Geoff’s Narrations are taking a little break
The GIST is a bit different…Scroll a bit down, and you will find it. 🙂
Another pulmonologist with an invasive testing machine (David Systrom was the first) enters the fray 🙂
There are a couple of reasons to celebrate seeing Inderjit Singh pump out long COVID studies: he’s a well-published Yale pulmonologist with an invasive exercise machine to play with. A leader in the invasive exercise field, Singh recently published an article, “The casting of invasive cardiopulmonary exercise testing: towards a common goal,” which, among other things, calls for increased use of iCPET to understand exercise intolerance.
Invasive exercise studies are so revealing because their ability to assess both arterial (oxygen rich blood coming from the heart) and venous (depleted blood after it has passed through the muscles) blood means they can tells what happened to the blood as it goes through the muscles during exercise. They can tell us if the muscles picking up sufficient amounts of oxygen or if blood is being lost during transit or is pumped out of the heart in sufficient amounts. Problems with all of these processes have been found in ME/CFS and long COVID.
In 2022, Singh teamed up with David Systrom, Aaron Waxman and others to show that the reduction in energy production found during exercise in long COVID was not due to heart issues but to “peripheral issues” such as blood flows and possible mitochondrial disruption and featured a hyperventilatory breathing pattern.
The gist is that people with ME/CFS and long COVID may be hyperventilating, i.e., breathing more rapid and deeper during exercise than normal in an attempt to get more oxygen into their muscles, and/or they might have autonomic nervous system problems.
The Gist
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Another pulmonologist with an invasive testing machine (David Systrom was the first) enters the fray 🙂
It’s great to see Yale researcher Inderjit Singh with his invasive exercise machine work in the long COVID field.
- The ability of invasive exercise studies to assess both arterial (oxygen rich blood coming from the heart) and venous (depleted blood after it has passed through the muscles) blood means they can tells what happened to the blood as it goes through the muscles during exercise.
- This is the first invasive exercise study to use metabolomics (the study of metabolism) in an invasive exercise study. Because metabolites power the Krebs cycle – which provides essential factors to the electron transport chain (which produces ATP) – a breakdown in metabolism could be behind the reduced energy production found in these diseases.
- The cardiovascular findings were as expected. They found that the muscles of long COVID patients were not getting normal amounts of oxygen (read energy). Because the muscles were not using up oxygen, the levels of oxygen found in the blood after it passed through the muscles was almost ten times higher than that normally found.
- Peak energy production was reduced and the long COVID patients began to rely on anaerobic energy production at an exercise level comparable to having to walk upstairs – far earlier than in healthy people. The pattern found suggested that mitochondrial problems were to blame.
- A “net extraction” of nine amino acids from the bloodstream suggested that the muscles of the long COVID patients had become depleted and were turning to the bloodstream to capture amino acids.
- A large increase in the consumption of purine inosine suggested, once again, that long COVID patients relied more on anaerobic metabolisms and suggested that it’s breakdown products were interfering with the mitochondria.
- A major takeaway from the study was its finding that both the aerobic and anaerobic energy production pathways in long COVID had been blunted.
- High levels of succinate suggested that a slowdown of the Krebs cycle might be causing succinate to accumulate in the mitochondria and subsequently get released into the bloodstream.
- The authors proposed that purine metabolism may serve as a potential novel treatment target but didn’t mention specific treatments.
- Asking several AI engines which purine inhibitors might be helpful in diseases with exercise intolerance/postexertional malaise uncovered a wide variety of drugs which might be helpful most of which I’d never heard of…Interestingly, the AI engines specifically mentioned ME/CFS, fibromyalgia and long COVID as diseases that might benefit from these drugs. See the blog for those drugs.
- Suramin – a drug which Dr. Naviaux has championed with regard to ME/CFS – was not among them because it’s a different kind of purine inhibitor. Suramin doesn’t block purine metabolism but blocks purine receptors from activating.
In 2023, in “Post-Acute Sequelae of SARS-CoV-2: More Than Deconditioning,” Singh and another Yale researcher put the brakes on the idea that long COVID was nothing more than deconditioning. Again, in 2023, Singh co-authored a paper comparing the exercise physiology of ME/CFS with long COVID.
Then, in November 2024, Singh’s invasive exercise study, “The metabolic and physiologic impairments underlying long COVID associated exercise intolerance,” employed metabolomics for the first time. Now Singh focuses on metabolism—a critical component of energy production. A lot of focus is on the mitochondria, but without metabolism, the mitochondria don’t have the resources they need to produce ATP.
Metabolic Slant
Before we get to the mitochondria, a long chain of metabolic events has to happen for the mitochondria to function properly. First, carbohydrates, fats, and proteins are metabolized or broken down into glucose, fatty acids, and amino acids, which are then broken down to produce ATP.
We often think of the mitochondria as the electron transport chain where ATP is produced, but it’s the Krebs or citric acid cycle that provides the electron donors the electron transport chain needs to produce ATP. Glucose, fatty acids, and amino acids feed the Krebs cycle, which takes place both in the cell’s cytosol and the mitochondria.
This problem with energy production in ME/CFS and long COVID could be due to metabolic problems that prevent the proper “feeding” of the Krebs cycle. A wonky Krebs cycle would not provide enough electron donors (FADH2, NADH) to the electron transport chain to produce the ATP needed for people with ME/CFS or long COVID to successfully in exercise.
Study Results
Cardiovascular Findings
Not enough oxygen being used by the muscles resulted in higher than normal levels of oxygen in the venous blood leading from the muscles.
Oxygen-Poor Muscles – Once again, we see a reduction in peak VO2 (peak energy production) caused by reduced peak EO2 or peak oxygen consumption; i.e., the mitochondria in the muscles were simply not using up enough oxygen. This is the oxygen extraction problem” that Systrom’s invasive exercise studies have found.
Oxygen-Rich Venous Blood – The reduced oxygen extraction in the muscles showed up as unusually high levels of oxygen in the venous blood. While this study did not have a healthy control group, the levels of oxygen found in the venous blood of the long COVID patients was almost ten times higher (26.5 ± 3.6%) than that normally found in healthy people.
When their peak VO2 plateaued, the muscles of the long COVID patients ran out of oxygen and started relying more on the less effective anaerobic energy production system to provide energy. The authors calculated that this turn to anaerobic energy production probably occurred at an exercise level comparable to having to walk upstairs. The pattern suggested that mitochondrial problems were to blame.
Metabolic Breakdown
Amino acids are usually pulled from the muscles. In the long COVID patients they were pulled from the blood stream as well – suggesting that the muscles have become exhausted.
Muscle Breakdown – The authors simply stated that a “net extraction” of nine amino acids was found and left it at that. A “net extraction” refers to more amino acids being taken from the bloodstream than released into it. Because amino acids are first taken from the muscles during exercise the net extraction suggested that the muscles of the long COVID patients had turned to the bloodstream in an attempt to renew themselves. If I’m reading it right, though, this finding appears to jive with another key finding in ME/CFS – that amino acids are being preferentially used in these diseases to feed the Krebs cycle.
Anaerobic Metabolism Emphasized—A global metabolic analysis indicating a large increase in the consumption of purine inosine suggested, once again, that long COVID patients relied more on anaerobic metabolism. Inosine is produced when ATP is rapidly broken down. The high consumption of inosine suggested that long COVID patients’ energy production systems maxed out early in the exercise session.
Inosine is catabolized ultimately into purines such as hypoxanthine and uric acid – suggesting that high hypoxanthine levels which have been associated with mitochondrial problems and reduced ATP levels – might be present.
Double Energy Hit – A major takeaway from the study was its finding that both the aerobic and anaerobic energy production pathways in long COVID had been blunted. The authors proposed that the findings “have important implications towards the development of potential pharmacotherapeutic interventions directed towards mitigating early reliance of anaerobic metabolism, which may include shifting, restoring, and/or enhancing mitochondrial oxidative phosphorylation capacity during exercise.
Succinate Sticks Out – A dramatic correlation between succinate in the venous blood and peak energy production was found (VO2 (r = 0.68; p= 0.0008). The authors suggested this could reflect post‐exercise glucose tolerance problems.
Succinate shows up! Look directly up to see where succinate enters the citric acid/Krebs cycle. (Image from Narayanese-Yassine, Mrabet_TotoBaggins; CC 3.0, Wikimedia Commons)
A familiar scenario may be playing out as well. While succinate can enhance ATP production in the electron transport chain, it also plays a role in the Krebs cycle. In hypoxic or low-oxygen conditions—the conditions this study suggests exist in the muscles during exercise—a slowdown of the Krebs cycle could cause succinate to accumulate in the mitochondria and subsequently get released into the bloodstream.
Itaconate Shunt Connection ????
The authors didn’t mention it, but the itaconate shunt inhibits succinate dehydrogenase (SDH), which breaks down succinate – resulting in increased succinate levels.
The two succinate elevations occur in different contexts: one results from metabolic activity during exercise, while the other results from inflammation. Could inflammation produced by exercise be propping up the succinate levels in ME/CFS patients and contributing to an itaconate shunt? I have no idea. 🙂
Purine Findings Suggest Treatment Options
In the end, the authors proposed that purine metabolism may serve as a potential novel treatment target but didn’t mention specific treatments.
High levels of ATP breakdown can have many consequences (Image from Jynto, CC0, via Wikimedia Commons)
The situation is complex given purines’ role in many processes and the variety of purine inhibitors found. However, purine inhibitors might be able to help situations where exercise intolerance is present and in conditions in which high levels of ATP are broken down. High ATP breakdown occurs when high levels of metabolic stress are present, causing the cell to break down more ATP than it synthesizes and can cause numerous problems.
Under these conditions, the muscle’s ability to relax and produce force is impaired. (Bob Naviaux, some time ago, stated that the low-energy state found in ME/CFS results in contracted, tense muscles.) Increased lactate and H⁺ ion production can cause intracellular acidosis. A predilection for protein misfolding can result in protein aggregations that gum up the works. All in all, high levels of ATP breakdown – which appeared to be happening in these long COVID patients – result in muscle fatigue, cellular stress, and metabolic imbalances.
We also might want to inhibit high levels of purine production because it can produce metabolites such as inosine and hypoxanthine that can be broken down into uric acid. Uric acid—which some ME/CFS/Long COVID doctors test for—enhances oxidative stress (the last thing anyone with these diseases wants more of) and muscle fatigue.
Purine Inhibitors
I asked ChatGPT AI and Perplexity AI about purine inhibitors and individuals with exercise intolerance or post-exertional malaise. ChatGPT AI suggested that the same kinds of purine inhibitors might be helpful for either condition.
Even though ME/CFS, fibromyalgia, and post-infectious diseases were the most commonly recommended diseases, I had not heard of most of these used to treat these disorders. All the drugs came with some cautions – but most seemed manageable.
Xanthine Oxidase Inhibitors (XOIs)
- Would work best in individuals with mitochondrial dysfunction or metabolic fatigue by reducing oxidative stress and improving energy efficiency
| Drug | How It Helps? | Who Might Benefit? |
|---|---|---|
| Allopurinol | Lowers uric acid and oxidative stress, improves nitric oxide bioavailability for better muscle oxygenation and endurance. | Individuals with mitochondrial dysfunction, chronic fatigue syndrome (CFS), fibromyalgia, or exercise-induced oxidative stress. |
| Febuxostat | Selectively blocks xanthine oxidase, reducing oxidative stress and ATP depletion without affecting other metabolic pathways. |
Purine Synthesis Inhibitors
- Best for people who need to manage chronic inflammation and immune overactivation, which can impair recovery and energy metabolism.
| Drug | How It Helps? | Who Might Benefit? |
|---|---|---|
| Methotrexate (low dose) | Reduces chronic inflammation and autoimmune responses that contribute to exercise intolerance. | Individuals with autoimmune disorders (RA, lupus, inflammatory myopathies) that impair exercise capacity. |
| Azathioprine | Suppresses excessive immune activation, preventing muscle and joint inflammation that limits exercise. | People with chronic fatigue, muscle inflammation, or post-viral syndromes (e.g., |
3. Adenosine Deaminase (ADA) Inhibitors
🔹 Best for: Boosting adenosine levels to enhance blood flow, ATP conservation, and reduce metabolic stress.
| Drug | How It Helps? | Who Might Benefit? |
|---|---|---|
| Pentostatin | Increases adenosine levels, leading to better vasodilation, oxygen delivery, and mitochondrial function. | Individuals with poor circulation, endothelial dysfunction, or metabolic fatigue (e.g., chronic fatigue syndrome, fibromyalgia, or long COVID). |
4. Purine Analog Nucleosides
🔹 Best for: Supporting mitochondrial function, ATP balance, and muscle recovery.
| Drug | How It Helps? | Who Might Benefit? |
|---|---|---|
| Ribavirin (purine analog) | Helps maintain nucleotide balance, preventing excessive ATP depletion. | Individuals with chronic fatigue, mitochondrial disorders, or viral-induced exercise intolerance. |
| Cladribine | Influences nucleotide turnover, possibly reducing exercise-related muscle degradation. | Endurance athletes or individuals with persistent muscle damage. |
Suramin?
Suramin (Image from Lanulos, Public domain, via Wikimedia Commons)
What about Suramin – the drug that Bob Naviaux has specifically targeted for ME/CFS and other post-infectious diseases?
Suramin is a different kind of purine-inhibitor. Instead of blocking purine metabolism, Suramin blocks purine receptors (P2X and P2Y) from signaling when signs of metabolic breakdown, such as ATP and ADP, are present. Bob Naviaux, if I remember correctly, believes that signals of metabolic stress, such as ATP and ADP, are causing the cells of ME/CFS patients to hunker down and exist in a low-energy state.
Suramin can also reduce the high levels of ATP breakdown (see above) found in ME/CFS, fibromyalgia, and long COVID-19. Overall, Suramin may be able to reduce high levels of ATP breakdown, improve energy efficiency, reduce inflammation, and protect neurons.
Great article Cort!!
What ever happened to Suramin? I vaguely remember the pharmaceutical company who manufactured it for African sleeping sickness, had purity issues. yet the WHO allowed it to be used in emergency situations for disease in Africa because the disease was worse than any side-effects from impurities. So it wasn’t pure enough to be allowed into clinical trials. Is that correct? And if so, surely they must have improved the purity by now?
I wonder if Bob Naviaux ever got a pure supply of it? or, if not did that hold up his studies? Because I remember he was wanting to use Suramin years ago in ME/CFS after a successful Autism trial.
An important point that people might not be aware of, is there is an overlap of multiple symptoms between autism and ME/CFS. (16 symptoms last time I looked) It’s almost like a ME/CFS type of illness is what triggered infant autism.
Imagine severe brain fog as an infant. It would be very difficult to form neuro pathways during that crucial developmental stage. Communication would be very difficult. Maybe the kids grow out of the ME/CFS stage so don’t display ‘Post Exertional Malaise’, but by then the damage is done to the brain due to the lost opportunity for early neural development.
And interestingly a percentage of autistic children do go onto develop ME/CFS as teenagers.
Also there is a higher number of autistic children (compared to the same number of healthy children) who developed long Covid. And psychiatrists in the UK wrongly assumed it was (yet again) behavioural, without realising there was already an overlap between ME/CFS and some forms of autism.
I asked him a couple of months ago I think it was about the trial – and did not get a response. I thought the trial was getting close when the pandemic started – and I wonder if it got thrown off. I don’t know what its status is right now.
Fingers crossed. This somehow sounds right: mechanism for the damage and possible treatments.
The measurements from exercise are all/mostly known results – and make sense with the lived experience of the diseases.
Without starting from zero.
I’m concerned about seeing a reliance on information from AI from a science-based publication. As we are all no doubt aware, generative AI is not intelligent. It’s simply a very fancy averaging machine. It can often return accurate information, but it can also very easily return inaccurate information and there will be no way to tell the difference. I am unsurprised to see laypeople asking AI for medical information, though I always warn them when I see them doing so. But for a scientifically minded organization to be depending on AI—and then *publishing* that AI-derived “information”—is incredibly worrying to me, and makes me trust the rest of the information I see here less. I hope you will address this in the future, because I and many others in the ME/CFS and Long Covid communities depend on your information! Which is why I hope you will ensure it is reliable moving forward by removing AI from your process or at the least having a verification process (with reliable, human-made information) for anything you get from AI. Please understand I mean this with all respect, this publication has been one of my primary sources of information since not long after I got Long Covid, and I hold you in the highest respect. That’s why this caught me so off guard.
Thanks JS for your nice words! I appreciate them.
This is quite an issue because I am finding AI VERY helpful. I really am.
I’m mostly using Pro Perplexity AI which provides citations and the questions I’m asking tend to be very technical as well. I would find it hard to drop it now.
For instance – a question “what does it mean when a net extraction of amino acids is seen during an exercise test?” brought up an answer which derived from dozens of published papers, a couple of books and two websites.
A question “what do high succinate levels during an invasive exercise test indicate?” used 28 scientific journals and one UCLA website.
A question “Could high succinate levels found during an invasive exercise study contribute to an itaconate shunt?” told me that it’s possible but no direct link has been established in the literature. That answer came from an assessment of over 20 published papers plus Health Rising. (I didn’t particularly like seeing Health Rising in there actually.)
I do sometimes see general websites including Health Rising and MEAction show up but the questions I
ask has Perplexity turn almost entirely to scientific papers.
The list of purine inhibiting drugs from ChatGPT Plus. That’s bit of an anomaly as I’ve mostly moved over to Perplexity AI Pro in part because it gives citations.
If you have any suggestions how I can make the best use of AI without compromising the integrity of the information please let me know either here or via email. One thing I can promise is to use AI generated information that’s derive from scientific papers – or a few select websites.
Thanks!
I feel a lot better about it knowing there are citations (and I’m assuming you’re checking those citations to make sure they’re actually saying what the AI summary says they’re saying). The most important thing with AI is verifying, so as long as you’re using those citations to confirm the info you’re being given, I feel much better about the information quality. Thanks again for the great work you’re doing!
Please, please check the references to verify that they actually support what AI is saying. AI does not always correctly synthesize or summarize information; it’s just really good at wording things in a way that it sounds like it knows what it’s talking about. Thanks for being upfront about what information is from AI so we can do our own research, but I also saw that and thought, “Oh! I had kind of hoped this was a responsible organization with accurate information.” I only recently signed up for the mailing list and, after reading an AI summary with no indication of medical review or oversight, lost some faith in the articles. (Again, though, being upfront about it is much better than posting potentially inaccurate information without any kind of disclaimer.)
Based on what you said, there may be too many websites to check, but a quick search to find medical articles related to the specific topic/assertion that was produced could help verify it, or if the AI makes it clear which references support specific assertions, you could click on those to confirm.
Are those links checked out? AI tools often make up credible sounding links that lead to a death end or link to existing papers that have completly different content then what the AI claims it has.
Even With citations you have to be careful cort. Watched a piece on this very issue where the citations either didn’t exist ir were fac smilies of ball park similar ideas.
Literally non of the citations but one were correct.
So better to double down in ang citations at this point
All well and good. How do I treat/try for my wife in the Akron Ohio with these novel pharmaceutical treatments?
Her gp is not up to date with your research. Two year long Covid. Nothing works.
Thank you
Joe juska
joejuska@gmail.com
Following, I have a similar question. The science is moving forward, but what do we, as patients, do to try to apply this?
Great Cort, thanks.
I remember your 2022 article, “A Gas Exchange Disease?” (https://www.healthrising.org/blog/2022/06/25/chronic-fatigue-syndrome-gas-exchange-disease/), and it came to mind recently.
A friend’s husband was admitted to the hospital in Feb. 2024 and diagnosed with elevated oxidant output (metabolic alkalosis). His PO₂ was 81.9 mmHg and SO₂ was 97.2% — but the test was reported as a venous blood sample. Whether it was venous or arterial wasn’t clarified, but if it was venous, those readings might indicate an issue with oxygen utilization at the tissue level.
He was prescribed allopurinol for hyperuricemia, but the treatment had an overall negative effect, likely due to his underlying Von Willebrand Factor issue (VWF 8 / Hemophilia A).
In my own case, I initially had a positive experience with methotrexate in 2022— I noticed improved muscle function and significant relief from lupus symptoms, to the point I thought it might be a breakthrough. However, after three weeks of using metex® PEN 17.5 mg once per week, I had to stop due to serious side effects: excessive bleeding (blood in both stool and urine), likely related to VWF types 2 and 5, and Antiphospholipid Syndrome (APS), along with sudden and excessive hair loss.
Based on this, I strongly recommend that patients ask for a VWF test before accepting certain medications, especially those with bleeding or thrombosis risk profiles.
I totally agree with the metabolic derangement theory Cort. I also think that there is a genetic component where our bodies compensate for years untill a high metabolic demand( infection, stress, trauma, inflammation, toxin) break this ability to compensate. I have recently discovered that I have a mutation in a gene causing PDH ( pyruvate dehydrogenase) deficiency. This would explain the inability to feed the Krebs cycle, the build up of lactic acid, the low oxygen extraction ( if the Krebs cycle is not functioning as it should) it would also explain the exercise intolerance, the immune disregulation due to perhaps lactic acidosis, the autonomic nervous system malfunction etc. If our bodies run on glycolysis we will produce only 2 net ATP instead of 36 from cell respiration. If pyruvate is not feeding the Krebs cycle then amino acids and fatty acids would need to fuel it. I do also have another genetic mutation which leads to reduced beta oxidation of fatty acids so for me it’s the amino acids that are left. Or at least this is my theory. For others it could be high insulin. If the insulin is elevated then the body is unable to use fats for energy so again it’s the amino acids that remain as fuel. My recent blood tests show elevated uric acid but I also see alot of this in a Facebook group about insulin resistance. I don’t still know how to overcome this block. I am still reading and researching. Sadly the increase in lactic and uric acid carry damaging effect for our vascular health. I now have small vessel damage which I don’t know how to repair. The issue with my theory is that these genetic mutations are very rare where ME/CFS is not. Do you have an idea when the biggest UK genetic study is due to report?
Hi Cort, thank you!
Your write: “The two succinate elevations occur in different contexts: one results from metabolic activity during exercise, while the other results from inflammation. Could inflammation produced by exercise be propping up the succinate levels in ME/CFS patients and contributing to an itaconate shunt? I have no idea. 🙂”
Yours is a good question – and we´d be closer to answering it if CPET measurements would be repeated in the subsequent PEM phase as the latter certainly has a different pathobiological underpinning as the trial phase. Don´t get me wrong: of course studying the immediate reaction to exercise is of great interest and value – but so is what happens in the body thereafter when it transitions into this highly specific clinical state of PEM.
Looking at 99.9 percent of ME/CFS research I sometimes wonder: is there a kind of phobia among researchers to collect data from patients during PEM? We´d be far better off in our understanding of ME/CFS if we had more comparative work on what the hell is different in these bodies when they are in their normal baseline – and when they are in the hell of PEM.
Great comment! I’ve wondered the same thing: why aren’t measurements being done in those later days, after the trial is over and patients are in full-blown PEM? I know my body is in a very strange state during PEM, very hard to describe, and then it dissipates on its own over the course of some days (or weeks) of rest.
Cort-keep using AI please. This was a solid article with a good addition about possible medications.. My son just used ChatGPT to review his mother’s medications. She had just seen a cardiologist who was not her own because she was in a very complicated medical crisis. ChatGPT said the medication this doctor had just prescribed was contraindicated (as it doubled a heart medication she was already on) plus some other issues. The pharmacy had filled the prescription. This gave him confidence to contact her own cardiologist’s office on an emergency basis. He was perfectly aware that AI could be wrong but in this instance it was spot on.
Hi Cort, Good blog. What you write gets to the core of our problem in the most objective way. I would like to note that the medication you mention such as Methotrexate and Azathioprine can have serious side effects and are not ideal. I know this from the experience of some people in my environment who have tried this. Even a low dose gave adverse effects such as becoming hypersensitive to infections.
That is the question..what did happen to suramin? It was my great hope and this is like 10 year old ideas….breaks my heart we just retread old groubd without truly establishing whether these things work
Yes…over the many decades I’ve been ill, I’ve witnessed different researchers thinking they are doing research that they think is new but if they would look back,they would see many of the research has already been gone through….big waste of sick peoples valuable time.
While many of us have nothing but time,we’d love to get on with our lives…what little bit we have left in many cases
I totally agree. I’m starting to think some of these findings are too radical for the stars quo because they’re literally showing its the environment that’s raking people out. Or rather big money toxins
It makes no sense to me that after naviaux completed the stage 2 surMin trial which was successful, that he just left it.
Similarly, the university of Bristol ( I think) had a professor trialling this similar purine therapies fir b.p. meds.
Then he and his work just disappeared
Bob naviaux, I belueve is working for nasa now. I’m hoping that the similar issues astronauts face with mitochondria etc that he gets backing and can extrapolate any therapies out to the general public maybe ggsts hus plan?
What I dont understand is layman like you and I have managed to dial in on these therapies years ago and have been urging scientists to look at these ideas
Then nea scientists show up thinking they’ve found the holy tail.
Don’t grt me wrong, I’m appreciative but also flabbergasted by the inertia
So… does this make hyperbaric oxygen therapy a good or bad idea?
“This is the first invasive exercise study to use metabolomics (the study of metabolism) in an invasive exercise study.” – Wasn’t Maureen Hanson first with the urine metabolomics 2-day CPET study? Or does “invasive exercise” mean something different (what does invasive exercise mean?) Thanks as always Cort!
Maybe you could add a brief explanation to the Gist…? Thank you very much!
I quickly ran the drugs through a German online apothecary and Wikipedia for prices and primary uses, with the following results (no guarantee for mistakes):
The first 4 drugs on the list are cheap (without looking further into their primary uses or side effects).
Pentostatin is an anticancer chemotherapeutic drug with – according to German Wikipedia – severe side effects.
Ribavirin is an expensive (3 digits) antiviral.
Cladribin is an expensive (4-digit) Multiple Sclerosis treatment, and is also a cancer chemotherapeutic.
Vaguely reminds me of an ME/CFS patient who reported online that she got better after (of all things) cancer chemotherapy.
☝️that’s why I decided to try fenbendozole
( anti-cancer) …and I can report my lymph lumps are shrinking.i don’t have cancer that I know of.
I took one single dose of ivermectin and had surprisingly good result. I’ve been around animals all my life so put my betting money on parasites