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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.

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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. xks201

    xks201 Senior Member

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    First of all L-Lactate and D-Lactate convert back and fourth to each other in the body. D-Lactate acidosis is real and can be induced by ingesting lots of lactic acid producing probiotics.

    There are two components to CFS IMO. Endocrine abnormalities and autotoxemia from infection (unwanted gut flora). Subclinical hypothyroidism IMO causes the immune dysfunction which sets up the autotoxemia and overall decline of every cell. I take 300mcg of T4 a day. Doctors today do not use enough t4. If you can't handle the side effects of T4 you need a beta blocker, but probably all of you could use more t4. I have tried t3 and it has such a ridiculously short half life that it just burns up whatever cortisol our weak adrenals can muster and leaves me at least more tired 30 minutes after the initial boost of energy I get, no matter what the dose. Iodine replacement is needed as well as selenium and Vitamin A.
  2. John H Wolfe

    John H Wolfe Senior Member

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    I got so far with that then overcomplicated it and gave up!

    I have now further developed my working hypothesis to take account of further readings, and in particular the recent work of Dr. Rowe. I've improved the article structure, am in the process of tightening up the discussion and have better developed/simplified the theoretical linkages between the main disorders in the Hypothesis section, as well as begun to develop a generalised checklist for protocol design :)

    Have now incorporated a little on this, via neuroendocrine stress

    Thanks for your input, I looked into the role of ANG II in POTS (as per your sig) and have also had a stab at incorporating that too

    PART VI: WOLFE HYPOTHESIS
    1) Primary Disorders & Vital Pathogenic Pathways: Prior to onset, at least one of the following primary disorder factors (often comorbid) place the CNS under strain via neurodynamic and lymphatic drainage dysfunction induced central sensitisation:
    A) CNS Central Sensitisation Syndrome (CSS):
    • Diminished neurodynamics e.g. dorsal defects, trauma, hypermobility
    • Potential for neuromuscular strain e.g. certain connective tissue phenotypes
    • Predisposition toward auto/hyper-inflammatory responses e.g. sensitivities
    B) Structural impediment of lymphatic circulation:
    • Idiosyncratic architecture of the spine (dorsal defects)
    • Acute spinal trauma
    • Other obstruction
    2) Triggers and Onset: 'Fast onset' ME/CFS is triggered when, in the presence of (a) primary disorder factor(s), (a) sufficiently acute and long lasting stressor(s) e.g. viral, bacterial, toxic, psychological trauma, physical trauma, surgery, or dehydration, tip(s) a patient's immune system into a chronic activation state
    'Slow onset' ME/CFS relates to the worsening of (a) primary disorder factor(s) over time, to the point where the patient enters a chronic activation state. This slow worsening often relates to phasic hormonal/growth-linked and lifestyle changes e.g. adolescence. Exacerbatory factors include all sources of peripheral-central sensitisation e.g. energy exhaustion and/or inadequate restorative sleep, deleterious eating and drinking habits, state of mind, and exposure to allergens, viral and bacterial infection, and toxins
    More often than not PWME who self identify as 'fast onset' patients can retrospectively identify signs of a 'slow onset' prior to an acute trigger event if they ponder carefully enough; thus we do not believe that 'fast' and 'slow' descriptives are necessarily indicative of heterogenous disorders, or representative of particularly distinct sub-groups
    3) Central Disorder Cascade:
    • Worsening of primary disorder(s) e.g. with an acute 'trigger' event
      • Chronic immune responses e.g. sustained B-lymphocytes/microglia activity
        • Chronic Activation State e.g. epigenetic B-lymphocytes/microglia changes
          • Chronic Systemic Inflammation e.g. thanks to inflammatory cytokines
            • (+) i) Enhanced stress gearing of the neurogenic sensitisation loop
            • (+) Chronic inflammation of the dorsal root ganglia
              • ≈ Increased congestion of spinal lymphatic drainage points
              • ≈ Concomitant increased volume of lymph passing through
                • ≈ Thoracic ducts swell and become varicose
                  • ii) Lymphatic drainage dysfunction
    i) Mounting central sensitisation ensues as afferent input from the increasingly irritable peripheral nerves becomes increasingly noxious. Increased resting muscle tone and aggravation of vascular and autonomic tone are a corollary of this nascent neurogenic disorder, which further modulates the (continued) impact of the onset 'trigger,' as well as that of any other complimentary pathogenic pathway e.g. ii)
    ii) Examples of direct impacts from i) include the impact of increased muscle tone on normal on 4th ventricular flow of CSF, and (central) lymphatic drainage, theoretically including the drainage of the lymph into the blood stream at the left subclavian vein e.g. a mild form of Thoracic Outlet Syndrome, which would have serious implications for lymphatic flow (chronic impediment of the chief circulatory aid: vacuum induction)
    4) Persistence:
    i) The cumulative cytokine-linked pro-inflammatory/sensitising effects of the above give rise to neuroendocrine disorder involving 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 inflammatory processes, metabolic functions, circulatory regulation and circadian rhythms
    Further Chronic Systemic Inflammation ensues, causing, for example:
    • Heightened antigenic, pseudo-antigenic and sensory sensitivity/reactivity
    • OI emerging/worsening, bringing feedback effects such as nerve and CNS blood supply deprivation/vasoconstriction, which ratchets up central sensitisation
    If the emergence of a chronic health disorder is accompanied by a period of relatively significant inactivity, as is often the case, and/or by a period in which a patient encounters (sporadic) neuromuscular strain, then a pro-inflammatory neurogenic sensitisation loop may take hold. This has the potential to up-rate severity of the primary factor: CSS, and hence the potential to determine the progression, and severity, of ME/CFS
    ii) Reduced (deep, lymphatic stimulative) respiration in ill health may further enhance the strain on the lymphatics. Over time the unidirectional valves that regulate flow within the thoracic duct (negating back-flow) become dysfunctional under such duress. Reverse drainage of lymph occurs and the CSF becomes polluted with toxic substances. These 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, causing (further) dysautonomia. This has feedback effects, examples include:
    Functional impairment of lymphatic circulation:
    • High ANG II levels in low flow POTS
      • ≈ Low bioavailability of nitric oxide
        • ≈ Less relaxation of smooth muscle lining of thoracic ducts
          • ≈ Functional impairment of Peristalsis of the thoracic duct
    Under-stimulation of lymph:
    • Shallow/chesty breathing
      • ≈ Attenuated respiration induced lymphatic circulation
    • Reduced regular medium to high intensity exercise
      • ≈ Attenuated skeletal muscle induced lymphatic circulation
      • ≈ Attenuated respiration induced lymphatic circulation
    • Thoracic hypovolemia (relating to blood volume/flow dysregulation [OI])


    Wolfe Hypothesis © John H Wolfe (2013)
  3. John H Wolfe

    John H Wolfe Senior Member

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    Updated Hypothesis presentation:

    "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) 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 Systemic Arousal
                • Neuroplastic changes
                  • ≈ Corruption of neural circuitry
                    • Sensory Processing Disorder
                    • ≈ Hypersensitivities
                    • The emergence of CSS
    Mounting central sensitisation ensues as afferent input from the increasingly irritable peripheral nerves becomes increasingly noxious (due, in part, to altered nociceptive signaling). Conditions of neuromuscular tension stimulate the release of inflammatory neuropeptides. 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. disrupted lymphatics:​
    • * ~ Increased congestion of spinal lymphatic drainage points
    • * ~ Concomitant increased volume of lymph passing through
      • ~ Thoracic ducts swell and become varicose
        • ~ Lymphatic drainage dysfunction
    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
        • Probable increased nerve sensitisation
          • Probable increased neurogenic sensitisation
            • Probable 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 from a)i include the impact of increased muscle tone on normal on 4th ventricular flow of CSF, and lymph transit, both to and, theoretically, from the lymphatic system (at the left subclavian vein e.g. a mild form of Thoracic Outlet Syndrome)​
    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) Fibromyalgia [FM]: We propose that FM shares the same core aetiology and pathophysiology outlined above but, compared with PWME, FM patients likely experience:​
    • Greater neurological sensitisation
    • Greater oxalate deposits
      • 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)
  4. John H Wolfe

    John H Wolfe Senior Member

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    How the hypothesis, and wider body of information contained within the rest of the article, translates in terms of avenues for investigation and treatment:

    "PART VI: REMISSION & RECOVERY
    All major sources of systemic stress/sensitisation must be addressed. The points below serve as a rudimentary checklist for protocol design, taking account of the intuitive implication of our model – as well as the growing body of evidence – for successful recovery strategies: a multi-faceted (integrative), individualised, and dynamic approach
    a) Attitude:
    • Optimism: Acknowledging the fact that recovery is within the power of the PWME
    • Determination: Committing to the cause of recovery, whatever changes are required
    • Self discipline: Ensuring that the strategy for recovery is consistently adhered to
    • Relaxed approach: Non-compulsive, patient, calm, expressive and not too introspective
    b) Physical Re-conditioning:
    i) Physical Under-stimulation:
    • Nerve/neuromuscular tension and strain targeted (indirectly) manual therapy
    • Regular progressive, yet dynamic and sustainable, physical activity regimens
    • Regular enjoyable mental activities, also pursued only to a sustainable degree
    • Focused respiration techniques e.g. retraining diaphragmatic breathing
    ii) Physical Overstimulation:
    • Avoidance of stimulants e.g. caffeine, intense computer games, argument
    • Careful consideration of pacing/’energy envelope‘ and rest requirements
    • Use of preparatory breathing techniques (mitigates against hypoxia)
    • Rigorous warm up and warm down procedures
    • Emphasis on exercising areas away from the core (minimises CSS, > PEM)
    • Emphasis on recumbent exercise (minimises orthostatic stress)
    • Emphasis on gentle exercise (max 50-60% of maximum HR)
    • Activity split into ‘bitesize’ chunks rather than prolonged sessions
    • Sensible supportive nutrition e.g. adequate protein & carbohydrate
    • Therapeutic effects of massage and hydrotherapy considered
    • Careful monitoring of PEM effects of exercise, with ongoing adaptation
    c) Circulation & Respiration:
    • Circulatory irregularities investigated and treated e.g. OI (NMH/POTS)
    • Poor respiratory habits eliminated e.g. costal breathing/hyperventilation
    • Avoidance of any source of toxicity, ‘man made’ or otherwise
    • Examination by a lymphatic drainage specialist e.g. at a Perrin clinic
    d) Nutrition:
    • Blood sugar balance, day and night e.g. only modest, consistent complex carb intake
    • Adequate protein intake e.g. minimum 75g per day
    • Adequate sodium chloride (salt) intake (in context of BP) e.g. as per OI regimens
    • Avoidance of certain substances e.g. FODMAPs, (pseudo)-antigens, toxins, stimulants
    • Full compliment of vitamins and minerals, especially B and C complexes
    • Full compliment of anti-inflammatory EPA & GLA oils
    • Antioxidant, detoxification, and allergy treatment as appropriate
    e) Mitochondrial energy:
    f) Other sources of systemic stress:
    • Any source of prolonged (lumbar) vertebral compression, shock or trauma
    • Any source of acute/prolonged nerve flexion e.g. flexion of ankles, hips, neck
    • Psychosocial disturbance e.g. avoid stressful situations, employ CBT/NLP
    • Sleep disorders, sleep disturbance, and sleeping environment
    • Other disorders, especially autoimmune diseases
    • Medicines to which one is intolerant e.g. Amitriptyline in some EBV patients"
    Wolfe Hypothesis © John H Wolfe (2013)
  5. Valentijn

    Valentijn Activity Level: 3

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    No.
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  6. Purple

    Purple Bundle of purpliness

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    Quickest and surest way to get permanently and severely crippled by the disease Myalgic Encephalomyelitis, as has been known for decades. By nature of PEM/PENE, this is cannot be sustainable - just the opposite in fact, and CUMULATIVE activity leads to loss of function which is often irreversible.
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  7. John H Wolfe

    John H Wolfe Senior Member

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    I appreciate that this is a hot topic but the many who have recovered, and many who are 'in remission' or (now) able to tolerate exercise/GET (including myself) are proof that it can be sustained in some cases if the conditions are right

    I would love to say I have a total understanding of precisely how to create the right conditions for exercise to become non-exacerbatory but I have probably only really covered the tip of that particular iceberg in my research

    My protocol does provide a number of avenues I believe to be key in opening many, possibly (hopefully) most, PWME up to (careful/dynamic) sustainable physical re-conditioning :)

    I would encourage you to read my research (most poignantly re: the ongoing study of Dr. Rowe) and protocol carefully and in their entirety, with an open mind. If you then have specific concerns/criticisms/ideas I would be more than happy to hear and discuss them
  8. Valentijn

    Valentijn Activity Level: 3

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    Exercise is not leading to recovery. It leads to intensified symptoms and a period of greater disability lasting days or weeks, in some cases months or years.

    If someone who actually had ME/CFS is able to exercise more, it's because they have recovered somewhat.

    Your entire effort is coming out like a typical GET/CBT spiel with a little dietary stuff on the side. If you want to get taken seriously, you need to take us seriously and re-evaluate your approach.
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  9. John H Wolfe

    John H Wolfe Senior Member

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    Often true, however for me, and many experts who know a great deal more than I about medicine, general health, and ME/CFS specifically, the belief that:

    Any exercise is necessarily harmful in all circumstances, where PWME are concerned

    ..is just as mistaken/potentially harmful as the belief that:

    Graduated exercise programs (alone) help ill people convalesce and should therefore be good for PWME

    Absolutely - the "right conditions" have been created for them to be able to physically rehabilitate

    It does not seem we are necessarily in disagreement. If you read my guide you'll note:

    "Virtually every PWME who has recovered or is in remission will tell you that restoring physical functioning and strength is an integral part of a successful recovery strategy. It is important to bear in mind that if you try to push yourself before your health and energy levels are stable you may do more harm than good however"

    Once again, with respect, I would invite you to read my research and protocol properly. From it you will gather that there are many systems that need to be cleared/desensitised in order for what is typically meant by 'exercise' to be tolerable, never mind therapeutic

    Perhaps I should have made it clearer that PART VI contains targets for protocol design (e.g. things for treatment programs to work towards), not immediate targets for patients per sae

    GET is where you end up once you are in recovery. My protocol focuses firstly on creating the right conditions, then on learning to listen to our bodies and pacing accordingly, and then the inference is that readers are free to make their own minds up as to which activities to pursue when, how regularly and for how long

    CBT is one of a broad variety of measures intended to reduce central (CNS)/peripheral-central (PNS-CNS) systemic stress; it's also a handy lifestyle tool - experientially, a good measure of self discipline seems integral to a speedy recovery. Attitude of mind is rather important as it 'sets the scene' for the other aspects of an efficacious protocol
  10. lansbergen

    lansbergen Senior Member

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    I do not.need exersice for that. The muscles i can use again I use for household chores that has to be done.

    You still have not understood that at a given moment some muscles can be used while others can not and that this can fluctate fast.

    Muscles I can use are strong enough. I do not have to train for it.
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  11. snowathlete

    snowathlete

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    It's hard to have an open mind to your view of exercise being good when you have experienced exercise at the lowest possible level and have been crippled by it for months and months.
    It's bad advice and insufficiently backed up by good science.

    I haven't read your other stuff. This is just a comment regarding exercise.
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  12. Kina

    Kina Moderation Team Lead

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    This protocol is similar to other ones I have come across. In a nutshell, Part IV is basicially saying:
    • Have a good attitude and have the right attitude.
    • do some GET
    • Get a massage, eat right, avoid toxins.
    • Take supplements.
    • Get some sleep.
    • Do some CBT.
    • Avoid stressful situations.
    • Avoid medications that you can't tolerate.
    You can't cure or put any physical disease into remission unless you address the underlying causes. Your language is full of blaming the patient. Referring to having the right attitude, self-discipline, making the right decisions smacks of if you fail at this, it's all your fault.

    The only protocol that will work is when the underlying causes are understood and can be treated effectively -- if it's viral, kill the virus; if it's autoimmune, treat the immune system etc.

    'Cleared/desenstized' - what does that mean? This protocol would be much better suited to a person suffering from chronic fatigue or burn-out because it seems to be another change your lifestyle approach and you will feel better kind of thing.






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  13. Valentijn

    Valentijn Activity Level: 3

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    I agree, and to expand on this slightly: deconditioned muscles are not an issue in ME. We can be unable to walk one day, and have a spontaneous remission where we can suddenly walk for hours. And then that slowly goes away and we're back to "normal".

    My muscles didn't recondition themselves overnight when this happened to me. It just happened. When I had to lay down for three weeks due to intense blood pressure problems, I was not weaker when I was finally able to stay standing up again. On the contrary, the extended rest left me temporarily stronger than before - at least, until I used up whatever reserves I'd managed to accumulate and ended up back at my "normal" level of ME dysfunctioning.
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  14. xks201

    xks201 Senior Member

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    It all looks good with pretty colors but show me someone you've treated with these ideas and then maybe I'll listen. There are plenty of theories about M.E.. But let's see a treated patient. lol
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  15. John H Wolfe

    John H Wolfe Senior Member

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    Indeed not, "physical activity" may constitute various tasks/pursuits

    If, by this, you mean that some muscles are under particular tension/particularly sensitised then I can assure you that I do understand this

    Physical rehabilitation (reconditioning of muscles, particularly leg muscles) has a positive impact on blood volume and blood pump muscle tonality. The extent to which this is beneficial depends on whether you have OI, and, if so, what type (of 'POTS')

    It may be that you personally are in relatively good physical condition and/or that such factors are less important in your case, in which case great :) but for most PWME, this is a major factor, and target for treatment, as per the approach of Dr. Rowe et al
  16. John H Wolfe

    John H Wolfe Senior Member

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    I understand it's hard but I am not an advocate of simple exercise as a cure all; instead I advocate smart activity, in the context of a protocol that focuses on creating the right conditions for recovery (to include alleviating the capacity for exercise to induce energy deficits and illness [arising from adverse stimulation e.g. linked to nerve sensitisation and/or lymphatic drainage dysfunction])

    The first part is your opinion, to which you are entitled, the second part is stating the obvious - the hypothesis, and composite theories, are still very much in their infancy and in my introduction I make it quite clear that the object is not to provide an irrevocable scientifically robust paper. The protocol is based upon an amalgamation of these things, plus study data, plus experiential/anecdotal evidence, plus fairly standard practice in integrative medicine and select, appropriate pieces of conventional wisdom from general medical/physical therapy disciplines
  17. John H Wolfe

    John H Wolfe Senior Member

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    Essentially yes, have an attitude that helps maximise wellness and your capacity for healing

    GET isn't off the table, and is a long term target for rehabilitation in my hypothesis article, but the protocol doesn't mention it except to say that it has come in for criticism. I've left the level of intensity of physical activity for patients to decide (advocating pacing in so doing)

    Yes, as appropriate

    Indeed you cannot, and indeed some of the lesser known, peripheral, or unknown underlying cause(s) may not be addressed in either article, but for me (and others) the articles provide fairly comprehensive platform for understanding the illness and some of the most fruitful means currently available to most of us to begin to unlock it :)

    This doesn’t mean people who have ME/CFS necessarily don’t have the right attitude, it’s just a checklist so that people can ensure they have as many things as possible ticked off (some may already be ticked)

    No-one deserves chronic illness, however as in all major illnesses, there are ways in which we may (inadvertently) help or hinder the healing process. There’s nothing accusatory or blameful about that, it’s just the facts of the matter

    Cleared of toxic/antigenic/inflammatory substances / desensitised due to the (subsequent) down rating of neurogenic sensitisation loops and hence the alleviation of peripheral-central sensitisation

    In other words, cleared of inflammatory agents and calmed to our cores

    It may well seem that way at first glance but it is part of a joined up approach that is designed to incorporate the key lessons (evidential, experiential, practical, theoretical and implicit) from the “amalgamation” of sources mentioned in my above post
  18. John H Wolfe

    John H Wolfe Senior Member

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    Deconditioning doesn't just relate to muscle function for normal movement, it has a host of unfortunate implications, perhaps chief among which is the impact on vascular function (circulatory abnormalities are widely viewed as being an important part of the pathophysiological puzzle)

    This kind of relatively stochastic variation in physical performance relates not so much, if at all, to deconditioning you're quite right; it relates, in my view, to factors such as: mitochondrial energy abnormalities, (associated) circulatory abnormalities, lactic acidosis, and adverse stimulation of the sympathetic nervous system in the context of issues such as nerve sensitisation and lymphatic drainage dysfunction
  19. John H Wolfe

    John H Wolfe Senior Member

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    You can lead a horse to water.. :rolleyes:

    I'm not asking people to put quasi-religious faith in my ideas, but merely to be open minded enough to be willing to explore them and the possibility that I could be right, if not in the round then about certain elements, and then perhaps to modify their personal protocols accordingly and reap the rewards! :)

    Rowe has a 2 year study underway, so hopefully we should see some encouraging results before long, which will further the evidence base for (an important, fairly unsubstantiated part of) my protocol

    Further, I get the impression that part of the reason Perrin Technique has been found to be helpful by many of those who have been able to persist with it, and why cognitive (re)programming (CBT/NLP etc) has been found to be effective in some cases, is because of the impact that they have on mitigating peripheral-central sensitisation (over time); my protocol incorporates these elements and is perhaps slightly more keenly focused on the peripheral sensitisation issue, and yet also more all encompassing (in terms of multiple, relatively comprehensive avenues for the alleviation of central sensitisation). This gives me reason to believe that there is something of an evidence base for its efficacy (or the efficacy of some of its constituent elements) already, and confidence that it will prove beneficial to myself and anyone who incorporates it into an appropriate personal approach
  20. xks201

    xks201 Senior Member

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    I'm not condemning you for proposing a theory, but I sure am interested as to the context of your knowledge. The world is full of researchers who sit in ivory towers and do not see patients and propose theories. Do you have CFS? Why are you researching this? Has this protocol worked for you? Overall it seems like you are proposing that toxins are overstimulating and inflaming the nervous system and this is true in cases of mold toxicity and Lyme. I am not exactly seeing a novel hypothesis here. If I am missing something let me know.
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