This post is based on years of recordings/notes from my visits with Dr. Cheney and his public talks. I’ve done the best I can to present this clearly and simply, but as he’s no longer here for me to run this by, please know this is merely my understanding of these issues as a layperson. Any changes in your regimen should be made with the supervision of your health care provider(s). A language note: While I prefer ME, Dr. Cheney used CFS or CFIDS, and in order to be clear about how he presented information, I’m going to use that everywhere applicable here.
In 2017, Dr. Cheney revised his thinking about the use of oxygen in CFS and began recommending low-dose nocturnal use of it to his patients. If you’ve been around the ME community for a while, it’s likely you’ve at least heard of what he termed “oxygen toxicity.” I don’t believe any Cheney patient has written publicly about the shift, and I thought someone should. Going from “oxygen toxicity” to recommending oxygen sounds like a complete turnaround, but was really only a partial one.
This is a bit longer than usual for me, so have some section links:
1. A Potted History of “Oxygen Toxicity”
2. Dr. Cheney’s Shift in Thinking
3. Interpreting the Nocturnal Pulse Oximetry Data
4. My Own Use of Oxygen
5. Life with an Oxygen Concentrator
6. Does it Help?
A Potted History of “Oxygen Toxicity”
To explain how he got from one view to the other, I have to first back up a bit, because his ideas about oxygen came from his interest in cardiac issues in the illness.
A 2003 paper by Peckerman and Natelson, in which impedance testing of people with CFS revealed reduced cardiac output, triggered Dr. Cheney’s interest in looking deeper at the heart. He was skeptical of the results and attempted to replicate them in his clinic. When he did, he found that his patients showed an even greater degree of reduction than the paper. This set him on the path of the echocardiogram investigations for which he became known.
One of the changes in cardiac function he discovered in his patients on echo was increased isovolumetric relaxation time (IVRT). IVRT is the time between the closure of the heart’s aortic valve and the inflow from the mitral valve. Increased IVRT is a normal finding when healthy people are at altitude and less oxygen is available; if you provide a healthy person at altitude supplemental oxygen, the IVRT decreases to normal.
Cheney, sensibly, thought that what he needed to do was supply his patients more oxygen, but when he put his CFS patients on four liters per minute of oxygen and then measured their IVRT, he found that in every case it increased rather than decreased.
He termed the oxygen-related increase in IVRT “oxygen toxicity.” I’m going to greatly simplify here: When the body uses oxygen in the production of energy, as a byproduct it produces superoxide, which has to be reduced to water. This is redox buffering. There are multiple mechanisms in the body by which this is done, but what Dr. Cheney told me was that in CFS, the body has a badly compromised ability to do the most efficient ones, and instead is compelled to down-regulate energy production to reach a point where the body can keep up with the superoxide byproduct. So he believed the increase in IVRT on oxygen was evidence of that down-regulation in energy production in action. He thought this down-regulation was an adaptation by the body to survive some unknown upstream insult, rather than the primary cause of CFS itself. (He later found support for this in Naviaux et al., 2016.)
Because of that contradictory finding, IVRT became key to his approach to the illness; at an appointment with him, you would have a long echocardiogram in which he would have you apply or take sublingually a series of substances, with a sonographer constantly tracking the shifts in your IVRT as the substance changed it and then it returned to baseline. Those substances that he found consistently increased the IVRT in patients he deemed harmful; those that decreased it he endorsed as potential treatment options, and based on your IVRT responses, he’d give you a personalized graph, indicating which ones he expected to be most fruitful.
But he decided in 2017 that “oxygen toxicity” had been not the best choice of terms. It’s a simple term, and it’s clear he originally felt it characterized the IVRT response to oxygen he saw on echo, but he came to believe it makes it sound like oxygen is always bad in CFS, and on that he changed his mind.
Dr. Cheney’s Shift in Thinking
One of Dr. Cheney’s admirable traits was that he was quite willing to revise his views based on new information. In 2017, he began encouraging patients to have nocturnal pulse oximetry data gathered, either by the loan of a device from a hospital oximetry lab or by the purchase of a consumer-grade device.
He found in those reports consistently lower baseline saturations than when patients were awake, and a pattern of further desaturations during deep sleep associated with spikes in pulse rate.
These results changed some of his thinking about oxygen.
He didn’t change his view that the downregulation of the body’s energy production was in response to the body’s reduced ability to deal with superoxide. He still referred to that as oxygen toxicity.
He did change his view about whether supplemental oxygen could be beneficial.
He continued to believe that too much oxygen had the potential to be deleterious because people with the illness couldn’t reduce superoxide effectively, and that meant carefully titrating the dose.
Interpreting the Nocturnal Pulse Oximetry Data
When he looked at the low nocturnal baseline saturations and further desaturations, he told me he believed they were happening due to hypo-perfusion in the central nervous system. As sympathetic tone fell during sleep and less oxygen was being supplied, the body would try to deal with the lack of oxygen supply by lowering demand first – thus the lower baseline saturation, followed by deeper desaturations. If that failed to bring the supply of oxygen and the demand for it in line with each other, the body would then respond by raising sympathetic tone to try to get more oxygen. Increased sympathetic tone means an increase in adrenaline. The adrenaline would get the heart’s left ventricles to squeeze harder or the heart to pump faster, supplying more oxygen.
If this sounds like a terrible see-saw, that’s what it is.
When he saw the pattern of desaturations and pulse rate spikes on oximetry results, he knew very well that it would cause all manner of sleep disturbances, especially a lack of deep sleep and unrefreshing sleep, which are highly characteristic of the illness. He said to me many times over the years, when we were trying to address my insomnia, “you can’t sleep on adrenaline,” and that was what the data indicated – to a greater degree than he’d previously suspected, apparently.
To fix this on the supply side, he began recommending nocturnal low dose oxygen and writing prescriptions for oxygen concentrators. It took nearly four years for me to take up this idea and decide to act on it.
He made many treatment suggestions to us as patients, and by the time he made this one, I’d first seen him eight years before and I’d seen a fair number of suggestions come and go. Some I’d picked up early on and they’d gone well; some I’d picked up early on and they’d gone badly, and I was gun-shy about being an early adopter again.
This felt like such a big shift in his thinking that I felt a little wary, and honestly, oxygen? Just its association with certain kinds of severe illness – illnesses I did not have – made me feel like it was a more serious intervention than I actually needed, or that maybe I should save it for a time when I was in a big downturn and needed a Hail Mary. I got to that point in late 2020.
My Own Use of Oxygen
Through the summer and early fall of 2020, I’d been doing the best I ever had since becoming bedridden; I was starting to think about whether I might be climbing toward the point that I would be entitled to call myself housebound. But I pushed a little too hard in two ways that fall: first I got in a disagreement with a now-late friend that they probably didn’t even notice, but it kicked up several hours of an adrenaline response in me, and then when my county grassroots group made it known they still had addresses that needed voting reminder postcards sent, I volunteered to do another batch.
I managed to deliver Pennsylvania, but at the cost of a serious crash.
As ever in my crashes, my sleep went promptly to pieces. With everything falling apart again, I decided it was time for that Hail Mary. I contacted Dr. Cheney on Thanksgiving about trying oxygen, and he wrote me a script for a concentrator on Black Friday. He recommended the Philips Respironics EverFlo. We paid out of pocket for it; he warned me that at saturations greater than 90%, insurance was unlikely to cover it, so we didn’t even try.
He counseled me to begin low and to raise the liters per minute to where I was getting nighttime saturations no higher than 97%. He said I could use anywhere from a half-liter per minute to five liters per minute, the top end of the concentrator’s output, but that he’d found a half-liter per minute to two liters per minute most common.
Life with an Oxygen Concentrator
When the machine, hose, and cannulas I’d ordered to go with it arrived, I got an ugly but unsurprising surprise: I couldn’t tolerate the vinyl hose and cannula. I had hoped against hope that this wasn’t going to be a problem, but I should have known it would be, as just being in the room with vinyl had previously been an issue. The hose and cannula stank in precisely the unignorable way that things do with multiple chemical sensitivity, and they made the oxygen itself stink of vinyl.
I really had no energy for problem-solving legwork, but managed to learn that some people with this issue use silicone hose. There was a company manufacturing it right in Pennsylvania, though I had to order their product from a plastics supplier elsewhere. With a vinyl hose typically one uses a connector, but I got silicone hose with a small enough internal diameter (1/8″) that I could just wriggle it onto the concentrator’s metal nozzle.
I found a company that makes silicone cannulas and bought one of those as well, but silicone doesn’t play nice with hair and it seeming to yank at individual strands as I shifted on the pillow was a non-starter. So instead, I laid the silicone hose as close to my nose as I could and called it good enough. I sleep with the door shut, so I figured I was probably eventually building up a therapeutic amount in the room, even if I wasn’t getting it delivered right into my nostrils. This has the benefit that I don’t seem to experience the nasal drying that goes along with oxygen.
An oxygen concentrator, I should say, is not a quiet thing. It makes constant, substantial chugging and puffing noises. We keep it in a corner of the kitchen and run a hose to my bedroom, both on the first floor. It will work with a hose of up to fifty feet in length, and that’s just about right to get to my bed. When we first got it I could definitely feel either the motor or transformer in it when it was on, even across the house, but I’ve improved enough that I don’t seem to be quite that electromagnetically sensitive at the moment. You do need a script to buy a reputable one; there are a lot of models out there for sale with shady descriptions that appear to be trying to evade this stricture, or offered on shady sites, but having tested none of them I can’t vouch for whether they do what they purport to or not.
Does it Help?
But the crucial question: Does it help? Hell yeah. Hell hell hell yeah.
The first thing I noticed was fewer awakenings. The next thing I noticed was that I seemed to have more resistance to post-exertional malaise. It’s made me markedly more resilient in that regard, and when PEM does happen, oxygen definitely blunts its severity. It’s not magic – I am absolutely sure that if I weren’t careful, I could still do myself harm – but it has made a big difference.
It made enough difference in that way that I now sometimes use it as a PEM reducer, when I have to do something that I know puts me at risk of it, like having an appointment. If I run the oxygen while I’m having a virtual appointment, or do a couple hours of it right when I come home from an in-person one, the payback is less bad.
I absolutely wouldn’t be without a concentrator now, given a choice. While it alone didn’t pull me out of the fall 2020 crash, in terms of overall symptomatic help, it’s right up there with pyridostigmine in a one-two punch of the most effective, most quality-of-life boosting interventions I’ve used. I wish I’d picked it up five years ago when Dr. Cheney was first recommending it.
thanks so much for sharing this info Jocelyn. I’m so pleased it has helped you. My SpO2 dropped after a hip operation where they broke my femur by accident, with an anesthesiologist who I l believe ignored the anaesthetic protocol I’d developed with the hospital based on Dr Lapp’s recommendations in the IACFSME Primer. It was a normal 98ish pre-op. They had me on O2 full-time at the hospital after the operation. After 3 days they told me that they didn’t want to take me off as my sats were still so low, but felt that keeping me on longer would be even worse.
It has been 89-91 since. Until I had a significant water leak at my condo at the beginning of Feb. Dealing with it and having to relocate to a hotel with my wheelchair and dog ment I had to overdo every day, which led to a declline in health and SpO2. Then each time I went back to the cndo I got sick – sore throat, phlegm, then later a combo os seats, chills, mild fever, headache……. So further health decline. My SpO2 has been averaging 86-89. I moved to respite care mid March. And now my family has taken my dog for the last week as even getting up and walking the 20 step to sit at the door for a few minutes to let her out was too much for me. But my sats haven’t started increasing yet.
I am investigating the cause of low sats with my new GP who knows nothing about ME and would like to keep it that way but I am going to have to gently educate her. I’ve had my lungs tested. And now she’s sending me to a respirologist for a spiromettry test. I was too sick to read up on what was best for us so this is perfect timing for me! I have a cpap already. 6 hours of 88 at night qualifies people for provincial coverage of oxygen therapy so that may be a silver lining.
Thanks again for sharing your experience and what Dr Cheney shared with you of his thinking.
Oh goodness, Leela, I’m so sorry to hear of your worsening; what a terrible set of circumstances and what a difficult trial. I hope you can get oxygen covered. If you or your doctor have any questions beyond this very simplified version, please let me know and I will be happy to dig into the information I have from Cheney for more detail.
I went with Dr Cheneys low oxygen at night some 4 years ago due to bad insomnia. I sent him my nocturnal oxygen and pulse readings and yes it was the up and down and he recommended me to try it. Had similar problems with vibration and noise, also found a place far away in the kitchen. but when I tried it I got pins and needles in the legs which did not let me fall asleep. I mentioned this to him, but since I could not be his patient here in the UK, he did not give me further advice. At least is was measuring having the concentrator at hand for the covid. Fortunately I did not need it. We all react differently, the usual story with ME. I do not want to discurrage other from trying it. There are firms where you can rent an oxygen concentrator for a week before buying. What I experienced started in the first night I was trying it. I tried it 2 more nights and then gave up.
I’m sorry it didn’t pay out for you, Inge. Those mystery symptoms in response to something that seems like it should be beneficial never stop being a bummer.