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

[thegodofpleasure]

That means that somewhere around a quarter of the studies funded by the CFIDS Association over the past five or six years have focused on pathogens. That hardly seems like a bias against viruses or pathogens.

It's certainly not a bias in favour of research into viruses or pathogens either - which, in the circumstances, we might justifiably have expected.

 

[Sam Carter]

It's certainly not a bias in favour of research into viruses or pathogens either - which, in the circumstances, we might justifiably have expected.

The circumstances being 20+ years of looking for, and not finding, a consistent and reproducible viral / retroviral / bacterial cause. Why would you expect research budgets to be channeled exclusively into unproductive areas of study?

 

[garcia]

The circumstances being 20+ years of looking for, and not finding, a consistent and reproducible viral / retroviral / bacterial cause. Why would you expect research budgets to be channeled exclusively into unproductive areas of study?

Err because pathogens cause disease?

 

[Sam Carter]

Err because pathogens cause disease?

Pathogens cause disease but ... err ... not all diseases are caused by pathogens.

 

[Cort]

Err because pathogens cause disease?

Because if you look at the research into retroviruses, EBV, HHV6 etc. you'll see alot of negative studies. That's started to change as researchers have refined their techniques and the science has improved. Pathogens got quite a bit of research ( at least for us ) at one time and it just bottomed out. In fact the CFIDS Association stopped finding any grants at one point (apparently because they weren't getting many at that point) and used their grant money to put on a State of CFS Conference in order to drum up some more leads. Lately pathogens have re-emerged as better candidates.

Its still very possible that pathogens cause some damage that causes CFS and then they fade away in some patients. That's what the Dubbo Studies suggest. On the other hand there's a good bit of anecdotal evidence from patients getting treated with antivirals - that difficult to detect pathogens are in play. Nobody,though, not the WPI or the HHV6 Foundation thinks there are good diagnostic tests for HHV6 or other infections in the central nervous system. This is a big problem. It and may very well take advances in technology before those infections become easily diagnosable.

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.

 

[V99]

A retrovirus is still a really good explanation for ME. Therefore, when a new one is identified it is worth having a look.

 

[acer2000]

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.

I think all of this research is very important. At bare minimum it lends credibility to the idea that CFS is a biological problem (which anyone who has it can tell you). However, people don't just one day have normal lives and then the next day have all the abnormalities that these studies show and the severe symptoms of CFS. Not without an intervening environmental cause, either a pathogen or a toxin.

So as long as these basic science studies are used with the ultimate goal of finding what the upstream cause is, they are great. If they are taken at face value and the disease is defined as a "collection of abnormalities" and nobody goes any further, these studies aren't serving their purpose and the value of the data is significantly reduced.

CFS, like many diseases in the past, looks way more complicated now than it will when the cause is found. And the cause will likely turn out to be simple and singular. Thats how the world works, its just not that complicated.

Thats my 2 cents anyways.

acer2000

 

[Sam Carter]

A retrovirus is still a really good explanation for ME. Therefore, when a new one is identified it is worth having a look.

I trust you will be championing research into HTLV-III & HTLV-IV then?

 

[V99]

I trust you will be championing research into HTLV-III & HTLV-IV then

Yes, of course

 

[Dr. Yes]

From v99:

Defreitas's research and XMRV are irrelevant to this point. No research could ever show that a retrovirus is not responsible for ME. The idea that science knows everything there is to know about retroviruses or anything is totally absurd.

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.

CBS, I think you have misinterpreted what v99 was saying. Garcia made the same point another way:

At the very least it is unscientific to say disease X *isn't* caused by a retrovirus unless you have categoric proof. If Suzanne Vernon does have such proof then I for one would like to see it.

Dr. Vernon's original statement was at least clumsy and inaccurate, and the implication, at least as written, is clearly that the inability of the CDC or others to find Dr. DeFreitas' retrovirus is positive evidence that retroviral infection is not involved in CFS. That implication is of course scientifically incorrect. Perhaps it was just a misstatement on her part, in which case she should correct it.

 

[Dr. Yes]

There are a number of problems with Dr. Vernon's proposal "Consolidate & Connect CFS Research", but I will focus here on the citation she uses for the following statement:

"After almost 20 years of accelerated research efforts examining the pathophysiological basis of CFS, no clear understanding of risk factors or the mechanisms underlying the key symptoms has emerged. These two decades have been marked by significant achievements in epidemiology (4-9) and by some advances in management (reviewed in 10-12). By contrast, the outcomes of pathophysiological research have generally featured delineation of what CFS is not - a muscle disorder, a retroviral infection, a recognised psychiatric disorder, a known autoimmune disorder, etc. Sadly, the endeavours seeking to define what CFS is, have been characterised by false leads and dead ends. That is, innumerable small, cross-sectional case-control studies have failed to support plausible hypotheses of an infective, immunological, neurological, endocrine or metabolic disorder (reviewed in 10, 11)."

Reference 11 is a 2003 review article by Afari and Buchwald in the American Journal of Psychiatry (http://ajp.psychiatryonline.org/cgi/content/abstract/160/2/221)
It is not the sort of article that I think the Science Director of our main patient advocacy organization should be citing at all, let alone as a good review of biological findings in CFS and of helpful 'management' strategies. Consider the following excerpts:

Generalized anxiety disorder and somatoform
disorder also occur at a higher rate in chronic
fatigue syndrome subjects than in the general population
(128, 133–135). In most (130–132), but not all cases (3,
136), the mood or anxiety disorder precedes the onset of
chronic fatigue syndrome.

Their references 131 and 132 are a couple heinous articles authored by Wessely and Peter Manu, respectively (Peter Manu was sort of the American precursor to Wessely and company).

By the way, Afari and Buchwald do provide a gem of a statement (in a good counter-argument, actually):

Although the distinctions
between physical and psychiatric illnesses often
are not useful or accurate, their differentiation is in part
the basis for a diagnosis of somatization.

That one statement sums up so much that is wrong with 'psychosomatic medicine' in general (including the astonishing lack of any science whatsoever in it) and with its application to CFS in particular!

However, they go on to present an argument that encapsulates much of the damaging beliefs that have led to the divide between the majority of ME/CFS patients and some at the CAA, CDC, CBT/GET advocates:

Attributions about the causes of an illness or its symptoms
are important in determining a patient’s response to
the illness (155). Patients with chronic fatigue syndrome
often attribute their illness to physical causes and minimize
psychological or personal contributions (148, 156,
157). For example, compared to patients with diabetes,
rheumatoid arthritis, and chronic pain, those with chronic
fatigue syndrome attributed their symptoms more often to
“a virus” or “pollution” and less often acknowledged a role
for their own behavior (56). Such causal attributions have
been related to an increase in symptoms (158) and functional
impairment (159, 160) and to worse subjective and
objective outcomes over time (161). It is noteworthy that
relatives also tend to attribute the patients’ symptoms to
somatic causes (157), and their beliefs and attributions
about chronic fatigue syndrome, as well as solicitous behavior,
may inadvertently reinforce patients’ illness behavior
(162). Although it has been suggested that somatic attributions
may be a risk factor for the development of chronic
fatigue syndrome (157), at the very least, they probably exacerbate
the illness and lead to greater disability.

They add:

Individuals with chronic fatigue syndrome employ a
variety of strategies to cope with the debilitating consequences
of fatigue. Overall, several studies suggest that
patients with chronic fatigue syndrome use significantly
more escape/avoidance strategies, compared with healthy
subjects (172), age- and gender-matched primary care
patients without chronic fatigue (173), or their nonfatigued
twins (174). Avoidance strategies, in turn, have
been associated with greater fatigue, impairment, and
other psychosocial disturbances in chronic fatigue syndrome
(175, 176). Thus, while not a cause of chronic fatigue
syndrome, maladaptive coping strategies can perpetuate
the illness.

I am both perplexed and deeply concerned that Vernon considered this paper an authoritative source for information on the lack of physical findings in CFS and, even more so, on the successful psychosocial approach to management of the disease! Are these views representative of Dr. Vernon's own on CFS, or on the CAA's as a whole??

 

[Dr. Yes]

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.

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!

 

[Robyn]

Oh but I like the (It's all in your head) diagnosis. It's kind of grown on me. NOT! I wonder if the MS patients liked being diagnosed with hysterical paralysis for over 50 years until they figured out it had a biological cause. If you aren't looking for a cause you won't find it. And this is not directed at the CAA. It's directed at the medical field in general because I feel they all share some responsibility for keeping us sick this long. They are the ones that need to wake up. The antidepressant haven't worked. In fact nothing has worked. You can't have this many people with these same set of symptoms and noone ever get's well. Doesn't take a rocket scientist to figure out there's a problem.

 

[V99]

Although the distinctions
between physical and psychiatric illnesses often
are not useful or accurate, their differentiation is in part
the basis for a diagnosis of somatization.

Sorry, I will not be very eloquent here, but that has to be one of the stupidest things I have ever read.

 

[V99]

It's directed at the medical field in general because I feel they all share some responsibility for keeping us sick this long.

I agree. It's been said before, but what ever happen to the science in ME.

 

[Robyn]

I agree. It's been said before, but what ever happen to the science in ME.

It's being held hostage by the pysch community.

 

[justinreilly]

Defreitas's research and XMRV are irrelevant to this point. No research could ever show that a retrovirus is not responsible for ME. The idea that science knows everything there is to know about retroviruses or anything is totally absurd. It is the fact, that the CAA gave up looking which is important. I would say the same about any organisation that would take such a naive approach to the biology of ME. They should have been looking. Will they be looking in the future if XMRV goes no where?

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.

CBS- I don't see what you're saying. What V99 said is that Vernon said that ME is not caused by a retrovirus and that Vernon's statement is unsupported. CAA and other orgs should have been on top of XMRV. I totally agree with her.

Cort- You stated that noone else (but WPI) was looking at XMRV so why single out CAA? I agree with V99 that every org should have funded this work. In this country the only orgs that fund any science on ME are WPI, CAA, NIH and CDC (and to a much lesser extent NCA) and we know we NIH and CDC have to be bludgened into funding any valid research, much less retroviral research.

Also, you are claiming again that CAA is funding XMRV research, but when questioned about this on the last thread, you said that you thought they weren't funding it (just providing samples) and good for them for getting someone else to fund it instead of them.

 

[justinreilly]

A retrovirus is still a really good explanation for ME. Therefore, when a new one is identified it is worth having a look.

I trust you will be championing research into HTLV-III & HTLV-IV then?

Yes, of course

I totally agree- all the new human retroviruses need to be researched re ME: HTLV III, HTLV IV, but especially XMRV, the 'related' MuLV's that Dr. Alter reported he found in humans in the NIH/FDA study, and DeFreitas retrovirus. It's crazy this is not being done.

 

[justinreilly]

I am both perplexed and deeply concerned that Vernon considered this paper an authoritative source for information on the lack of physical findings in CFS and, even more so, on the successful psychosocial approach to management of the disease! Are these views representative of Dr. Vernon's own on CFS, or on the CAA's as a whole??

Yes! This is outrageous.

 

[justinreilly]

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!

Beautifully put, Dr. Yes! I fully agree. I think CAA's current research program is good. That said, I think it would be a better use of resources to look more into etiology esp retroviruses. As long as we keep doing research along the lines of what CAA has been doing, we will always just be drowned out by the propaganda of the psychs, CDC and NIH, we will have no traction as always and things will change much too slowly.