rvallee
Senior Member (Voting Rights)
Something I've been meaning to work out for a while. For any theoretical model explaining the mechanisms of ME/CFS, there are necessary conditions that must be met, without which a model simply cannot account for the data. What are those? Especially with a purpose to falsify flawed models and hypotheses.
Basically it would serve as a checklist for any theoretical model, where if it fails to meet one of those conditions, it can safely be discarded. This isn't about hunches or personal hypotheses, but about making sense of the data. In science, when data contradict a model, the model must be thrown out. We now have more data than ever, thanks to Long Covid.
For example, we know that several pathogens can trigger ME/CFS, thus any model relying on a single pathogen (e.g. HIV -> AIDS) can be ruled out. Similarly, bacteria can also cause ME/CFS, and so it cannot be about a single type or family of viruses or bacteria. The idea that a pathogen never before encountered by humans is also popular, but can also be discarded either way, especially as reinfections with COVID can also cause ME/CFS, as can the very first one.
Another example, a traditional biopsychosocial model is that it's deconditioning. Well, deconditioning cannot fluctuate, and a necessary condition for a theoretical model of ME/CFS is that fluctuations are not just common, but can be very rapid, cumulative and occur even as a result of mild fitness training. Deconditioning simply cannot account for that, and thus can be dismissed as a valid hypothesis.
Similarly, people who have never heard of ME/CFS, or even of chronic illness in general, as well as people who did but did not believe in them, can develop ME/CFS, which discounts any anxiety/fear model with anticipation of possible lifelong illness affecting behavior.
Many very fit people have developed ME/CFS, which discounts any model involving prior sedentary behavior, or inability to understand or work out how to be active, having to be 'coached' into 'learning simple walking' and other things.
Even when obviously triggered by an infectious illness, severity of acute illness does not seem to predict likelihood or severity of the illness, this is overwhelmingly obvious with COVID. Also, even when not obviously triggered by an infectious illness, subsequent infectious illness often makes it worse, including mild ones. However, sometimes mild infections can make the illness better, usually temporarily. Any model has to, if not account for it, at least not contradict it.
ME/CFS affects men and women, children and adults, and so any valid theoretical model cannot require things like hormonal changes happening later in life. Similarly, there have been poor studies showing elevated childhood adversity, but people with perfectly happy childhoods have also developed it, by which this hypothesis can be safely discarded.
Cognitive exertion can be a trigger for PEM/PESE, just as much as physical exertion, and so any valid model cannot depend on physical exertion involving only muscles or locomotion.
Remission and recovery can be spontaneous, even rapid, which discounts many hypotheses that can only unfold over the long term, and vice-versa. Some remissions and recoveries unfold over many months and years, and any valid model must account for it, or at least not make those data impossible.
The heart of the scientific method is falsification. For example, any hypothesis requiring that only women can be affected can be thrown out by finding a single man. Finding false positive evidence is often easy, but isn't the way to do science. Rather, we posit things that are impossible if a model is true, and if found, then we can discard it.
Let's do some effing science!
Basically it would serve as a checklist for any theoretical model, where if it fails to meet one of those conditions, it can safely be discarded. This isn't about hunches or personal hypotheses, but about making sense of the data. In science, when data contradict a model, the model must be thrown out. We now have more data than ever, thanks to Long Covid.
For example, we know that several pathogens can trigger ME/CFS, thus any model relying on a single pathogen (e.g. HIV -> AIDS) can be ruled out. Similarly, bacteria can also cause ME/CFS, and so it cannot be about a single type or family of viruses or bacteria. The idea that a pathogen never before encountered by humans is also popular, but can also be discarded either way, especially as reinfections with COVID can also cause ME/CFS, as can the very first one.
Another example, a traditional biopsychosocial model is that it's deconditioning. Well, deconditioning cannot fluctuate, and a necessary condition for a theoretical model of ME/CFS is that fluctuations are not just common, but can be very rapid, cumulative and occur even as a result of mild fitness training. Deconditioning simply cannot account for that, and thus can be dismissed as a valid hypothesis.
Similarly, people who have never heard of ME/CFS, or even of chronic illness in general, as well as people who did but did not believe in them, can develop ME/CFS, which discounts any anxiety/fear model with anticipation of possible lifelong illness affecting behavior.
Many very fit people have developed ME/CFS, which discounts any model involving prior sedentary behavior, or inability to understand or work out how to be active, having to be 'coached' into 'learning simple walking' and other things.
Even when obviously triggered by an infectious illness, severity of acute illness does not seem to predict likelihood or severity of the illness, this is overwhelmingly obvious with COVID. Also, even when not obviously triggered by an infectious illness, subsequent infectious illness often makes it worse, including mild ones. However, sometimes mild infections can make the illness better, usually temporarily. Any model has to, if not account for it, at least not contradict it.
ME/CFS affects men and women, children and adults, and so any valid theoretical model cannot require things like hormonal changes happening later in life. Similarly, there have been poor studies showing elevated childhood adversity, but people with perfectly happy childhoods have also developed it, by which this hypothesis can be safely discarded.
Cognitive exertion can be a trigger for PEM/PESE, just as much as physical exertion, and so any valid model cannot depend on physical exertion involving only muscles or locomotion.
Remission and recovery can be spontaneous, even rapid, which discounts many hypotheses that can only unfold over the long term, and vice-versa. Some remissions and recoveries unfold over many months and years, and any valid model must account for it, or at least not make those data impossible.
The heart of the scientific method is falsification. For example, any hypothesis requiring that only women can be affected can be thrown out by finding a single man. Finding false positive evidence is often easy, but isn't the way to do science. Rather, we posit things that are impossible if a model is true, and if found, then we can discard it.
Let's do some effing science!
).
