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Professor Julia Newton: Research Presentation: Transcript and Video: November 2012

Discussion in 'General ME/CFS News' started by Firestormm, Jan 15, 2013.

  1. voner

    voner Senior Member

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    Firestormm,

    thank you for taking the effort to write a transcript of that video. Reading the transcript and watching the video has been very useful and enlightening for me. Dr. Newton does a good job of taking complex information and breaking it down into simple terminology for laypeople. I also found it very hopeful that she is teaming up with the immunologist in some of her current research. she is digging for the root cause!

    I took notes and wanted to share some quotes from the transcript that struck me. some of it has been discussed in this thread and some has not.(bold emphasis added by me).......
    1. "in a non-CFS/ME world it is well recognised that the lower your blood pressure is the worse you will perform on memory tests. And the more your blood pressure drops when you stand up the more likely your memory is to decline over time."
    2. "we’ve been able to show repeatedly – in two series of CFS/ME patients and in fatigue-associated chronic diseases – that if you have fatigue or CFS/ME the acid you generate in your muscles is significantly higher and you have greater difficulty getting rid of that acid once you stop exercising. And between bouts of exercise your pH doesn’t go back to normal."
    3. "we can reverse that accumulation of acid in patients with CFS/ME by adding dichloroacetate to the cell culture where the muscle cells have been exercising.
    4. "when we did muscle MRI we found there were two distinct groups of patients. There are people who generate huge amounts of acid and there are people who don’t. And actually we believe that the type of exercise that these two different groups do, needs to be different. There’s a huge literature from the exercise physiology field that showsthat actually some types of exercise may make one of those two types of muscle MRI abnormalities, worse. So, we believe that we ought to do a study whereby we get people’s muscle MRI and find out which group they belong to and then we tailor the exercise for the Activity Management – I don’t like the word ‘exercise’ because I know it raises antibodies in people – but that the Activity Management that they are then encouraged to participate in, is different according to what their muscle looks like....."
    5. "you know I always think about CFS being a big umbrella and that underneath it POTS is one box, orthostatic hypotension is another box, and there will be x number of boxes….....
    Dr. Newton is identifying measurable subgroups in her patients!!
    It makes a lot of sense to me to starts using different terminology for what everyone keeps on calling "exercise". Dr. Newton's use of the term "activity management" seems to me to be a far more accurate and much less misleading term.
    I have some questions to throw out.
    1. Anybody have any information about currently available pharmaceuticals or herbal substances that worked to balance the pH of the blood? As discussed earlier in this thread, the blood of her patients was too alkaline when at rest pre-exertional, and to way too acidic after exertion.....
    2. In point 2, she says there are two different types of patients. the ones who have way too much acid may relate to muscle pain/neurologic pain associated with chronic fatigue syndrome and fibromyalgia patients and the other patients be ones without associated pain? she does not mention anything about pain in her presentation....
    Firestormm, SOC and Valentijn like this.
  2. Firestormm

    Firestormm Senior Member

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    Am pleased and grateful to you Voner in posting some key extracts. Worth thinking about and not everyone here is able to wade through a lengthy transcript or listen to the presentation. Will have a ponder on your questions and might pull some more out of the presentation to help get her main points across.

    But yes, it does seem that she might have uncovered (and importantly quantified) reasons behind why some of us can do more in terms of physical exercise of the muscles and others not so much - and why recovery from said exertion might vary considerably across the patient cohort. Although why this acid is produced in the first place (in the quantities that it is and not absorbed readily) remains a mystery I think.

    This could be part and parcel of Post Exertional Malaise. Be great to have an explanation for that phenomenon finally - even if only in part. And her colleague at Newcastle - well I'd like to hear more about his work. Another biological fingerprint would be extremely gratifying to see and could also point the way to more effective and tailored treatment.

    Take care.
    Sasha likes this.
  3. jimells

    jimells Senior Member

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    This is very similar to my own experience. This past November I experienced a partial remission for about a month. During that time I was cutting firewood with a chainsaw - hardly an activity one would expect from a 'deconditioned' person. I wasn't doing this eight hours a day, of course.

    The remission is now over and I'm back to resting on the couch 20 hours a day. I will likely have to wait another year for the next remission. :(
    currer likes this.
  4. Shell

    Shell Senior Member

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    Jimells, I am so sorry. In the head game a remission and then another relapse is a hard battle to fight. But as Churchill was want to write; KBO. (keep bugg'ring on).
  5. barbc56

    barbc56 Senior Member

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    That sucks, to put it bluntly. So sorry.:(

    I wonder if being able to rebound so quickly might also have to do with how long a person has been disabled/bedbound/inactive? I would think it makes sense that the longer the disability the longer to get up to speed, but what do I know? I have to be deconditioned to a certain extent but that is a by product of my fatigue. It's just so hard to sort this out. I absolutely am not saying that I don't believe what people are reporting. Have there been any studies on this?

    Barb
  6. lansbergen

    lansbergen Senior Member

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    As far as I know it is ignored.

    Would about 20 years be long enough?

    It is not getting up to speed. It is suddenly normal functioning skeleton muscles
    Valentijn, alex3619 and currer like this.
  7. currer

    currer Senior Member

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    At my worst I was bedbound for two years and then roombound for a further three. I then experienced a rapid improvement and went out walking and living much more normally without experiencing any "deconditioning" in my return to full activity.

    I believe deconditioning to be a medical myth, and irrelevant to the experience of previously fit and healthy young people.

    Deconditioning is only relevant to the elderly in my opinion, who are weak due to old age and cannot compensate for loss of daily exercise.

    Deconditioning as an explanation is similar to "medical facts" about obesity, diet lifestyle and health.
    They are "explanations" to cover up for lack of real understanding of causes of disease and ill health.

    I have no time at all for "deconditioning" as an explanation in ME.

    Jimells and lansbergen are right about this.
    jimells and Shell like this.
  8. alex3619

    alex3619 Senior Member

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    We cannot rule out deconditioning as an unproven possibility, or for subsets. However the sudden extreme changes in at least a subset of us are against deconditioning. Given that such changes can also apply to the brain, sometimes simultaneously, how does deconditioning account for sudden brain changes? It is not like the brain is a muscle, and deconditioned muscles do not become conditioned then deconditioned again in merely hours.

    Some kind of biochemical change occurs, though the trigger might be neurological, immunological or metabolic. Then the change goes away.

    Very few hypotheses about ME can account for this, and none that I am aware of deal with it directly. Its not easy to study either. This is an occasional phenomenon, not something that is constantly present. The only way I can think of to investigate it would be a prospective study. Take 100 patients, do regular biochemistry on them, then when they undergo remission, send someone to collect bloods from them immediately. You might have to follow these patients for many years however in order to get enough information using this approach.

    In my partial remissions though its over a course of one to two hours that they occur, they last typically for about six hours, then fade over the next one to two hours. Several have occured after I ate an avocado and chicken sandwich, which saw me testing this with regular chicken and avocado sandwiches for a while. Alas, its not reproducible like that.
    Valentijn likes this.
  9. ukxmrv

    ukxmrv Senior Member

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    I'm not sure how deconditioning could explain these finding in ME by Dr Melvin Ramsay

    1. Variability and fluctuation of both symptoms and physical findings in the course of a day.

    and this finding in remission

    2. It is quite common to find that muscle power is normal during a remission and in such cases tests for muscle power should be repeated after exercise.

    or this

    3. The chronic case of M.E. can take two different forms. In the first there is a recurring cycle of remission and relapse. In three doctors who contracted the infection between 1955 and 1958 the endless alternation of remission and relapse, still continues. In my experience a remission can last as long as 3 years. Marinacci and Von Hagen record one of seven years. The second form of chronic M.E. is more tragic in that no remission occurs. The patient lives a very restricted existence, unable to walk more than a short distance and that with considerable difficulty, unable to read for any length of time and in many cases subject to disturbance of sleep rhythm and/or vivid dreams and always the almost invariable frequency of micturition, hyperacusis and dizzy spells. A few of these chronic cases are compelled to sleep upright as a result of permanent weakness of the intercostal and abdominal recti musculature.

    and Dr Klimas exercise regime would appear to be against this finding

    4. A unique form of muscle fatiguability whereby,even after a minor degree of physical effort, 3,4,5 days or longer elapse before full muscle power is restored.

    The subgrouping problem could maybe be solved in part by seperating patients who have ME (as per Ramsay) to start with.
    Shell likes this.
  10. alex3619

    alex3619 Senior Member

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    Item 4 is consistent with the deconditioning model as proposed, ukxmrv. Not so the other points.

    A point of the exercise studies is they show there is a probable threshold of exercise, which is very low in even moderate patients, beyond which damage and long term effects occur. However under that threshold there is no damage. Deconditioning occurs due to lack of exercise due either to avoidance of exercise or to damage caused by exercise (which might not really be deconditioning.) So the loss of muscle power is after effort beyond a threshold, and it is claimed the threshold can be meaured.

    So its not just a theory of deconditioning, its a theory of weakened muscle which is made rapidly and persistently worse after crossing a threshold. Now the claim that the muscles can be deconditioned might be right for some, not just for lack of exercise, but because whatever goes wrong with overexertion damages muscle function. That loss of function results in something that looks like deconditioning, even though it may not be classic deconditioning.

    Its the remissions themselves that I find the most compelling in arguing against deconditioning as a univeral argument for anything ME related. I currently cannot think of a way in which deconditioned muscle, if using the usual definition of deconditioned, can explain this. What might explain it is if "deconditioning" is in fact chemical suppression of function. This fits the data, but then it moves the definition of deconditioning back to my position on some kind of chemical disturbance, and not due to lack of exercise. Biochemistry can change fast, then change back. Deconditioning and conditioning are very slow by comparison.

    The only concern with arguing about sudden remission and relapse, is that while we lack full understanding of the biochemistry and only have a limited understanding of some of the mechanisms, some might argue this is evidence of psychological causation (even though there is in fact no objective evidence for psychological causation).
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  11. beaverfury

    beaverfury beaverfury

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    1. "we can reverse that accumulation of acid in patients with CFS/ME by adding dichloroacetate to the cell culture where the muscle cells have been exercising.
    http://en.wikipedia.org/wiki/Dichloroacetate

    Lactic acidosis
    The dichloroacetate ion stimulates the activity of the enzyme pyruvate dehydrogenase by inhibiting the enzyme pyruvate dehydrogenase kinase.[5] Thus, it decreases lactate production by shifting the metabolism of pyruvate from fermentation towards oxidation in the mitochondria. This property has led to trials of DCA for the treatment of lactic acidosis in humans.[6][7][8][9]
    A randomized controlled trial in children with congenital lactic acidosis found that while DCA was well tolerated, it was ineffective in improving clinical outcomes.[7] A separate trial of DCA in children with MELAS (a syndrome of inadequate mitochondrial function, leading to lactic acidosis) was halted early, as all 15 of the children receiving DCA experienced significant nerve toxicity without any evidence of benefit from the medication.[8] A randomized controlled trial of DCA in adults with lactic acidosis found that while DCA lowered blood lactate levels, it had no clinical benefit and did not improve hemodynamics or survival.[9]

    Bugger! :(

    DCA does not occur in nature. It is a trace product of the chlorination of drinking water and is produced by the metabolism of various chlorine-containing drugs or chemicals.

    Thought i might just drink a glass of water and fix it.
  12. beaverfury

    beaverfury beaverfury

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    I'm liking nicotine too. Though i think its just cause it gets me out of it :love::love::love: ..
    I think its making my hair fall out though!

    The coming and going of energy is quite weird. Sometimes i can beat the heck out of a punching bag, other times i cant lift myself off my chaise lounge. The fluctuations make it difficult to convince others that i have severe energy problems. It looks like a matter of will to an outsider
  13. Valentijn

    Valentijn Activity Level: 3

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    Agreed ... a psychological (psychosomatic) model would fit with the remissions, but that would fail to explain objective signs which the deconditioning model is used to (poorly) explain. A major roll for deconditioning is disproven by remissions, and a major roll for psychosomatization is disproven by those objectively observable signs (muscle twitching, ataxia, blood sample abnormalities after exertion, altered vO2max, etc).

    This is probably why BPSers have to rely on such a broad definition of CFS, and even then they misrepresent symptoms rather badly. If PEM and remissions were an integral part of the illness they are studying, instead of just simple chronic fatigue, their theories would be clearly inappropriate.
    alex3619 likes this.
  14. Research 1st

    Research 1st

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    Having read some people's great enthusiasm about this research I wanted to add my two cents if I may as people might not fully understand the great difficulties it presents in terms of aiding the dire situation of people with ME and severe grade CFS.

    First of all, this research is not 'ME' research. It is organic chronic fatigue research only.

    The cohort (group of patients) being studied are only meeting Fukuda CFS (CDC) criteria. This is most important to note as because of this criteria of CFS in use, a neurological causation for chronic fatigue (and viral) for the cohort is excluded. Ergo, none of this research is describing ME sufferers. Yes the Newcastle research will include ME sufferers, but by default of heterogeneity phenomena not by design. As we know well, ME cannot be diagnosed using simple exclusionary tests. It requires many complex tests Vs Fukuda CFS. These tests are not available to the vast majority of people - SPECT brain scan etc. ME thus remains undetected in society, unresearched and not believed in by many if not most.

    Although the cohort in a UK study like this meets Fukuda CFS, UK patients are not diagnosed with Fukuda CFS criteria themselves. Instead a Department of Health criteria is used, one they constructed for themselves and one not officially recognised outside of the UK NHS. This is called 'CFS/ME'. This diagnosis doesn't exist medically because....

    Like Fukuda CFS, 'CFS/ME' is not a medical diagnosis, but a clinical diagnosis made by the physician. This is why in the UK, as with Fukuda CFS criteria, the medical profession is skeptical to the reality of ME existing as no 'proof' exists when diagnosing their patients they are actually genuinely organically sick. Sad to say, if I was in a doctors shoes and not aware of the muddling of ME with CFS, I would agree with them also. (Doctors want and need tests, they want and need evidence. This is how the practice medicine).

    British 'CFS/ME' diagnosis amounts to [1] worsening of symptoms after exertion, [2]unrelenting chronic fatigue that significantly impacts on people's lives, [3]this fatigue is not relieved by rest and [4]memory problems [5] one or more additional symptoms. Yes, I said that correctly, one additional symptom. Misdiagnosis is thus rife. People with seizure disoders are being told they have CFS/ME, people with poor sleep, people with practically any reason you can think of that have unexplained 'chronic fatigue' that is explained using basic tests. (Thyroid, heart disease, Diabetes etc).

    Why does this matter? Because the research cohort of people wanting to perform biomedical research is effectively ruined from the get go. Skeptics know this. Naturally I am not a skeptic of CFS (unexplained fatigue) or ME, but I know that simple diagnostic criterias are laughed at by skeptics and rightly so. (There is no science behind a 'diagnosis of exclusion'). So the muddle is circular and on and on it goes.

    'CFS/ME' can then deconstruct into: chronic fatigue syndrome, or ME for peoples own biased reasons which includes researchers. Most people aren't aware of this when meeting people in person (or online) who use the label ME, or believe they have ME because they were diagnosed with CFS or CFS/ME by a British doctor.

    ME is a neurological disorder, so neurological pathology must be present at time of diagnosis. The British ignore this and their NICE guidelines advise against detecting people with neurological ME, by suggesting patients shouldn't be given a TILT table test routinely - ironically the very thing Dr Newton is pressing for and why Dr Newton would like the update to the NICE guidelines to be altered to include this. This is good to hear and a positive step if the guidelines are altered.

    Dr Newton is trying her best with other researchers and is on the side of people with physical organic 'fatigue'.
    But.....in this research presented in this thread there is no control group to assess outcomes, thus even if there was a 'pure' ME cohort (with an accept and official diagnostic test for ME such as Diabetes), it would be premature to conclude anything positive from the results. Scientists know this, we know this.

    A lack of a control group would likely be caused by a lack of funding. Additionally, do be aware that the Medical Research Council (MRC) in the UK will not accept ME as a biomedical single cause disease (such as MS), and thus will not fund 'ME' research and only generic chronic fatigue. The MRC have also blocked biomedical research, this was revealed in a document in the UK National Archives I believe, or another source. (I forget which). Wessely has also threatned the UK DWP not to seperate ME from CFS by defining ME as neurological. That is in the UK National Archives also. Clearly for reasons we are not to know, the original ME patients just like the original Autistics, are unique. They are not syndromes, and they are not spectrum disorders. CFS and 'High functioning Autism' changed all that. (As with CFS, many could claim to be aspergic with enough practice). Fukuda CFS and Asperger's is diagnosed by a theory and by behaviours/beliefs. Not by science findings.

    We will not see an MRC funded 'CFS/ME' Rituximab paper in 2013. We will hear of a Sjogren's Syndrome 'fatigue' paper. Quite scadellous if you have ME, but entirely logical and fair if you 'believe' in CFS/ME being an organic 'fatigue' disorder and not a non HIV-AIDS causing neuroinflammation and early death. Hence in the mindset of these people, they thought choosing a Sjorgren's cohort was a good idea. A good idea if you believe 'fatigue' is the core problem.

    Those with cronic severe chronic neurological ME will tell you that 'fatigue' is not their core problem. Instead they will mention barries to normal functioning such as: Episodic paralysis, convulsions, chronic pain worsened by activity, immune activation (raised lymph glands, sneezing, sore throat) immune supression (repeat infections), CNS dysfunction and OI, cardiac abnormalities, rare cancers, bone disease (osteoporosis and arthritis/degeneration of the spine, bones holding teeth ), hormonal disturbances such as hypoglycemia and low cortisol/ADH/Aldosterone and cognitive impairment that may be as bad as a mild dementia, and lastly multiple vitamin deficiences, low blood volume and disabling vertigo/dizyness and neuropsychiatric disturbances such as anxiety/emotional liability. Many more I'm sure.

    Dr Newton is a 'fatigue' researcher. She is not an 'ME' or a 'CFS' doctor, and is nothing as experienced in immunology as the likes of Dr DeMeirleir, Dr Peterson, Dr Cheney, Dr Bell who are experts in their field for decades. Autonomic 'fatigue' certainly exists in ME, but it is just one part of the picture. An outcome of having ME, not the cause.

    ME is a multi-sysytemic-disease which for some is fatal at an early age, and for many is severly debilitating and will make you homebound for life. You cannot exercise people back to wellness with ME who have so many provable dysfunctions (using tests) no more than you can gently flash lights in the eyes of people with a seizure disorder to make them 'adjust'.

    You can rehabilitate people who have beliefs using CBT and Pacing to encourage them to increase activity, hence 'some' with CFS (Fukuda) recover using CBT. You can rehabilitate ex atheletes and people without on-going disease using paced activity scheduling who ran their body into the floor with over exertion, stress, or EBV but are now better just run down and need to take things gradually. What you wont do is take excess acid out of long term severe grade PWME's muscles and find they recover.

    The Low NK function, the OI not associated to inactivity (it comes on when people are active) the bone disease, the endothelial damage, the glial cell flammation is still there. Personally speaking, I am worried that POTS is appearing to being redrawn by some into OI. OI is OI, not POTS. OI can be experienced by a NASA astronaught, but this isn't a chronic Dysautonomia, this is a symptom of low gravity that people on earth don't even experience. We all know ME involves a hyper sympathetic nervous system tone. Yet ME also involves an absent parasympathatic nervous system tone also. This significant finding cannot be explained by beliefs in a virus or a mystery ailment leading to fear of activity. There is no science behind deconditioning causing this either. The science points to a damaged CNS and chronic neuroinflammation. Autopsy studies of people diagnosed with severe grade CFS and ME in the UK do show evidence of neuroinflammation. Thus the cause for severe CFS and neurological ME is likely an immune disease causing neurological damage over time due to poorly understood inflammatory proceses. De-conditiong theory (for neurological ME) thus falls on its face as does reversing a multitude of demonstratable organic dysfunctions by monitoring your pulse rate and keeping within an oxygen threshold..

    For ME patients with their feet on the ground and not a spacecraft, there remains a total lack of service provision to engage with people who believe in organic ME.There is no 'CFS' team in Newcastle UK patients can meet, there is a psychiatric rehab team that works with people who have unexplained chronic fatigue. Yes there is a group of people who are researching physical chronic fatigue but Dr Newton has a group of designated patients she studies long term, every other 'ME' patient does not have access. Like all other UK residents you get psychiatrically treated as this is the way the British run CFS/ME. One size fits all: Graded exercise, cognitive behavioural therapy for the 'belief' in ME.

    With the troublesome use of generic chronic fatigue in biomedical 'ME' research, one selects Fukuda CFS cohorts and can never come to a finite conclusion what this research is finding because the researcher doesn't know themselves! Canadian consensus definition and or ME International consensus defintion is far superior. You will see the MRC will never allow this critieria to be used, because then the likelyhood of an 'ME' cohort being detected and studied, increases.

    The entire UK NHS system in all state Hospitals must follow accepted protocol, what they call 'evidence based medicine', which is actually non evidence based psychiatry based on a theory of activity avoidance. Newcastle NHS website shows Newcastle Health Trust views ME as the umbrella fatigue disorder (multiple disorders of non organic caused chronic fatigue) and recommends psychiatric intervention as a therapy.

    So to conclude, it is positive to see a group of people (very rare in the UK) doing biomedical research, however, one should resealise that the research cohort is only generic chronic fatigue and not a neurological cohort, or an immune supression cohort. Scientifically this means we can garner very little information for its relevance for people with chronic neurological ME. This keeps the UK government happy, and the MRC who fund the Wessely School even more happy.

    Definately when looking at any CFS or ME research, always check the cohort. If it is Fukuda you will never find the cause as to the reason of your illness (biological or psychological), because the people studied are very mixed bag of individuals with differing reasons to be ill.

    To this day, both the CDC in America and their British counterparts still refuse to acknowledfe 'sub-sets' of CFS and label these subsets accordingly. This wastes precious money, time and consequently patients lives. For some, CFS is a walk in the park, for others a deadly outcome.

    Health agencies CFS phobia and ME denial says all you need to know. Celebrating biomedical Fukuda CFS research for neurological ME is like celebrating being handed an umbrella with holes in it. That includes Rituximab studies. Fluge and Mella's study was over 80% Canadian Criteria though. We need the British to follow suit now, but they won't. Approaching 45 years after ME was officially recognised by the W.H.O and even after the British banned blood/tissue donations due to a suspected viral/prion link we still are using CDC 'outbreak' denial criteria/Reeves mass hysteria criteria and this is a tragedy for both science and patients.

    Prion disease also comes in cluster outbreaks for unknown cause. Food for thought, or maybe vaccine for NF-KappaB. If the UK state really thought you needed CBT and exercise for ME they'd not have a tissue ban in place so you cannot donate and infect other people .

    Human tissue doesn't pass on faulty illness beliefs proposed by the Wessely School as maintaining CFS. Retroviruses, viruses, prions and other infectious agents do.Biomedical 'Chronic Fatigue' research from Newcastle or any other 'fatigue' team won't ellucidite the answer to those pressing fundamental questions, ever.
  15. Firestormm

    Firestormm Senior Member

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    Wow. That's a lot to wade through. I thought you were the CFIDS AA for a moment with a name like that. Research 1st is their website is it not? The entry criteria of any study might be 'Fukuda' but that then dismisses the expert ability of Newton and others to diagnose - don't you think?

    After all it was Newton and colleagues who produced the study that highlighted the misdiagnosis rate - at 40% - of those referred to her with an initial (mis) diagnosis. A study that was largely welcomed by all 'communities' and subsequently this concern about misdiagnosis was confirmed by a further study here from last year.

    You are correct of course - at the present time - as throughout history - NOBODY can diagnosis 'ME' or 'CFS' with an objective test and NOBODY has come up with a viable suggestion of one or an aetiology that explains what we are faced with. We are where we are and the better the expert (the more awareness and knowledge) the greater the chance that anything that can be explained and has been missed will be picked up, identified and treated separately.

    In Britain - and increasingly in the US - the diagnosis name is either ME or CFS. That is what the '/' means. You and your doctors can call it what you like. Until an aetiology is established - through sub-categorisation - there is no claim that any nomen is more relevant than the next or that the 'diagnosis' can be supported by definitive evidence.

    But let's not go back to that bloody rigmarole. Newton here is talking about abnormalities observed WITHIN the cohorts she has investigated. Not all of them have Autonomic Dysfunction for example, which will be a separate - perhaps - diagnosis to their 'ME' - or POTS for that matter - or Heart abnormalities - or specific and quantifiable muscle/acid/exercise problems.

    To even suggest that ME = inflammation = autonomic dysfunction and muscle related exercise intolerance is clearly beyond what the current research suggests. And those who use 'ME' as a preference cannot in all honesty claim the right to their condition - their health - being the result of neurological inflammation than anyone else who's diagnosis name happens to be CFS.

    Within the 'pot' of patients with a diagnosis named either ME or CFS there will be some who exhibit clear signs of neurological abnormality and/or symptoms. There will be some who - upon autopsy - will have some pathological organic abnormality within the brain of the basal ganglia perhaps (but this hasn't been clearly demonstrated as something applicable to inflammation or to the brain or to a specific cohort or as a cause for symptoms experienced or as a specific disease that might or might not be 'ME').

    We cannot say whether any of this - or all of them - equate to those with POTS or with Autonomic Dysfunction or with even the biological fingerprint of 'fatigue' that may or may not be forthcoming.

    I still do not understand how those who make these claims intend for people with 'ME' to be allocated their own cohort when entering clinical studies - separated from those with 'CFS'. Where's your aetiological model? How will you determine someone with 'ME' from someone with 'CFS'? Or a 'neurological cause' from a 'non-neurological' cause? She is studying Autonomic Nervous System Dysfunction.


    What if as a patient you are identified as having autonomic dysfunction and as a result of the research - and subsequent treatment - it removes (or reduces) the 'brain fog' and memory problems and even weird headaches and disequilibrium (which is where the research is heading)?

    If the research identifies a treatment that when applied to those with e.g. autonomic dysfunction and it helps to clear up all these reported 'ME' symptoms (as well as 'CFS' symptoms by the way) - then where's the inflammation?

    We don't know where this research is leading. That's kind of the 'fun' thing about research. Inflammation may indeed have a role - it might be part of the untreated biological processes that perhaps Newton has identified - we don't know - it might not. Other than inflammation, I don't see where your 'this isn't neurological research' is coming from?

    You also mentioned a 'lack of control group'. Well on the slides I looked at, control groups were featured. Also featured were other chronic illnesses with which she drew direct comparisons in her research. In the MRC funded studies you can bet that there WILL be control groups. They wouldn't permit anything else.

    If her - and other - research confirms these initial findings and we progress to a treatment for what has been identified - then we might also see RCT's. But let's not get ahead of ourselves. This was a presentation. All the relevant slides carried the names of the published papers.

    Check them out. I haven't yet been able to. I'll list them all if you like when I get a moment.

    edit:
    re: basal ganglia and autopsy stuff
  16. alex3619

    alex3619 Senior Member

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    Logan, Queensland, Australia
    Cohort issues will always remain a problem until we have a diagnostic test. Now the irony is that the discovery of a diagnostic test for an ME-like illness, whether its POTS, NMH or OI related, is good for ME. This is because that part of the cohort can then be separated out and treated differently - they can no longer argue for inclusion by using vague definitions. The existence of a defined physiological disease subgroup also helps fight psychobabble - its one more example, to add to the huge list, of where they were wrong.

    We do need to be aware though that Newton's research is mainly about different forms of OI, and there is no guarantee that these forms match strict epidemic ME, which in turn may be more than one illness - nobody knows. However they are likely to match some subgroup, and every subgroup we can separate out is a step forward.

    Patients with ME are not necessarily excluded under an Oxford CFS definition. They should be but they not only is ME often not recognized, and useful tests not carried out, but symptoms are often just ignored. I expect some ME patients to creep into any large Oxford CFS cohort.

    I seriously doubt that Julia Newton's cohort matches ME, but I cannot rule out the possibility that not every subgroup fails to match ME. We need more data.

    Further there is a political victory here. If the Newton et. al. research gets substantive robust results, then we have more evidence for advocacy that biomedical research is what is needed, not psychosocial research. That can be used, perhaps, to get more leverage for studies on strictly defined ME. Also the lessons learned in the OI research, even if its not valid for ME, may help us to figure out how ME is different.
    Valentijn likes this.
  17. Firestormm

    Firestormm Senior Member

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    Cornwall England
    You can't enter into research that is seeking to explain and quantify symptoms with a preconception of a disease that may or may not exist distinctly. The MRC has called for proposals - and made funding available - to further investigate the neuropathology:

    As they have for other areas:

    This additional call was put out in July 2012 although as yet no news has been forthcoming that suggests any application has been made or has been successful. Doesn't mean that any MRC project is the right call or that it will result in the right research.

    It may be that the accumulation of research does one day include 'inflammatory mechanisms' but whether or not this will be sufficient - when coupled with all the other evidence - to suggest that 'ME' is a distinct neurological condition of which inflammation plays a key role is still too early to call.

    Without this kind of evidence - to form a distinct aetiology - it is very unfortunate that a separate cohort of 'ME' not 'CFS' patients cannot be drawn. But there we are. It is what it is. At this time 'ME' is the same as 'CFS'.

    Encephaloymyelitis might prove to be an inappropriate name for whatever the aetiology - represented by the symptom manifestations in a distinct cohort - turns out to be. There are some patients - lest we forget - who do not feel that they have the symptoms suggested by 'fatigue' or post-exertional malaise or autonomic dysfunction or etc. etc.

    Personally, I prefer to use the acronym ME and favour Encephalopathy (a term also recognised by NICE and MRC etc) when asked about it. It is a personal preference. But I don't have a particular issue with hearing people and researchers using the term CFS or using Fukuda either.

    Each of the criteria advanced under whatever nomen capture (in my opinion) all of those who are on forums and all of the friends that I associate with - so there is no difference in the absence of objective tests. It is all opinion-based.

    What I don't feel anyone can claim is that Encephalomyelitis is evidence-based as descriptions of a distinct and testable disease (Encephalopathy being neurological and indicating neurological symptoms but less specific).

    We might get there. We might not. If it were easy to have been achieved it would have been done by now even with the interference and obfuscation that many of us I suspect might legitimately feel has held back progress.
  18. barbc56

    barbc56 Senior Member

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    Just to clarify, I have never believed our condition is caused by deconditioning. This would be an interesting subject if it weren't happening to us, eh?

    Absolutely!! I could add to that psychological diagnosis can sometimes be prone to the. That happened to me when it turned out I was hyperthyroid even though I have close relatives with the same thing.This was before I was diagnosed and a long time ago.

    I have also had several incidences of a medical disorder unrelated to this and was attributing the symptoms to me/cfs. Unfortunately, when these were cleared up I only found a minimal improvement but at least I had the conditions taken care of as they could have progressed. It's just so hard to sort all this.
  19. jimells

    jimells Senior Member

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    northern Maine
    For myself, I don't think I am experiencing a sudden normal functioning of muscles. I suspect a sudden more normal functioning metabolism, as in I suddenly have more ATP, or a better ability to use it. It's like buying water-free high-octane gas, or cleaning the terminals on a corroded car battery.
  20. jimells

    jimells Senior Member

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    northern Maine
    Yes, absolutely, this is what happens to me, usually about once per year, generally for about a month.

    How strange. And I'm sure no doctor you have seen has ever paid the slightest attention to this.

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