Occasionally a theory has popped up that (at least some cases of) MECFS (and other chronic syndromes/diseases) could be due to chronically elevated endogenous carbon monoxide (CO) levels (disregarding the triggering mechanism for now). This is the theory of toxicologist Albert Donnay, who first reported back in 2000 that inhaled CO poisoning might be a common cause of CFS, FM, MCS, and GWS. The symptoms of each overlap considerably. But there is a dearth of data on patients’ CO levels, despite it being easily measured. We don’t know if MECFS patients have abnormally high (or low) levels. Both very low and high levels of CO are harmful, and can be fatal if not resolved. While CO poisonings due to inhaled gas are somewhat well known, it’s not as well known that the body both creates, stores in tissues, metabolizes, and exhales CO, maintaining a balance under healthy conditions. Various substances, lifestyle behaviors, and even medical treatments can raise or lower internal levels. But if high levels are not resolved, health issues occur. Could this be what’s occurring in some MECFS patients?
If Mr. Donnay’s intriguing theory is incorrect, then there must be at least one clear difference, such as symptoms, or better yet, an objective test or biomarker, that clearly distinguishes them. It is not a DLCO test, for example, which is low in both groups. So what if anything does distinguish them? Are there studies in which people with ME/CFS consistently get results that are significantly different from the results of people who have high levels of CO and/or endogenous Heme Oxygenase (HO) activity?
We’re hoping that contributions to this thread may shed some light on this.
If Mr. Donnay’s intriguing theory is incorrect, then there must be at least one clear difference, such as symptoms, or better yet, an objective test or biomarker, that clearly distinguishes them. It is not a DLCO test, for example, which is low in both groups. So what if anything does distinguish them? Are there studies in which people with ME/CFS consistently get results that are significantly different from the results of people who have high levels of CO and/or endogenous Heme Oxygenase (HO) activity?
We’re hoping that contributions to this thread may shed some light on this.