Jen Brea: My ME is in remission

[rvallee]

It has to be navigated correctly, people like one liners and easy answers, the PACErs saying well the whole film is crap because she didn't have ME hence PACE is right will gain loads of traction if we are not ready for it and we don't navigate this keeping in mind it will be used against us.

I'm sure they will, but their own ideological model would have guaranteed Jen would never have gotten this surgery.

Wouldn't be a smart move. Pretty sure they'll make it, but it's a dumb argument that actually demonstrates how incompetent and indifferent to our well-being they are.

Jen is the highest profile ME patient in the world. Or was, maybe. And she is making a miraculous recovery. As has Jeff and others. The psychosocial ideologues claim to not be interested about cause and etiology because they're all about rehabilitation. And here are stories of misdiagnosed (or distinct subset) patients who have made a significant recovery and... zero interest. None.

If we take their claims of wanting to help us at face value, these are people who have dedicated their career to "rehabilitating" severely ill people and they show no interest whatsoever in a possible case of significant recovery by the highest profile patient in their field of expertise. Whether it's a subset or a misdiagnosis is irrelevant, by the MUS model of ME, these cases were "textbook" cases of CFS, thanks to the extremely vague and muddied definition they unleashed onto the world.

Which frankly yet again shows they are full of shit but it's way too on the nose, they can't even bother faking interest in possible significant breakthroughs about a disease they "own" by way of being the creators of the current dominant paradigm. The same with a potential diagnostic test by the nanoneedle, absurdly claiming that a diagnostic test isn't particularly needed despite diagnosis being THE most significant obstacle to progress. That's shocking incompetence.

Cautious optimism is definitely warranted and my opinion is cases like Jen demonstrate subsets of differential diagnoses, which is explicitly recommended against in the psychosocial model. Nevertheless, this is significant because their model applied to those cases. It shows that there is a subset out there of people suffering severe chronic disability who could be helped and the "experts" in the field show no interest whatsoever.

Could not more blatantly show they are charlatans. So maybe they will try to score a goal, but it will yet again be an own goal.

 

[Mij]

I'm curious as to how taking Valcyte for years is no longer needed for a 'persistent viral infection' after CCI surgery? My conclusion is that it wasn't helpful in the first place?

 

[rvallee]

But we are not talking about a new idea. We are talking about whether or not CCI is associate with a clinical picture that overlaps with ME/CFS (likely to use the word fatigue. CCI has been known about for at least 100 years. The clinical picture has been in the textbooks for 100 years. Nothing new.

One possibility is that if there are more... "believable" from the perspective of physicians... symptoms in CCI then there would not be the focus on fatigue, which is just as invalid in ME anyway. It's not the main symptom and should never have been so prominently discussed as "it".

The psychosocial lot has focused obsessively on fatigue at the exclusion of everything else, not because it is such a prominent feature of the disease but because it is so extremely vague and easy to confound. It was talked about before CFS but ME was mostly known as a flu-like syndrome. We wouldn't even be talking so much about fatigue without it being pushed and promoted by ideologues, something that likely did not happen with CCI if other symptoms stood out more.

So if that ideological push did not happen with CCI, then we should expect the literature to not be filled with a symptom that can, even though it shouldn't, be used to mean just about anything and in fact is being abused precisely to create confusion and mix everything in the MUS ideological framework.

 

[Inara]

an arbitrary cut off considered normal. The question is whether the cut off has been put in the right place

But this is a problem with every normal range. Assuming a Gaussian distribution makes it only slightly better - and while there exist outliers in a Gaussian distribution, for most doctors they don't.

 

[Jonathan Edwards]

But this is a problem with every normal range.

Exactly, so being diagnosed with CCI does not necessarily mean that there is a significant craniocervical problem ('CCI').

 

[Inara]

Exactly, so being diagnosed with CCI does not necessarily mean that there is a significant craniocervical problem ('CCI').

But then being diagnosed with anything doesn't necessarily mean something. Where does that take us? And what's medicine's answer to that?

 

[Hip]

I'm curious as to how taking Valcyte for years is no longer needed for a 'persistent viral infection' after CCI surgery? My conclusion is that it wasn't helpful in the first place?

My tentative and very speculative hypothesis (sorry if some don't like these!) is that Jen and Jeff's recovery may actually have been due to viral clearance brought about by the CCI/AAI surgery.

In both cases, their POTS immediately resolved after surgery (POTS is objectively measurable). POTS is due to autonomic dysfunction, so it seems that the surgery instantly fixed the dysautonomia. I suggest the mechanical brainstem pressure may have been impeding autonomic nerves, causing dysautonomia.

But the ME/CFS symptoms took longer to clear, weeks to months.

New research indicates that the immune response is controlled by both the sympathetic and parasympathetic nervous systems, so my speculation is that the instant resolution of dysautonomia after surgery may, in turn, have caused immune function to improve, thereby clearing viral infections (and/or resolving possible exaggerated or dysfunctional immune responses to these infections), thus putting ME/CFS into remission.



This autonomic-immune connection hypothesis was originally suggested by Jeff:

It could also be that the brain stem compression disrupts the autonomic nervous system so that the immune system can't clear viral and/or bacterial infections normally.

 

[Jonathan Edwards]

But then being diagnosed with anything doesn't necessarily mean something. Where does that take us? And what's medicine's answer to that?

I don't really understand what you are querying. Marky asked if being diagnosed with CCI means you have CCI. I was pointing out that the definition of CCI may be both arbitrary and subject to unreliability from place to place or scan to scan. Similarly a man might be diagnosed as anaemic with an Hb of 13.5 by an alternative practitioner keen to prescribe expensive herbal remedies, when he is not anaemic in any sense that matters.

The solution is good quality control. The reason to publish the cases said to have CCI is so that we can all be sure of the quality control.

 

[Trish]

But please can we avoid ME advocacy groups giving prominence to speculative hypotheses based on a few individual cases. I fear it does our cause harm.

Do you have evidence to indicate that such stories work against advocacy efforts? On the one hand you are asking for proper evidence regarding ME/CFS treatments, and asking people not to make unproven speculative hypotheses. But then you put forward an unproven hypothesis of your own! Can't have it both ways!

That made me smile. You're right, I don't have evidence that giving prominence to speculative hypotheses harms advocacy. That's why I said 'I fear ....' not 'It will...'

However I do think if any ME advocacy organisation were to give prominence in advocacy to any hypotheses based on a few cases, that makes them no better than other advocacy organisations that promote, for example, LP as a cure for ME based on a few cases, or ME organisations that publish stuff on their websites like 'some patients find graded exercise therapy helpful'. I think that undermines our efforts to be taken seriously by politicians and scientists.

 

[JES]

I'm curious as to how taking Valcyte for years is no longer needed for a 'persistent viral infection' after CCI surgery? My conclusion is that it wasn't helpful in the first place?

If I remember correctly, Jeff had exactly the same thing as Jen, massively elevated viral titers (against EBV?), but all this cleared up after the CCI surgery. Medicine has a very poor understanding of how the ANS works. I have spoken with lots of doctors and they just shake their head whenever I bring up my ANS problems / dysautonomia. ANS is obviously involved in maintaining/regulating a huge number of bodily processes, including regulating the immune response.

 

[Hip]

That made me smile. You're right, I don't have evidence that giving prominence to speculative hypotheses harms advocacy. That's why I said 'I fear ....' not 'It will...'

Glad it raised a smile. I was in a playful mood when I wrote it!

But ME 'symptoms' are not caused by persistent viral infections.

The jury is still out on that. There are researchers who discount viral theories of ME/CFS, but others who pursue them.

 

[Milo]

What throws me back is that patients themselves influence others to obtain a diagnostic test or a treatment. We have seen this over and over throughout the years, and there are a few reasons for this:

- The lack of physicians or medical specialty looking at ME patients on a daily basis.
- Patients that have been burnt so many times by unknowledgeable or unwilling to investigate physicians
- Patients sick so many years, unable to pay for health care that is not covered
- Seemingly the lack of legitimacy of this illness has amongst physicians.
- There seems to be a lack of leadership (though this is changing) from physicians and researchers and perhaps a lack of traction with their peers, and most clinicians work in silo.
- patients reading science litterature and experimenting on themselves.

So patients end up doing their own things to save themselves. Occasionally or rather rarely patients go on to get better. Often times there is a skepticism from their peers when this happens.

But in the wider medical community, this is not how things usually work. When there are discoveries, the communications happen through scientific publishing and through conference presentations. This triggers further hypothesis and funding bodies allocate money to research that particular hypothesis formally.

That system seem totally broken for us. Moreover, there might be several years before science can determine whether there is a correlation or a subset of ME patients that have CCI. That wait time is not necessarily attractive to patients who have been sick for decades.

 

[Jonathan Edwards]

If I remember correctly, Jeff had exactly the same thing as Jen, massively elevated viral titers (against EBV?), but all this cleared up after the CCI surgery. Medicine has a very poor understanding of how the ANS works. I have spoken with lots of doctors and they just shake their head whenever I bring up my ANS problems / dysautonomia. ANS is obviously involved in maintaining/regulating a huge number of bodily processes, including regulating the immune response.

Hang on, I don't mean to be difficult but this to me makes no real sense.

High viral titres are a sign of immunity to the virus. If the immune response was reduced and antibody levels fell that would be a bad thing. We don't want our antibodies to EBV to 'clear up'. Medicine has a reasonably good understanding of how much control the autonomic nervous system has on thing like immunity. Cutting the vagus nerve does not seem to be too much of a problem with immunity. Antibodies are produced by plasma cells in bone marrow that have as far as we can tell almost no sensitivity to any environmental control. They just chuck out antibody until they are forced out by other plasma cells wanting the space.

I am not surprised that doctors shake their heads when people talk of Dysautonomia because all the talk of Dysautonomia around ME does not add up to me. I am not at all clear that POTS is Dysautonomia. It seems just as likely it is a response to low blood volume. The fact that the heart rate increases indicates that the autonomic nerves are working well.

And if we have a poor understanding of how the ANS works how do we know it is obviously involved in regulating all this stuff? That doesn't seem to add up.

 

[lansbergen]

High viral titres are a sign of immunity to the virus. If the immune response was reduced and antibody levels fell that would be a bad thing. We don't want our antibodies to EBV to 'clear up'.

As I recall it, viral titres and antibody titres are not the same thing

 

[roller*]

should be easy, when jen (coxsackie?) and jeff (EBV?) would publish the lab-chronology of titers (measurable things) they claim improved - before and after treatment...

should be clear to them, that there is considerable community-interest in precision on this.

what virus did the 3rd interviewed pwmecfs (mattie) have ?

 

[Milo]

should be easy, when jen (coxsackie?) and jeff (EBV?) would publish the lab-chronology of titers (measurable things) they claim improved - before and after treatment...

should be clear to them, that there is considerable community-interest in precision on this.

what virus did the 3rd interviewed pwmecfs (mattie) have ?

Is this people’s court?

 

[roller*]

Is this people’s court?

you think, we better not ask ?

 

[dreampop]

Would getting the NIH study to check for CCI also help? They would have a more neutral perspective and a healthy cohort. Because I’m not sure how a single case report would add a lot of clarity. I trust the details and veracity @JenB has given

 

[JES]

High viral titres are a sign of immunity to the virus. If the immune response was reduced and antibody levels fell that would be a bad thing. We don't want our antibodies to EBV to 'clear up'. Medicine has a reasonably good understanding of how much control the autonomic nervous system has on thing like immunity. Cutting the vagus nerve does not seem to be too much of a problem with immunity. Antibodies are produced by plasma cells in bone marrow that have as far as we can tell almost no sensitivity to any environmental control. They just chuck out antibody until they are forced out by other plasma cells wanting the space.

I agree that high titers don't imply a "persistent active infection", which is the term that someone used few posts above. And yeah, it wouldn't be good if they antibodies completely cleared up, thanks for correcting that.

According to what Naviaux mentioned in a Q&A, high antibody titers could still be pointing towards a problem, even if there is no active infection as such. That problem factor would be the ANS or rather something in the brain that was corrected after CCI leading to resolution of a dysfunctioning ANS, which is of course nothing but a hypothesis. I quoted the relevant part of Naviaux' response in the following:

Third, latent and reactivated viral and bacterial infections can occur, but in the case of ME/CFS that has lasted for more than 6 months, this may be the exception rather than the rule. We have learned in our autism studies with Dr. Judy Van de Water that supertiters of antibodies do not mean new or reactivated viral replication. Supertiters of IgG antibodies mean that the balancing T-cell and NK cell mediated immune activity is decreased. This is a functional kind of immune deficiency that causes an unbalanced increase in antibodies.

The doctors I spoke to have no idea about the autonomic nervous system, they all just shake their head. I even got the diagnosis "autonomic dysfunction" following a TILT table test, which makes even less sense if there are no ANS problems in POTS. Either way, there seems to be a lack of understanding about what the ANS does and doesn't do, at least in my country.

 

[Milo]

you think, we better not ask ?

My comment suggested indeed that it is none of our business, and if these individuals volunteer this information, that’s ok but they should not be obligated in any way to provide further infomration.

It sometimes feels like patients are pressing for proof in order to decide for themselves whether this hypothesis has credibility and it is not how science works.

Disclosure: I myself received off-label treatments that were promising but did not pan out. And I have been told by other patients that it didn’t work because I didn’t have ME.