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

[Robyn]

Here's more on viruses affecting the heart from Dr. Lerner. This is a 3 part series on cardiac infections and CFS.

http://www.youtube.com/watch?v=JGd1frMB9X0&feature=related

http://www.youtube.com/watch?v=IRC86TXzDpk&feature=related

http://www.youtube.com/watch?v=Ri2696OrFNc&feature=related

 

[Cort]

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

That's not the issue in my opinion. Of course they could be - I was responding to the idea that our researchers and research groups are missing the big picture because they're not all concentrating on viruses.

These chronic diseases get hundreds of millions of dollars a year in funding - researchers are obviously are looking for the answers - whether they involve viruses or something else but the ultimate answers - even in well studied chronic disease - are obviously not easy to find. They are 'chronic' because they can't figure them out or figure out how to treat them so as to make them disappear. This is really difficult stuff - certainly not the kind of stuff you can figure out with the kind of funding that we get.

XMRV is so exciting because it potentially presents a much easier target; kill the virus, heal the body.....its so simple.

 

[judderwocky]

The fact that so many viruses and pathogens are involved is why a retrovirus would make so much sense though... Pointing to the other viruses only makes the case for retroviruses even stronger IMO.

CDC spokesperson ..... Dr. Phillip Lee in 1996 on whether he thought it was a retrovirus
skip to 11:00 min in ....


http://vimeo.com/13048135

 

[V99]

I'm not sure what your point is on the reference?

ME did not disappear from the literature, it just added CFS to the end. The Canadian criteria on ME/CFS is ME. They just added the CFS part because of the CDC, Wessely, etc. corruption of the disease. After all it is the disease we are all talking about, not the symptom chronic fatigue.

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.

 

[Cort]

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?

Maybe she didn't realize that you were only going to focus on that specific one and ignore the rest of them

 

[Dr. Yes]

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.

But you're confusing clinical diagnosis with basic research. There is no need to actually find a particular pathogen in ME/CFS patients in order to infer that they are causative or co-causative, to make them central to an explanatory hypothesis, and to focus research efforts from that perspective. The reason we must infer a major role for them is that the majority of us became ill in what is to all appearances an infectious episode, and/or present clinically with ongoing signs and symptoms of pathogenic processes or immune reactions indicative of a response to pathogens. That is the key component of the whole history of ME/CFS, starting with the epidemics and continuing with analyses of sporadic cases. The tragic side of that history has been the marginalization of the overwhelming evidence for pathogenic involvement, and of the subsequent dilution of case definitions and research efforts. We ourselves should not contribute to that marginalization.

And again, my argument is not that we should study HHV-6 all day. It is that we should concentrate on investigating processes that could be related to pathogen activity in general. There are many hypotheses that could explain most of the symptoms of ME/CFS, but those that do not involve pathogens cannot account for the known epidemiology of the disease nor for the other, abundant evidence of pathogenesis. That does not mean all research focuses on looking for pathogens; in fact, most of it may well end up on mitochondrial/ metabolic dysfunctions, as in Rich van K's hypothesis. But we do have to go with what we know, and approach such issues (and design research programs) from the perspective of AT LEAST initial pathogenesis or we risk never fully understanding the mechanisms we are studying. And if, as much evidence suggests, there is persisting, active pathogen involvement in ME/CFS, then it's essential to our search for treatments that we keep that a focus of ME/CFS research.

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 pathogens of interest don't even show up in spinal fluid studies very often.

The point is that you assume the presence of pathogens so that you look for evidence of pathogenesis, immune inflammatory processes, or related CNS damage in the first place. If you do not assume the presence of pathogens or pathogen damage, you won't look for any of that stuff and will keep grasping at disparate signs or symptoms, coming up with one partial hypothesis after another, and hope that you hit on the key one eventually (and that you will know it when you see it). That's akin to stumbling around in a dark room, hoping you bump into a lamp, when it would make more sense to use what you know about the usual layout of rooms to guide you in the search for that lamp.

What I am arguing for essentially is greater scientific parsimony in the overall approach to ME/CFS research. That means focusing on the simplest explanations based on all the evidence at hand. And that in turn means keeping pathogenesis in the primary explanatory model of ME/CFS.

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!

Yes, that is why I also argue for more research into brain imaging and neurology in general. That could give us at least the evidence of structural damage as they found in MS, or dysfunction as they've recently found in Gulf War Illness. It would be easier to get funding for such research, and to know where to look once funds are procured, if the research consensus was shifted back to ME/CFS being a physical disease involving pathogens. That original focus has been muddied and blurred because of a faulty assumption that the inability to identify clearly causative pathogens meant pathogens were less likely to be the cause. Absence of evidence is not evidence of absence, as they saying goes; as another one goes, if it walks like a duck and quacks like a duck, it's probably a duck. The proper scientific approach is to base hypotheses on available evidence, and for all the world, ME/CFS looks like a disease involving pathogens, with no other causative agents that can explain both the pathology and clinical/ epidemiological history. Despite so far being unable to figure out which pathogens are involved and how, that remains the correct perspective until an equally (or more) powerful hypothesis comes along.

The most convincing evidence of pathogen involvement is probably anecdotal and published reports of patient success when using them [antivirals (ed.)]

The most convincing evidence of pathogen involvement lies in the epidemiology and clinical presentation of ME/CFS.

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.

Researchers in general will only investigate what is pertinent to their area of interest. That in itself has led to the "piecemeal" approach. But coordinated research efforts, such as those by the CAA or WPI, should be guided by a hypothesis or set of hypotheses that allow for greater focus and, overall, more intelligently designed science than we would otherwise expect.

Must take a long break now- if anyone sees me posting on this thread again please shoot me.

 

[judderwocky]

But you're confusing clinical diagnosis with basic research. There is no need to actually find a particular pathogen in ME/CFS patients in order to infer that they are causative or co-causative, to make them central to an explanatory hypothesis, and to focus research efforts from that perspective. The reason we must infer a major role for them is that the majority of us became ill in what is to all appearances an infectious episode, and/or present clinically with ongoing signs and symptoms of pathogenic processes or immune reactions indicative of a response to pathogens. That is the key component of the whole history of ME/CFS, starting with the epidemics and continuing with analyses of sporadic cases. The tragic side of that history has been the marginalization of the overwhelming evidence for pathogenic involvement, and of the subsequent dilution of case definitions and research efforts. We ourselves should not contribute to that marginalization.

And again, my argument is not that we should study HHV-6 all day. It is that we should concentrate on investigating processes that could be related to pathogen activity in general. There are many hypotheses that could explain most of the symptoms of ME/CFS, but those that do not involve pathogens cannot account for the known epidemiology of the disease nor for the other, abundant evidence of pathogenesis. That does not mean all research focuses on looking for pathogens; in fact, most of it may well end up on mitochondrial/ metabolic dysfunctions, as in Rich van K's hypothesis. But we do have to go with what we know, and approach such issues (and design research programs) from the perspective of AT LEAST initial pathogenesis or we risk never fully understanding the mechanisms we are studying. And if, as much evidence suggests, there is persisting, active pathogen involvement in ME/CFS, then it's essential to our search for treatments that we keep that a focus of ME/CFS research.


The point is that you assume the presence of pathogens so that you look for evidence of pathogenesis, immune inflammatory processes, or related CNS damage in the first place. If you do not assume the presence of pathogens or pathogen damage, you won't look for any of that stuff and will keep grasping at disparate signs or symptoms, coming up with one partial hypothesis after another, and hope that you hit on the key one eventually (and that you will know it when you see it). That's akin to stumbling around in a dark room, hoping you bump into a lamp, when it would make more sense to use what you know about the usual layout of rooms to guide you in the search for that lamp.

What I am arguing for essentially is greater scientific parsimony in the overall approach to ME/CFS research. That means focusing on the simplest explanations based on all the evidence at hand. And that in turn means keeping pathogenesis in the primary explanatory model of ME/CFS.


Yes, that is why I also argue for more research into brain imaging and neurology in general. That could give us at least the evidence of structural damage as they found in MS, or dysfunction as they've recently found in Gulf War Illness. It would be easier to get funding for such research, and to know where to look once funds are procured, if the research consensus was shifted back to ME/CFS being a physical disease involving pathogens. That original focus has been muddied and blurred because of a faulty assumption that the inability to identify clearly causative pathogens meant pathogens were less likely to be the cause. Absence of evidence is not evidence of absence, as they saying goes; as another one goes, if it walks like a duck and quacks like a duck, it's probably a duck. The proper scientific approach is to base hypotheses on available evidence, and for all the world, ME/CFS looks like a disease involving pathogens, with no other causative agents that can explain both the pathology and clinical/ epidemiological history. Despite so far being unable to figure out which pathogens are involved and how, that remains the correct perspective until an equally (or more) powerful hypothesis comes along.


The most convincing evidence of pathogen involvement lies in the epidemiology and clinical presentation of ME/CFS.


Researchers in general will only investigate what is pertinent to their area of interest. That in itself has led to the "piecemeal" approach. But coordinated research efforts, such as those by the CAA or WPI, should be guided by a hypothesis or set of hypotheses that allow for greater focus and, overall, more intelligently designed science than we would otherwise expect.

Must take a long break now- if anyone sees me posting on this thread again please shoot me.

Just to throw this out.... MS is increasingly linked to HERVs and Retroviruses as well..... its not completely unknown what causes this in MS...

 

[Hope123]

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. .

This is OT but I wanted to correct this.

Scientists are looking into why certain people develop diabetes and other don't -- many reasons are brought forth, including genetics, obesity, etc. BUT eating more sugar in and of itself is not a cause. I have taken care of people with diabetes and diabetes runs in my family despite that the relatives affected have eaten healthy, exercised, and are actually on the thin side. Yes, if you have diabetes, eating an unhealthy diet, including a lot of sugar, will worsen it but there are plenty of people with a sweet tooth who do not get diabetes.

From American Diabetes Association: http://www.diabetes.org/diabetes-basics/diabetes-myths/

Myth: Eating too much sugar causes diabetes.

Fact: No, it does not. Type 1 diabetes is caused by genetics and unknown factors that trigger the onset of the disease; type 2 diabetes is caused by genetics and lifestyle factors. Being overweight does increase your risk for developing type 2 diabetes, and a diet high in calories, whether from sugar or from fat, can contribute to weight gain. If you have a history of diabetes in your family, eating a healthy meal plan and regular exercise are recommended to manage your weight.

 

[judderwocky]

This is OT but I wanted to correct this.

Scientists are looking into why certain people develop diabetes and other don't -- many reasons are brought forth, including genetics, obesity, etc. BUT eating more sugar in and of itself is not a cause. I have taken care of people with diabetes and diabetes runs in my family despite that the relatives affected have eaten healthy, exercised, and are actually on the thin side. Yes, if you have diabetes, eating an unhealthy diet, including a lot of sugar, will worsen it but there are plenty of people with a sweet tooth who do not get diabetes.

From American Diabetes Association: http://www.diabetes.org/diabetes-basics/diabetes-myths/

Myth: Eating too much sugar causes diabetes.

Fact: No, it does not. Type 1 diabetes is caused by genetics and unknown factors that trigger the onset of the disease; type 2 diabetes is caused by genetics and lifestyle factors. Being overweight does increase your risk for developing type 2 diabetes, and a diet high in calories, whether from sugar or from fat, can contribute to weight gain. If you have a history of diabetes in your family, eating a healthy meal plan and regular exercise are recommended to manage your weight.

Being overweight predisposes you to getting diabetes... THAT is a fact.

It is also a fact that if you do not control your diabetes and eat sweets it makes it worse.

Why do you have a problem with me saying this?

A lot of people get diabetes because they don't watch what they eat. They allow themselves to turn into balloons and then run around wanting our overworked medical professionals to catter to their poor eating habits.

I mentioned specifically some people get it for other reasons... Some however are irresponsible.

My ex-grandfather in law... knew he had diabetes... he could have managed it much better... instead he ate whatever he wanted, and had to have his toes amputated. That was his choice.

Please read my words more carefully.


"Obesity is a frequent cause of insulin resistance and poses a major risk for diabetes. Abnormal fat deposition within skeletal muscle has been identified as a mechanism of obesity-associated insulin resistance. We tested the hypothesis that dietary lipid deprivation may selectively deplete intramyocellular lipids, thereby reversing insulin resistance. Whole-body insulin sensitivity (by the insulin clamp technique), intramyocellular lipids (by quantitative histochemistry on quadriceps muscle biopsies), muscle insulin action (as the expression of Glut4 glucose transporters), and postprandial lipemia were measured in 20 morbidly obese patients (BMI = 49 8 [mean SD] kg m−2) and 7 nonobese control subjects. Patients were restudied 6 months later after biliopancreatic diversion (BPD; n = 8), an operation that induces predominant lipid malabsorption, or hypocaloric diet (n = 9). At 6 months, BPD had caused the loss of 33 10 kg through lipid malabsorption (documented by a flat postprandial triglyceride profile). Despite an attained BMI still in the obese range (39 8 kg m−2), insulin resistance (23 3 μmol/min per kg of fat-free mass; P < 0.001 vs. 53 13 of control subjects) was fully reversed (52 11 μmol/min per kg of fat-free mass; NS versus control subjects). In parallel with this change, intramyocellular—but not perivascular or interfibrillar—lipid accumulation decreased (1.63 1.06 to 0.22 0.44 score units; P < 0.01; NS vs. 0.07 0.19 of control subjects), Glut4 expression was restored, and circulating leptin concentrations were normalized. In the diet group, a weight loss of 14 12 kg was accompanied by very modest changes in insulin sensitivity and intramyocellular lipid contents. We conclude that lipid deprivation selectively depletes intramyocellular lipid stores and induces a normal metabolic state (in terms of insulin-mediated whole-body glucose disposal, intracellular insulin signaling, and circulating leptin levels) despite a persistent excess of total body fat mass. "

http://diabetes.diabetesjournals.org/content/51/1/144.abstract

The point i am making, is that when one of these individuals comes into the clinic, the doctor knows the issue is predominantly one of diet, exercise, and essentially discipline. If they fix that, the illness goes away.

I dont mean to belittle the experience of those like my friend .... it was obvious how frustrating the disease was, and how he had to take into account soo much... i wouldn't want to have to manage anything like that, and it was certainly not his fault or related to his diet in anyway.

I'm only bringing it up... because its not "mysterious" how some people get diabetes. When a really overweight person comes into an office with tons of insulin and blood sugar issues and their toes have poor circulation. They don't scratch their heads and say "gee... how could this happen, they were so healthy otherwise!"

similarly... when somebody comes in with skin cancer.... also common in florida... and they have clearly been frying themselves to a crisp outside for the last twenty years.... its probably a result of the sun exposure.....

I only brought this up, because I think diabetes is sometimes a poor comparison to CFS... yes, some questions still remain for some individuals... but for a lot of them the doctor knows what the problem is...

for those with "unexplained genetic or other issues".....

Once again.... Disseminated viruses are being found increasingly responsible.... a lot of damage can occur to the pancrease from low level viral infections....


A lot of "weird" human diseases seem to be coming down to various forms of inflammation caused by low grade viral infections... a lot of these are endogenous/retroviral.... some just infect cell clusters that are spared from the immune system...

there are genetic links, most likely because the people all share the same deffective surface protein / anti body/ receptor or whatever

 

[omerbasket]

Listen, people, there are many many responds here, but the fact remains the same. Dr. Vernon said that this is not a disease caused by a retrovirus, even though she has no proof for it, and even though many scientists that know the disease would have raised retroviruses, even before the "Science" paper, as a possible cause.
Not only that, she says that CFS is "not a retroviral infection", but that it is not a "recognised psychiatric disorder".
In the big words and in the little ones - her bias is clearly shown. And what's also shown is at least one little reason for her to dismiss XMRV as the cause of ME/CFS: Because a very short-time before the "Science" paper, she literally said that it is not.

 

[Angela Kennedy]

I think, judderwocky, the problem is in the claims made about obesity and diabetes or obesity and health per se are not based on great evidence, and are often based on a victim-blaming ideology that has some similarities to the way ME/CFS patients are treated. Even your own writing here is a bit 'these are the FACTS!' presumptive when there are various problems in the claims made, flaws in the methodology etc. etc.

I would really suggest you read two sources if you can. One is a the 'junkfood science' blog by Sandy Swarcz which shows some of the flawed 'science' going on in claims around 'obesity' and health and other health issues (though it's not perfect- it's far superior to Ben Goldacre's blog). The other is the book by Michael Gard and Jan Wright The Obesity Epidemic: Science, Morality and Ideology (2005) Routledge, London.

 

[ukxmrv]

I think Angela and many of the posters here make good points.

The chance is that Dr Vernon is wrong. A Retrovirus XMRV may be the cause of CFS and ME or it may be a contributing factor.

Saying that CFS is not a retroviral infection may be just plain wrong.

We can argue about the semantics of it but as a long term patient who lived through the Defreitas/ Holmes saga I was very disappointed when research stopped in that area. I wanted it to continue and if it had we may have had an answer earlier on.

If XMRV does turn out to be the cause of CFS and ME, then Dr Vernon was wrong. That's a big deal to me. I only have one life and I want people in positions of authority (and who get paid for it) to make the right decisions and the right comments.

Dr Vernon needs to explain why she didn't find the cause and why money was not put in that area - if XMRV is shown to be the cause.

If XMRV turns out to be wrong, then I would like to see research into other possible retroviral causes. I've always expected it to be something like this.

 

[Gemini]

The reason we must infer a major role for them [pathogens] is that the majority of us became ill in what is to all appearances an infectious episode, and/or present clinically with ongoing signs and symptoms of pathogenic processes or immune reactions indicative of a response to pathogens. That is the key component of the whole history of ME/CFS, starting with the epidemics and continuing with analyses of sporadic cases. The tragic side of that history has been the marginalization of the overwhelming evidence for pathogenic involvement, and of the subsequent dilution of case definitions and research efforts. We ourselves should not contribute to that marginalization.

Dr. Yes,

Excellent, brilliantly written summary of our history & where we should be focused! Thank you!

Take that break now but don't go far away!

Gemini

 

[Cort]

Listen, people, there are many many responds here, but the fact remains the same. Dr. Vernon said that this is not a disease caused by a retrovirus, even though she has no proof for it, and even though many scientists that know the disease would have raised retroviruses, even before the "Science" paper, as a possible cause.
Not only that, she says that CFS is "not a retroviral infection", but that it is not a "recognised psychiatric disorder".
In the big words and in the little ones - her bias is clearly shown. And what's also shown is at least one little reason for her to dismiss XMRV as the cause of ME/CFS: Because a very short-time before the "Science" paper, she literally said that it is not.

Listen Omerbasket - the fact is that you are mischaracterizing Dr. Vernon's statement - in effect you are putting words in her mouth. She was said that the research to date does not indicate this is a retroviral infection (that was well before XMRV) and she used 130 plus citations as 'proof
of that.

I think you're wrong about many researchers thinking CFS was caused by a retrovirus. Remember there were only two human infectious retroviruses found before XMRV and only one major one (HIV). Do you think the research world has not been scouring disease after disease for evidence of another retrovirus after what happened with HIV (and HTLV)? Well, they have been doing that for decades and until last year they didn't find a single one. So while you may think it was so obvious - I don't think it was obvious at all - that only the third human infectious retrovirus would pop up in CFS or any other disease.

 

[Cort]

But you're confusing clinical diagnosis with basic research. There is no need to actually find a particular pathogen in ME/CFS patients in order to infer that they are causative or co-causative, to make them central to an explanatory hypothesis, and to focus research efforts from that perspective. The reason we must infer a major role for them is that the majority of us became ill in what is to all appearances an infectious episode, and/or present clinically with ongoing signs and symptoms of pathogenic processes or immune reactions indicative of a response to pathogens. That is the key component of the whole history of ME/CFS, starting with the epidemics and continuing with analyses of sporadic cases. The tragic side of that history has been the marginalization of the overwhelming evidence for pathogenic involvement, and of the subsequent dilution of case definitions and research efforts. We ourselves should not contribute to that marginalization.

And again, my argument is not that we should study HHV-6 all day. It is that we should concentrate on investigating processes that could be related to pathogen activity in general. There are many hypotheses that could explain most of the symptoms of ME/CFS, but those that do not involve pathogens cannot account for the known epidemiology of the disease nor for the other, abundant evidence of pathogenesis. That does not mean all research focuses on looking for pathogens; in fact, most of it may well end up on mitochondrial/ metabolic dysfunctions, as in Rich van K's hypothesis. But we do have to go with what we know, and approach such issues (and design research programs) from the perspective of AT LEAST initial pathogenesis or we risk never fully understanding the mechanisms we are studying. And if, as much evidence suggests, there is persisting, active pathogen involvement in ME/CFS, then it's essential to our search for treatments that we keep that a focus of ME/CFS research.


The point is that you assume the presence of pathogens so that you look for evidence of pathogenesis, immune inflammatory processes, or related CNS damage in the first place. If you do not assume the presence of pathogens or pathogen damage, you won't look for any of that stuff and will keep grasping at disparate signs or symptoms, coming up with one partial hypothesis after another, and hope that you hit on the key one eventually (and that you will know it when you see it). That's akin to stumbling around in a dark room, hoping you bump into a lamp, when it would make more sense to use what you know about the usual layout of rooms to guide you in the search for that lamp.

What I am arguing for essentially is greater scientific parsimony in the overall approach to ME/CFS research. That means focusing on the simplest explanations based on all the evidence at hand. And that in turn means keeping pathogenesis in the primary explanatory model of ME/CFS.


Yes, that is why I also argue for more research into brain imaging and neurology in general. That could give us at least the evidence of structural damage as they found in MS, or dysfunction as they've recently found in Gulf War Illness. It would be easier to get funding for such research, and to know where to look once funds are procured, if the research consensus was shifted back to ME/CFS being a physical disease involving pathogens. That original focus has been muddied and blurred because of a faulty assumption that the inability to identify clearly causative pathogens meant pathogens were less likely to be the cause. Absence of evidence is not evidence of absence, as they saying goes; as another one goes, if it walks like a duck and quacks like a duck, it's probably a duck. The proper scientific approach is to base hypotheses on available evidence, and for all the world, ME/CFS looks like a disease involving pathogens, with no other causative agents that can explain both the pathology and clinical/ epidemiological history. Despite so far being unable to figure out which pathogens are involved and how, that remains the correct perspective until an equally (or more) powerful hypothesis comes along.


The most convincing evidence of pathogen involvement lies in the epidemiology and clinical presentation of ME/CFS.


Researchers in general will only investigate what is pertinent to their area of interest. That in itself has led to the "piecemeal" approach. But coordinated research efforts, such as those by the CAA or WPI, should be guided by a hypothesis or set of hypotheses that allow for greater focus and, overall, more intelligently designed science than we would otherwise expect.

Must take a long break now- if anyone sees me posting on this thread again please shoot me.

Sorry to keep this going but I think you've just stated what is already happening. Researchers do take note of the viral pathogenesis associated with CFS and they have for many years. Research into CFS was dominated for quite a while by the search for viruses and immune abnormalities. That never really panned out which is something to think about. Yes there are immune abnormalities in CFS but can the immune abnormalities found in CFS thus far explain the disability found in this disorder? I would say, with the exception of RNase L. - which the research world has ignored - not really. You don't have the massive immune dysfunction in CFS that you see in other infectious disorders. Immune studies, with the exception of RNase L. and natural killer cells, are also, to my recollection, pretty inconsistent. Yet the immune system is the 1st place you would go to unravel an infection.

History - You're asking for more parsimony but in doing so you're missing quite a bit of history. The research community did, in fact, demonstrate considerable parsimony at one time with a good portion of the research devoted to finding pathogens and demonstrating immune abnormalities consistent with a pathogen. We seem at times to think they're kind of slow and stupid - or imply that anyway - why don't they just focus on pathogen related issues? Its so obvious! But the research community recognized that infectious onset was typical of CFS and that was the first thing they plowed money into it. They found some interesting stuff but nothing they felt could explain ME/CFS and they started shifting some of their attention elsewhere.

Trends in CFS Research - Check out this paper I did looking at trends in CFS research over time about five years ago. From 1988 to almost 2000 immune research (except for psychology) dominated the research agenda of ME/CFS researchers. 2000 was when, I believe, the CAA held its state of Science conference to gather new leads because the field had become so stagnant. As of 2004 immune research was still an important avenue but the areas like the brain were now quite important. It would be interesting to update that paper.

http://www.aboutmecfs.org/Rsrch/TrendsCFSResearch.aspx

Now there's interest in the vascular system and the autonomic nervous system and, of course, the HPA axis - each of which could be affected by a retrovirus. Dr. Mikovits just wrote that the immune, neurological and autonomic nervous systems are all affected in both CFS and AIDS. That in itself demonstrates how difficult it is to devise a 'pathogen oriented research program that does not focus on the pathogen itself. With regards to a retrovirus, since the retrovirus could conceivably cause problems everywhere, you end up searching everywhere - which is what is happening in the field today.

By the way Annette Peterson recently stated that the big pathogen arrays the WPI has been using found evidence of each pathogen ( HHV-6 a, HHV-6 B, HHV-7, EBV, CMV) in no more than 10% of CFS patients. That means that you have a wide variety of pathogens, each of which occurs in a fairly small subset of CFS patients. The pathogen arrays did not pick up evidence of any other pathogens consistently. The only pathogen the WPI has consistently found in CFS is, ironically, XMRV.

We already know that gamma retroviruses often have neurological effects, that XMRV is turned on by the HPA axis and that it can insert itself into the walls of blood vessels - it could be that researchers have been studying the pathogenesis of XMRV for a long time in CFS without knowing it.

 

[omerbasket]

Listen Omerbasket - the fact is that you are mischaracterizing Dr. Vernon's statement - in effect you are putting words in her mouth. She was said that the research to date does not indicate this is a retroviral infection (that was well before XMRV)

No, Cort. You are putting here words in her mouth. She said didn't say that the research to date does not indicate this is a retroviral infection. She said that it indicates that it is not a retroviral infection. Actually, she even used stronger words than "indicates that".

Now, regarding "that was well before XMRV"... Well, that was in July 2009... The "Science" study was published just three months afterwards, and was in press three months before (in April 2009). I don't know if she knew about it - but I think it's a very reasonable option that she did know about it. Again, I don't know, but I don't dismiss that possibility. I even uploaded links on this thread that shows that Dr. Mikovits, in an interview in April 2009, implemented that they found the specific viruses that are related to ME/CFS.

I think you're wrong about many researchers thinking CFS was caused by a retrovirus. Remember there were only two human infectious retroviruses found before XMRV and only one major one (HIV). Do you think the research world has not been scouring disease after disease for evidence of another retrovirus after what happened with HIV (and HTLV)? Well, they have been doing that for decades and until last year they didn't find a single one. So while you may think it was so obvious - I don't think it was obvious at all - that only the third human infectious retrovirus would pop up in CFS or any other disease.

I don't know how many people looked for retroviruses in ME/CFS in those years. I know that William Bell believed that a retrovirus would explain it all. I know that he, Elaine Defreitas and others have found a retroviral link, which was quickly dismissed by Reeves and the CDC. I don't know what "130 plus citations" as proof of ME/CFS not being a retroviral infection you're talking about (and by the way, you can bring millions of citations and still prove nothing), but I guess much of this statement would be based on the CDC "not replicating" DeFreitas results (and not even trying to replicate her study...). Now, I'll post again the link to the video that judderwocky have posted on this thread earlier:
http://vimeo.com/13048135

Do you want to know on who's studies does Dr. Vernon, who worked at the CDC, is basing this unscientific opinion (that is described by her as a fact)? On the studies of the man who said this:

"Dr. William Reeves, the man incharged of investigating chronic fatigue for the CDC told us over the phone that:
1. There is no viral cause for this problem.
2. There are no immune system abnormalities in patients with chronic fatigue.
3. There are no clusters.
So when asked about the illness in Lake Tahoe, he said that was hysteria."

Anyway, Dr. Vernon can give any number of references that she'd like to. But I don't see a way of proving that retroviruses are not the cause for ME/CFS, and even if there was a way, her references doesn't prove anything. Upon that you can add the fact that she should know how much dirt and lies there are in the studies about ME/CFS, especially those done by the CDC.
When you take that, and take people that are real scientists, such as Dr. Bell and Dr. DeFreitas, who says that a retrovirus might be the cause of ME/CFS and that anyway it really fits, you have no reason whatsoever to say that it isn't the cause. I mean, she didn't even say that "MOST of the studies done until now didn't find a retroviral link" (while she forgot to mention DeFreitas study that did find it). She just said that the studies until now show that ME/CFS is not caused by a retrovirus. I mean, Dr. Philip Lee, which was than an assistant to the secretary of health, said that he thinks it is caused by a retrovirus or a virus.

Now, not only that Vernon has no evidence of ME/CFS not-being-caused by a retrovirus - and we did have, even in July 2009, evidence that it is caused by a retrovirus - by stating it is not caused by a retrovirus she also disregards that there are many many studies connecting XMRV to viruses. A retrovirus is a virus, and if it can be HHV-6, EBV, CMV, enteroviruses etc., why can't it be a retrovirus? What kind of scientist says something that he has no proof for? If we would look away for a moment from the fact the Dr. Vernon disregarded the clues that ME/CFS might well be "a retroviral infection", we should remember that a good scientist would never say "It is not that", when he have no proof for that. I mean, the scientific world the that ulcers cannot be caused by a bacteria, because of the high level of acids in the stomach. But then came Helicobacter Pilory and told us otherwise.
And what kind of scientist that works for a patient advocacy group - a group that must be the first one to tell everyone that ME/CFS sufferers suffer from a organic disease and definitley not a pshychiatric one - would say that ME/CFS is "not a retroviral infection" - altought it was never proven, and might very well be soon proven wrong - and would than say that it is just not a "recognised psychiatric disorder"?

 

[V99]

Listen Omerbasket - the fact is that you are mischaracterizing Dr. Vernon's statement - in effect you are putting words in her mouth. She was said that the research to date does not indicate this is a retroviral infection (that was well before XMRV) and she used 130 plus citations as 'proof
of that.

I think you're wrong about many researchers thinking CFS was caused by a retrovirus. Remember there were only two human infectious retroviruses found before XMRV and only one major one (HIV). Do you think the research world has not been scouring disease after disease for evidence of another retrovirus after what happened with HIV (and HTLV)? Well, they have been doing that for decades and until last year they didn't find a single one. So while you may think it was so obvious - I don't think it was obvious at all - that only the third human infectious retrovirus would pop up in CFS or any other disease.

If you pretend that XMRV never happened the research would still not tell you that a virus or retrovirus was not responsible for ME. Researchers may have been scouring for signs of another retrovirus, but they have hardly looked at ME patients, or other disease with an unknown cause. The signs and symptoms common to this disease do point towards a virus or retrovirus, no matter what fictitious entity the CDC created. We know so little of the world, but humans still find a way to convince themselves that certain avenues are closed, even when the evidence suggests this to be incorrect.

 

[Cloud]

"By the way Annette Peterson recently stated that the big pathogen arrays the WPI has been using found evidence of each pathogen ( HHV-6 a, HHV-6 B, HHV-7, EBV, CMV) in no more than 10% of CFS patients." That means that you have a wide variety of pathogens, each of which occurs in a fairly small subset of CFS patients. The pathogen arrays did not pick up evidence of any other pathogens consistently.

Cort, could you please provide a link to this statement. Thank you

 

[gracenote]

Here's an interesting quote. Obviously, something changed after this.

http://www.me-cvs.nl/index.php?pageid=3024&printlink=true&highlight=lyme

from The Elusive CFIDS Retroviruses by K. Kimberly Kenney

CFIDS Chronicle, Summer 1993

The Association's commitment to continuing its retroviral research program remains strong. Recent reports from independent investigators of retroviruses isolated from CFIDS patients lend new credibility to the study of the relationship between novel retroviruses and CFIDS. We are proud that the Association and its members have taken the lead in funding this research and remain hopeful that it will elucidate the nature of CFIDS.

 

[omerbasket]

"By the way Annette Peterson recently stated that the big pathogen arrays the WPI has been using found evidence of each pathogen ( HHV-6 a, HHV-6 B, HHV-7, EBV, CMV) in no more than 10% of CFS patients." That means that you have a wide variety of pathogens, each of which occurs in a fairly small subset of CFS patients. The pathogen arrays did not pick up evidence of any other pathogens consistently.

Cort, could you please provide a link to this statement. Thank you

Anyway, if you find, let's say 10% of patients to be positive for CMV, and 9% of patients to be positive for HHV-6, it can be that 5% of the 9% that are positive for HHV-6 are also positive for CMV. So you might well have, let's say, just 15%-20% of the 101 patients positive for other infections.
Anyway, as she said: They found that every which infection was present in no more than ~10% of the patients. Only XMRV was found to be present in 98% of the patients.