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You may wonder why the CAA treats XMRV the way they do... So:

Angela Kennedy

Senior Member
Messages
1,026
Location
Essex, UK
Sorry, I will not be very eloquent here, but that has to be one of the stupidest things I have ever read.

Yes. The 'in part' was comical especially. The whole edifice of 'somatization' is based on the distinction between 'physical' and 'psychiatric' (meaning 'mind' problems), with a privileging of the 'mind' over the body, the body a mere brute envelope. All very Cartesian dualistic- you know, the thing the psychs all claim to 'transcend'?
 

Angela Kennedy

Senior Member
Messages
1,026
Location
Essex, UK
But the only unifying hypothesis I can think of that can account for all those abnormalities, without requiring new understandings of human biology, is one of pathogenic causation or co-causation. And as acer2000 pointed out, those things by themselves represent a diffuse constellation of potential markers with only limited insight into pathophysiology.

The CAA has been fishing for biomarkers too exclusively for too long; there are many problems with this approach, including the poor definition of the disease itself (even Fukuda would include overlapping, unrelated conditions) and therefore of 'true' patient cohorts, but also the basic problem that the search parameters are too wide... Looking for biomarkers is like looking for a needle in a colossal haystack (i.e. the sum of possible biological parameters interacting with the sum of biological and environmental variables). It would make far more sense for an organization with a very limited research budget like the CAA to formulate, based on available biomedical research, a set of co-existing hypotheses for the pathophysiology of ME/CFS and to look for evidence of the causal mechanisms posited by those hypotheses. This is exactly what the WPI did. Instead, the CAA - and many other researchers - have tended to investigate rather peripheral associations between disease and certain biological parameters that do not encompass a central hypothesis of disease causation and that in themselves would, at best, only suggest a possible correlating pathophysiology. As I said this has been the sort of piecemeal approach prevalent in the research community as a whole towards CFS, but the CAA was in the position to do what the WPI ultimately did: to focus on investigating a particular hypothesis of what is going on in ME/CFS, particularly one involving viral pathogenesis, for which the biomedical evidence (despite what Dr. Vernon asserts in the linked article) has always been the strongest.

The CAA research strategy has been to cast a wide net and look for anything that correlates to (rather vaguely defined) illness in CFS patients, but with necessarily limited funding this has never seemed to me like an efficient approach. And even in the search for biomarkers they seem to have ignored two of the most compelling findings in ME/CFS research: abnormal SPECT, PET, and fMRI scans, and low circulating blood volume. To complement the work being done by the WPI and others, I would love to see the CAA expand efforts to look for these abnormalities in CCC-defined cohorts. The studies with Drs. Medow and Shungu hint in this direction, but are again essentially looking for different markers.

My apologies for spamming!

A beautiful summary of the problems that have dogged the 'research' strategy for 'CFS' for so many years, Doc.
 

omerbasket

Senior Member
Messages
510
There is no rational response to this. It borders on religious fanaticism that cannot be reasoned with. You've summed up your unwillingness to have a rational conversation quite nicely.
If you say that saying that the scientific world today doesn't know everything, and can't prove that retroviruses are not the cause for something (show me the way you can prove such a thing. And how surprisingly, suddenly you discover a new retrovirus and all your "proofs" from the past worth absolutley nothing), then you don't know science, and if you were a scientist you would do much more harm than good.
We, humans, have to remember we still don't know it all. If we won't remember that, we would never get even close to knowing it all.

Cort - Everything you say might strengthen the thought that retrovirus is not the cause, but in no way it proves it. Especially when we know who were the people that strengthen the idea the retrovirus are not the cause (i.e. people who say that ME/CFS is pshycological), and Dr. Vernon should also know that.

Now, if that's what she agrees to write, than she probably thinks that or, if it was possible, have an even stronger opinion about retorviruses not being the cause for ME/CFS.
Now, imagine that XMRV wasn't to be found connected to ME/CFS by the WPI. Do you think that a researcher like Dr. Vernon, who had already decided the retroviruses are not the cause for ME/CFS, would have even thought about studying the new retrovirus that was found in prostate cancer patients?
Well, it's a fact that there have been three years since the publication of the findings in prostate cancer until the publication of the findings in ME/CFS, in which she did not try to study that possibility. But she probably wouldn't have done it ever, because, she have already decided that "CFS is not [...] a retroviral infection".
 

V99

Senior Member
Messages
1,471
Location
UK
Originally Posted by V99
I agree. It's been said before, but what ever happen to the science in ME.

if you're looking in the scientific literature there basically are no published studies on ME after 1985 and just a handful of small papers - mostly doctors clinical notes prior to then. Its always been a niche topic - and a very small niche at that.

Seriously? What disease are you talking about. I'm sure everyone with that diagnosis in the UK, and everyone who knows that they have that disease, will be very happy that this conversation is not about them. ME is not a niche topic!

CFIDS would be considered niche, if that really was a discussion worth having.

Out of interest how did the patients advocacy groups end up with CFIDS and not ME?
 

V99

Senior Member
Messages
1,471
Location
UK
I would note that that paper apparently had at least 132 references. i think one has been mentioned. Do you have any idea how representative it is? Have you checked out any of the others?

Yes, they have been checked. It is still used as a reference.
 

Dr. Yes

Shame on You
Messages
868
if you look at the studies that Dr. Vernon has integrated in with each other I think you'll see that she's attempting to tie in blood pooling in the gut, reduced blood flows to the brain (causing all sorts of symptoms) and I believe Shungu's mitochondrial problems in the brain (complicated enough that its hard to remember). That group of studies as a whole is very hypothesis driven and quite ingeniously done. Its rare that different research teams collaborate so closely - so closely, in fact, that they can adjust their research protocols relative to other teams findings to take advantage of them (Before they publish).

But what could be the underlying cause of those three phenomena? What is the explanatory hypothesis? I do see in the integration of those studies the suggestion of a hypothesis for related pathological mechanisms, but not one that clarifies the cause of those mechanisms. To me it seems that piecing one's way back from those mechanisms to the root could take a very, very long time; the disease pathologies in ME/CFS are so numerous and complex. I am concerned that with this approach alone we could wind up pulling on strings and getting tangled up for years more. If there was generous national funding for ME/CFS research I might be less worried but given that there is hardly any I would prefer that the focus of our specialist research organizations (at least) be on exploration based on a hypothesis of causation, which I still believe may be simpler than the "Outside-->In" approach. Offhand I can't think up a causation hypothesis that can explain the full biomedical picture of ME/CFS that does not involve pathogens and related immune reactivity. The one study out of six recently funded by the CAA focuses on EBV in vivo, but how does that study tie in with the others to form an explanatory hypothesis or model?

There are countless biological parameters that would be very interesting to investigate, that might also show correlation to the symptoms or severity of ME/CFS, and that might reveal something else that is noticeably wrong with us. But surely the larger percentage of funding should remain related to the pathogen/immune connection, which has always been the most abundant and obvious evidence of a physical disease in patient histories and clinical presentation. Taking that as a starting point (at least by one hypothesis of causation) we can then allow it to direct us where and what to investigate next, given the other noted elements of the clinical picture (PEM, OI, sleep disturbance, allergies and MCS, etc, etc). If, for example, a viral cause or co-cause is posited, one would be more likely to look for the root of ME/CFS hypovolemia or OI in microvascular damage that could be caused by viruses or by excessive cytokine activity than, say, to look for shortages of an enzyme that converts dopamine to norepinephrine (or defects in that enzyme's gene). Both studies would be interesting, but with limited funds (and time, in more ways than one) it makes more sense to pursue studies that flow from a hypothesis with explanatory power.

I'm not sure the WPI's research efforts, other than XMRV, will satisfy you either.
Their proposed studies, including those not related to XMRV, make good use of limited funds, in my opinion. What they don't do, and likely can't do by themselves, are brain imaging and circulatory studies (which I hope the CAA continues to address and expand upon). The main point, though, is that they wound up finding XMRV because they were focusing on pathogens in the first place. I would say to take that as your working hypotheses (pathogens/immune abnormalities), and let that guide where and how you look next. That doesn't mean you only do research on potential causes, but that your project selection is informed by that hypothesis, even when it focuses on other ME/CFS signs and symptoms (like PEM).

from CBS:
As for FMRI specifically, I have been told that this is being investigated further (not necessarily by the CAA - personal communication as a potential subject and discussion of my subjective experience with CFS doc). If I hear more on this I'll let you know.
Thanks...and good luck!
 

bakercape

Senior Member
Messages
210
Location
Cape Cod. Mass
Then why does she say

I don't like CAA, but I agree with Caledonia. Vernon is just reporting what the thrust of the various papers has been. In science speak, you sometimes just report what papers say. The fact that some of them might be wrong is simply understood unless you say otherwise - "Dr blah *convincingly* demonstrated..." or "Blah blah had been the common belief since whenever, but in a series of strong papers it was demonstrated that...". Biomed PhD classes, which I dabbled in briefly without being enrolled, consist largely of everyone discussing papers and trying to rip them up. And I think most students are fairly surprised, as I was, by just how many papers can be ripped up or semi ripped up by old hands who know the game. I had certainly known that some papers were wrong, but I didn't quite realize just how many were totally unconvincing, or at least questionable, from at least one defensible perspective. So, the potential wrongness of all past findings is drummed into everyone's head over and over.

"It's not a recognized psychiatric disorder." Leaving the possibility open that it is a psychatric disorder that we just don't recognize.

Why does she not say it is not a " recognized retroviral infection" She just closes the door and says it is not one.

Here in we see her bias!
 

froufox

Senior Member
Messages
440
Very well said again Doc!!

But what could be the underlying cause of those three phenomena? What is the explanatory hypothesis? I do see in the integration of those studies the suggestion of a hypothesis for related pathological mechanisms, but not one that clarifies the cause of those mechanisms. To me it seems that piecing one's way back from those mechanisms to the root could take a very, very long time; the disease pathologies in ME/CFS are so numerous and complex. I am concerned that with this approach alone we could wind up pulling on strings and getting tangled up for years more. If there was generous national funding for ME/CFS research I might be less worried but given that there is hardly any I would prefer that the focus of our specialist research organizations (at least) be on exploration based on a hypothesis of causation, which I still believe may be simpler than the "Outside-->In" approach. Offhand I can't think up a causation hypothesis that can explain the full biomedical picture of ME/CFS that does not involve pathogens and related immune reactivity. The one study out of six recently funded by the CAA focuses on EBV in vivo, but how does that study tie in with the others to form an explanatory hypothesis or model?

There are countless biological parameters that would be very interesting to investigate, that might also show correlation to the symptoms or severity of ME/CFS, and that might reveal something else that is noticeably wrong with us. But surely the larger percentage of funding should remain related to the pathogen/immune connection, which has always been the most abundant and obvious evidence of a physical disease in patient histories and clinical presentation. Taking that as a starting point (at least by one hypothesis of causation) we can then allow it to direct us where and what to investigate next, given the other noted elements of the clinical picture (PEM, OI, sleep disturbance, allergies and MCS, etc, etc). If, for example, a viral cause or co-cause is posited, one would be more likely to look for the root of ME/CFS hypovolemia or OI in microvascular damage that could be caused by viruses or by excessive cytokine activity than, say, to look for shortages of an enzyme that converts dopamine to norepinephrine (or defects in that enzyme's gene). Both studies would be interesting, but with limited funds (and time, in more ways than one) it makes more sense to pursue studies that flow from a hypothesis with explanatory power.



Their proposed studies, including those not related to XMRV, make good use of limited funds, in my opinion. What they don't do, and likely can't do by themselves, are brain imaging and circulatory studies (which I hope the CAA continues to address and expand upon). The main point, though, is that they wound up finding XMRV because they were focusing on pathogens in the first place. I would say to look that as your working hypotheses (pathogens/immune abnormalities), and let that guide where and how you look next. That doesn't mean you only do research on potential causes, but that your project selection is informed by that hypothesis, even when it focuses on other ME/CFS signs and symptoms (like PEM).

from CBS:


Thanks...and good luck!
 

Cort

Phoenix Rising Founder
With regards to orthostatic intolerance and pathogens.

It could also be autonomic nervous system problems - problems with blood flow regulation. Dr. Vernon is exploring a hypothesis where problems in the gut effect blood flows to the brain. There is also the low blood volume issue - where does that come from. That are lots of chronic diseases -in fact i would think most chronic diseases do not have a pathogen involved - they come from, i guess, breakdowns in the system's over time caused by ??????. I think they know what's happening on the surface but they don't know why. Do they know why diabetics stopped producing insulin? For the genetically caused diabetes I would guess yes but for the other types I really don't know.
 

richvank

Senior Member
Messages
2,732
On the other hand there is alot of good evidence of low blood volume, vascular problems, natural killer cell problems, cortisol issues, increased oxidative stress, metabolic abnormalities, etc. Shungu, who is funded by the CFIDS Association, just found evidence of mitochondrial problems in the brain. There are LOTS of other things to study as well.

Hi, Cort and the group.

I would like to note that all of the phenomena you have listed here, including the new Shungu results, are explained by the GD--MCB hypothesis for CFS. Information on it is available on your site and at www.cfsresearch.org

Best regards,

Rich
 

urbantravels

disjecta membra
Messages
1,333
Location
Los Angeles, CA
I think dysautonomia can explain quite a number of things, certainly including OI.

Type I diabetes is thought to be an autoimmune reaction - the body attacks the pancreatic cells that produce insulin, usually in childhood. (I have a friend who has "Type I" diabetes because he was in an auto accident and his pancreas was damaged. Doesn't really count as normal Type I diabetes but is treated the same way - he has an insulin pump etc.)

Type II diabetes is brought on gradually, there is a genetic propensity to develop it, but it develops in the presence of lifestyle factors - overeating, obesity, carb/sugar heavy diets, etc. Over time the cells throughout the body develop a resistance to insulin and the body tries to produce more to compensate. At an advanced stage, the pancreas can "burn out" from these efforts and you may need insulin in Type II diabetes.

Most infectious diseases do not become "chronic" because they either kill you, or eventually get cleared from the immune system after making you sick and doing whatever damage they are going to do. Some types of infections can find a place to hide out in the body - herpes zoster (shingles), herpes simplex - and periodically re-emerge to wreak havoc. Malaria does something similar, with periodic re-emergences (but it is a parasite, not a bacteria or virus).

A retrovirus, unfortunately, is forever. It becomes part of your genome. HIV has gone from being a death sentence to a manageable chronic condition via great advances in antiretroviral drug therapy - but they can't clear it from your system, just keep it continually suppressed.
 

Cort

Phoenix Rising Founder
But what could be the underlying cause of those three phenomena? What is the explanatory hypothesis? I do see in the integration of those studies the suggestion of a hypothesis for related pathological mechanisms, but not one that clarifies the cause of those mechanisms. To me it seems that piecing one's way back from those mechanisms to the root could take a very, very long time; the disease pathologies in ME/CFS are so numerous and complex. I am concerned that with this approach alone we could wind up pulling on strings and getting tangled up for years more. If there was generous national funding for ME/CFS research I might be less worried but given that there is hardly any I would prefer that the focus of our specialist research organizations (at least) be on exploration based on a hypothesis of causation, which I still believe may be simpler than the "Outside-->In" approach. Offhand I can't think up a causation hypothesis that can explain the full biomedical picture of ME/CFS that does not involve pathogens and related immune reactivity. The one study out of six recently funded by the CAA focuses on EBV in vivo, but how does that study tie in with the others to form an explanatory hypothesis or model?

There are countless biological parameters that would be very interesting to investigate, that might also show correlation to the symptoms or severity of ME/CFS, and that might reveal something else that is noticeably wrong with us. But surely the larger percentage of funding should remain related to the pathogen/immune connection, which has always been the most abundant and obvious evidence of a physical disease in patient histories and clinical presentation. Taking that as a starting point (at least by one hypothesis of causation) we can then allow it to direct us where and what to investigate next, given the other noted elements of the clinical picture (PEM, OI, sleep disturbance, allergies and MCS, etc, etc). If, for example, a viral cause or co-cause is posited, one would be more likely to look for the root of ME/CFS hypovolemia or OI in microvascular damage that could be caused by viruses or by excessive cytokine activity than, say, to look for shortages of an enzyme that converts dopamine to norepinephrine (or defects in that enzyme's gene). Both studies would be interesting, but with limited funds (and time, in more ways than one) it makes more sense to pursue studies that flow from a hypothesis with explanatory power.thanksas soon

Their proposed studies, including those not related to XMRV, make good use of limited funds, in my opinion. What they don't do, and likely can't do by themselves, are brain imaging and circulatory studies (which I hope the CAA continues to address and expand upon). The main point, though, is that they wound up finding XMRV because they were focusing on pathogens in the first place. I would say to look that as your working hypotheses (pathogens/immune abnormalities), and let that guide where and how you look next. That doesn't mean you only do research on potential causes, but that your project selection is informed by that hypothesis, even when it focuses on other ME/CFS signs and symptoms (like PEM).

from CBS:


Thanks...and good luck!

The Pathogen question in CFS is dogged by a fundamental problem- there are problems with diagnosis regarding every pathogen that is of interest in CFS. Its kind of remarkable actually; there are lots of pathogens for which diagnostic protocols are well worked out but this is not true for any of the pathogen in CFS that I can think of - we specialize in the controversial pathogens. So when you say, let's just focus on pathogens you're immediately hit with a stumbling block. It sounds like a great idea but its just not very easy.

HHV6- prime candidates for investigation in CFS. There are good tests for HHV6-A and Dr. Peterson has said that, HHV-6 A is the prime focus in CFS but it's possible that HHV-6 B is hat is doing the damage in the central nervous system. HHV6 is a pathogen searching for a disease - something that clearly drive Robert Gallo, a codiscoverer I believe, crazy. At the HHV6 onference he said there's no way HHV-6 could be causing all the disorders that people are attributing to it and that itself is harming the field. He felt the HHV-6 fieldwould never be legitimizeduntil it started focusing on a few disorders. The HHV6 foundation has been working on a diagnostic test for years - they recognize that that is the key element that's missing.

EBV - is not that different. Dr. Montoya believes some diagnostic tests are illuminating that other researchers believe don't tell you anything. Ronald Glazer and Dr. Lerner believe that EBV functioning has been truncated in CFS causing it to spit out proteins that are causing the problem but the rest of the field thinks this is voodoo science and it is not being picked up on. (The CAA is funding his investigation that an aberrant form of EBV is at the heart of CFS. THey are also funding research into HERV's - which they believe could interact with herpesviruses and cause CFS. - two causal pathogen studies)

Enteroviruses - Dr. Chia believes that the diagnostic testing for enteroviruses was simply off -due to no one's fault - for decades. He finally found one diagnostic lab that he felt was doing the right kind of testing. Unfortunately his findings have not spurred on others to look for enteroviruses.

Dubbo - then you have the Dubbo studies suggesting that the infection caused by each of they studied is actually resolved; the pathogen is taken care of but that an overly aggressive immune response somehow turns CFS on.

Another Big Roadblock - Then there's the problem with central nervous system infections. How do you, short of biopsying a person's brain which is illegal or doing an autopsy find them? The pathogensof interest don't even show up in spinal fluid studies very often.

The pathogen field lacks clarity on a very basic level. You have to solve some of the methodological problems before you can really begin to get at them in a credible way. What you have is a nice theory that makes sense but alot of difficulty determining if it's true - particularly if the pathogen is found in the brain.

Cautionary note - If you've followed multiple sclerosis research a bit then you know that the proximate cause of MS - demyelination of the neurons - has been known for decades and they've looked at different pathogens just as long. They've been digging into neurons for decades - and they are still arguing a) if a pathogen causes it and b) if it does which one does......this is after decades of intense effort!

The most convincing evidence of pathogen involvement is probably anecdotal and published reports of patient success when using them. Infortunately we don't have any statistically rigorous, well designed studies on antiviral treatment in CFS - not one. THere's not one placebo-controlled, blinded, good study on antiviral treatment in CFS. So there's really nothing for the academic world outside of CFS to latch onto.

The big pathogen arrays the WPI is using will surely be very helpful as well but they are a pretty recent development and the The WPI has not, I don't think ?, published anything on their pathogen array studies and from what we hear is that they are basically finding herpesviruses - so no real surprises.

We're lucky that XMRV has captured so much interest because you get the idea that maybe they're gonna figure out whether that virus is playing a role.

Pathogens may very well be it but its a tough field. You could argue, XMRV accepted, it would be better to devote one's resources to uncovering the downstream problems because you might have a better chance of affecting them. (Not talking about XMRV here).

I think researchers are pretty smart. I think they are trying to get as close to this disease as they can with the amount of money they have - unfortunately that money is really lacking. If they had more money I think you would see a lot more comprehensive studies that attempt to explain the big picture in CFS.
 

richvank

Senior Member
Messages
2,732
A retrovirus, unfortunately, is forever. It becomes part of your genome. HIV has gone from being a death sentence to a manageable chronic condition via great advances in antiretroviral drug therapy - but they can't clear it from your system, just keep it continually suppressed.

Hi, urbantravels.

Have you heard about the study abstracted below?

Best regards,

Rich


J Med Virol. 2009 Jan;81(1):16-26.
Immunotherapy of HIV-infected patients with Gc protein-derived macrophage activating factor (GcMAF).

Yamamoto N, Ushijima N, Koga Y.

Division of Molecular Immunology and Immunotherapy, Socrates Institute for Therapeutic Immunology, Philadelphia, Pennsylvania 19126-3305, USA. nobutoyama@verizon.net
Abstract

Serum Gc protein (known as vitamin D3-binding protein) is the precursor for the principal macrophage activating factor (MAF). The MAF precursor activity of serum Gc protein of HIV-infected patients was lost or reduced because Gc protein is deglycosylated by alpha-N-acetylgalactosaminidase (Nagalase) secreted from HIV-infected cells. Therefore, macrophages of HIV-infected patients having deglycosylated Gc protein cannot be activated, leading to immunosuppression. Since Nagalase is the intrinsic component of the envelope protein gp120, serum Nagalase activity is the sum of enzyme activities carried by both HIV virions and envelope proteins. These Nagalase carriers were already complexed with anti-HIV immunoglobulin G (IgG) but retained Nagalase activity that is required for infectivity. Stepwise treatment of purified Gc protein with immobilized beta-galactosidase and sialidase generated the most potent macrophage activating factor (termed GcMAF), which produces no side effects in humans. Macrophages activated by administration of 100 ng GcMAF develop a large amount of Fc-receptors as well as an enormous variation of receptors that recognize IgG-bound and unbound HIV virions. Since latently HIV-infected cells are unstable and constantly release HIV virions, the activated macrophages rapidly intercept the released HIV virions to prevent reinfection resulting in exhaustion of infected cells. After less than 18 weekly administrations of 100 ng GcMAF for nonanemic patients, they exhibited low serum Nagalase activities equivalent to healthy controls, indicating eradication of HIV-infection, which was also confirmed by no infectious center formation by provirus inducing agent-treated patient PBMCs. No recurrence occurred and their healthy CD + cell counts were maintained for 7 years.

PMID: 19031451 [PubMed - indexed for MEDLINE]
 

akrasia

Senior Member
Messages
215
When the CAA decided to marginalise the Incline Village and Lyndonville cluster cases, accepting increasingly diluted definitions of the illness, they denied a crucial dimension that should have been driving their research: the illness was infectious, if not actually contagious.

The Holmes definition of CFS, a weapon in the larger project of the demolition of m.e., was an act of deliberate disinformation. How in the light of what happened to Cheney and Peterson's patients, the ostensible templates for the Holmes definition, could this not be seen as transmissible?

If, at the very least, you had evidence coming out Nancy Klimas's lab in the early 90's, of the presence of reverse transcriptase and a retrovirus blooming on Mike Holmes(a very different Holmes) photographs of slides, something Klimas often cites, how could the retrovirus project just be sidelined without a good explanation of why this was happening?

Abandoning the search for a pathogen allowed the wooly thinkers and psychobabblers to run amok. If nothing else, a firm stand expressing a belief in the presence of ongoing infection could have served as a bulwark against a lot of very malign nonsense. You can have a theory of causation that awaits confirmation by research. Why leave a vacuum?

I also have contributed to the CAA's research project, because I thought that some of the things they are exploring worthwhile. I gave with great reservation because of some of the issues outlined by contributors to this thread and my lack of faith in the CAA to stay consistent. You cannot cultivate a view I outlined above and play host to Peter White in your magazine, without extraordinary conceptual contortion and compromise. Committing to a infectious explanatory model would have made this impossible.

If I say something is not a "recognized" psychiatric illness, then I'm leaving the door open that it might be one day. And if I follow this up by quoting from a CFS "specialist", who has a very strong interest in factitious illness, I'm inviting a great deal of suspicion. Why would you do that? Given Suzanne Vernon's problematic lineage she should avoid the merest suggestion of a psychiatric etiology. Does she not realize that some of us are going to follow up on her references?
 

thegodofpleasure

Player in a Greek Tragedy
Messages
207
Location
Matlock, Derbyshire, Uk
With regards to orthostatic intolerance and pathogens.

That are lots of chronic diseases -in fact i would think most chronic diseases do not have a pathogen involved - they come from, i guess, breakdowns in the system's over time caused by ??????.

How can you be sure that they are not caused by an unknown pathogen ?
That is surely the key point at issue here.
 

Cort

Phoenix Rising Founder
Seriously? What disease are you talking about. I'm sure everyone with that diagnosis in the UK, and everyone who knows that they have that disease, will be very happy that this conversation is not about them. ME is not a niche topic!

CFIDS would be considered niche, if that really was a discussion worth having.

Out of interest how did the patients advocacy groups end up with CFIDS and not ME?

I don't think you are read my post clearly. I was referring to the scientific literature - papers published in medical journals. Go into Pubmed type in myalgic encephalomyelitis and then go back to before 1985 (when chronic fatigue syndrome became the name) and then look at how much research was done on this disease. There's very, very little on ME in the published literature - that was what I stated I was referring to.
 

judderwocky

Senior Member
Messages
328
With regards to orthostatic intolerance and pathogens.

It could also be autonomic nervous system problems - problems with blood flow regulation. Dr. Vernon is exploring a hypothesis where problems in the gut effect blood flows to the brain. There is also the low blood volume issue - where does that come from. That are lots of chronic diseases -in fact i would think most chronic diseases do not have a pathogen involved - they come from, i guess, breakdowns in the system's over time caused by ??????. I think they know what's happening on the surface but they don't know why. Do they know why diabetics stopped producing insulin? For the genetically caused diabetes I would guess yes but for the other types I really don't know.

Yes. My mother managed the Diabetes center here in central florida for a long time. I volunteered there a lot in high school. Most of the diabetes patients have diabetes because they ate too much sugar their entire life and won't exercise. There are some very unfortunate individuals who have developed the condition from viral infections, genetic conditions, etc.... but a number of the individuals that came into the clinic, it was simply a life of ZERO discipline. I definitely have sympathy for those that were/born developed it from no fault of their own - a friend of mine in highschool.... a national level swimmer... had diabetes... it was very difficult for him and he had to work on it.... unlike others

Case in point - my ex-grandfather in law. Had diabetes. Would never check his sugar. Never wanted to have to deal with it. He would shovel cake and sweets into his mouth everytime my grandmother would turn around. This was characteristic of a lot of the individuals that came in these clinics. There are blood tests that can give a doctor an idea of how well a patient has been managing their blood sugar (i think they get a picture of several weeks) and they frequently are doing nothing for the disease. Many of them simply want a pill that will make them better without having do deal with the long term effects. Diabetes is tough work: you have to watch everything and show remarkable discipline. Unfortunately many of these patients confuse discipline with taking a medication.......

As far as blood flow issues go.... they do these studies on a number of conditions. Just about anybody with a chronic condition is going to have some sort of blood flow issues somewhere. I just don't think its going to show causality or provide anything more useful than it has in any other disease group... yep you got some blood issues, nope, probably not the cause.

for instance:

http://www.ncbi.nlm.nih.gov/pubmed/20536743
http://www.ncbi.nlm.nih.gov/pubmed/20629257
http://www.ncbi.nlm.nih.gov/pubmed/20616885
http://www.ncbi.nlm.nih.gov/pubmed/20555149
http://www.ncbi.nlm.nih.gov/pubmed/19940398

As a side note i find it interesting that these diabetes patients would continue to get treatment over and over again while doing nothing to help themselves... yet CFS patients get nothing and are usually desperate and will do anything a doctor tells them.
 

Cort

Phoenix Rising Founder
So I found this on another thread and it looks like it's possible that a retrovirus could cause cardiac problems. Couldn't that also explain the blood flow issue?

Infection of Cardiomyocytes and Induction of Left Ventricle Dysfunction by Neurovirulent Polytropic Murine Retrovirus

http://jvi.highwire.org/cgi/content/abstract/81/22/12307

Of course, viruses could cause all of it. Goff suggested that there are many well known diseases viruses could be causing that are not linked to viruses now. That in itself demonstrates how difficult it can be to pin down a virus as a causal factor - he was talking about diseases that the federal goverment spends hundreds of millions of dollars a year researching....

.XMRV is a different story - its a new virus and we'll see how prevalent it is in different disease groups.