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Wolfe Hypothesis ~ Key causative processes involved in CFS/CFIDS/M.E.

Does this theory seem plausible?

  • Yes

    Votes: 9 23.7%
  • Didn't read it

    Votes: 5 13.2%
  • Not sure I fully understand it

    Votes: 5 13.2%
  • No

    Votes: 19 50.0%

  • Total voters
    38

John H Wolfe

Senior Member
Messages
220
Location
London
I did indeed read your article
I'm afraid you rather jumped the gun/missed the point - the best appreciation of my thinking re: the nature of the illness comes not from reading the protocol that is based on that thinking, but the literal embodiment of that thinking: my hypothesis article (the principal subject of this thread/OP)

It also lacks information about established medical treatments for known ME symptoms, which is a major disservice to your proposed audience
I'm more interested in helping myself/others overcome what I believe to be the core disease process(es) than tackling symptoms (in the short term/relatively superficially), although many of the pointers do provide routes to improving symptoms (in the short term) too

Your "conceptual model" includes references to some ME/CFS researchers, but lacks reference to or even acknowledgement of a substantial amount biomedical research into ME
Feel free to suggest some more :)

It would benefit from acknowledgement that many of us with ME (not the symptom "chronic fatigue") achieve 50-60% of our potential maximum heart rate sitting in a chair
Done, thanks for the suggestion
 

John H Wolfe

Senior Member
Messages
220
Location
London
Why do you use the name John H. Wolfe, VMD, PhD who is a researcher at The Wistar Institute?
I used the name John H Wolfe for my stage name as John is the name of my maternal grandfather (childhood idol), H stands for Horatio (the greatest naval officer/arguably the greatest war hero that ever lived), and Wolfe is the name of the General (who faught the French in Canada) with whom my family has connections on my father's side (and also a cool name)

Any correlation with any other 'John H Wolfe's are coincidental :)
 

John H Wolfe

Senior Member
Messages
220
Location
London
I think what Val and others are getting at is that your protocol and advice doesn't appear, to at least some of us, to reflect the reality of me/cfs as defined by the ICC, CCC, or even Fukuda and that naturally leads to people wondering if you really have it
Well that makes sense/is not unreasonable. I have made it fairly clear what I am talking about when I discuss ME/CFS in these resources however in the introduction to the article that this thread is principally about, hence my comments that I do not feel the need to further elucidate

I understand you don't want your diagnosis questioned
That was not my contention, personally I am a very open and candid person and don't really mind (hence I didn't duck Kina's interrogation etc)

More generally however, I think it extremely distasteful/callous to question the diagnosis of another on a forum like this without being invited to do so and can imagine that such a tac could cause great anguish

are you saying that in the future youre going to try and make money out of your protocol, or will that not happen?
I have no plans to try to make money out my research/theorisation/advice no, this work and my desire to share/develop it is motivated purely out of a desire to help maximise wellness/prospects for remission/recovery among PWME
 
Messages
15,786
I'm more interested in helping myself/others overcome what I believe to be the core disease process(es) than tackling symptoms (in the short term/relatively superficially), although many of the pointers do provide routes to improving symptoms (in the short term) too
Could you succinctly set out what you believe the "core disease process" is and how you think your suggestions will cure it?
Feel free to suggest some more :)
The problem is that your theories are unsupported, and contested by many people - you are the one who needs to support them, not us.
 
Messages
15,786
I am aware of the definitions and some of their distinctions, I simply do not see it as necessary to cater for them in the presentation of my protocol at this stage.
If you're designing a treatment, you need to define who it is for. As someone who's somewhat into film and such, I think you would be able to see the need to define who your audience is intended to be.

Oxford and CCC definitions are completely different. A great many people who qualify as Oxford patients do not have ME/CFS as defined by CCC. Vastly different symptoms are required in each definition, and each has different exclusionary requirements. To say that your guide is for all CFS patients is meaningless - there is no such thing, absent a clarification of which "CFS" you are talking about.
 

John H Wolfe

Senior Member
Messages
220
Location
London
I can't really say that I am close to being convinced that the Perrin Technique is a valid treatment for ME/CFS
My own view is that it is helpful in so far as it can help bring about remission as it involves techniques that improve not just lymphatic drainage/systemic detoxification but also improves the neural sensitisation picture (which I believe lies at the core of our illness) by (somewhat inadvertently) neuromuscular tension/functional mobility

I really can't say much though because I haven't participated in this technique
I have, and for me it seems a helpful, if incomplete and rather hard going, treatment and protocol

Just as an aside, if you are trying to keep your real name private, it's quite easy to find what it is with a simple search
I’m not don’t worry, if that were the reason for the pseudonym I’d have said. Out of interest, how did you perform this simple search?

I just can't get my head around your hypothesis and/or theory and I am still not clear what it is
Essentially my theory currently relates the core pathology of ME/CFS to a background process of peripheral nerve sensitisation ~ sensitising both the central and sympathetic nervous systems

Any systemic stress layered atop that background process further enhances central/sympthatic disarray and hence worsens symptoms. Hence, for me, the route out of ME/CFS is the alleviation of the background process along with the avoidance of systemic stress from any source in so much as is possible

For research to be relevant and valid, it must be about people with ME with a clearly defined criteria and it must rule out those who do not have ME. Much of the research is very poor in this respect
Agreed, it’s best to be sure that the research relates to ME/CFS, rather than just CFS or chronic fatigue in so far as is possible. This is something I should work on as I develop the piece and will certainly have to work on should I wish to get published, fair point

Did you identify any specific sources in my article that concern you in this regard or was it just a general impression you got?

You would have to suggest multiple drugs in your protocol because it addresses multiple issues related to multiple physiological systems
I’m sure you can appreciate that this is where pharmacological interventions get extremely complicated/potentially hazardous, and that kind of advice is beyond the paygrade of most qualified pharmacologists, never mind ‘armchair researchers’!

I was asking simply if you thought there was anything different or unique about your protocol
My protocol is the practical embodiment of my efforts. I think that the theory that informs it is indeed unique, and the combination of/implicit relative import of the ‘targets’ are of course likely to be unique because of this, but I am quite aware that a lot of the constituent elements have been proposed in some shape or form, at some stage, in some place, by some person, over the years

This does not mean it is flawed advice, it simply means it shares similarities with certain aspects, or certain treatments, that have had mixed effects on patients in the past

you come across as being very defensive and angry when members criticize your protocol or hypothesis
If some of my responses have been somewhat short it is because of the level of unnecessary/unprovoked antagonism/rudeness I have faced in some of the posts – any ‘neutral’ would tell you that. I haven’t risen to it, I’ve kept a cool head and stayed calm, and relatively civil. Any neutral will confirm this

we need more research with strict adherence to researching subjects using the proper criteria for inclusion
Agreed, but to abandon literature reviews, meta analysis (of empirical/experiential data), and conceptual models based thereupon would be to miss a trick

when people question you, you tell them to go read your protocol even though they have
If they question me on the specifics then I engage with them, if they level general (emotive) ‘impressions’ (suppositions/presumptions) at me that do not reflect consideration of the material in the round then they’re unlikey to meet with a particularly favourable response

Perhaps you could accept that some of your views and conceptualizations may be incorrect and/or damaging to PWME
Absolutely, at no point have I suggested I am some infallible authority on the disease process(es) or associated implications for treatment

What is it that would make me read yours and try yours over others?
That isn’t really for me to say is it, I don’t know you, you position (experience with the illness/expertise in associated areas) or what motivates you

On a more general level, I would hope that a conceptual model indicative of a great deal of research and joined up thinking, combined with a broad basis for treatment options (most of them fairly simple/free/self administered) would present an appetising prospect to most patients ~ with the implication that they digest the information for themselves, reach their own conclusions, and cherry pick if necessary, as appropriate

It's sensible in terms of helping to maximize health status
At least we can agree upon this

it is likely not helpful for ME patients to get better
I’m not sure I follow. Surely if it is sensible in helping maximise health then it is (more) likely (than not) to be helpful (if not a cure all) at least in some cases?

Please provide some research that definitively shows that we can 'hasten our recovery' by following a protocol such as yours
I would love to, and should I continue with this work that would doubtless be an objective. Needless to say, clinical studies are not exactly the next stepping stone when you are just starting out in health research as a private individual with limited contacts/resources

From your statement, I do get a sense that you really don't understand ME very well
Perhaps you could explain why that is?

Well then, don't get angry and annoyed when people criticize your approach
I am neither angry nor annoyed, I don’t waste energy getting worked up over the comments of anonymous strangers, don’t worry, but nor do I ‘lie down for people’ (who bare me contempt)

What do you actually mean by 'systemic stress'
Essentially it covers direct and indirect stimulation of important systems e.g. nervous/immune systems, or exhaustion/degradation of related support mechanisms e.g. nourishment/restorative rest of these systems, that induces/produces (directly or otherwise) inflammatory/sympathetic/hormonal ‘stress’ responses

if anything these people should develop ME because their systems are in melt-down and have been for years
That depends, if neural hyper-sensitivity syndrome is not in the background for long enough/sufficiently pronounced then, given the relations espoused in my hypothesis, it seems logical to suppose that these patients would be unlikely to develop ME/CFS

You should 'bog' yourself down in the diagnostic criteria if you are going to write about ME/CFS
Please see the introduction to my article. I’m open to any specific suggestions for further refinement

My point is that some of us lead very healthy lifestyles but are still extremely sick. You seem to be unable to accept this
Not sure where you got that idea from? I lead a very healthy lifestyle and am not yet recovered myself!

There are identical protocols out there
Can you link me to some of them please?

Why not aim it at people diagnosed with ME/CFS via either the CCC or ICC rather than the whole world
I aim it at people who have ME/CFS, whether they have been diagnosed or not, by this criteria or that. What’s important to me is that the advise is congruent with what I know/believe about the illness ME/CFS (as outlined in the introduction to my hypothesis article). Of course I am happy to further refine this outline for clarity if I see a compelling reason to do so but otherwise I’m content
 

John H Wolfe

Senior Member
Messages
220
Location
London
Lifestyle is not the answer to the core processes of my disease
Indeed it is not; it is one part of the answer to the question of how to facilitate the unwinding of a core process of ME/CFS (central sensitisation/sympathetic stimulation linked to neural hyper-sensitivity, and associated aggravating factors that cause systemic stress), that I (rightly or wrongly) believe to be the core process
 

John H Wolfe

Senior Member
Messages
220
Location
London
Could you succinctly set out what you believe the "core disease process" is and how you think your suggestions will cure it?
See the post above, and also my response to Kina

The problem is that your theories are unsupported, and contested by many people - you are the one who needs to support them, not us
Where did I say anyone needs to support my theory? All I ask is that people who may benefit are open minded enough to take a look, ideally a good look, and form their own views free from any presumption or stigma; also more usefully from my POV: discuss, and help develop, elements where appropriate
 

John H Wolfe

Senior Member
Messages
220
Location
London
If you're designing a treatment, you need to define who it is for
People with ME/CFS

Oxford and CCC definitions are completely different
Does the Oxford definition refer to 'ME/CFS'? Nope. That said, most of the advice may also be helpful for 'CFS'/'chronic fatigue' patients more generally

As for differences between CCC and ICC, at present I don't see them as particularly important in the context of my theory, and hence advice, as I do not view the chronological aspect/nuances in disease presentation as necessarily being indicative of distinct core processes (something I think I have already explained)

That said, I should probably include PENE in my hypothesis article - strikes me as being more apt than the mere inclusion of the term: PEM

To say that your guide is for all CFS patients is meaningless
When did I say that? It's for, as in intended/designed for PWME (ME/CFS), but anyone who may benefit from it is of course welcome to refer to it, to include people with fairly ordinary health (it's a 'wellness' guide after all)! :)
 

Mij

Messages
2,353
Sorry I don't follow; in my protocol I state I have had experience with (living with) ME/CFS for over a decade

You were diagnosed with ME or CFS? I'm reading through your site and you are addressing issues such as candida, diet, toxic stress, sleep issues. etc I'm not following you either. Everyone here is very "open minded" btw. we've addressed all these issues that you are presenting hundred times over.
 

John H Wolfe

Senior Member
Messages
220
Location
London
Updated main theory presentation:

PART VI: WOLFE HYPOTHESIS
1) Aetiology: ME/CFS is the descriptor applied to the symptomatological manifestation of advanced Neural Hyper-Sensitivity Syndrome (NHSS), typically arising among people with:
  • Neurodynamic restrictionse.g. dorsal defects, trauma, hypermobility, P53 inactivation
    • A Hyper-inflammatory predisposition e.g. allergies, sensitivities, asthma, eczema
2) Onset Themes: Fast onset‘ ME/CFS is triggered when (a) sufficiently acute stressor(s) e.g. microbial, toxic, psychological trauma, physical trauma, surgery, dehydration, tip(s) Nerve Hypersensitivity linked central sensitisation (NHS-CS), over some threshold chronicity level​
Slow onset‘ ME/CFS relates to the gradual worsening of NHS-CS over time, often in relation to phasic hormonal/growth-linked, and lifestyle/behavioural themes e.g. adolescence and the impact of related growth spurts, increased computer/desk usage induced hip and neck flexion, and (lumbar) spinal destabilisation/vertebral compression, on tension/sensitisation in the PNS. Other exacerbatory factors include energy exhaustion and/or inadequate restorative sleep, deleterious eating and drinking habits, state of mind, and exposure to toxins, antigens, and pseudo antigens
Most ‘fast onset‘ patients can retrospectively identify signs of a ‘slow onset‘ prior to an acute trigger event if they ponder carefully enough; hence, given the above, we do not interpret ‘fast‘ and ‘slow‘ descriptives as being indicative of heterogenous disorders​
3) Pathophysiology:
a) Core Disorder Cascade:
  • Worsening NHS-CS e.g. with an acute ‘trigger’ event
    • Sustained immune responses e.g. B-lymphocytes/microglia activity
      • Chronic Activation State e.g. epigenetic B-lymphocytes/microgliachanges
        • Chronic Systemic Inflammation e.g. thanks to inflammatory cytokines
        • (+) ~ The impact of viruses that remain ‘latent’ in the dorsal roots (EBV)
        • (+) ~ Nerve sensitisation arising from other sources e.g. behavioural
          • ≈ Escalation of the neurogenic sensitisation loop
          • (+) Chronic inflammation of the dorsal root ganglia *
            • Chronic Systemic Arousal
  • * ~ Increased congestion of spinal lymphatic drainage points
    • ~ Thoracic ducts swell and become varicose
      • ~ Lymphatic drainage dysfunction
** Mounting CS ensues as afferent input from the increasingly irritable peripheral nerves becomes increasingly noxious due, in part, to altered nociceptive signaling (reduction in threshold/increase in responsiveness of nociceptors), intra-neural blood flow, and neuromuscular tension induced inflammatory neuropeptide activity. This further modulates the impact of the onset ‘trigger’, as well as that of any other complimentary pathophysiologic pathway to chronification of NHS-CS; we term this chronicity: Neural Hyper-Sensitivity Syndrome (NHSS)
b) Chronicity and Persistence:
i) Neuroendocrine Disorder: The cumulative sensitising effects of the above give rise to altered hormone metabolism, production, and removal leading to neurotransmitter disorder and associated dysregulation of the HPA & HPT Axes. Once dysautonomia takes hold many important systems break down e.g. normal immune/inflammatory, metabolic, circulatory and circadian rhythm processes​
Further Chronic Systemic Inflammation ensues, causing, for example:​
  • Heightened antigenic, pseudo-antigenicand sensory sensitivity/reactivity
    • ~ Potential for CS escalation with continuing/future exposure to relevant agents
  • Emergence or worsening of OI (hypotension/hypovolemia/’low flow POTS’)
    • ~ Reduced intra-neural blood volume/flow
      • ~ Increased nerve sensitisation
        • ~ Increased neurogenic sensitisation
          • ~ Escalation of CS
If, as is often the case, the emergence of a chronic health disorder is accompanied by a prolonged period of relative inactivity, and/or by a period in which a patient encounters significant acute, or less significant ongoing, neuromuscular strain, then a pro-inflammatory neurogenic sensitisation loop may take hold. This has the potential to escalate CS, and hence the potential to determine the progression, and severity, of ME/CFS​
ii) Lymphatic Drainage Dysfunction: Examples of direct impacts of neurogenic sensitisation include the impact of increased resting muscle tone or ‘tightness’ on 4th ventricular flow of CSF, and lymph transit both to and, theoretically, from the lymphatic system e.g. a mild form of Thoracic Outlet Syndrome at the left subclavian vein
Behavioural factors such as reduced physical activity, and hence (deep) respiration, under conditions of chronic ill health may further enhance the strain on the lymphatics thanks to the resultant under-stimulation of lymph:​
  • Shallow/costal breathing
    • ≈ Attenuated respiration induced lymphatic circulation
  • Reduced regular exercise
    • ≈ Attenuated skeletal muscle induced lymphatic circulation
    • ≈ Attenuated respiration induced lymphatic circulation
Over time the unidirectional valves that regulate flow within the thoracic duct (negating back-flow) may become dysfunctional under such duress. Reverse drainage of lymph may then occur, causing contamination of the CSF and other fluids and tissues. Toxins may make their way up to the blood brain barrier where they may permeate, acting on exposed portions of regions of the brain e.g. the basal ganglia, most poignantly the hypothalamus, causing (further) dysautonomia. This has functional feedback effects, examples include:​
  • High ANG II levels in low flow POTS
    • ~ Low bioavailability of NO
      • ~ Less relaxation of smooth muscle lining of thoracic ducts
        • ~ Functional impairment of peristalsis of the thoracic duct
  • Thoracic hypovolemia (relating to blood volume/flow dysregulation [OI])
    • ~ Attenuated arterial pulsation action on thoracic duct flow
c) Central Sensitisation Syndrome (CSS): Quite apart from, or on top of, any localised peripheral hypersensitivity, abnormal central (sensory/sympathetic) responses to normal inputs from anywhere in the anatomy (Central Neuropathic Pain Disorder), may become the norm in certain cases. This is believed to come about thanks an increase in the excitability of neurons within the CNS triggered by elevated nociceptor activity and linked to subsequent, sustained changes in the strength of synaptic connections between nociceptors and neurons of the spinal cord associated with Activity-Dependent Synaptic plasticity
4) Gender Bias: The female:male ratio in ME/CFS is roughly 4:1, we put this partly down to:​
  • Distinct hormonal profiles
    • ~ Higher risk of ANS dysfunction (precise mechanisms unknown)
    • ≈ Higher levels of relaxin, which allows joint mobility, in females
      • ≈ Females are more likely than men to have hypermobile joints
        • ~ Higher potential for diminished nerve mobility with puberty
      • ≈ Females have inherently less stable sacrums
      • ~ Higher potential for local neuropathic pain disorder
  • Greater potential for development of sensitivities (e.g. allergic) with age in females (Kelly & Gangur, 2009; Wormald, 1977)
  • Enhanced limbic systems in females
    • Enhanced potential for emotionality under adverse/emotionally charged conditions
5) Fibromyalgia [FM]: We propose that FM shares the same core pathophysiology outlined above but, compared with PWME, FM patients likely experience:
  • Greater (complication of) mitochondrial dysfunction (Castro-Marrero et al., 2013)
  • Greater neurological sensitisation e.g. of the somatosensory system and SNS
    • ~ Greater ‘crosstalk’ between sensory nerves and SNS
      • ~ Escalated Sympathetically-mediated Pain
        • ~ Escalated nociceptive signaling
          • ~ Enhanced potential for CSS
            • ~ Enhanced dysesthesia
            • ~ Enhanced allodynia
            • ~ Enhanced hyperalgesia
  • Greater oxalate depositse.g. as a function of:
    • High systemic calcium:magnesium ratio (a function of diet/deficiencies)
    • High systemic oxalate (a function of diet/clearance abnormalities)
    • Any other predisposition for relatively high oxalate aggregation
Wolfe Hypothesis © John H Wolfe (2013)
 
Messages
15,786
See the post above, and also my response to Kina
The only I answer I get is "read my other stuff". Your other stuff is very long, spammy and full of annoying colors. I want the short and sweet version - and if it's not capable of being concisely summarized, why not?
Where did I say anyone needs to support my theory? All I ask is that people who may benefit are open minded enough to take a look, ideally a good look, and form their own views free from any presumption or stigma; also more usefully from my POV: discuss, and help develop, elements where appropriate
You are making numerous authoritative statements, which are contrary to the experiences of most patients. If these are based solely on your individual experiences as a fatigue patient, with nothing else backing them up, then you need make it clear that your opinions have no real basis which is relevant to ME/CFS patients.
 

SOC

Senior Member
Messages
7,849
Sorry, I've read through it but I still don't where you mentioned that you were diagnosed with ME or CFS. You've been sick for one decade and seem pretty functional to me for a young lad? Keen Sportsman? Are you watching or actively participating? ;) Yeah, I'm not following you at all.


In post #95 in this thread, the pseudonomynous John H Wolfe says:
Diagnosed with 'CFS' by my GP when I returned to the UK in Summer 2004

• Self diagnosed with ME/CFS in Spring 2012

Does that answer your question? ;)
 
Messages
15,786
My own view is that it is helpful in so far as it can help bring about remission as it involves techniques that improve not just lymphatic drainage/systemic detoxification but also improves the neural sensitisation picture (which I believe lies at the core of our illness) by (somewhat inadvertently) neuromuscular tension/functional mobility
You have no useful authority to back up your theories - not research, not collected patient experiences, not even science. Just your individual opinions as a fatigue patient.
Essentially my theory currently relates the core pathology of ME/CFS to a background process of peripheral nerve sensitisation ~ sensitising both the central and sympathetic nervous systems
How does this sensitization account for PEM? OI? Abrupt remissions? Relapses? Worsening symptoms? Co-infections? Inflammation? Muscle twitches? What evidence is there that sensitization exists and is a causative factor in ME/CFS patients?

"Sensitization" seems to be a simple non-answer which involves a lot of vagueness. It's a nice way to dodge a very hard question which brilliant and dedicated scientists haven't found despite decades of searching.
Any systemic stress layered atop that background process further enhances central/sympthatic disarray and hence worsens symptoms. Hence, for me, the route out of ME/CFS is the alleviation of the background process along with the avoidance of systemic stress from any source in so much as is possible
More vague hand-waving.
Agreed, it’s best to be sure that the research relates to ME/CFS, rather than just CFS or chronic fatigue in so far as is possible. This is something I should work on as I develop the piece and will certainly have to work on should I wish to get published, fair point
Yes, until that happens your opinions are doomed to get torn apart rather easily.
I’m sure you can appreciate that this is where pharmacological interventions get extremely complicated/potentially hazardous, and that kind of advice is beyond the paygrade of most qualified pharmacologists, never mind ‘armchair researchers’!
Now this gets confusing, because you have repeatedly said that we have everything we need to heal, and once we get rid of whatever causes our "stress response" by following your guide, then we can get "out of ME/CFS". You are either over-selling the capability of your treatment to heal anyone, or you are just paying lip-service to physiological issues to avoid being verbally decapitated on the spot. But it cannot be that both 1) your guide is sufficient to heal anyone, and 2) there are real physiological dysfunctions occurring that require other treatment.
My protocol is the practical embodiment of my efforts. I think that the theory that informs it is indeed unique, and the combination of/implicit relative import of the ‘targets’ are of course likely to be unique because of this, but I am quite aware that a lot of the constituent elements have been proposed in some shape or form, at some stage, in some place, by some person, over the years
Try any CBT clinic or new age idiot who has read too much about CBT/GET theories regarding ME/CFS.
This does not mean it is flawed advice, it simply means it shares similarities with certain aspects, or certain treatments, that have had mixed effects on patients in the past
It means we've seen it before, tried it extensively, and it doesn't work. Your theories are a failure, and if you had done your homework before getting started, instead of creating very broad conclusions based on your personal experiences, you could have avoided getting into this whole mess to begin with.
Agreed, but to abandon literature reviews, meta analysis (of empirical/experiential data), and conceptual models based thereupon would be to miss a trick
You actually need to read the research - the reviews and meta analyses are insufficient, if you want to use them to support some sort of theory.

Absolutely, at no point have I suggested I am some infallible authority on the disease process(es) or associated implications for treatment
Even if that were true, you are still badly over-estimating your knowledge of ME/CFS. Do your homework first next time - actually get involved with the community and read the literature and join in the discussions before presenting yourself as enough of an expert to create a treatment protocol.

On a more general level, I would hope that a conceptual model indicative of a great deal of research and joined up thinking, combined with a broad basis for treatment options (most of them fairly simple/free/self administered) would present an appetising prospect to most patients ~ with the implication that they digest the information for themselves, reach their own conclusions, and cherry pick if necessary, as appropriate
If any research was involved in your theories, it was the wrong research, and rather hastily and superficially read. Also, some of your suggestions for treatment are dead wrong and likely to be harmful. That is a huge problem, and you seem unwilling to fix it.
I aim it at people who have ME/CFS, whether they have been diagnosed or not, by this criteria or that.
Sorry, this isn't ever going to work. Pick a frigging criteria. Otherwise your advice is about as worthless as something meant to "cure" both cancer and MS patients. Just like those two groups, the different groups of "CFS" patients have little in common. If your only criteria is "chronic fatigue" then you might as well include a dozen or so illnesses, because chronic fatigue is a very common symptom - it is not a disease.
 

SOC

Senior Member
Messages
7,849
I think perhaps the root problem here is that we're expecting some science behind a scientific theory. That may be a bit much to expect from an undergraduate with a background in film-making and acting. Research, logic, problem-solving and the fundamental principles of science are not usually a part of that curriculum. For example, "Background research" or "literature search" mean entirely different things in science and liberal/fine arts. Both are valuable, but need to be used in the appropriate context.

Opinions and personal experience are great resources for fiction writing. Scientific writing needs research, evidence, verification, and so on.