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'.