Shiqiru
Established Member
Firstly, I would like to clarify the use of AI. The attached image includes my original Chinese response to you, as well as the AI's evaluation and the beginning of my English reply. I have some English proficiency for slow and general conversations, but for professional, lengthy English expressions, I need the assistance of AI translation (specifically Gemini 2.5 Pro). When dealing with complex content, to ensure clear communication, I also use AI to improve efficiency; for instance, the section headings AI provided for my content were helpful, so I've kept them. I always re-translate the AI-generated English back into Chinese using translation software to proofread it. My message last night might have been sent late (1 AM), or perhaps out of politeness, I added AI generated opening English sentences that were not present in my original Chinese text. Going forward, I will try my best to only use the direct English translation of my own words.Your responses look increasingly like AI products @Shiqiru and that puzzles me. To be honest I don't see any of this adding up in relation to MECFS. Fatigue in MECFS is not the fatigue of normal parlance. Poor oxygenation is one of a hundred causes of symptoms called fatigue but until there is more convincing evidence I see no reason to thi k it has anything to do with MECFS.
For a theory to work you need to consider all the things that don't fit as well as the ones that might fit. To me the things that don't fit loom much larger when it comes to implicating energy metabolism, and especially oxygen access in MECFS.
As an anecdote, I regularly ski at 3500 meters in the Alps and walk at up to 5000 metres in the Andes. I don't recognize any particular relation between altitude and fatigue, just breathlessness and "the wall".
You mentioned an experience that I am very eager for. I'd like to share a bit of my own story. In 2006, the summer before my senior year of university, I was learning to swim and developed what seemed to be a respiratory infection. Out of concern for my training schedule, I didn't stop. My symptoms gradually worsened. For over a year afterward, I experienced severe chronic coughing and joint pain, especially at night. The cough subsided after about a year, but after graduating and moving home, the joint pain, particularly in my neck, worsened due to a cold and damp living environment (it still flares up now with colds or weather changes).
However, compared to ME/CFS, I consider myself fortunate: I found ways to alleviate my symptoms. By moving to a warmer place and carefully keeping myself warm, my cold sensitivity and joint pain gradually came under control, to the point where they are barely noticeable in normal life. But the cost is that in May, when others start wearing short sleeves, I might still need a light down jacket, and I sleep wearing elbow and thin gloves.
My wife, after several COVID infections, developed characteristic features of lupus. Fortunately, it was diagnosed early and is currently well-controlled, with minimal impact on her life. I won't list other long-term symptoms among those close to me after respiratory infections.
From my own experiences and through learning about post-infection conditions, I've come to realize that these post-infection symptoms, often involving the immune system, are incredibly diverse, and their combinations are equally varied (like my own: cough, cold sensitivity, joint pain, where cough and joint pain were independent in time and pathology). Why do similar triggers (infections) lead to such different outcomes? Is there a common mechanism? I tend to support this point. This is a crucial question, but researchers in this field have conducted years of related research and currently do not have a clear answer.
What we can do now is mostly symptomatic treatment or management. For me, being cold triggers joint pain, so I prioritize warmth, which largely solves my problem. But for ME/CFS, there seem to be few effective symptomatic relief measures, which is truly regrettable. However, from the perspective of disease progression, ME/CFS might represent a more severe stage (perhaps akin to arthritis progressing to joint deformation, or leading to other severe conditions like heart symptoms) where the early stages were simply not adequately perceived. This is where a precise, quantifiable tool becomes vital, and ORC is one of the few with this potential. For diseases like ME/CFS, where symptomatic relief is so challenging, researching common mechanisms of post-infection syndromes becomes even more critical.
Speaking of post-infection syndromes, respiratory post-infection sequelae are probably the most widespread and frequent, given the scope and speed of spread, and the recurring frequency of events like COVID and influenza. A question that cannot be avoided when studying the mechanisms of post-infection syndromes is the connection between the acute and chronic phases of infection. For respiratory infections, that's where ORC changes come in. From my test results, every test subject's ORC decreased during the acute phase and recovered to baseline during convalescence.
Although current explanations for ORC reduction, such as diffusion impairment or shunting (which are indeed partial causes), struggle to establish a clear link with chronic symptoms, lung diseases have a characteristic: experimental difficulty. It's currently unclear whether other factors jointly determine ORC reduction (ORC is new, so it might lack immediate persuasive power; for severe cases, SpO2 reduction is clear). However, damage to the microenvironment, such as microclots and impaired red blood cell deformability, are very promising directions. These could establish the connection between the acute and chronic phases of infection.
Despite the diversity of chronic symptoms, there might be strong correlations in symptom development, for instance, a connection at the underlying immune system processes. Because ORC is universal in the acute phase and potentially highly prevalent in the chronic phase of some post-infection sequelae, coupled with its other characteristics, it could become an excellent research tool. A breakthrough in understanding the common mechanisms of post-infection syndromes might begin with a focus on one symptom. ORC has this potential. For example, Akiko Iwasaki's group's 'A causal link between autoantibodies and neurological symptoms in long COVID' still uses activity levels, cognitive tests, and pain thresholds to evaluate symptoms in animal experiments. This might be why a brilliant preprint like that hasn't been formally published for over a year – ORC could be a potential supplement or alternative.
Three years ago, I designed this testing method. Two years ago, by using it on a small scale, I obtained very promising test data. Seeing top-tier research still using evaluative metrics like activity levels, cognitive tests, and pain thresholds – which I find less precise, objective, accurate, and quantifiable – fueled my motivation to promote this testing method. Due to my current inability to conduct larger-scale tests through traditional academic publication routes, my progress has temporarily stalled. Coming to S4ME and engaging with users here has become one of my few remaining options.
For an unvalidated testing method, receiving this much attention here has already been very gratifying. I admit that without a significant amount of testing, I cannot definitively confirm that ORC is effective for ME/CFS; I can only analyze its potential effectiveness. I now also understand more deeply the doubts and difficulties that ME/CFS patients might have regarding ORC testing. Thank you, Jonathan Edwards, for helping me understand these aspects better.
To further promote ORC, I'll add a more point. ORC can also be introduced to healthy family members, who can test it when conditions allow. On one hand, this helps them understand their own body's state, and on the other, it establishes a precise, normal personal baseline. This could then become a useful reference during the acute phase of any future respiratory infections.