neurophusion
New Member
@Learningandlistening. Perhaps the reason members of this forum thought you abandoned the debate is because you stopped posting here and announced on Twitter, "I'll be stepping away from this specific topic on social media for the next few months."?
Contrary to what seems to be a common caricature, the presence of ME/CFS symptoms do not suddenly make people inherently close-minded about the potential of mind-body approaches, this doubt develops after humiliating reality checks delivered by the nature of this illness.
The negative stance towards the biopsychosocial model applied to ME/CFS is not a "non-negotiable truth", it is a working conclusion drawn from spending many hours assessing the evidence through the lens of critical thinking and rational skepticism. This conclusion can change when convincing evidence is presented, and it is concerning that we are expected to significantly lower the standards because you think "mind-body therapies are quite difficult to trial". There is no reason why brain retraining cannot be subject to clinical trials.
As far as I can tell, this forum consists of people who largely engage in equal opportunity skepticism: low quality biological research gets grilled here like everything else.
All the CBT/GET proponents had to do to be more convincing about their approach to ME/CFS is to employ a stringent diagnostic criteria and show clinically useful improvements on objective outcome measures. Yet they failed to do so after three decades, therefore we will continue to dispute their claims.
Furthermore, the underlying rationale of brain retraining can be tested using biological measures as objective proxies for the processes that are supposedly mediating subjective symptoms.
Your WIRED article mentions discussions with mindbody proponent Vegard Bruun Wyller. Did he mention that in the early 2010s he was involved with research into the use of low dose clonidine to inhibit the sympathetic nervous system activation that was supposedly driving the sustained stress arousal feedback loop? While the drug worked to inhibit catecholamines, CFS patients became worse at the endpoint, not better, suggesting that the increased sympathetic nervous system activity (if actually present) is a compensatory mechanism.
It makes sense that an illness characterised by post-exertional malaise or exacerbation of symptoms after stressors (physical, cognitive, emotional) could benefit from managing such stressors or responses to it, but that is not the same as the illness being primarily perpetuated by internal psychological factors stuck in a feedback loop of the stress response.
Contrary to what seems to be a common caricature, the presence of ME/CFS symptoms do not suddenly make people inherently close-minded about the potential of mind-body approaches, this doubt develops after humiliating reality checks delivered by the nature of this illness.
The negative stance towards the biopsychosocial model applied to ME/CFS is not a "non-negotiable truth", it is a working conclusion drawn from spending many hours assessing the evidence through the lens of critical thinking and rational skepticism. This conclusion can change when convincing evidence is presented, and it is concerning that we are expected to significantly lower the standards because you think "mind-body therapies are quite difficult to trial". There is no reason why brain retraining cannot be subject to clinical trials.
As far as I can tell, this forum consists of people who largely engage in equal opportunity skepticism: low quality biological research gets grilled here like everything else.
All the CBT/GET proponents had to do to be more convincing about their approach to ME/CFS is to employ a stringent diagnostic criteria and show clinically useful improvements on objective outcome measures. Yet they failed to do so after three decades, therefore we will continue to dispute their claims.
Furthermore, the underlying rationale of brain retraining can be tested using biological measures as objective proxies for the processes that are supposedly mediating subjective symptoms.
Your WIRED article mentions discussions with mindbody proponent Vegard Bruun Wyller. Did he mention that in the early 2010s he was involved with research into the use of low dose clonidine to inhibit the sympathetic nervous system activation that was supposedly driving the sustained stress arousal feedback loop? While the drug worked to inhibit catecholamines, CFS patients became worse at the endpoint, not better, suggesting that the increased sympathetic nervous system activity (if actually present) is a compensatory mechanism.
'Sustained Arousal' Hypothesis Not Sustained: Wyller's Clonidine Trial for Chronic Fatigue Syndrome Fails - Health Rising
Specifically, we suggest that CFS is caused by sustained arousal. Wyller Brun Wyller’s drug/behavioral approach to chronic fatigue has been controversial in Norway. Embraced by many in the medical community there it’s emphasis on psychological factors has dismayed many in the ME/CFS community...
www.healthrising.org
It makes sense that an illness characterised by post-exertional malaise or exacerbation of symptoms after stressors (physical, cognitive, emotional) could benefit from managing such stressors or responses to it, but that is not the same as the illness being primarily perpetuated by internal psychological factors stuck in a feedback loop of the stress response.
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