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Dr Avindra Nath (NIH intramural study) to give Solve webinar, 21 April

viggster

Senior Member
Messages
464
But do they understand PEM sufficiently to know who has it and who doesn't? Do they know what the symptoms of PEM are? Do they know when PEM starts? Do they know how to distinguish PEM from other forms of exercise intolerance or DOMS? I'm concerned that they're going to claim "I feel tired after exercise" is sufficient to establish that PEM is present.

And calling it "post-exertional fatigue" seems like a pretty bad start, regarding understanding it. It. Is. Not. Fatigue. It's bodywide pain, it's a headache, it's painfully swollen lymph nodes, it's crashing blood pressure and rising heart rate, it's ataxia ... etc. NOT FATIGUE. If they can't even get that much right, we really are screwed.


Agreed. They're being very dismissive regarding concerns of multiple control groups and small sample sizes. How about they have their biostatistician run the relevant computations to figure out what sort of results they'll need to get a statistically significant result? Currently it looks like it's going to be very difficult to find any "significant" abnormalities after correcting for so many comparisons being made.
I don't understand why patient selection is so misunderstood. NIH has clarified many times - patients will be referred from experienced clinicians. How does Dr. Klimas know someone has PEM? Do you trust her and the others to make a diagnosis?

As for how many patients are needed to get results, that depends on how far askew from normal those results are. Ron Davis looked at one patient and saw one mitochondrial factor so far out of whack he thinks it's important and will be publishing on it.
 
Messages
15,786
Do you trust her and the others to make a diagnosis?
Not the ones who are on record supporting the use or efficacy of GET. They are not all Nancy Klimas.

As for how many patients are needed to get results, that depends on how far askew from normal those results are.
Yes, and they can calculate how many patients they need to have a reasonable shot at getting statistically significant results when comparing dozens of results with 2 control groups. This is something pretty basic which should be done before throwing millions of dollars into a study.
 

viggster

Senior Member
Messages
464
Not the ones who are on record supporting the use or efficacy of GET. They are not all Nancy Klimas.


Yes, and they can calculate how many patients they need to have a reasonable shot at getting statistically significant results when comparing dozens of results with 2 control groups. This is something pretty basic which should be done before throwing millions of dollars into a study.
What evidence do you have that hasn't been done?
 

viggster

Senior Member
Messages
464
Not the ones who are on record supporting the use or efficacy of GET. They are not all Nancy Klimas.


Yes, and they can calculate how many patients they need to have a reasonable shot at getting statistically significant results when comparing dozens of results with 2 control groups. This is something pretty basic which should be done before throwing millions of dollars into a study.
Also, those kinds of stats are typically run for late-stage drug trials where the approximate treatment effect is known and then you calculate how many people you need in your study to see that effect. This is a discovery study, and many many comparisons will be made across the groups, but there's no good way to know up front how strong of an effect might be at play for each variable.
 
Messages
15,786
Also, those kinds of stats are typically run for late-stage drug trials where the approximate treatment effect is known and then you calculate how many people you need in your study to see that effect.
They're also often run for other trials, including CBT/GET psychobabble trials. If they can manage, the NIH sure as hell can too.

Several of these researchers involved with the NIH project have deliberately sabotaged their own biological research in the past by throwing in too many small control groups, and a bunch of pointless extra tests.

This is a potentially very serious problem, and your dismissal of people's legitimate concerns is just undercutting your own credibility. At least admit there might be a problem which needs to be addressed instead of crossing our fingers for good luck and hoping it all turn out all right.
 

viggster

Senior Member
Messages
464
They're also often run for other trials, including CBT/GET psychobabble trials. If they can manage, the NIH sure as hell can too.

Several of these researchers involved with the NIH project have deliberately sabotaged their own biological research in the past by throwing in too many small control groups, and a bunch of pointless extra tests.

This is a potentially very serious problem, and your dismissal of people's legitimate concerns is just undercutting your own credibility. At least admit there might be a problem which needs to be addressed instead of crossing our fingers for good luck and hoping it all turn out all right.
Now you're just insulting me. See ya later.
 
Messages
15,786
Now you're just insulting me. See ya later.
You're making claims on a subject matter of which you do not seem to have even a basic understanding, and are not providing even a basic explanation of why this study would have sufficient statistical power.

I don't believe that you have bad or dishonest intentions, but you're taking a hardline pro-authority stance on an issue which you clearly don't understand. That does undermine your credibility ... again, not due to dishonesty, but due to making unequivocal claims which contradict some basic statistical concepts.
 
Messages
2,087
This is a potentially very serious problem, and your dismissal of people's legitimate concerns is just undercutting your own credibility. At least admit there might be a problem which needs to be addressed instead of crossing our fingers for good luck and hoping it all turn out all right.

You're making claims on a subject matter of which you do not seem to have even a basic understanding, and are not providing even a basic explanation of why this study would have sufficient statistical power.

@Valentijn i understand your frustration but my interpretation is that @viggster was expressing an opinion.
I have my own concerns about the trial and I'm sure everybody does. But everyone should be able to express their opinion and if that opinion is so out of place that is causes offence, then by all means form a rebuttal.

But I didn't see anything hardline or pro-authority in the posts i read.

Sadly i do believe sooner or later we are all just going to have to cross our fingers and hope. It is unlikely that the NIH will change anything major at this stage.

If people have serious concerns over the referral process then this should be the avenue to campaign against.
But a well thought out strategy would be required, not an all out war.

The concerns seem to be around the Dr.s would prescribe GET. Any Dr. who prescribes GET in my mind is completely ignorant of ME/CFS. Do we need to highlight the IOM report, the work of Tuller, the MEA survey to these Dr.s and ask them for a statement ? Any other suggestions ? Exclude any patient who claims exercise helped them - but maybe there are patients who do very light exercise and they find it somewhat beneficial.
I think it is more or less impossible to guarantee 100% accurate patient selection.

At some point we are either relying on the patient or the Dr. for their honesty.
How will we know every patient had a viral onset ?
 

Bob

Senior Member
Messages
16,455
Location
England (south coast)
And calling it "post-exertional fatigue" seems like a pretty bad start, regarding understanding it. It. Is. Not. Fatigue. It's bodywide pain, it's a headache, it's painfully swollen lymph nodes, it's crashing blood pressure and rising heart rate, it's ataxia ... etc. NOT FATIGUE. If they can't even get that much right, we really are screwed.
But your observations don't apply to all patients. It's not my own experience. We're a heterogeneous group, and you're describing one subset. For the first ten years, I experienced no pain, no headaches, no blood pressure issues, no heart rate issues, etc. I had straightforward exhaustion (otherwise described as fatigue), brain fog (loss of mental vitality, and temporary loss of memory recall), and malaise. The best description I could come up with for my symptoms was "flu-like malaise" which is inclusive of all of my symptoms. The biggest problem for me was the severity of those symptoms, the relentlessness, and the severe reactivity to exertion (PEM). So I don't strongly object to the term "post-exertional fatigue" as long as the "post-exertional" aspect is properly understood, observed and defined. The problem here is that we clearly have different cohorts (both described in the IOM report) that need recruiting.
 
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Bob

Senior Member
Messages
16,455
Location
England (south coast)
But do they understand PEM sufficiently to know who has it and who doesn't? Do they know what the symptoms of PEM are? Do they know when PEM starts? Do they know how to distinguish PEM from other forms of exercise intolerance or DOMS? I'm concerned that they're going to claim "I feel tired after exercise" is sufficient to establish that PEM is present.
I agree - this is a vital aspect of the study.
 

Bob

Senior Member
Messages
16,455
Location
England (south coast)
Agreed. They're being very dismissive regarding concerns of multiple control groups and small sample sizes. How about they have their biostatistician run the relevant computations to figure out what sort of results they'll need to get a statistically significant result? Currently it looks like it's going to be very difficult to find any "significant" abnormalities after correcting for so many comparisons being made.
Yes, and they can calculate how many patients they need to have a reasonable shot at getting statistically significant results when comparing dozens of results with 2 control groups. This is something pretty basic which should be done before throwing millions of dollars into a study.
But I don't think this is like an ordinary study, is it? It's a deep study rather than a broad study. They're looking for clues, upon which basis to recruit more participants. If they find any potential abnormalities, then they will scrutinise them further. Nath even said that a single outlier can be interesting to investigate further. As Brian said, it's possible to find significant abnormalities in a single patient (n=1).
 
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Bob

Senior Member
Messages
16,455
Location
England (south coast)
Basically, I think it's all an issue of trust, or a lack of trust. If we simply don't trust them, then we don't trust them, and everything they do will be seen through a prism of distrust and suspicion. I'm not saying that's the wrong reaction, but Nath seems very serious about this study. If we don't trust them, then there's not a great deal more we can do, is there, in terms of practical advocacy? I agree about the issue of understanding PEM, and perhaps that's something we could help educate them about, but I'm not sure how we'd do that.
 
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duncan

Senior Member
Messages
2,240
There are several problems, and the real work hasn't even begun. I think it only good sense (and maybe good Science) to observe that now is the time to intercede and make changes before any potential additional missteps occur that cannot be undone.

There is no credible justification for inclusion of the psychobabblers. None. No good can come from their inclusion. But bad can. So one has to wonder why are they there in the first place, and now that we have identified them as a problem, and no adequate explanation for their presence has been forthcoming, why are they still involved? Literally months after they were identified as offensive and unnecessary, why are they still there??

The selection process. IF any clinicians can't even understand PEM...if they are actually prescribing GET to our sick, how can we expect them to differentiate between tired people who DO improve with exercise, and pwME who suffer because of it? Isn't letting such clinicians populate this study opening the door for studying the wrong people? Isn't this precisely what the CDC and other organizations and groups have done in the past? Like the Wichita study?

Why does the lead investigator seem to conflate ME/CFS with fatigue? Not just any investigator, but the individual charged with running the show? I like this guy! I think he brings some serious credentials to bear in this process. But if he is starting the process with what might be a serious and fundamental misunderstanding about the nature of our disease, what might that mean for the study governance? Does he just think he is studying tired people? Small wonder then that he is okay with the psych contingent...

Why are we still looking at a Lyme control? With only 40 patients being examined, there should only be pwME, and healthy controls.This is basic stuff. For that matter, why is the individual who is responsible for all Lyme research listed as a contact - not just an investigator, but as a contact?

We are told time and time again that the NIH wishes to work with patients as a team, but not a lot of teamwork has been evidenced yet. Who will be the patient representatives, and what will be the extent of their role? They should be able to interview prospective candidates to help ensure true ME/CFS sufferers are being examined. Is this in the cards?

These are serious issues. Perhaps they are not so serious for some in Bethesda, but we have seen this played out before over the last 30+ years, and it hasn't ended well for us very often.

As many have suggested, it might be good going forward that the NIH actually addresses in detail more of our concerns. For starters, I'd like to know that other than the removal of the FMD control, what patient study process recommendations have the NIH embraced and not just paid lip service to - and what are their intentions relative to other issues? It shouldn't be good enough to say "Why should the NIH listen to us", or "We should be thankful that they are even giving us their attention", or "We should be grateful that they are even considering us as really sick".

We need to be heard precisely because we ARE the sick, and they have gotten that wrong for far too long.
 
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Bob

Senior Member
Messages
16,455
Location
England (south coast)
I'm still catching up with the discussions, above. I see that I've repeated some stuff that's already been said.

@Valentijn, I think you're being unfair to @viggster, and have misinterpreted him. I agree with his observations about the nature of the trial. This isn't the usual type of study. It's an initial observational study, whereby n=1 (a single patient) can potentially give interesting results to follow up. Ron Davis is doing a similar small, but deep, study isn't he? Because it's an observational study, there's no hypothesis upon which to base a statistical analysis, so the study can't be underpowered or overpowered. Or that's my understanding.

Also, those kinds of stats are typically run for late-stage drug trials where the approximate treatment effect is known and then you calculate how many people you need in your study to see that effect. This is a discovery study, and many many comparisons will be made across the groups, but there's no good way to know up front how strong of an effect might be at play for each variable.
 

duncan

Senior Member
Messages
2,240
I am talking about recommending a gradually increasing exercise regimen as therapy. Check out Podell's blog. I provided a link to it earlier in this thread, I think. Did Lapp allude to it in his presentation? I can also think of one other that USED to, but not sure if he still does.

But all it takes is one. I don't even know if the patients will be equally divided by clinician, or if proximity will play a greater role. Proximity = dollars.
 
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Research 1st

Severe ME, POTS & MCAS.
Messages
768
Complete silence on the matter, and the high likelihood that such calculations would confirm that two control groups is a really really bad idea for a small study.

Val, you have it correct as ever, thank you for your explanation and Duncan also understands the situation we are in.

In more basic terms (as I don't have your brain power!) I thought I'd explain a little also to people who don't understand and think that it's a case of patient trust. It isn't a case of patient trust, it's about scientific accuracy (pre study selection of what it means to be an 'ME/CFS' patient to the NIH and scientific integrity (post study promotion of the results and what this means in relation to what Science knows already about ME and CFS).

So here we go:

Point 1: Who & Where Dr Nath et al, gets the blood from matters as Fatigue clinics aren't representative of ME patients:

The undisclosed human Retrovirus findings which backed Mikovits's findings of retroviruses (not XMRV) in CFS humans wasn't permitted to be made public. The finding went against the whole idea that Mikovits is a bad scientist and we don't need expensive ARV's. ARV's in CFS is a political nightmare to fund, CFS being perhaps 20x more prevalent than AIDS. For those unaware, Dr Montoya's group had retroviruses at 85% positive rate. CDC know this, NIH know this. The data will never be made public and it will be left to private researchers to pick up the pieces, which may senselessly cost more lives of people with severe ME, especially involving cancer.

So we stick with the manuscript. Non infectious, Chronic Fatigue Syndrome of any cause not explained by basic tests:

Why is this important or related in any way to the NIH Dr Nath study? Well, the other group tested for retroviruses (from an 'expert' CFS clinician) did not have retroviruses - will this negative retrovirus group fatigue clinic now be sending blood, again, to represent 'ME/CFS' in the small but complex NIH study? If so, we know its a fix to erase ME in favour of Chronic Fatigue.

Hence it matters, massively, who and where the blood is from. With a CFS diagnosis, different conditions are out there, under the labels ME and CFS or ME/CFS. Different condition alter Scientific data, and so it alters the politics.
The CDC know this, the NIH know this.

Point 2:
People with severe ME are made very ill by even gentle GET.
People with depression and F48.0 Oxford Chronic Fatigue failed to recover with GET.
GET is thus useless and doesn't work, not a surprise as the idea was created by psychiatrists for CFS as a form of aversion therapy (fear of exercise).

Of concern Dr Lapp and Dr Bateman and others advocate for CBT and GET, gentle, but still promote it.
This means their patients benefit from it and tolerate it. Yet we know, ME patients don't tolerate it. It thus matters, hugely, if the NIH blood samples are coming from Dr Bateman/Dr Lapp or others with FATIGUE CLINICS - because clearly, they benefit from gentle graduated exercise, and people with ME - don't.

It is thus critical to the integrity of the proposed NIH study with Dr Nath et al, to understand when producing any form of influential or definitive study (which clearly it aims to be):

*What signs of disease the patients have you got the samples from

*What doctors collected the samples

*How long have the patients been ill for

*How badly affected are they.

*What conditions other than CFS do they have
? (We'll get back to this in a moment, hence it's in red text).

*What makes them worse/better.

*What medications are they on and what medications can they tolerate.


Point 3:

Different clinicians see different patients. All doctors have personal bias, including in ME CFS research, it's part of being human. If you ask Wessely to select 100 'ME' patients and test them for infections and inflammation you will get a very different outcome than if you ask Dr Peterson - however, both can publish their work under the title CFS, ME or ME/CFS - even if the two different doctors are looking at two different groups of people with unrelated health problems.

The CDC know this, the NIH know this.

What do we know?
Dr Cheney and Montoya's patients are more sick that someone attending a Fibromyaliga/Chronic Fatigue clinic like Dr Bateman's. That is a given, because of the therapies available at the clinics differ.

We also know that publishing a paper does not make you an 'ME CFS expert'. There has been talk recently, for example, that Dr Lipkin is an 'expert researcher' in CFS. He is not. The same goes for claiming that doctors who draw blood from patients in fatigue clinics are 'expert clinicans in ME'. Again, they are not expert in ME because they see 1000's of people with Chronic Fatigue only, not the sort of patients Dr Byron Hyde sees in Canada.

A true expert on ME has decades of research and clinic expertease, looking at people very ill. People like Dr De Meirleir. These are true ME experts, and these are the people who the NIH should have selected to give blood samples. Of course, they are not invited and also took no part in a game they know from experience, is rigged - such as the IOM contract, which Dr Bateman supported. So far, All government studies have been rigged for 'ME/CFS' and 'CFS', in terms of not revealing a ME cohort within ME/CFS, and 'CFS' because the government allied researchers use as weak diagnostic criteria as possible, rather than the opposite. Naturally, they never find much.

Conversely, people who fly, train, car, ambulance themselves to see people like Dr De Meirleir, consistently show the same abnormalities over and over again: Intracellular infections, Orthostatic Intolerance and Autonomic Dysfunction and Inflammation of a Cytokine expression nature.

Tragically for ME science research consistent findings in CFS (likely ME) are not required to present in any 'Groundbreaking' government study and are not required to be present in the Dr Nath study either - before patient selection, before the blood draws - which they should be. If they aren't? Then you are simply analysing blood from people with unexplained chronic fatigue, aka Fukuda CFS. The CDC know this, the NIH know this.

Sadly, this will happen by default because this is what the government want. Non inflammatory ME to equate to ME. - thus deleting ME, thus deleting inflammation, thus deleting a retrovirus or Chronic Lyme being 'disovered' to be what organic, CFS is, all along.

Point 4:
Why does this all matter regarding the Dr Nath et al, (NIH study)and why are patients, sensibliy and rightly emotionally invested in demanding quality research which some claim is simply a lack of trust rather than logic?

The public don't know about ME within CFS and don't care. The public do not decide an outcome of a study, but they aid discrimination. Ignorant doctors who believe CFS is mind-body problem don't care either and use the press to worsen discrimination. Hence ME, a disease not dissimilar to MS, doesn't officially exist in society.

The ME CFS patients whose own lives have been destroyed do know and do care. Hence Val and Duncan's points.


Point 5:
My most important point is in red text above, that if you scroll up you will read mentions we don't know what other conditions the patients have: This is hugely important, and I'll tell you why:

To the terrible cost to the patients, CFS ME researchers can exclude patients who have explained reasons for Chronic Fatigue including in important research studies. What this means, is largely, people with ME cannot be researched, because their multiple co-morbidities exclude them from becoming: CFS/ME or ME/CFS.

If you have any of the following due to having ME, you will likely be excluded from the NIH study, or indeed any other.
Is this saying again this is some big mean nasty bad plot? No. But it explains to the unaware how the results of any CFS research (which sticks to this rule) will find little or no differences comparing CFS to neurotic patients which Wallit knows and why Wallit was included:

ME and organic CFS sufferers report and can develop:

Allergies
Arthritis
Asthma
Autonomic Dysfunction (POTS)
Cancer
Diabetes
Gynecological and female related disorders such as PCOS
Heart failure (Mitochondrial)
Infections
Inflammation
Low blood volume
Nutritional Deficiencies
Sleep Disorder
Thyroid disorder, Low Cortisol.

Any of the above (and many more I haven't written) will remove you from a diagnosis of Fukuda CFS, because the above are explained reasons for Chronic Fatigue. CFS fatigue should be unexplained, hence the removal of the above. By doing this, the dreadful disease ME is hidden which is why Straus and British Psychiatrists colluded together, to create the CFS. We will see in a minute what Straus really thought of CFS patients behind closed doors.


Point 6:

The results of a government based 'ME' paper (that isn't one), but can be claimed to be so by the 'results':

The results of the NIH study can be 'spun' by spin doctors as they always have been before, despite the huge consequence to the patients who won't respond to what the CDC promote (CBT/GET/Antidepressants) because they have ME and not a problem with Chronic Fatigue related to anything you pick out of a hat (Fukuda CFS, Oxford CFS).

CFS and ME/CFS are a mixture of conditions due to CDC intentionally mixing in unexplained fatigue with ME (they created CFS after all), and intentionally non screening (pre and post diagnosis CFS sufferers) for explained reasons for suffering related to ME pathology (CFS criteria only uses basic tests, not specialist tests that PWME are positive on) - such as TILT test..

This was done intentionally to remove ME from CFS research with the blessing of British psychiatrists and vaccine manufacturers who stated they wanted to replace ME with any cause of fatigue, CFS. Vaccine manufacturers to this day, celebrate and congratulate the Wessely School destruction of ME, and promotion of CFS as a mental illness by giving them awards. The CDC know this, the NIH know this. Some of us, know this, because we have long memories, because we are old!

By mixing in alleged mentally ill people with ME people, we see research finding inconsistency or 'no association' (usually) from government studies. A prime example of this was the recent Dr Lipkin and Dr Hornig paper, that found no Cytokine expression after 3 years oddly declaring this to be a huge finding in 'ME/CFS'. No inflammation after 3 years though, does not happen in ME so their paper was invalid when relating it to ME.

Instead, ME is associated to chronic cytokine expression, as Dr Montoya's paper (that is blocked from being published) shows, countless CFS papers have shown previously, and patients who test their own blood discover also. Dr Montoya's blocked paper shows massive cytokine inflammation in the more severely affected, to the extent he has biomarkers to screen for mild Vs more severe - the elusive subsets. This work of Dr Montoya's of 'medicalising' CFS, goes against everything the NIH are saying with Lipkin who is going for no cytokines after 3 years and thus no inflammation. Retroviruses will cause high levels of Cytokine expression - as was discovered by multiple groups, but denied by the government - hence Dr Lipkin will not disclose or discuss Dr Montoya's 85% positive retrovirus finding, years after Judy Mikovits was excommunicated.


Point 7:
CFS research without biomarkers failing to screen patients before their inclusion in a study (to check they have possible ME) can never determine a cause of ME. Why? The study results of CFS research using weak fatigue based inclusion criteria creates further heterogenous groups, unrelated conditions - this is then called 'ME' by Government agencies. This 'phenomena' in CFS research is what keeps all patients perpetually imprisoned. The CDC know this, the NIH know this - but do it anyway from habit, because no one is brave enough in government to suggest they stop (because they think the patients are mind-body tired people) so it won't hurt them.

Without clinically evaluated signs of disease to determine if it is likely someone has ME (within the idea of ME/CFS) one cannot possibly say with confidence or scientific accuracy that the results of any study represents ME, if the patients who's blood is sampled or brain is scanned does not have any signs of ME present.

Point 8:

Why does this matter, not just to us, but to Science?

ME is a specific disease, a brain injury, a neurological condition. CFS is not required to demonstrate any neurological signs, and thus the misdiagnosed without ME, can end up in an influential or definitive government study on CFS or 'ME/CFS', who don't have the condition ME or bilogical CFS either. The CDC know this, the NIH know this. The UK MRC know this with their PACE trial.

This is why, ultimately, it's critical that the samples tested for Dr Nath's NIH study are from people with well described organic ME. BUT they won't be. Why? Cinician bias, then will decide, if the 'specialist' think, the person has it - because of their own interpretation of what 'it' is. This isn't Scientific.
We need tests run, before the NIH blood samples are collected from potential PWME but tests cannot be run, as then if abnormal the person doesn't have Fukuda CFS - by the rules of what CFS is, hence it is insane to call any research or any condition: 'ME/CFS or CFS/ME' with any real confidence as it would be equally inaccurate to call a condition MS/Lupus because both involve Chronic Fatigue but aren't the same conditions!

Point 9:

Breaking the stalemate, with checkmate:

No Government funded study, such as the NIH will honestly include the same inflammatory ME patients with retroviruses (Montoya's patients) - but they will instead use FATIGUE CLINICS to get the data from and find nothing, or find inconsistency. Hence we find people's valid, sensible, and science based concerns over the NIH who have a history of neglecting CFS patients. When was their last large scale study on general CFS? 20 years ago?

Point 10: (Conclusion):

No matter how honest or nice Dr Nath is as Scientist (I'm sure he's both), it's who the CFS patients are, where they come from (clinics) how sick they are (severity) and what abnormalities they have before being selected for study inclusion, which determines the quality of a study purporting to be about 'ME/CFS' sufferers and their immunological status.

So far, ALL government agency CFS studies have failed miserably to do anything to change the 10 problem points I have listed and it's private researchers or who know the signs of ME, who tend to get results.

This needs to change, and no amount of window dressing or 'assurances' to patients mean anything, it's all study design and being transparent about study design and wanting to be a pioneer in science that gets you results.

However, doing that usually gets your paper un published, or your position in jeopardy for not towing the line.

Will anyone show bravery this time from NIH in trying to expose ME, instead of covering it with a fatigue blanket?
 

Riley

Senior Member
Messages
178
I am talking about recommending a gradually increasing exercise regimen as therapy. Check out Podell's blog. I provided a link to it earlier in this thread, I think. Did Lapp allude to it in his presentation? I can also think of one other that USED to, but not sure if he still does.

But all it takes is one. I don't even know if the patients will be equally divided by clinician, or if proximity will play a greater role. Proximity = dollars.

You seem to be devoting a tremendous amount of energy to a problem that is hypothetical and speculative.
 

duncan

Senior Member
Messages
2,240
Well, @Riley, I could tell everyone that I was prescribed, personally, this therapy by two clinicians on the list, but that's just hearsay.

So I tried to provide some objective perspective.

Regardless, I should think the topic worthy of our attention, given the gravity associated with the results of picking the wrong patients to be studied.