1. Patients launch a $1.27 million crowdfunding campaign for ME/CFS gut microbiome study.
    Check out the website, Facebook and Twitter. Join in donate and spread the word!
Leptin
Andrew Gladman reflects upon the recent IACFS/ME conference and the buzz surrounding a small molecule, leptin.
Discuss the article on the Forums.

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

Discussion in 'General ME/CFS Discussion' started by John H Wolfe, Sep 13, 2012.

?

Does this theory seem plausible?

  1. Yes

    9 vote(s)
    24.3%
  2. Didn't read it

    5 vote(s)
    13.5%
  3. Not sure I fully understand it

    5 vote(s)
    13.5%
  4. No

    18 vote(s)
    48.6%
  1. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    36
    London
    I have ME/CFS, have done for 10+ years, did limited amounts of reading/discussion in the past but only started research in earnest last autumn (around which time I made this thread to chart the development of my ideas)

    I returned to the research a couple of months ago and have subsequently developed my theory a great deal (toxicity does feature but that's more of a sideshow now, and there's a lot more to it than that)

    To maximise my chances of recovery, and to help others recover too, by developing and refining an effective protocol (on an on-going basis)

    It's still in its infancy, some of the most important parts have only been added in recent weeks

    Further (explanatory) context..

    Subsequent to that post, I have also attempted fairly routine (and certainly nowhere near as strenuous as the kind of physical activity I am able to tolerate) direct nerve mobilisation glides (like stretches) on two occasions (in the absence of other stimuli) and suffered markedly disturbed sleep and payback (core feeling of illness, discomfort in back, cognitive deficit, weakness) for about a day afterwards, consistent with Rowe's finding - indicative of neurogenic sensitisation ~ stimulation of the SNS
  2. lansbergen

    lansbergen Senior Member

    Messages:
    987
    Likes:
    446
    I do not. They do not work.

    After 27 years and been at the point of dying? Get real.

    If I had followed your advice i would not have survived let alone improved the way I have.
    snowathlete and Valentijn like this.
  3. xks201

    xks201 Senior Member

    Messages:
    606
    Likes:
    178
    Well it is nice to see that you are trying to help yourself and others. It just slightly enrages me when someone who does not have this disorder claims that positive thinking will cure it. I do not see how anyone could be considered anything but positive by default when stuck in a bed living for years on end unable to function normally and having not slit one's own wrists yet. lol

    I used to propose all sorts of theories on this website. Now I simply claim what has worked for me. We all know that there are nervous system imbalances present. Those may be from hormone imbalances/deficiencies in some - or from other causes, possibly genetic - altering the metabolism and production of things like serotonin and other neurotransmitters.

    I found out my pituitary basically was unable to produce adequate growth hormone. The implications of going for potentially years with untreated growth hormone deficiency at a somewhat young age relative to when most disease strikes people are really unknown to the medical community.

    So it is hard to say what came first - the chicken or the egg. In some cases there is clear cut evidence of a foreign pathogen or toxic exposure which help narrow the cause and cure.

    In my body I have chosen not to focus on pathogens. I could chase viruses all day. I have not seen anyone recover solely from antiviral treatments, even when they were shown to have a viral load of something. Though, my story is different than yours and you may not have what I have, in any case, and I'm glad whatever you are doing for yourself is helping.

    But I must preface this by saying that to claim that your hypothesis is an answer to every case of M.E. or CFS is a common thread I see that I do not like. I'm not sure if you are claiming this or not but I think that this disease would be a lot better understood now if people and researchers stopped looking for one common cause. So many things can cause it. Therefore the treatment is not going to be the same for everyone. A lot of people's treatment may look completely different from others' treatment.

    I more than anyone was hopeful to see even a 10% improvement. But almost anything can do that. We need to not settle for slight improvement. Either you are treated or not. Either you can function at the level you need to survive in this world or you can't. And I'm not discouraging you from writing. What you are doing is great. If anything it is keeping you motivated to survive. I did it too. But to call one thing "The" Hypothesis and insinuate that it is "The" answer to basically what is a set of symptoms that a hundred things is potentially a lie if sold that way.
    Valentijn likes this.
  4. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    36
    London
    Ah, I see. So you have select muscle groups that work for household chores/daily activities but not for other activities?

    Could you possibly expand on why you feel this is the case?
  5. xks201

    xks201 Senior Member

    Messages:
    606
    Likes:
    178
    I will just say that I have tests backing up everything I have found wrong with myself. It is easy for me to make claims that something cured me - but I do not believe it if I cannot at least prove the science. I hate to be like this but I think its necessary for us to do if we want to differentiate between scientific knowledge and a proposed theory. And of course all knowledge isn't deductive...as in just randomly spotting an abnormality on a lab test and deducing it to a cause. An inductive reasoning process went into why I ran those tests to begin with. Either way I verified the information. No doubt anyone can benefit from massage and positive thinking and whatever but to what degree is that really worth mentioning to a patient who has tried it and cannot benefit? I guess I am contradicting myself to a degree because if it works for you, that's great and keep doing it. But I am not going to propose a theory is going to fix everything based on something that makes everyone feel better.
    Valentijn likes this.
  6. lansbergen

    lansbergen Senior Member

    Messages:
    987
    Likes:
    446
    You still don't get it.

    One day some muscles work and on other days other muscles work. I use the muscles that work.

    I have to eat and drink so I use the mucles that work to do things that make that possible.

    When I could not swollow even drinking was not possible.

    I will not respond to your psychobable why I do feel that is the case. They simply refuse to do what I want them to do. If that is too difficult for you to understand, so be it.
    Purple and Valentijn like this.
  7. Kina

    Kina Moderation Team Lead

    Messages:
    5,114
    Likes:
    3,435
    Ontario, Canada
    I have a very positive attitude. In fact, many comment to me that they don't know how I stay so positive despite my health status. It still puts the blame back on the patient -- if they haven't maximized their wellness and capacity, then it's their poor attitude that is contributing to them still being as ill as they are. :mad::mad:

    Rehabilitation -- are we sickness addicts? :D :eek: We don't need to be rehabilitated, we need physiological treatments that address the underlying issues not exercise, stress relief, CBT etc.

    Appropriate?

    Understanding of the illness? It is poorly understood and some in-roads are being made presently towards a rudimentary understanding. Simply writing down all the suspected mechanisms has nothing to do with providing 'appropriate' treatments. You are providing suggestions that have been offered by many, nothing new here except you choose to call it your hypothesis and suggest a protocol. What exactly is your hypothesis other than ME/CFS has many diverse suspected causes and you can 'rehabilitate' yourself with non-treatments. Yes, you can have any chronic disease and maximize your health status by cleaning up your diet, taking in proper nutrition, avoiding stress but it doesn't cure ME/CFS or any chronic disease. All you are doing is addressing lifestyle choices. ME is not a lifestyle choice (I seem to be saying that a lot lately, I might make in my siggy :D)

    What if the underlying cause is not inflammatory agents? What if it is a viral infection causing sensitization, or poorly functioning immune system causing a cascade of effects etc. None of your suggestions even come close to addressing that. It's the same old, same old. And after one does everything to clear the 'inflammatory' agents which is about as nebulous as clearing toxins and find their cores are not calmed, then one can conclude that what they have done did not work and something significantly complex is occurring.

    It still seems to be a change your lifestyle approach kind of thing. If a person is burned out, stressed out, not eating properly, constantly tired from the lifestyle they are leading, then yes these things can be applied but I am just failing to see how this approach can actually do much for ME. It's really unfortunate that tired, burned out people are getting misdiagnosed with ME/CFS because then they try these things and write a book to sell on the internet about how they were cured not realizing they were misdiagnosed and No I am not suggesting this what you are doing. It's just we get reams of this kind of stuff and in the end it usually doesn't work out. I do believe after initial diagnosis, people will try anything. Then after a while when nothing has any significant effects, they realize the complex nature of the disease and look elsewhere for answers other than changing the lifestyle. The real treatment is not going to come from this kind of thing, it's going to come from cutting edge science coming up with exactly what to target not just a mish mash of lifestyle changes. There also seem to be some subsets where some of things help but most with ME find that working on underlying issues helps with the underlying issues but not with the core symptoms of ME.

    I may sound harsh and I am not trying to be but when you have made enough lifestyle changes and tried different protocols based on nutrition and supplements and you keep coming down with infection after infection, you come to the realization that it's just not working. I can't fix my immune system via diet, exercise, supplements, massage, correct thinking, CBT etc, etc. I have done much and I am much 'healthier' than I used to be but I am also much sicker. A cancer patient can do all these things but in the end they still have Cancer -- nobody tells they are not going to have cancer or are going to be rehabilitated if they do certain things.

    IF you have a hypothesis, then you need to test it -- rigourously.

    The explanation section of ME/CFS isn't too bad as it's an amalgamation of lots of theories about ME/CFS. It's the protocol that is lacking because it's not addressing the underlying causes -- it's an attempt to apply lifestyle bandaids.
  8. snowathlete

    snowathlete

    Messages:
    2,017
    Likes:
    2,054
    UK
    You may not find my comments constructive, but you're posting your hypothesis and I'm resonding to your content - specifically your request for an 'open-mind' regarding exercise, which is pretty unrealistic when you know some people have had very damaging experiences involving exercise in ME/CFS.

    You advise exercise which I think is bad advice because of the evidence we already have on the topic; It can seriously harm people. It's one thing to have a hypothesis and include views that may be unpopular, but when it goes against existing knowledge about the potential harms of such advice, and you ignore that, you have to expect negative feedback.
    Valentijn and Purple like this.
  9. roxie60

    roxie60 Senior Member

    Messages:
    1,580
    Likes:
    443
    Central Illinois, USA
    It certainly lists many of the overlapping experiences many of us have reported. No wonder Drs have trouble believing us.
  10. alwayshopeful

    alwayshopeful

    Messages:
    74
    Likes:
    32
  11. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    36
    London
    I’m not surprised!


    PWME demonstrate remarkable stoicism and many also have demonstrably optimistic traits, however some of us do get stuck in a rut with defeatist thinking (in fairness it’s hard not to when faced with an invisible illness that few in positions of authority seem to accept exists, with no consensus on causation nor a definitive cure)


    Yes indeed, have done little on the genetic side to date but added a few bits yesterday, including our gene expression linked subnormal serotonin reservoirs


    Associated with insufficiently restful sleep or do you think it a core deficiency?


    For me (hyper)inflammatory disposition (arising from the factors noted in the article) comes 'first' in this context, many systems/processes (including sleep) then suffer, development then suffers, and stress states emerge, particularly under conditions of neurogenic stimulation and/or exposure to other stimuli such as those you mention


    Me either, although I’ve seen people recover from antiviral treatments combined with exercise and nutrition programs, and if you have the chance to read my article in depth there are plenty of clues as to why this might be. This is not to say that I think antiviral treatment is necessary for recovery btw, for me the precondition re: chronic infections is that immunodeficiency is undone (by reducing systemic stress long term and avoiding troughs associated with neurogenic stimulation/overexertion/sleep insufficiency/exhuastion etc)


    CFS is not, but I believe ME/CFS (with no co-morbidity of other disorders e.g. psychiatric/sleep disorders) does have a common ‘rough’ pathophysiological picture, and that fibromyalgia may well share this mechanistic pathway, albeit with extra bits added on (see the bottom of PART VI)


    100% agree. I posited a common pathway, not a common cause (mode, or point of entry, onto that pathway)


    Again I agree, which is why I didn’t just stop at doing basic reading up when, finally, I took the time to ascertain whether I did in fact have ME/CFS. Although I see ignoring/rejecting opportunities to gain 5%, or 10%, here and there outright as tantamount to closed mindedness to the point of self harm


    That said, I am aware, and agree, that it's pretty unwise to 'get ones hopes up' re: the many and varied somewhat 'alternative' treatments out there, ahead of actually gauging efficacy for oneself

    When I say the hypothesis, I mean the theory proposed in my pathophysiological article, I would never be so bold/foolish as to claim it was THE answer!- at this stage it’s little more than a fairly well researched, but certainly not particularly scientifically rigorous or (yet) well known/supported, conceptual platform, still under development
  12. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    36
    London
    The fastest route to 'the answer' (for oneself) is to combine what our illness has taught us since onset, how we feel, how certain aspects of lifestyle make us feel, how others self report as feeling etc, with hypothesis testing of a more scientifically robust nature, yes

    With respect, if you take the time to read my articles you will see that there is a great deal more to it than that

    Following my protocol requires an individualised approach, with efforts in each sphere according closely with the precise target. There will be some for whom certain approaches prove, or at least seem, inappropriate or ineffective, however I rather doubt there are many people on the planet who have approached the spheres covered in the way in which I advocate if/as appropriate and found zero (positive) impact

    For example, I can see why Perrin Technique (PT) massage may work for some and not for others, it improves lymphatic drainage but it only partially addresses neurogenic sensitisation. A patient who has/works towards a lifestyle broadly consistent with a protocol such as mine will likely go into remission and possibly put it down to PT alone, when in fact the elements in their lifestyle that cover the other spheres e.g. carefully tailored nutrition, exercise (including stretching), fluid intake etc are actually, also, vital to their recovery. Conversely, a patient who relies on PT alone and has a lifestyle otherwise noncompliant with a protocol such as mine is unlikely to find physical therapy effective and will hence likely report it as either ineffective or, more likely, another case of 'does more harm than good' (as lymphatic drainage places the body under enhanced strain in detoxifying)

    "The points below serve as a rudimentary ‘target’ checklist for protocol design" - this means a basic, potentially incomplete checklist. There is no claim in either article that my conclusions/advice are all encompassing (if only!) :)
  13. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    36
    London
    I see, so muscles recruited for other tasks have become in some way inoperable, or deconditioned?

    I meant 'why do you feel this is the case' as in 'what do you put this down to'?

    I think I understand - are you saying you have a problem with motor coordination/proprioception (sense of the relative position of neighbouring parts of the body and strength of effort being employed in movement)?
  14. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    36
    London
    That’s great to hear :)

    A dangerous, unfair, and counter-productive, assumption to assert indeed!

    (Physical)

    Agreed re: psychological support as appropriate, although (past entry into remission stage) physical reconditioning accompanies recovery in most instances, so I cannot agree that we do not need exercise

    Yes, deemed to be appropriate at the individual level e.g. CBT/NLP is appropriate for those with psychological issues/blocks but less of a priority for those without them

    If you take the time to read my hypothesis article you’ll realise that a great deal more has gone into it than that. This assertion is both inaccurate and unnecessarily rude/hostile

    A lot of the basis for the hypothesis relates to composite theories many of which have been proposed by others at various stages, yes. Most new theories come about due to an element of hypothesis stacking. I’m not entirely sure what you are trying to achieve by berating my efforts in this way

    If your tone was less aggressive I might be inclined to go to greater lengths to explain but frankly you have exhausted my good will. If you really want to find out then, again, I suggest you read PART VI

    Where have I proposed a cure for ME/CFS?

    It’s all of these things in many cases (they are interlinked, clues throughout the article, particularly PART III)

    I simplified for you, there is a great deal that can/must be done to achieve these macro-principals (as indicated in both articles)

    Lifestyle is likely key to providing the best conditions for recovery in most patients, yes

    Once one gets to grips with the notion that ME/CFS are complications/symptoms arising in relation to central sensitisation (~systemic stress) passing some threshold level, it's a short hop to being able to intuitively 'reverse engineer' the logic behind the notion of reducing systemic stress as being key to unlocking the illness

    I am well aware of these themes and have tried many alternative therapies and one or two ‘wonder cures’ myself over the years, hence I am well aware of the natural skepticism surrounding new theories/protocols

    This is likely because they work on a single/small number of presenting issues. We do not, typically, have the energy or expertise to fully investigate, research, and treat multi-sphere disorders both presenting, non presenting and latent. My articles are an attempt to move in the direction of lowering systemic stress across the board, through intelligent design, so as to help myself, and others, unlock the illness – something that must logically be best achieved by an integral approach if one buys into the notion of ME/CFS as being based out of multi-system ‘stresses’

    Indeed they do not, but they do (hopefully) encourage people to explore all the options, and many approaches besides specific, targeted, drugs have demonstrable efficacy re: best chances of a full recovery from cancer

    Indeed one does, in so far as is possible, and as soon as possible
  15. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    36
    London
    Correct me if I'm wrong?

    Imagine life lived in an urban environment after a road traffic accident involving a pedestrian.. most affected people will, given time, and the right support where necessary, learn to face their fear of automobiles and grasp with ease the concept that so long as they are careful and look both ways/listen, their quality of life will improve when they re-conquer the fear of crossing

    Just because something is repeatedly shown to be bad when done in a certain way, does not mean that it is necessarily bad in all forms, for all people, all of the time. Hopefully we can agree upon this

    What makes you think I have ignored the reality that is PEM? A quick ctrl + f of my articles should tell you otherwise
  16. Valentijn

    Valentijn Activity Level: 3

    Messages:
    5,857
    Likes:
    7,916
    Amersfoort, Netherlands
    No. A major muscle can simply stop responding.

    Example: I'd just walked through an airport, stood in lines, nearly collapsed due to OI, and finally got onto the airplane. We got into the air, and I tried to cross one leg over the other to help a bit with the OI. But my leg just sits there like a stupid lump of flesh when I tell it to lift.

    It's not that it's too painful to lift, or too shaky ... it simply won't move. After an hour or so I can lift it again. During all of this, the other muscles in that leg seem to function - I can move my leg around a bit, but can't lift it. And my other leg I can lift as normal during the entire episode.

    Something similar seems to happen on a regular basis, though less extreme. Ataxia is a common issue when walking, and it's my experience that some of the minor muscles involved in walking (and keeping a smooth gait) are not working. The major muscles can compensate somewhat, but we're still shuffling along with a weird jerky motion. Same thing for going down stairs - with some muscles not joining in to make the descent smother, it becomes difficult and puts a lot of pressure on the knees.

    When ATP is in short supply, certain muscles get priority access to it, IIRC. This may be why we can usually still walk around and function somewhat, while still being very disabled by the symptoms.
  17. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    36
    London
    Updated Hypothesis presentation:

    PART VI: WOLFE HYPOTHESIS
    1) Aetiology: ME/CFS is the descriptor applied to the symptomatological manifestation of Central Sensitisation Syndrome (CSS) associated with neuroendocrine disorder and arising commonly in relation to the predisposing factors:
    • Neurodynamic restrictions e.g. dorsal defects, trauma, hypermobility, P53 inactivation
      • Predisposition toward hyper-inflammatory responses e.g. sensitivities, asthma
    'Fast onset' ME/CFS is triggered when (a) sufficiently acute stressor(s) e.g. microbial, toxic, psychological trauma, physical trauma, surgery, dehydration, tip(s) central sensitisation over some threshold chronicity level​
    'Slow onset' ME/CFS relates to the gradual worsening of central sensitisation 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​
    2) Pathophysiology:
    a) Core Disorder Cascade:
    • Worsening central sensitisatione.g. with an acute 'trigger' event
      • Sustained immune responses e.g. B-lymphocytes/microglia activity
        • Chronic Activation Statee.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. toxic/behavioural
            • ≈Escalation of the neurogenic sensitisation loop
            • Chronic inflammation of the dorsal root ganglia *
              • (+) ~ Chronic Neuropathic Pain Disorder
              • (+) ~ Chronic Systemic Arousal
                • ≈ Dysautonomia
                • Emergence of CSS **
                  • ~ 'Crosstalk', between sensory nerves and SNS
                  • ~ Neuroplastic changes
                    • ≈ Corruption of neural circuitry
                      • Sensory Processing Disorder
                      • ≈ Hypersensitivities
    • * ~ Increased congestion of spinal lymphatic drainage points
    • * ~ Concomitant increased volume of lymph passing through
      • ~ Thoracic ducts swell and become varicose
        • ~ Lymphatic drainage dysfunction
    ** Mounting central sensitisation ensues as afferent input from the increasingly irritable peripheral nerves becomes increasingly noxious due, in part, to altered nociceptive signaling, 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 central sensitisation (the emergence of CSS) e.g. chronic lymphatic drainage dysfunction (above)​
    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 CSS 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 CSS
    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 CSS, 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
    3) 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
    4) Fibromyalgia [FM]:We propose that FM shares the same core aetiology and pathophysiology outlined above but, compared with PWME, FM patients likely experience:
    • Greater mitochondrial dysfunction (Castro-Marrero et al., 2013)
    • Greater neurological sensitisation e.g. of the somatosensory systemand SNS
      • ~ Greater 'interference', or 'crosstalk', between sensory nerves and SNS
    • 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)
  18. Valentijn

    Valentijn Activity Level: 3

    Messages:
    5,857
    Likes:
    7,916
    Amersfoort, Netherlands
    Let's try a different metaphor:
    Imagine you've lost both legs in a traffic accident. You get out of the hospital, and your doctor, family, friends, and co-workers complain that you spend too much time sitting around. They ask you why you aren't running marathons and climbing mountains anymore. Most of them start avoiding you, after you respond unfavorably to suggestions that if you would just get out more, or start running short marathons again or climbing little mountains, you'd have legs again in no time.
    It's bad for all patients with CCC or ICC ME/CFS who have not yet recovered. No ME/CFS symptoms are the result of avoidance or sensitization, and I find your suggestions regarding that to be extremely uninformed, harmful, and offensive.

    Stop trying to "fix" us and please have a look at yourself first.
    aimossy and Purple like this.
  19. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    36
    London
    Aha, so a problem with motor control. I suppose this could be associated with the neurological abnormalities that Natelson discusses, possibly involving "corruption of neural circuitry" associated with motor control. What do you think?

    In my article I link this to neurotoxic, amyloidic impacts, but it could also be a function of the above - particularly relating to neurogenic sensitisation (irritable nerve) linked SNS/sensory 'interference' or 'cross talk' (fight or flight side of the nervous system confusing/getting confused by the sensory side of the nervous system). Any thoughts?

    I've always had a funny gate too! Interesting

    Indeed, and tissues/organs, most notably the brain:

    "Peters et al. (2004) further suggest that being as the brain, which is the most energy intensive organ pound for pound, is relatively limited in its capacity to store/produce energy, hence under conditions of chronically low mitochondrial energy availability it usurps glucose from other tissues"
  20. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    36
    London
    My dear we still have our legs! :)

    I agree that it is often counter-productive if the conditions are not right, but I see increases in activity as being correlated with recovery once a patient is in remission, both experientially and theoretically

    Circulatory abnormalities like OI for one, is compounded by inactivity e.g. it can lead to vascular/leg muscle deconditioning and lower blood volume. Lymphatic circulation is also impacted by inertia and inertia-linked respiratory habits

    Can you elucidate? I'm afraid I don't see how

    I'm not trying to "fix" anyone dear, merely positing a theory and associated protocol ideas to aid wellness and potentially boost chances of recovery in those open minded enough to entertain these ideas

    How do you mean?

See more popular forum discussions.

Share This Page