Dr Cheney looking into low dose oxygen therapy at night

[keenly]

Sample of email from Dr Cheney as part of his concierge program.

'An interesting technological advance has recently shed light on sleep disturbance in CFS. This new technology allows for continuous monitoring of blood oxygen saturation all night long during sleep (www.pulseoximeter.org/cms50f.html) for $112 as well as tissue perfusion (www.pulseoximetersplus.com/quest-sleep-unit-wrist-pulse-oximeter-pc-68b/) for $275. The technology consists of a pulse oximeter on the finger tied to a wrist band that records the data while the patient is sleeping in their own environment.

A recent analysis of such data in one of my CFS cases was very informative at several levels. The patient collected sleep data using this technology (www.pulseoximeter.org/cms50f.html) on three consecutive nights with the first two nights having no changes and thus demonstrating good reproducibility night over night. On the third night, she removed her EMF protective shields consisting of under-pillow tektites (https://en.wikipedia.org/wiki/Tektite) and an Earthcalm Sanctuary Bracelet (www.earthcalm.com/emf-protection-pendants-bracelets). There was a notable and negative shift towards more desaturation within the critical first two hours of sleep without the EMF protective devices and her sleep was more impaired. Note that these devices do not so much block external EMF but rather modify the Schumann Resonance Effects of earth’s on electromagnetic field which has a day-night variation in amplitude (see https://en.wikipedia.org/wiki/Schumann_resonances).

Independent of the EMF effects observed, the technology demonstrated an increase in significant desaturations below 90% during the first two to four hours of sleep and a lower baseline saturation as well during the first two hours of sleep. It is noteworthy that this patient, as is most often the case in CFS, demonstrated almost no desaturation over baseline after a 30-second, end-expiratory breath-hold which means she has a very low oxygen throughput into cells and thus is in a very low energy state at the cell level. A low energy state based on mitochondrial down-regulationviii will lower the cardiac output which is seen in virtually all disabled cases of CFSvi. Lower cardiac outputs can increase the incidence of hypoperfusion which will then drive desaturation to compensate for hypoperfusion to avoid oxygen supply-demand mismatching which is fatal to cells. In addition, hypoperfusion in the brain will cause arousal via increased sympathetic tone and will destroy restful sleep. Hypoperfusion is most likely to be seen in the first two to four hours of sleep which is the deepest sleep and where CNS depression is at its greatest. CNS depression can reduce sympathetic tone that can help compensate for hypoperfusion and thus exaggerate desaturations which is what was documented with this CFS patient.

What this all means is that we may need to consider low dose oxygen (@ 1-2 lpm) to improve sleep and to be used especially during the initial hours of sleep to avoid excessive desaturation and resulting arousal which will destroy any chance for refreshing sleep and improved redox buffering (ie GSH/GSSG ratios) which restful sleep provides and at the core of CFS. Before we take such a step, I need to prove that 1-2 lpm of oxygen can be buffered by CFS patients using IVRT response criteria on the echo. We know that they cannot buffer oxygen @ 4 lpm by IVRT criteria but I suspect that most can buffer 1-2 lpm. We also need to consider EMF defense which appears to impair sleep as well'.

 

[MikeJackmin]

One patient? Three night's sleep?

 

[trishrhymes]

@keenly can you give us the source of this information? And is there any further information about other patients, or studies?

 

[keenly]

@keenly can you give us the source of this information? And is there any further information about other patients, or studies?

Dr Cheney sent it to me as a sample of the emails one can receive when they pay to join his consierge service.

 

[Little Bluestem]

The technology consists of a pulse oximeter on the finger tied to a wrist band that records the data while the patient is sleeping in their own environment.

I tried to get on of these from the local (very rural) medical supply store several years ago without success.

 

[anciendaze]

I think there will be more to this story. Some background:

Dr. Cheney, in addition to a number of enthusiasms which may not pan out, has done careful studies of heart function in patients with ME/CFS, beyond looking for traditional heart damage. He found there was a consistent increase in IVRT (isovolemic relaxation time). The time for heart muscle to relax limits the rate of filling of the left ventricle. This means reduced output even if ejection fraction is good.

You also see such an increase in healthy people suffering from hypoxia, like mountain climbers. The difference is that ME/CFS patients show a paradoxical response to supplemental oxygen during the test. It actually causes IVRT to increase, while in mountain climbers there is a decrease in IVRT with oxygen.

This points to a block in oxygen metabolism at a later stage where metabolic byproducts are being cleared. Evidence of PEM is consistent with this.

Continuous monitoring of O2sat during sleep can detect small drops in oxygenation which do not count as official sleep apnea. If we have disturbed autonomic function while upright, it is not stretch at all to assume disturbed function while asleep, when the autonomic function takes over while higher centers of the brain are either less active, or doing things unrelated to physiological needs of the rest of the body. The common observation of normal sleep paralysis during REM sleep is an example of how the rest of the body tries to ignore irrelevant activity in the brain.

Cheney's next step seems to be to treat drops in O2sat during sleep with low-dose supplemental oxygen, just to the point of relieving measured transient episodes of hypoxia during sleep, even if the patient does not meet ordinary diagnostic requirements for sleep apnea. It is important to realize that excess oxygen can make the problem worse, even if the patient avoids becoming dependent on supplemental oxygen. You only want to provide enough to promote normal sleep physiology.

I've just checked Harrison's Handbook of Physiology*, and found remarkably little on the metabolic activity of sleep despite considerable detail on endocrine and neurological activity. From a metabolic standpoint it is not even clear why people need sleep, since some phases of sleep are as active as waking.

This strikes me as a reasonable experiment which does not require new pharmaceuticals, etc. So far as I can determine, at this distance from the source, every step is subject to measurement.

There is the initial finding of increased IVRT during echocardiograms, and the paradoxical response to oxygen in patients for whom this is appropriate. There is the finding of episodic hypoxia actually measured during sleep, even if other evidence of apnea is absent. The result of successful treatment should be a decrease in IVRT measured during echocardiograms as a result of metabolic recovery during normal sleep.

This kind of thing does not require millions of dollars and committees of experts. It could also benefit individual patients in a matter of weeks.

* This title was a mistake. I meant Harrison's Principles of Internal Medicine 18th edition.

 

[Sushi]

The technology consists of a pulse oximeter on the finger tied to a wrist band that records the data while the patient is sleeping in their own environment.

My cardiologist is about to have me do a home sleep study which will measure oxygen as well as other markers. It seems to be the new standard for sleep studies--do it at home with a kit because no one sleeps well in a lab. There are a number of companies that supply home sleep study equipment. Tomorrow I'll find out the one that I'll be using.

 

[keenly]

My cardiologist is about to have me do a home sleep study which will measure oxygen as well as other markers. It seems to be the new standard for sleep studies--do it at home with a kit because no one sleeps well in a lab. There are a number of companies that supply home sleep study equipment. Tomorrow I'll find out the one that I'll be using.

Excellent.

 

[keenly]

I think there will be more to this story. Some background:

Dr. Cheney, in addition to a number of enthusiasms which may not pan out, has done careful studies of heart function in patients with ME/CFS, beyond looking for traditional heart damage. He found there was a consistent increase in IVRT (isovolemic relaxation time). The time for heart muscle to relax limits the rate of filling of the left ventricle. This means reduced output even if ejection fraction is good.

You also see such an increase in healthy people suffering from hypoxia, like mountain climbers. The difference is that ME/CFS patients show a paradoxical response to supplemental oxygen during the test. It actually causes IVRT to increase, while in mountain climbers there is a decrease in IVRT with oxygen.

This points to a block in oxygen metabolism at a later stage where metabolic byproducts are being cleared. Evidence of PEM is consistent with this.

Continuous monitoring of O2sat during sleep can detect small drops in oxygenation which do not count as official sleep apnea. If we have disturbed autonomic function while upright, it is not stretch at all to assume disturbed function while asleep, when the autonomic function takes over while higher centers of the brain are either less active, or doing things unrelated to physiological needs of the rest of the body. The common observation of normal sleep paralysis during REM sleep is an example of how the rest of the body tries to ignore irrelevant activity in the brain.

Cheney's next step seems to be to treat drops in O2sat during sleep with low-dose supplemental oxygen, just to the point of relieving measured transient episodes of hypoxia during sleep, even if the patient does not meet ordinary diagnostic requirements for sleep apnea. It is important to realize that excess oxygen can make the problem worse, even if the patient avoids becoming dependent on supplemental oxygen. You only want to provide enough to promote normal sleep physiology.

I've just checked Harrison's Handbook of Physiology, and found remarkably little on the metabolic activity of sleep despite considerable detail on endocrine and neurological activity. From a metabolic standpoint it is not even clear why people need sleep, since some phases of sleep are as active as waking.

This strikes me as a reasonable experiment which does not require new pharmaceuticals, etc. So far as I can determine, at this distance from the source, every step is subject to measurement.

There is the initial finding of increased IVRT during echocardiograms, and the paradoxical response to oxygen in patients for whom this is appropriate. There is the finding of episodic hypoxia actually measured during sleep, even if other evidence of apnea is absent. The result of successful treatment should be a decrease in IVRT measured during echocardiograms as a result of metabolic recovery during normal sleep.

This kind of thing does not require millions of dollars and committees of experts. It could also benefit individual patients in a matter of weeks.

 

[anciendaze]

I feel the need to warn people that Dr. Paul Cheney is a fairly sick man who is not even seeing patients in the vast majority of cases handled by his clinic in the past. He had a heart transplant many years ago, and is in good shape for a survivor of nearly complete heart failure. He has a remarkable mind which considers things other doctors ignore, but when you are in such unknown territory this comes with the possibility of making mistakes. He is cautious enough that I don't know of anyone actually harmed by these experiments. (You need to contrast this with the typical series of uncontrolled experiments run by doctors who believe the problem is psychological. "All these patients need are antidepressants and a pair of running shoes." There are patients who have been given 30 different psychotropic medications -- and a graduate course on side effects.) I wouldn't be surprised to learn there are patients who feel otherwise about Cheney. If you try something with great hopes, and the result falls short of expectations, it is easy to believe you have been harmed. Just about every suggested treatment has fallen short of expectations.

Now I want to get to the core of what makes this possible treatment different: it is fully testable. You can't argue that the problem is a matter of uncertain diagnosis. He only applies this to patients who show the long IVRT he looks for on an echocardiogram. (Measuring IVRT is well recognized by cardiologists, even if there are disputes about significance.) If a patient sent to him does not exhibit this characteristic, that patient is not a good candidate for this treatment. He is also measuring episodic hypoxia during sleep, independent of conventional diagnosis of sleep apnea. If the patient does not exhibit these episodes during sleep then supplemental oxygen is not an appropriate treatment.

Results of his experiments should also not depend on assessments of psychological factors. He is looking for a decrease in IVRT and an increase in cardiac output. He could be wrong, but this suggested approach is fully testable without any new technology or science.

 

[anciendaze]

I'm getting feedback from communication outside PR which indicates some misunderstanding. At the risk of repetition I will add some emphasis to the above.

It is important to note here that this is not evidence that "more oxygen is better". I've already mentioned the paradoxical response above. If a patient has trouble clearing the byproducts of oxygen metabolism normally, producing more such byproducts will not improve matters. This could be what is going on in PEM.

(You might also ask divers why oxygen rebreather apparatus acquired such a bad reputation. Oxygen is not always a morally "good" chemical.)

I've said above that evidence of dysautonomia while awake should raise suspicions that autonomic function is impaired during sleep. The obvious natural inference about breathing is that you feel an urge to breathe when you are short of oxygen in your lungs. This makes sense, but is simply wrong. Human physiology works a different way, but we don't notice the difference under common circumstances.

There was a tragic accident at Kennedy Space Center in which three engineers died. They were trying to inspect the inside of a Shuttle External Tank stored there, not realizing it was filled entirely with nitrogen. (There were multiple individual and organizational errors in this, but that is not my purpose in telling the story.)

Since 80% of the air you breathe is already N2, you should not expect to notice a difference in smell or taste from 100% N2. The obvious warning of breathing pure nitrogen would be shortness of breath. This did not appear until the victims were suffering effects of hypoxia because the stimulus to breathe is controlled by partial pressure of CO2, and breathing pure nitrogen clears CO2.

If people who should be alert for problems can be so completely taken in by a complete absence of O2 while conscious, with safety only a few feet away, no one should be surprised if a damaged autonomic system fails to properly maintain control of breathing to prevent episodes of hypoxia during sleep.

 

[PatJ]

I wondered what the perfusion index was on the Quest unit, and why that unit is more expensive. Amperor Direct has this information about the perfusion index (my italics in the quote below):

Perfusion Index or PI is the ratio of the pulsatile blood flow to the non-pulsatile static blood flow in a patient's peripheral tissue, such as finger tip, toe, or ear lobe. Perfusion index is an indication of the pulse strength at the sensor site. The PI's values range from 0.02% for very weak pulse to 20% for extremely strong pulse. The perfusion index varies depending on patients, physiological conditions, and monitoring sites. Because of this variability, each patient should establish his own "normal" perfusion index for a given location and use this for monitoring purposes.

Perfusion index is normally monitored with pulse oximeters. PI is also a good indicator of the reliability of the pulse oximeter reading. For most pulse oximeters for general use, the reading is unreliable or unavailable if PI is at or below 0.4%. There are oximeters, such as those from Masimo, designed for extreme low PI. Most people that use an oximeter at home would not need a perfusion index indicator because they are considered to be in general good health. A perfusion index adds a lot of sensitivity to the oximeter sensor thus adding to the cost of the oximeter.

 

[keenly]

I'm getting feedback from communication outside PR which indicates some misunderstanding. At the risk of repetition I will add some emphasis to the above.

It is important to note here that this is not evidence that "more oxygen is better". I've already mentioned the paradoxical response above. If a patient has trouble clearing the byproducts of oxygen metabolism normally, producing more such byproducts will not improve matters. This could be what is going on in PEM.

(You might also ask divers why oxygen rebreather apparatus acquired such a bad reputation. Oxygen is not always a morally "good" chemical.)

I've said above that evidence of dysautonomia while awake should raise suspicions that autonomic function is impaired during sleep. The obvious natural inference about breathing is that you feel an urge to breathe when you are short of oxygen in your lungs. This makes sense, but is simply wrong. Human physiology works a different way, but we don't notice the difference under common circumstances.

There was a tragic accident at Kennedy Space Center in which three engineers died. They were trying to inspect the inside of a Shuttle External Tank stored there, not realizing it was filled entirely with nitrogen. (There were multiple individual and organizational errors in this, but that is not my purpose in telling the story.)

Since 80% of the air you breathe is already N2, you should not expect to notice a difference in smell or taste from 100% N2. The obvious warning of breathing pure nitrogen would be shortness of breath. This did not appear until the victims were suffering effects of hypoxia because the stimulus to breathe is controlled by partial pressure of CO2, and breathing pure nitrogen clears CO2.

If people who should be alert for problems can be so completely taken in by a complete absence of O2 while conscious, with safety only a few feet away, no one should be surprised if a damaged autonomic system fails to properly maintain control of breathing to prevent episodes of hypoxia during sleep.

Hence LOW DOSE.

 

[Gingergrrl]

I wondered what the perfusion index was on the Quest unit, and why that unit is more expensive. Amperor Direct has this information about the perfusion index (my italics in the quote below):

Pat, Do you use a pulse oximeter at home with the perfusion index feature and if so, do you find it adds anything helpful?

 

[PatJ]

I use a CMS50D+ finger meter (which shows SpO2, pulse rate, and plethysmograph.) Supposedly it has a perfusion index but I can't see it on the display, although it does show a bar that bounces according to pulse strength.

As I understand it, the perfusion index is useful for finding the best finger to use for the sensor, and when recording and graphing data the perfusion index can help to determine data quality (below a certain PI the SpO2 readings may be unreliable.) Consider what might happen when recording overnight: if you move around too much then the sensor may be loosened and the SpO2 value would change. If the sensor records the perfusion index then you may be able to tell that a low PI means the sensor was mispositioned during part of the night and the SpO2 values aren't reliable for that period.

This thread has me thinking about recording SpO2 etc. values overnight. The CMS50D+ is a little clunky for that (although it works for some people) so I'm looking into a wrist based unit that uses a separate finger sensor for more comfort and accuracy while sleeping. The CMS50I and IW look good, record the perfusion index, are supported by SleepyHead (3rd party software so a person isn't stuck with the default software) and are available on eBay.

Couple of useful definitions:
Perfusion index - "Numerical representation of your pulse strength. Higher number corresponds to stronger pulse strength."
Plethysmograph - "Visual representation of your heartbeat. Consistent waveform represents good blood flow detected."

 

[anciendaze]

When I talked about Harrison's Handbook above, I meant Harrison's Principles of Internal Medicine. I've let that stand too long to simply pretend it was never mislabeled.

What I'm now asking others out there on the forum is if they can find anything indicating a metabolic role for sleep in traditional medical literature. If my impression is correct this is a gaping hole in the physiology being taught to young doctors. If you know otherwise, please correct me.

Coupled with the results by Naviaux and company on undiagnosed metabolic problems in ME/CFS (or depression, though those problems seem different,) this raises the possibility of research which does not require tandem mass spectrographs or a great deal of sequencing nucleic acids or polypeptides. It doesn't replace those, but it is another approach to crack the problem.

 

[Gingergrrl]

I use a CMS50D+ finger meter (which shows SpO2, pulse rate, and plethysmograph.) Supposedly it has a perfusion index but I can't see it on the display, although it does show a bar that bounces according to pulse strength.

Thank you for this info and I may ask you more about it later . Are you finding it useful so far?

The CMS50I and IW look good, record the perfusion index, are supported by SleepyHead (3rd party software so a person isn't stuck with the default software) and are available on eBay.

So do you have to purchase software or an App for your phone that is separate from the pulse ox? I will have to look into this more. My illness began with tachycardia in my sleep and I'd wondered at that time if my 02 was dropping and the tachy was to wake me up? I no longer get tachy in my sleep (vs. more traditional POTS symptoms when I am awake) but at the same time, I have no idea if my 02 is actually dropping in my sleep and have not measured this.

 

[PatJ]

Are you finding it useful so far?

For quick checks it's useful. It's quite sensitive to HR so the pleth graph is detailed/fine resolution. I can easily see what happens to my heart rate when I stand up by watching the BPM increase while the pulse strength indicator starts bouncing higher; then I can watch my heart rate stabilize as I remain stationary. All this happens in a few seconds.

So far my SpO2 has been within the normal range (always above 95) which surprised me since I sometimes feel like my brain is starved for oxygen, but I suppose that just because there is oxygen in the blood doesn't necessarily mean it's being properly used.

I've read in other threads that Valentijn uses a pulseox to stay below a certain BPM threshold to avoid PEM.

So do you have to purchase software or an App for your phone that is separate from the pulse ox?

A basic non-recording fingertip pulseox won't need any software since it's built in. A recording unit will come with software. The quality of the software can vary significantly for the vendor, even if they use the same re-branded hardware. Having the option to use 3rd party software like SleepyHead (which is opensource) is useful for some people.

I've ordered a CMS50I from eBay. I'll give feedback once it arrives and I have a chance to test it for a few days and nights. I got the CMS50I instead of IW (wireless/Bluetooth) because I didn't think I would use the wireless and it almost doubles the cost of the unit.

 

[anciendaze]

I have long had a pulse oximeter, but one without recording, which prevents me from using it while asleep. I do not see significant drops in O2sat while awake, but then I am not using it when I start to "gray out" after standing too long. I wouldn't be able to read the result anyway. Another problem is that it would probably malfunction when my hands turn cold.

During exercise the O2sat does not seem to drop. There is no problem getting oxygen into blood, the problem comes later, probably in clearing byproducts of oxygen metabolism. It would make sense that this is what pushes us into anaerobic metabolism at ridiculously low thresholds. I'm not aware of research beyond the recognition that we do have low thresholds, and these get lower after maximal exertion, and stay longer for at least 24 hours. Nobody seems to know what is taking place metabolically when this happens.

What I do find is a long recovery time for heart rate. In fact my main use of the meter is not for O2sat, it is to avoid activities which prolong the time for heart rate to recover after exertion. This is the best simple measure of condition I have found.

I'm still asking people to notify me about medical textbooks or even research papers which explain what sleep accomplishes metabolically. From a naive perspective all of us are familiar with people reporting poor physical energy after a bad night, and a feeling of increased energy after a good night's sleep.

There is a great tendency in medical literature to describe psychological benefits of sleep without discussing measurable metabolic changes resulting from sleep. We might then expect someone like a chess grandmaster to suffer a drop in performance after a bad night, but it is harder to explain poor performance in physical endurance competitions. (You can always use the non-quantifiable idea of "will power", but this universal explanation is unsatisfactory precisely because it can explain anything without being otherwise measurable.) If there is no metabolic benefit from good sleep the recognized drops in performance in endurance sports after a bad night are inexplicable.

Before doctors dismiss my reports of waking up feeling like I have just run a marathon as psychological distortions, I'd like to know if they can measure any physical change resulting from good or bad sleep. It would be nice to know some physical reason people need sleep.

One impression I get from detailed explanations of "The Physiology of Sleep and Waking" is that this is a terribly complicated activity which no one should attempt at home without expert supervision. This sounds like a way to avoid saying "we don't have a clue what sleep accomplishes".

 

[PatJ]

It would be nice to know some physical reason people need sleep.

To complicate things even more:
1) Buddhist nuns and monks who meditate deeply for long periods each day often need very little sleep (ie. 4 hours per night). Why does a meditatively calm mind and body contribute to a reduced need for sleep?
2) Some very productive people are known for functioning on very little sleep (3-4 hours per night). Are their bodies (and/or minds?) more efficient?