John H Wolfe appreciate your ambition
Thanks, and thanks for your input
I wonder if it possible to identify groups of patients that respond to similar treatments?
I believe so, yes. Indeed the most efficacious application of broad protocols like mine involves a certain amount of (implicit) 'categorisation' of patients, although the difficulty here is relying on self-reporting and limited test procedures - many issues can be hidden/difficult to disambiguate e.g. mild gastro intestinal disorders/idiopathic gluten sensitivity, untested OI, unconscious behavioural/postural risk factors, buried emotional trauma
The approach I take personally is to test for whatever seems like it could feasibly be an issue and examine/address all sources of systemic stress at a basic level (as per the checklist/protocol) so as to ensure I've got as many bases covered as possible. This may seem daunting/exhausting for PWME, particularly the more seriously affected, but once you have a routine/reminders in place it's not particularly onerous in terms of time/mental energy
Some people do well on abx, some on antivarls, some on methylation
Indeed. Chronic infection is often at the heart of (if not exactly the core process, in my estimation, concerning) ME/CFS. Viral infections are typically closest to the core in my view, although acute/secondary chronic bacterial infection are also associated with chronicity e.g. autoimmune inflammation arising from gastro-intestinal disorders
Methylation cycle type issues are associated with onset/relapses in most PWME, beyond B12 utilisation difficulties/free radical activity it may represent a critical pathway to mitochondrial failure for example, which would appear, in turn, to be something of a biomarker for ME/CFS
All of this appears however, to be secondary to sensitisation arising in relation to restricted neurodynamic and (associated) core hyper-inflammatory profiles. In other words, treating secondary disorders with abx/antivirals/glutathione/B12 etc is therapeutic on both the level of the target systems and more broadly in terms of reducing systemic stress and hence central sensitisation, however these interventions alone may not prove sufficient to go beyond remission to
sustained recovery, unless accompanied by factors that are designed to, or (in many cases) inadvertently, address other factors associated with noxious neurogenic stimulation/other source inflammation
be good if we could narrow treatments in to groups to predict what kinds of patients respond to what treatments?
Absolutely, the conventional approach to treat only those symptoms that are clearly presenting, and only when the patient absolutely insists, with reference to GPs and non-ME/CFS oriented specialists, is inadequate. It would be helpful if treatment planning took a more holistic approach, at least in terms of identifying the most relevant targets for (further) investigation and treatment within a broad panel of options (such as that embodied in
Part VII)
For instance some do well on glycine and some don't. Why is that? and can it be predicted somehow?
I've yet to investigate the role of amino acids in any great detail but I imagine it would relate to the relative influence of associated deficiencies vs. other sources of systemic stress and diminished capacity to compensate for systemic stress, in the context of individual patient profiles