HBOT for ME/CFS/CFIDS

HBOT- Has a course of this treatment helped you?

  • Yes It helped a bit

    Votes: 2 12.5%
  • Yes It helped Moderately

    Votes: 4 25.0%
  • Yes It helped a lot and I feel much better

    Votes: 4 25.0%
  • No It made me worse

    Votes: 0 0.0%
  • No, I felt no difference in symptoms, but did not worsen symptoms

    Votes: 5 31.3%
  • I felt so bad on HBOT that I was forced to stop before I finished my course of treatment

    Votes: 1 6.3%

  • Total voters
    16

Silencio

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believe hard chamber treatments are limited to 90 minutes sometimes with a 15-min air break in the middle.
They are designed to get you 60 mins of oxygen treatment at 2.4ata depth. Ten mins to dive w no mask, ten min break from pure oxygen at bottom, but while still at depth breathing the chamber air, and then ten mins back to surface w no mask.
 

Moof

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I think it's important to say what pressure, what gas you were breathing, and how long each session lasted.
Funnily enough, I contacted the local MS centre last week about possibly renewing my membership to do HBOT again. I had to stop the original course because I was still working at the time, and just couldn't find the extra energy to travel to the centre, battle the claustrophobia, and endure the noisy environment. (I have ASD as well as ME, and struggle with sensory sensitivity.)

If it's still available to non-MS patients and I can afford it, I'm planning to do another course. They offer dives to various depths, starting low and building up, and I'm sure I'd be able to get accurate information about the pressure and gases. I'll post about it if I'm able to go ahead.
 

Wayne

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The logic of HBOT is that any biochemical reaction that uses oxygen as a substrate can be driven faster.
Makes sense--here's another layer of logic. I have a home mHBOT unit, which I bought for a variety of reasons, one of those to treat Lyme. I'd read some pretty incredible Lyme testimonials of successful treatment, apparently because Lyme bacteria thrive in the body where there's less or no oxygen, such as cartilage, joints, brain, etc. The highest concentrations of oxygen is normally in the blood, but when using HBOT, you get increased levels of oxygen literally everywhere, which can eradicate (oftentimes) hidden infections.

I'm guessing you'll be back to normal pO2 in minutes, but I've not found data on this despite looking pretty hard.
One thing I noticed in the beginning of doing mHBOT was that my face would become flushed afterwards, and would sometimes last for several hours. I don't know why, but one reasonable explanation would be that there was more oxygen in my system. Just a hypothesis, but thought I'd mention it, as oxygen levels might stay higher than just a few minutes. I actually suspect they do.

multiple sessions only make sense if there is some cumulative benefit.
I've done both hard chamber at 2.0 ATA, and soft chamber at 1.3 ATM. I did several sessions at 2.0, and at one point realized it felt too intense. My last couple of sessions were at 1.75, which felt better. I sometimes wish my 1.3 ATA chamber would go a little higher, which I might be able to finagle at some point. I suspect my "ideal" pressure would be 1.5 ATA. The woman I bought my chamber from said that to get the benefits of a higher ATA than 1.3 ATA, just stay in the chamber a little longer. Whether that's true or not, I can't say. She seemed to think it was ALL about increased oxygen, and not about the pressure, even though higher pressures would increase oxygen levels faster.

If anyone has experience 2.4 ATA HBOT for longer treatments, I'd like to know. I've heard you can sleep in a soft chamber - so longer treatments but lower pO2.
I use my chamber almost daily, and go to sleep 90%+ of the time. My average times in the chamber is probably about 45 minutes, but probably range between 30 minutes and an hour. After several months of regular use, I feel I've been able to sense when my body has had enough on a given day, and even occasionally when to skip a day. I've become a believer in doing long-term lower ATA treatments vs. shorter term higher pressure treatments (which can apparently become stressful to the body after a while).

If anyone has added supplemental oxygen to a soft chamber, please let me know.
I use supplemental oxygen in my chamber. I had gotten 3-4 sessions in a clinical setting (1.3 ATA soft chamber) without using supplemental oxygen, so was able to do a bit of a comparison. Though I feel I got good results without the oxygen, I much prefer having the supplemental oxygen, and feel it's more effective.

From my perspective, the most important difference between the two chambers is the duration of treatment.
I would tend to agree. I've come to believe--at least in most cases--a person can get the same (or very close to the same) benefits from a soft mHBOT chamber as they can from a hard HBOT chamber.
 
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20 years ago I had hard chamber sessions of 60 minutes duration, 5 days at a time. ...Then a few months rest before the next course of 5 days. Gas was pure oxygen. I also had IV vitamin C - 40 grams prior to each dive. Not sure now of the pressure. I had to fly to another city to have treatments and I stopped after a couple of years.
I noticed improvements in sleep quality and energy levels while having treatment and for a time after, but these benefits didn't last long term.
 

used_to_race

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Since we've been thinking a lot about HBOT as a possible means of escaping the IDO metabolic trap, let me say a few things about HBOT that I've learned by reading and talking to physicians and patients.
Has there been any additional discussion on the forums of this topic? I had heard Dr. Davis was thinking about this but didn't know it was much more than a thought experiment.

One other point regarding the survey... If you've experienced improvement, it would be helpful to indicate if that improvement was just as you left the chamber or if the improvement was still noticeable at the time you began the next session. This would be a good sign that cumulative benefit is possible.
Before I get into your other points I want to mention up top that I never feel any different upon exiting the chamber. I've been doing mHBOT 5-7 times a week for about an hour since around May 2018 and I am pretty sure all benefits have been cumulative. This aligns with most of the other accounts I've heard and read from people who have some post-infectious chronic illness and benefited from mHBOT. Importantly, a key feature of most of these experiences (including mine) is that consistent benefits don't become apparent for a few months or even a year. Like I said, I started in spring 2018 and wasn't confident the HBOT was helping until early 2019. I did add in other medications in the meantime which makes things less clear. I have not tried going a long period of time (a week or, more interestingly, 1-3 months) without doing HBOT, but that might shed some light on whether these perceived cumulative benefits are reversible or lasting. What do you think about this Dr. Phair?

To my knowledge you are basically breathing compressed air, so only 20% or so oxygen.
The gas coming out of the oxygen concentrator (into the mask which is worn inside the chamber) is 100% oxygen to my knowledge. However the chamber itself is filled with air and must mix with the oxygen coming out of the mask to some degree, as it is not sealed. So the patient is likely breathing very oxygen-rich air, but I would only be guessing if I were to offer a percentage. Maybe there's a device I can use to measure this, but I wouldn't really know where to look. I want to clarify that most people using mHBOT at home are breathing this compressed, concentrated oxygen through a mask, so there is definitely increased oxygen going into the lungs compared to just compressed air.

I measure a pressure inside my chamber of (measured using phone barometer) 1.285ATA or 976 mmHg. Using the alveolar gas equation and assuming 40% as the fraction of inspired oxygen (looks like partial pressure of water is constant with respect to pressure right?), I get:

PaO2 = (976- 47) * 0.4 - 40/0.82 = 322.8 mmHg

compared to sea level conditions given in the link above which yields around 100 mmHg. If we assume no mask and 21% oxygen in the chamber, we still get around 150 mmHg, so it's a big improvement over sea level but not that significant compared to with mask. If you were to go to 2.4 ATA and 100% O2, you'd get well over 1600 mmHg. How partial pressure of oxygen relates to intracellular oxygen concentrations and thus potential substrate action upon IDO1 is a matter for folks more learned than myself (or at least those with more time). I know, for example, that hemoglobin is basically saturated at sea level conditions anyway, so there is a binding capacity that can't be exceeded for this. This would be affected by our evolution at sea level and above I assume, so perhaps we have evolved to have certain rates of absorption of our cell walls, certain binding capacities of intracellular molecules, or whatever else. But if it's just oxygen in solution inside the cell, then I think there would be a big difference - again assuming we can bring the extra oxygen through the cell membrane at a decent rate which may not be the case, perhaps supporting a test of longer mHBOT sessions of hours or more.

Other theories could easily have good reasons to try HBOT as well.
Could you elaborate on this when you get a chance? I have my own thoughts but would love to hear yours.

If someone knows how long it takes to get back to normal pO2
This seems like it would take only minutes (or less), as you said. I wonder if it has been measured in the context of diving studies, but divers coming up too fast will have nitrogen coming out of solution in their blood very quickly. So unless the intracellular environment is special, I think any dissolved gases that were acquired during HBOT will come out of solution within a minute or so.

Without knowing the Km values of the enzymes I think a good rule of thumb would be to maximize the product of pO2 and duration with due consideration for the balance of potential risk and potential reward.
I think divers say not to exceed 0.5 bar of pO2 for very long, but mHBOT doesn't get too close to this limit. I would feel okay spending hours in the HBOT. The limiting factor for me is that it gets kind of hot and gross in there if you spend too long inside. Summer in LA is not the best time to test this out...

Lastly, have you considered the effects of Ozone Therapy and whether it might offer similar benefits as far as intracellular oxygen concentration? I haven't looked into it much but that could be interesting.

Thanks for your thought-provoking post.
 

used_to_race

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One thing I noticed in the beginning of doing mHBOT was that my face would become flushed afterwards, and would sometimes last for several hours. I don't know why, but one reasonable explanation would be that there was more oxygen in my system. Just a hypothesis, but thought I'd mention it, as oxygen levels might stay higher than just a few minutes. I actually suspect they do.
This is probably from nitrogen coming out of solution in your facial capillaries and causing flushing rather than oxygen staying in solution. Do you get flushed when inside the chamber as well or just upon coming out? If it happens only upon exiting then it probably isn't due to oxygen.

I've done both hard chamber at 2.0 ATA, and soft chamber at 1.3 ATM. I did several sessions at 2.0, and at one point realized it felt too intense. My last couple of sessions were at 1.75, which felt better. I sometimes wish my 1.3 ATA chamber would go a little higher, which I might be able to finagle at some point. I suspect my "ideal" pressure would be 1.5 ATA. The woman I bought my chamber from said that to get the benefits of a higher ATA than 1.3 ATA, just stay in the chamber a little longer. Whether that's true or not, I can't say. She seemed to think it was ALL about increased oxygen, and not about the pressure, even though higher pressures would increase oxygen levels faster.
I think at 2.0 and 1.75 ATA you'd be risking getting mild oxygen toxicity after more than 30 minutes or so, it could have been that. You can replace the relief valves at the foot of the chamber with ones that are calibrated to open at 1.5, but then your seams or zippers might fail. I can send you a link to the product if you want.
 

Wayne

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So the patient is likely breathing very oxygen-rich air, but I would only be guessing if I were to offer a percentage.
I don't know if this is helpful, but the woman I bought my mHBOT chamber from told me that if I don't use a cannula with the oxygen that's coming into the chamber, I can still get as much as 80% of the increased oxygen without using the cannula.

I can send you a link to the product if you want.
I would love to have a link to that. The woman I bought my chamber from said that they're are built to exceed 1.5 ATA, so I have no worries about that whatsoever. Apparently, 1.5 ATA is common in Europe, and they built their chambers to withstand that amount of pressure. -- My mHBOT brand is Summit to Sea.
 

used_to_race

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I would love to have a link to that. The woman I bought my chamber from said that they're are built to exceed 1.5 ATA, so I have no worries about that whatsoever. Apparently, 1.5 ATA is common in Europe, and they built their chambers to withstand that amount of pressure. -- My mHBOT brand is Summit to Sea.
I don't think HBOT in general is that common anywhere, lol. Nevertheless, here is the link to the part. I seem to have misremembered, they give a range for the opening psi of the valve. 1ATA is 14.7psi. The chamber adds about 4psi using P/N B-51019-1 in that link. If you replaced those valves with P/N B-51019-2 you'd get right around 1.5ATA. Personally I wouldn't do this, I think the zippers or windows would fail a lot faster. But if you can afford subsequent repairs I'd say it's a cool experiment.
 

perrier

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Has there been any additional discussion on the forums of this topic? I had heard Dr. Davis was thinking about this but didn't know it was much more than a thought experiment.



Before I get into your other points I want to mention up top that I never feel any different upon exiting the chamber. I've been doing mHBOT 5-7 times a week for about an hour since around May 2018 and I am pretty sure all benefits have been cumulative. This aligns with most of the other accounts I've heard and read from people who have some post-infectious chronic illness and benefited from mHBOT. Importantly, a key feature of most of these experiences (including mine) is that consistent benefits don't become apparent for a few months or even a year. Like I said, I started in spring 2018 and wasn't confident the HBOT was helping until early 2019. I did add in other medications in the meantime which makes things less clear. I have not tried going a long period of time (a week or, more interestingly, 1-3 months) without doing HBOT, but that might shed some light on whether these perceived cumulative benefits are reversible or lasting. What do you think about this Dr. Phair?



The gas coming out of the oxygen concentrator (into the mask which is worn inside the chamber) is 100% oxygen to my knowledge. However the chamber itself is filled with air and must mix with the oxygen coming out of the mask to some degree, as it is not sealed. So the patient is likely breathing very oxygen-rich air, but I would only be guessing if I were to offer a percentage. Maybe there's a device I can use to measure this, but I wouldn't really know where to look. I want to clarify that most people using mHBOT at home are breathing this compressed, concentrated oxygen through a mask, so there is definitely increased oxygen going into the lungs compared to just compressed air.

I measure a pressure inside my chamber of (measured using phone barometer) 1.285ATA or 976 mmHg. Using the alveolar gas equation and assuming 40% as the fraction of inspired oxygen (looks like partial pressure of water is constant with respect to pressure right?), I get:

PaO2 = (976- 47) * 0.4 - 40/0.82 = 322.8 mmHg

compared to sea level conditions given in the link above which yields around 100 mmHg. If we assume no mask and 21% oxygen in the chamber, we still get around 150 mmHg, so it's a big improvement over sea level but not that significant compared to with mask. If you were to go to 2.4 ATA and 100% O2, you'd get well over 1600 mmHg. How partial pressure of oxygen relates to intracellular oxygen concentrations and thus potential substrate action upon IDO1 is a matter for folks more learned than myself (or at least those with more time). I know, for example, that hemoglobin is basically saturated at sea level conditions anyway, so there is a binding capacity that can't be exceeded for this. This would be affected by our evolution at sea level and above I assume, so perhaps we have evolved to have certain rates of absorption of our cell walls, certain binding capacities of intracellular molecules, or whatever else. But if it's just oxygen in solution inside the cell, then I think there would be a big difference - again assuming we can bring the extra oxygen through the cell membrane at a decent rate which may not be the case, perhaps supporting a test of longer mHBOT sessions of hours or more.



Could you elaborate on this when you get a chance? I have my own thoughts but would love to hear yours.



This seems like it would take only minutes (or less), as you said. I wonder if it has been measured in the context of diving studies, but divers coming up too fast will have nitrogen coming out of solution in their blood very quickly. So unless the intracellular environment is special, I think any dissolved gases that were acquired during HBOT will come out of solution within a minute or so.



I think divers say not to exceed 0.5 bar of pO2 for very long, but mHBOT doesn't get too close to this limit. I would feel okay spending hours in the HBOT. The limiting factor for me is that it gets kind of hot and gross in there if you spend too long inside. Summer in LA is not the best time to test this out... above

Lastly, have you considered the effects of Ozone Therapy and whether it might offer similar benefits as far as intracellular oxygen concentration? I haven't looked into it much but that could be interesting.

Thanks for your thought-provoking post.
I'm very glad ozone was brought up; the best ozone machine is the hocatt; your whole body is immersed in this apparatus. This machine did result in a marginal improvement. I was rather surprised to learn that it is very hard to find practitioners who have the hocatt. Even in California! I called around LA and could not find it. Forget about Canada--not a chance. But this is a very interesting machine. It is /was around 35 thousand dollars if not more when I enquired years ago. But it seems to require someone on the outside, a technician, monitoring the person. It gets rave reviews and I do not understand why more physician don't have it. There is another gas that this machine releases besides ozone.

We also have ozone sauna, and no benefits. But the hocatt is not your ordinary ozone sauna at all.
I wonder what Dr Phair thinks of this.
https://hocattusa.com/how-it-works/
 

HTester

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Before I get into your other points I want to mention up top that I never feel any different upon exiting the chamber. I've been doing mHBOT 5-7 times a week for about an hour since around May 2018 and I am pretty sure all benefits have been cumulative. This aligns with most of the other accounts I've heard and read from people who have some post-infectious chronic illness and benefited from mHBOT. Importantly, a key feature of most of these experiences (including mine) is that consistent benefits don't become apparent for a few months or even a year. Like I said, I started in spring 2018 and wasn't confident the HBOT was helping until early 2019. I did add in other medications in the meantime which makes things less clear. I have not tried going a long period of time (a week or, more interestingly, 1-3 months) without doing HBOT, but that might shed some light on whether these perceived cumulative benefits are reversible or lasting. What do you think about this Dr. Phair?
@used_to_race What I think about this is that you've taught me a lot I need to know. One of the great things about PR and S4ME is there is such a wealth of experience out there, I can just post what I'm thinking and find out if someone's experience can rule it out. Thank you for this provocative post. I'll be thinking about how it could be cumulative for a long time.
 

HTester

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I know, for example, that hemoglobin is basically saturated at sea level conditions anyway, so there is a binding capacity that can't be exceeded for this.
This is exactly correct. HBOT in any form is aiming to increase pO2 in plasma and then the gradient of pO2 from plasma to cells will be shifted up so that intracellular pO2 cannot fail to be increased for the duration of the therapy.

looks like partial pressure of water is constant with respect to pressure right?
As soon as air is just a little way down the trachea it is saturated with water vapor, hence its partial pressure is constant. Made me smile broadly to see a reference to the alveolar gas equation. Did you know about alveoli prior to having to learn this stuff to do HBOT rationally?
 
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@HTester

Hi Dr. Phair,

very severe patient here, my family has a portable chamber.

Do you see any specific dangers in trying this treatment? I am not looking for a „yes, it is safe“, I know you can not know, I am looking for specific things that you see could be an issue?

What about more oxygen and the potential of even higher oxidative stress?

ty!
 

used_to_race

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This is exactly correct. HBOT in any form is aiming to increase pO2 in plasma and then the gradient of pO2 from plasma to cells will be shifted up so that intracellular pO2 cannot fail to be increased for the duration of the therapy.
Do we know anything about these gradients or the resulting intracellular pO2? I gather from the news about metabolic trap stuff so far that measuring anything intracellularly is very hard in general. Assuming the metabolic trap hypothesis is valid, do we have some idea of how much pO2 must change in order to "un-clog" IDO1 inside the cell? Presumably one could calculate the rate of clearance of tryptophan as a function of pO2 to predict the outcome of a treatment like mHBOT.

As soon as air is just a little way down the trachea it is saturated with water vapor, hence its partial pressure is constant. Made me smile broadly to see a reference to the alveolar gas equation. Did you know about alveoli prior to having to learn this stuff to do HBOT rationally?
I used to be a competitive cyclist and was living in Colorado for some time trying to make professional racing work out, so I came across the equation when looking into doing some training camps at higher altitude and so forth. Not sure if this is relevant but I initially got sick when I was spending a lot of time above 3000m, and ever since I started looking into HBOT I felt like maybe that had something to do with my onset. Putting it in terms of the metabolic trap, if IDO1 functions more poorly at high altitude due to lower pO2 inside the cells, then the threshold for tryptophan inside the cell to activate the trap in a predisposed individual is lower than at sea level. For me, the stimulus seems to have been EBV infection, but maybe living at altitude and trying for a few weeks to train and race despite feeling sick could have put me over the edge. I wonder if there are more cases of ME/CFS per capita in high-altitude places with a lot of non-native individuals living there, such as the Rocky Mountain States in the US.
 

HTester

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Do we know anything about these gradients or the resulting intracellular pO2? I gather from the news about metabolic trap stuff so far that measuring anything intracellularly is very hard in general. Assuming the metabolic trap hypothesis is valid, do we have some idea of how much pO2 must change in order to "un-clog" IDO1 inside the cell? Presumably one could calculate the rate of clearance of tryptophan as a function of pO2 to predict the outcome of a treatment like mHBOT.



I used to be a competitive cyclist and was living in Colorado for some time trying to make professional racing work out, so I came across the equation when looking into doing some training camps at higher altitude and so forth. Not sure if this is relevant but I initially got sick when I was spending a lot of time above 3000m, and ever since I started looking into HBOT I felt like maybe that had something to do with my onset. Putting it in terms of the metabolic trap, if IDO1 functions more poorly at high altitude due to lower pO2 inside the cells, then the threshold for tryptophan inside the cell to activate the trap in a predisposed individual is lower than at sea level. For me, the stimulus seems to have been EBV infection, but maybe living at altitude and trying for a few weeks to train and race despite feeling sick could have put me over the edge. I wonder if there are more cases of ME/CFS per capita in high-altitude places with a lot of non-native individuals living there, such as the Rocky Mountain States in the US.
Measuring things intracellularly is difficult mostly because the the concentrations of interest are in the uM or even high pM range. Since intracellular volume is on the order of 100 - 300 fL, you can multiply the two together and not get very much mass. To overcome that difficulty, you have to measure the total mass in a couple million cells. This is challenging because the plasmacytoid dendritic cells in human blood are somewhere between 0.1% and 1% of the PBMCs. Moreover, it's often tough to get blood from a CFS patient's vein and patients often have had experiences that require they limit the number of tubes they donate. It's a tricky balance. The lower limit of detection in a modern mass spec instrument is ~1 pmol. The lower limit of detection in a state of the art mass spec is ~10 fmol. We have only limited access to a 10 fmol instrument.

Do we have some idea of the pO2 necessary? No. We know the Km(O2) for IDO1 at normal [Trp]. We do not know the Km(O2) in the substrate inhibition regime. In truth, we do not even know that the "Trp-binds-first-and-impairs-O2-binding" theory is correct. An alternative theory is that high Trp binds to an allosteric site on IDO1 and inhibits the enzyme. In my talk at the Stanford Symposium in a couple weeks I'll show the structure of the IDO1 catalytic site; to me it seems reasonable that O2 just cannot get to the heme when Trp gets into the pocket first.

High altitude? Like you, I've been wondering this for years. There are very few docs with the experience to diagnose CFS even in the big coastal cities, so the logistics of answering the per capita question are daunting.
 

HTester

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@HTester

Hi Dr. Phair,

very severe patient here, my family has a portable chamber.

Do you see any specific dangers in trying this treatment? I am not looking for a „yes, it is safe“, I know you can not know, I am looking for specific things that you see could be an issue?

What about more oxygen and the potential of even higher oxidative stress?

ty!
@bread. The HBOT physicians worry about high pO2 because of possible convulsions. I don't know the mechanism of this. From my perspective, if the trap is correct, the biggest danger is inextricably tied to the reward. If you or we succeed in reducing Trp below the critical point (defined in our paper) then it is possible (maybe even likely) that there will be a sudden overshoot in the flux of kynurenine production and therefore in its downstream metabolites, some of which are neuroactive. I don't know if this overshoot will feel like heaven or hell, but at least in current model simulations, the overshoot appears to be the price you have to pay to escape the trap. Patients I know would pay any price.

Yes, there is surely the potential for greater oxidative stress. There are risks. We are on the edge of what's known.
 
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@bread. The HBOT physicians worry about high pO2 because of possible convulsions. I don't know the mechanism of this. From my perspective, if the trap is correct, the biggest danger is inextricably tied to the reward. If you or we succeed in reducing Trp below the critical point (defined in our paper) then it is possible (maybe even likely) that there will be a sudden overshoot in the flux of kynurenine production and therefore in its downstream metabolites, some of which are neuroactive. I don't know if this overshoot will feel like heaven or hell, but at least in current model simulations, the overshoot appears to be the price you have to pay to escape the trap. Patients I know would pay any price.

Yes, there is surely the potential for greater oxidative stress. There are risks. We are on the edge of what's known.

Thank you!

Can you give severe patients a hint of when approximately you will have results from the spectrometer? For many, including myself this would be very important to understand to gain some peace of mind, you can tell me it will be a year from now and it will be easier than waiting 2 weeks and not knowing it is only weeks. It is also important to understand for many because we have to weigh things against each other, in my case I am on the brink (I am overexerting for weeks on this forum as I feel I need more data points to achieve a decision of what to do next, the last 5 treatments made me worse) and do have also CCI and I am not sure would survive this surgery but on the other hand will have to try at some point.

So I hope your trap is correct and do surgery then, this is a potentially life altering decision, so every bit of information does help making it.

I hope you understand that I do not want to push you but I do have to ask, everything else would be madness from my point of view.

Let me know if you need more blood from a severe to very severe patient, have sent blood internationally before!

Also, are you aware of Wim Hof? His technique is the opposite of what we want to achieve, considering IDO trap, correct?

This is a study about hus technique:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4034215/


ty for everything.
 
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Do we have some idea of the pO2 necessary? No. We know the Km(O2) for IDO1 at normal [Trp]. We do not know the Km(O2) in the substrate inhibition regime. In truth, we do not even know that the "Trp-binds-first-and-impairs-O2-binding" theory is correct. An alternative theory is that high Trp binds to an allosteric site on IDO1 and inhibits the enzyme. In my talk at the Stanford Symposium in a couple weeks I'll show the structure of the IDO1 catalytic site; to me it seems reasonable that O2 just cannot get to the heme when Trp gets into the pocket first.
Is the hypothesis that a higher plasma pO2 might drive O2 into cells without changing the O2 carrying capacity of hemoglobin? Many folks with ME/CFS state that their blood volume is reduced, and, given people's OI problems, we are told to increase fluid and salt intake. I've wondered if EPO would be helpful, though rather than increasing plasma pO2 it would increase O2 carrying capacity of the blood. Different than what you are saying with HBOT, but maybe not completely unrelated.
 
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In my talk at the Stanford Symposium in a couple weeks I'll show the structure of the IDO1 catalytic site; to me it seems reasonable that O2 just cannot get to the heme when Trp gets into the pocket first.
Is it also possible that a virus or other trigger caused a change in the nuclear proteins regulating IDO1 expression so that its protein levels are decreased, thereby increasing Trp concentrations in the cell, then IDO2 isn't helpful at clearing Trp because of the 1-2 damaged genes (and therefore IDO2 protein)?

Edit: "IDO2 isn't helpful at clearing" *high Trp *levels because......"
 
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Is the hypothesis that a higher plasma pO2 might drive O2 into cells without changing the O2 carrying capacity of hemoglobin? Many folks with ME/CFS state that their blood volume is reduced, and, given people's OI problems, we are told to increase fluid and salt intake. I've wondered if EPO would be helpful, though rather than increasing plasma pO2 it would increase O2 carrying capacity of the blood. Different than what you are saying with HBOT, but maybe not completely unrelated.
With EPO you just make more red blood cells, increasing their concentration in the blood with respect to other things like plasma and WBCs or whatever. The binding capacity of hemoglobin stays the same. So you might be able to increase the oxygen carried in the bloodstream by a decent amount this way, but the missing piece of information is: which factors affect the amount of oxygen that can enter the cell?

In any case I think the first step is to confirm and demonstrate the metabolic trap hypothesis. Once this is done, you'd have to verify whether increased oxygen availability inside the cell will actually allow IDO1 to function again.

With regard to the blood volume stuff, it would be interesting to measure a patient's blood volume (via dilution) and hematocrit/RBC count before and after treatment with fludrocortisone. Specifically why does lower blood volume cause problems? If you're just adding fluids and it makes people feel better, then I wouldn't think the issue is oxygen delivery or delivery of some other essential compound.