the start of the blog, we also have an exercise study that suggests that people with ME/CFS are doing everything they can, breathing-wise, to shove more oxygen into their blood.
Any researchers up for an ME/CFS 129Xe MRI lung study?
These oxygen/breathing studies are so interesting and relevant to me. I have lifelong, cough variant asthma that wasn’t diagnosed until I was in my mid 40s—and airway remodeling had already produced severe obstruction on lung function tests. Now on inhalers and other meds, I have moderate obstruction. My everyday functioning has been less than most who have moderate COPD then further damage from flu, pneumonia and sepsis resulted in needing oxygen supplementation. That ME could be complicating all this is something I hope may lead eventually to treatment to improve both lung function and exercise intolerance. Thank you for your work to keep up aware of research and clinical findings.
Really interesting. There has to be an extra-added ME component that adds to the exercise intolerance and been suggested that the breathing issues during exercise result from a metabolic dysfunction in the muscles (!). Now we see clear evidence of microcirculatory problems in long COVID. I would be shocked if some similar isn’t happening in ME/CFS. Long COVID, after all, may primarily be a vascular disease – which would fit ME/CFS to a tee.
It gets ever more interesting.
Cort,
I know this slightly off topic. But, has anyone ever reported that their POTS and other neurological symptoms started while they lived at Camp Lejeune, N.C.. Mine did. Toward the end of my father’s tour there, I passed out twice playing basketball. At first, the Doc’s were convinced that I had a cardiac problem. Eventually the Neurologist’s realized that I had, what at the time, was called “Idiopathic Orthostatic Hypotension”. That started my long, strange journey through the bowels of the NIH, as my Dad was then stationed across the street at The Bethesda Naval Hospital. Over the next 25 years I slowly developed all of the typical ME/CFS symptoms. (I was of course told that I was “crazy”, like most of us have! Despite the fact that I have documented small fiber neuropathy.) Has anyone else ever reported a similar pattern? We’re discovering that all the bases are contaminated, but Congress just opened the door for the Lejeune “non-cancer” survivors to also file suit. I’m 100% certain that those benzene, TCE, and vinyl chloride derivatives “whacked” my immune system. Many of my friends died of bladder, liver, and kidney cancer. But, unfortunately, they lived on the base longer than I did.
I haven’t heard of that but you know we’ve barely scratched the surface of ME/CFS. We only have a few prevalence studies and nothing nationwide for sure. Given the toxins that I’m sure permeate many of the bases, I would be shocked if there weren’t many people like you. The military has always ignored that kind of stuff…
It sounds like dysautonomia came first – and then evolved into ME/CFS. Dr. Bateman at the conference said she knows many people who kind of drifted into ME/CFS over time.
Cort, Thanks for all of the “heavy lifting” that you have one for us, by reporting the research in such an understandable manner. I have often said that you were an angel, sent on a mission. I think that we are lucky that you attended such fine Bioscience school like U.C Santa Cruz. You can find your way through the clutter.
:). Thanks! Unfortunately ME/CFS stopped me from completing my degree at UCSC. What a memorable place that was for me, though. So many possibilities. Nothing in my education before or since could touch it. Just the atmosphere of the place was remarkable.
I have that form of asthma too!
It’s allergic too.
Steroids would mess me up, which is what doctors wanted me to take – daily. I couldn’t comprehend how they wanted to harm me in order to control/manage the astgma. I said screw this, then went on my own, and found that eliminating wheat eliminated the asthma.
That was… a good 15 years ago.
Maybe allergic triggers can vary for each person.
All of these oxygen delivery problems, make me wonder if Hyperbaric Oxygen is understudied/under-researched. At Dr. Nancy Klimas’s lab they are employing HBOT to treat Gulf War Vets with cognitive decline. The patient’s feel it is working. Dr. Scott Sherr in New York feels that HBOT therapy helps regrow blood vessels in the brain, lungs, and heart. HBOT apparently forces the bone marrow to produce more stem cells that instigate tissue damage repair (no research citation on these claims.) Michel Phelps claims that a normal 48 hour recovery is cut to 4 hours with HBOT. Joe Namath knew that his many concussions were radically effecting his cognition. He claims that ~30 HBOT sessions reversed that damage completely. HBOT saturates the plasma to the point where you do not need erythrocytes (red blood cells), to fuel cells with oxygen.
I didn’t know about Klimas! Interesting about Joe – he was real trouble there for a while. We have a blog coming up on HBOT shortly.
Rich do you know if Dr Nancy is using hard shell or soft shell HBOT ? Joe Namath said he used the hard shell chamber ( 3.0 or above.)
I have had ME/CFS for thirty-two years – and I don’t have any obvious lung problems (adapted to reduced energy long ago?).
I’m more curious to hear what, if anything, can be done about this problem – I’m past working age, so it won’t save my working life except for the writing I’ve undertaken as a replacement (when I can).
And if the damage is permanent, it will help many more people get the disability benefits they should have.
But a treatment/cure needs to be based on knowledge of what the problem actually is, because I tolerate very few medicines, and won’t take anything not absolutely essential. And proven for whatever my particular constellation of symptoms is.
At least this – like so many other theories – sounds plausible.
I don’t have obvious lung issues either but I’m pretty clear that my breathing isn’t what it could be. I had to walk about a mile in high heat recently. About halfway through I noticed that my breathing was all over the place – it was like it was straining to find some equilibrium.
Yes I believe this applies to my mecfs- I have noticed a change in my breathing and a desire/need to elevate my legs so I believe oxygen transfer and blood vessels are at play. I would participate in a 129xe mri study though it looks like most of the machines are currently located on the east coast? https://cpir.cchmc.org/XeMRICTC
Thanks, Nancy! I had no idea that consortium exists. Too bad we don’t see one in Harvard (yet) where David Systrom might have access to one. I don’t recognize any of the researchers but hopefully, some are involved in long COVID work here. How nice it would be – and how much sense it would make to have an ME/CFS control group. A similar finding would make a huge difference for this field.
So how should we breathe ….slow , fast , shallow or heavy, with whatever limitations we have to cause minimum long term damage to ourselves?
No wonder I find breathing exercises so challenging.
i still pant as i write this as no matter what i do, ONE sneeze and i’m outta breath, huff puff everyday and the weakness with it is horrible! I WANNA BREATHE!
I do wonder where PEM, and especially PEM caused by non-exercise stress fits into all of this. I was just reading about microtubules, structures inside cells which have multiple functions and when disturbed can cause many different seemingly unrelated maladies It is very technical reading and I don’t want anybody to think that I am implying that these are our problem.
Sometimes I think that we are looking at the gross (macro) probable causes (by which I mean the big obvious ones–like breathing) and that possibly the cause(s) could be on a more micro level–hidden. Makes me think about Ron Davis’ ‘factor X’ in the blood stream…
For myself, its almost like I have a battery which if mildly depleted, takes a couple of days to fully recharge. It doesn’t matter if the depletion is by exercise or non-exercise activities. Now what body process has that kind of cycle?
Not enough oxygen (instead relying on anaerobic energy) also causes excess lactic acid in the blood – something noted in the blood of pwme for decades.
I’d love to be in this sort of study. Before I knew I was more than just “out of shape”, I used to hold my breath when playing tennis, which was either an attempt to force more oxygen into my blood or a Valsalva maneuver to try to increase my blood pressure. Nowadays, like Dee, I feel out of breath when I sneeze.
@Tim
so that’s why we hold our breath!!!
thank you for two explanations
I can relate to this microcirculatory problem so easily, and have a bit of corroborating evidence.
In a echocardiograph I had ‘central hypovolemia inferred’. I have severe POTS.
I have barely any visible finger prints, which Dr Cheney thought is an indication of microcirculatory problems. I feel better after a hot shower, which I guess dilates the blood vessels. I also get unprovoked bleeding from below the nail of the left big toe. Would this indicate some damage to the blood vessels.
It seems to make sense to me. Hoping they find out more about this.
I have had post-viral syndrome three times: in 1994, 2000, and 2022. The type of virus does not seem to be relevant, the symptoms are the same. The explanation in this article (i.e., microcirculatory) makes more sense than anything else I have read and would explain the results of recent breathing tests and labs which suggest breathing obstruction and blood clots, although my doctors have been unable to find the culprit. So happy to see new diagnostic machines are making their way into the system.
Has anyone read Ramsey’s Disease by Leslie O. Simpson & Nancy Blake? Seems similar.
Leslie O. Simpson is a retired hemorheologist from New Zealand who has researched the red blood cells of patients with myalgic encephalomyelitis (ME). According to Simpson’s research in the 1980s and 1990s the red blood cells of ME patients show shape deformities that cause impaired microcirculation of the blood in the capillaries.
https://me-pedia.org/wiki/Leslie_Simpson
i asked the local masterton hospital labs if they could do some of the dark field blood tests for me to see how my cells looked ,when i first got my PVCFS
sadly they couldnt without referals
Mostly for me it was cos the timeline for my illness fitted in with his mycoplasma damaging the cells from the inside (ie they feed on the HDL and created a “layer” around the healthy cells to protect themselves…which meant body ramped up defenses to stop something they couldnt get to …and also caused the heart issues…..USA CFS site did a member survey from 10000 plus members 1/3 got their CFS from the flue 1/3 got it from vaccinnes and 1/3 from heartattacks )
which all fitted my timeline …Flu that went viral HA a yr later and CFS on top of it
hadnt heard any mention of Dr Simpsons work for ages
(all above is from like 15 yrs ago incase my memories got things muddled 😛 )
I always wondered if the Mycoplasma no one could find was hiding inside the bones …ie where the red blood cells are formed …thus invading the cells as they developed
Mum was one of the original Tapanui flu victems i think cos her Fibromyalgia seemed to have come in around that time once we had the forsight to be able to look back (ie her symptoms were all put off as “womans issues” by all her different Drs for like 15 20 yrs b4 a final diagnosis
Yes!
Acacia, I am so happy you mentioned the missing fingerprint issue. I also have this and up to one third of Dr. Cheney’s patients had missing fingerprints. Why is no one researching this interesting and unusual marker?
I, too, have lost my fingerprints. I’ve had two rounds of ME-CFS in my lifetime. And I had deep vein blood clots in my early twenties and almost died from the allegedly safe Pill.
I found out back then I have Factor V Leiden, a blood clotting disorder which makes me prone to them.
But it was many years later when I figured out on my own (confirmed by three separate Geneticists at three different institutions) I also have Ehlers Danlos Syndrome. I suspect it’s my EDS, a genetic flaw in my collagen, which is behind my fingerprint disappearance. But maybe it’s microcirculation issues, too.
Given my past, I use Lumbrokinase, Nattokinase and Serrapeptase on rotation. These supplements work against clots. At this point in history, I’m doing all I can think to do to prevent them.
I’ve also avoided taking the ClotShot for the very same reason. One of my Doctors practically begged me to take it; I told him it made no sense to let a spike protein dense mystery injection into my already severely damaged body. I use prophylactic Ivermectin, wear masks when in public buildings, gargle and rinse my sinuses when back home (all per the FLCCC protocol) and have avoided Covid thus far. I also use NAC which is said to protect against clots in addition to its many other benefits.
We live in an astonishing time. I assume most here have previously or are currently suffering from ME-CFS and/or long Covid. I hope everyone hangs in there and never gives up hope. As weak as we may be, we’re still exceptionally strong, enduring people.
EARTHWORMS!! Yes, you read this right. Lumbrokinase is an enzyme synthesized from earthworms. It may be a safer alternative to other pharmaceutical blood thinners in the treatment of hypercoagulable states in ME/CFS.
This is an excerpt from The Townsend Newsletter, but there are also many studies in PubMed on lumbrokinase.
https://www.townsendletter.com/article/lumbrokinase-an-enzyme-for-more-than-just-circulatory-health/
“However, since chronic infection and chronic inflammation tend to create a hypercoagulable blood state,(31,32) some clinicians may feel that lumbrokinase’s true benefit is in reducing hypercoagulation-associated complications.”
Because my blood has been thick since the beginning of this illness, on the advice of my doctor, I have been taking a half dose of lumbrokinase for about two weeks and just started the full dose today. I have noticed some ability to walk longer without the heavy limbs feeling and shortness of breath, but it is too soon to see what the full impact will be. I will let you know.
My MD, who has been an ME doctor for decades, recommended this. I have yet to try it.
Nice! Had never heard of this. Another thing to add to my list of things to try.
Are you only taking Lumbro? What about Nattokinase and Serrapeptase? Those are also natural anti-coagulents.
Shortness of breath (in particular when coming close to exertion limits) is something that came on following corona vaccine for me. It feels as if the oxygen breathed in does not get absorbed by the body (I am double vacced with Pfizer). I don’t think I had it before with ME/CFS.
It makes me wonder if this kind of oxygen disturbance, if it might be caused for example by something like spike-related microclotting?, could be something specific for LongCovid rather than ME/CFS.
(There is a preprint that showed spike S1 persistence in postvacc individuals https://www.researchsquare.com/article/rs-1844677/v1 (Caveat: I did not check fpr myself how they checked whether partiticipants did not have Long Covid, as I think some Long Covid infections can be antibody negative.) Also, if I understood correctly, there are papers discussing a possible role of spike protein in clot formation).
But of course I cannot say for sure whether the onset of new symptoms following Covid vaccine are really related to something Covid specific (such as persistence of elements of the virus or specific immune reactions to elements of the virus), or whether they are just onset of new ME/CFS symptoms following strong immune reaction to the vaccine.
The fascinating thing about this is that it seems to be consistent with a theme in people like me with fibromyalgia. The problem of maintaining our body temperature appears also is based on dysregulation of shunting of the small vessels, caused in fibromyalgia by the extra and damaged small nerves that operate those shunts. This small nerve problem in my opinion is basic to virtually every problem we have. From vision to teeth to pain etc.
Agreed! The possibilities are huge.
I’m 73 and have had fibromyalgia for over thirty years. I have not had Covid or ever smoked, but I have the same erratic breathing patterns described above after intense exercise. When Covid started, I bought an oximeter which showed an oxygen level of about 97-98%. There must be enough oxgen, but there must be a malfunction perhaps at the mitochrondrial exchange level.
Great question. So why are pulse ox levels ok? Mine have never been great but they’re not dangerous. Maybe one idea is that we’re hyperventilating or breathing strangely in order to drive more oxygen into the lungs and bloodstream – and we are succeeding for the most part – but that’s also reducing CO2 levels – which cause a whole host of problems – many of them synonymous with ME/CFS and long COVID.
Other than that – I agree – there’s probably something going at on the level of the muscles.
One of the first things my daughter told me when she became ill with ME/CFS was “I feel like I can’t breathe.” We investigated asthma and got an inhaler, but that didn’t help much. She was a long-time dancer in great physical shape. The more she exercised, the worse she got. She also had blood drawn and tested by Simpson in his early research–showed the deformed blood cells. But her father (42 years older) also got tested (as part of the controls) and also had the deformed cells. He had several chronic conditions but not CFS. Her heart/lung exercycle test in the 2000’s showed the highest disability level about 4 years after her illness began.
A lack of Nitric Oxide (NO) may contribute significantly to these microcirculatory problems. NO relaxes vessels and makes red blood cells more deformable (so they can pass through the smallest blood vessels). NO is also anti-thrombotic.
(Sorry I sent the comment before it was finished)
NO also supports the exchange of oxygen and CO2 and it increases the efficiency of mitochondria.
When there is a severe lack of NO, this will result in thrombosis, hampered blood flow, less energy, probably even lack of oxygen in the smallest blood vessels (e.g. the brain?). Extreme lack of NO may hinder the exchange of oxygen.
The problem with extreme lack of NO is, that it is difficult to turn around. Because the release of NO from other molecules is prevented by a lack of NO ….
I found a work around to this catch-22 problem. I want to investigate this with long COVID patients but it is impossible to find a doctor who wants to cooperate on this.
If a lack of NO is indeed the main problem, therapies to use anti-coagulants or therapies to filter out micro clots etcetera will never give optimal results.
i mentioned this in a thread the other day
Ive been boosting my NO with Beetoot Juice in my breakfast smoothy and also via dark chocolate (70 per cocoa mass or higher types)
the back of the Tongue has Bacteria which is there specifically to produce NO in the body so sucking on a chunk of Dark chocolate seems logical to me 🙂
Beetroot juice bulking has been done by olympic record teams for the last 20 yrs or so supposedly..
Also NO D3 and i think Meletonim/Seretonum are vital in a lot of those energy processes
ie Get your 30 mins a day in the sun every day and especially the bright sunlight pre 9 AM and avoid bright lights after 9Pm to help regulate body clock/and sleep patterns
Additionally on NO production via Tongue bacteria
just watched an interesting youtube vid
In it she showed studies which found using antibacterial mouthwash 1-2 times daily wiped these beneficial bacteria out ..thus reducing NO production
Another study showed it was beneficial to brush/scrape the tongue reguarly (without toothpaste) ….this reduced harmful bacterias which “killed off” the beneficial bacterias
She couldnt find any studies on whether brushing with fluride toothpastes effected the good bacterias thou
But main points were Dont use antibacterial moothwashes and Do brush the tongue ,to help the beneficial NO production tongue bacterias
Does this explain why this study might have found positive results?
Combining L-Arginine with Vitamin C Improves Long-COVID Symptoms: The Nationwide Multicenter LINCOLN Study
Raffaele Izzo 1 , Valentina Trimarco 2 , Pasquale Mone 3 , Teresita Aloè 4 , Massimo Capra Marzani 5 , Antonio Diana 6 , Giovanni Fazio 7 , Mario Mallardo 8 , Mauro Maniscalco 9 , Giuseppe Marazzi 10 , Nunzia Messina 11 , Simone Mininni 12 , Chiara Mussi 13 , Girolamo Pelaia 14 , Alfio Pennisi 15 , Pierachille Santus 16 , Francesco Scarpelli 17 , Francesco Tursi 18 , Alessandro Zanforlin 19 , Gaetano Santulli 20 , Bruno Trimarco 1
Affiliations expand
PMID: 35868478 PMCID: PMC9295384 DOI: 10.1016/j.phrs.2022.106360
Free PMC article
Full text links Cite
Abstract
Introduction: Recent evidence suggests that oxidative stress and endothelial dysfunction play critical roles in the pathophysiology of COVID-19 and Long-COVID. We hypothesized that a supplementation combining L-Arginine (to improve endothelial function) and Vitamin C (to reduce oxidation) could have favorable effects on Long-COVID symptoms.
Methods: We designed a nationwide multicenter clinical study (LINCOLN: L-Arginine and Vitamin C improves Long-COVID), in which a survey assessing several symptoms that have been associated with Long-COVID was administered to COVID-19 survivors; effort perception was measured using the Borg scale. Patients were divided in two groups, with a 2:1 ratio: the first group included patients treated with L-Arginine + Vitamin C, whereas the second group was treated with a multivitamin combination (alternative treatment). Before administering the survey, patients completed 30 days of treatment.
Results: 1590 patients were initially enrolled, of which 1390 completed the study. Following a 30-day treatment with L-Arginine + Vitamin C, the survey revealed that patients in this treatment group had significantly lower scores compared to the other group. There were no other significant differences between the two groups. When examining effort perception, we observed a significantly lower value (p<0.0001) in patients receiving L-Arginine + Vitamin C compared to the alternative-treatment arm.
Conclusions: Taken together, our findings indicate that the supplementation with L-Arginine + Vitamin C has beneficial effects in Long-COVID, in terms of reducing its typical symptoms and improving effort perception.
The severity of my CFS/Fibro varies in waves. When it is bad, my eyes become hypersensitive to light and my ears to sound. I cannot eat or drink anything without my head pounding, and my skin becomes very sensitive (and painful) even to the touch of bed sheets. This could be explained by (fragile) small nerve fibers damaged and/or irritated by insufficient micro-vascular blood/oxygen supply. Note that this problem could also tire muscles quickly (ie. No energy stamina). It could further explain an intolerance to virtually any kind of stimulation, as stimulation (even such as digestion, seeing light, or hearing sound) requires and depletes oxygen/energy. I have also noted that when my skin becomes painful after only a minute or two lying in the same position in my bed, the only thing that may reduce the pain (and permit sleep) is slow, purposeful deep breathing. To me, this suggests that cellular hypoxia may be implicated. I speculate that micro-vascular insufficiency could underlie all of my (many other) symptoms, and. it could be primary to the gassing problems identified in this research. (And TY very much Cort).
Cfs is primarlily an environmental illness.
Mito function according to their surroundings.
Air hunger which we all know and suffer from is a real frontrunner symptom.
In my case it always increases as my diet is more acidic and if i drink acidic liquids
It’s alleviates symptoms when I clean up fluid intake.
It’s serum acidity/alkalinity issue.
Of course MD will tell you that’s quackery but I have this a long time and can read.it like a book.
These links might help explain why, and what to do about it :
https://www.researchgate.net/publication/340027241_Suppression_of_NLRP3_Inflammasome_by_Erythropoietin_via_the_EPORJAK2STAT3_Pathway_Contributes_to_Attenuation_of_Acute_Lung_Injury_in_Mice
https://www.researchgate.net/post/Covid-19_Erythropoietin_EPO_deficiency_syndrome2
https://www.nature.com/articles/s41419-020-2276-8
In addition, there is the problem of red blood cells :
https://www.researchgate.net/publication/357172246_Activation_of_Sphingomyelinase-Ceramide-Pathway_in_COVID-19_Purposes_Its_Inhibition_for_Therapeutic_Strategies/comments
which also can be prevented with EPO:
https://www.researchgate.net/publication/44629882_Ceramide_in_Suicidal_Death_of_Erythrocytes
My above comment is only aimed at Long Covid.
Whether it also applies to ME, I am not certain.
https://www.healthrising.org/treating-chronic-fatigue-syndrome/drugs/erythropoietin-procrit-for-chronic-fatigue-syndrome-mecfs/
Or
You can follow up to see if this study was published
https://grantome.com/grant/NIH/U01-AI045940-03-1
There’s probably more if you look for it
My lung function and CT scans all normal but being short on breathe is my worst symptom. Even if they find the microcirculation is impaired in lungs it me Cfs pots etc. What can they even do about it?
I’m at 14 sessions of hyperbaric oxygen therapy currently, 4 more planned next week from a 20 session course. At the first session I felt like my body was drinking oxygen in like it was parched. That stopped after a couple of sessions and the main impact was feeling tired. However the brain fog seemed to improve a bit about 10 sessions in and I could walk back from local shops without 3 stops en route.
I was deteriorating before this course of treatment so 20 sessions is not going to be a cure but I’m planning one session a week afterwards and will see how that goes. If I am permitted to do so (waiting list for treatment) I may try asking for more sessions.
Fingerprint sensors never recognise my fingers.
Fascinating….Systrom said he knows of other patients with the same experience and he can envision how it might work….Big question – is it a temporary fix or will it last longer. Even if its temporary its pointing an arrow at something.
I have an oximeter in case I caught covid. My sats have never been anything to worry about although I havent tried measuring them when attempting to exercise.
I’ll try and remember let you know if if lasts. I’m hoping if I have a session each week then it will continue to have an impact – and if not maybe they’ll let me have more sessions, I can possibly get to cancellations. I’ve been ill for many years, I’d hope if this was offered to people who were recently diagnosed or less ill to start with it might be more effective.
Any updates on this? Anyone finding therapies that are working to ease the air hunger / Shortness of breath?
I’ve only had covid once a far as testing goes; that was in August. In November I had surgery. I quit breathing for 20 minutes after surgery. After surgery I was sent home with oxygen.
Now it’s April and I still use oxygen regularly. Pulmonary lung function is fine. On the first visit with the lung fictitious, he had me do three laps around; when I stopped, my o2 was 79 and slowly climbe6 back up.
I’ve had a chest CT scan, chest xray, an echo, a brain MRI, and wore a heart monitor for two weeks. Everything comes back normal.
If I don’t use oxygen constantly, I get dizzy spells, headaches, light headed, short of breathe; but the worst part is the chest pressure.
Lung doc is at a loss. 😪
Tammy
There are some new hypotheses about what is going on in lungs. We have a blog on one coming up.
Anything I can do in the meantime? Is this the new normal? Big questions that may be impossible to answer I’m sure.:-(