Chronic Fatigue Syndrome and Retroviruses: Jumping the Gun

When I first heard that a retrovirus had been identified as a possible cause of chronic fatigue syndrome, I withheld judgment and awaited further developments. When I heard that two subsequent studies had failed to replicate the findings of the first, I assumed that the first had been a false alarm and would be disregarded. Not so.

 It’s a classic case of wishful thinking outweighing good judgment. One unconfirmed report of an association between the XMRV virus and chronic fatigue syndrome (CFS) resulted in a rush to test for the virus, speculation about possible implications, and even suggestions for treatment. And the subsequent negative studies did little or nothing to reverse the trend. 

XMRV is Xenotropic murine leukemia virus-related virus. In the past, there were reports that this retrovirus was associated with prostate cancer, but then other reports found no link. In 2009 a study was published in Science, “Detection of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome” by Lombardi et al., reporting an association with CFS:

we identified DNA from a human gammaretrovirus, xenotropic murine leukemia virus–related virus (XMRV), in 68 of 101 patients (67%) as compared to 8 of 218 (3.7%) healthy controls.


Later, the researchers reported that up to 95% of CFS patients test positive with antibody testing. The study did not prove a causal relationship. The authors suggest that the retrovirus may reactivate other viruses, such as herpes viruses (the opposite is also possible). There could be many different viruses behind CFS/ME. And it could be that XMRV is an incidental finding secondary to the immune dysfunction  in CFS/ME. Two subsequent studies in the UK, here and here, also looked for the virus in CFS patients but both failed to find it.  

CFS is still a controversial diagnosis. Some observers have implicated psychological factors and somatization. Sufferers are on the defensive, wanting to validate CFS as a real physical entity. The finding of a virus was just what they were hoping for. They want to believe in it, and their emotions have clouded their judgment.

A battle has erupted between retrovirus believers and non-believers, each side attacking the other’s research and accusing them of bias. Some of the criticisms are based on virological laboratory procedural details that I am not competent to judge. Some of the other criticisms are about things I can understand.

The Science study came out of the The Whittemore-Peterson Institute. This institute was founded by a couple (the Whittemores) whose daughter had CFS and who was treated by Dr. Peterson with an experimental antiviral drug.   They are clearly biased towards finding a viral etiology. The researchers in the UK were similarly accused of bias towards finding a psychological etiology. Accusations of bias may be credible but don’t necessarily mean that the bias contaminated the results. Another criticism is less credible: the UK studies used a different set of criteria for diagnosing CFS.  Even if you think that some of the UK subjects didn’t qualify as having CFS, if even a few of them had CFS and the virus was really associated with it, the virus should have shown up in at least a few subjects. Critics have tried to rationalize away the negative findings in the UK by suggesting that the virus occurs regionally and is absent in the UK; but then if the virus were the cause of CFS, there wouldn’t be any CFS in the UK. 

So far we have one study for and two against the association of XMRV with CFS. More studies are underway that should settle the debate. If the virus is there, it will be found by other labs and a consensus will eventually develop as to whether there is an association. If an association is confirmed, there will still need to be further research to determine what the association means and whether there is a causal relationship. The logical response is to stay tuned, not to leap prematurely into testing and treatment.

Tests are already commercially available. One is offered by VIP Diagnostics, a company owned by the Whittemore family. It costs $450 and uses the same methods as were reported in the Science article. The website discloses that the tests have not been approved by FDA for diagnostic purposes and that medical expertise is required for test interpretation. The lab pays a royalty to the Whittemore-Peterson Institute for each test it performs.

In his Nov. 3, 2009 Lyndonville Times newsletter, Dr. David Bell offered this cogent advice:

I am reluctant to suggest to anyone that they spend big bucks for a commercial test now. We do not know if a particular test is accurate, and even if it is accurate we do not know what it means, and even if we did know what it meant we would not know what to do with it.

 That pretty much says it all. Nevertheless, patients are flocking to be tested. If they test positive, they can feel vindicated. If they test negative, they can rationalize that they may actually be positive but have a viral load too small to be picked up on the test at the moment; they might even rationalize that they are better off than if the test had shown a larger viral load. Win/win. 

 Antiretroviral treatments are already being proposed by some doctors. Most proposals are based on the drugs used for HIV/AIDS, on the assumption that antiretroviral AIDS drugs would be equally effective for the XMRV retrovirus. But that might well be a false assumption, and these are powerful drugs with worrisome side effects, not the sort of thing that you would want to try “just in case.”

Other concerns have been raised by the CFS community. Is XMRV sexually transmitted like HIV/AIDS? If you have chronic fatigue syndrome or another XMRV-related condition, should you take special precautions with your sexual partners, even if you’re in a committed relationship? Should you opt for not breastfeeding your children? Should you not even have children? 

I can understand the desperation of these patients. I can understand their need to believe anything that would validate their suffering. I can understand their motivation to try anything that might bring them relief. But I don’t want to see people wasting money on useless tests, I don’t want to see mothers unnecessarily worrying about whether it is safe to breastfeed their children, and I don’t want to see people suffering side effects from drugs they don’t need. A cautious wait-and-see approach is dictated by common sense and by an understanding of how often initial scientific research findings turn out not to be true. Like remarriage after divorce, the overblown enthusiasm for the XMRV/CFS connection is a triumph of hope over experience.

Posted in: Basic Science, Science and Medicine

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41 thoughts on “Chronic Fatigue Syndrome and Retroviruses: Jumping the Gun

  1. ZenMonkey says:

    “Even if you think that some of the UK subjects didn’t qualify as having CFS, if even a few of them had CFS and the virus was really associated with it, the virus should have shown up in at least a few subjects.”

    This has exactly been my suspicion, but as a layperson I’m not qualified to make this assertion. Thank you for addressing it.

    I’m a CFS patient who would love nothing more than to see XMRV turn out to be a smoking gun that can be cured with antiretrovirals. But not until the science is there. Even more than you, if I may say so, I empathize with my fellow patients…and I am really worried about the fallout from this near-hysteria over XMRV before there’s anything even resembling a scientific consensus on it. I’m also disappointed in the scientific “names” in CFS who are enabling the hysteria instead of reminding patients how science works.

    Thank you so much for writing this column.

  2. BillyJoe says:

    “XMRV is Xenotropic murine leukemia virus-related virus. ”

    All I can make out of XMRV is Xenotropic Murine Retro Virus.

  3. Draal says:

    “Critics have tried to rationalize away the negative findings in the UK by suggesting that the virus occurs regionally and is absent in the UK; but then if the virus were the cause of CFS, there wouldn’t be any CFS in the UK. ”

    You have assumed that there is only one cause of CFS. Is that true?

  4. passionlessDrone says:

    Hello friends –

    The bigger problem here is that the competing studies are using very, very different populations defined as having CFS. The two negative studies were both undertaken by psychologists who have a large vested interest in CFS being seen as a condition of behavior, as opposed to biology. Obviously, the WPI study has its own set of biases, with the testing now available.

    By way of Smurf @ In the Pipeline:

    Here is the WPI patient selection (in supplementary materials):

    “Patient samples. Banked samples were selected for this study from patients fulfilling the 1994 CDC Fukuda Criteria for Chronic Fatigue Syndrome (S1) and the 2003 Canadian Consensus Criteria for Chronic Fatigue Syndrome/myalgic encephalomyelitis (CFS/ME) and presenting with severe disability. Samples were selected from several regions of the United States where outbreaks of CFS had been documented (S2). These are patients that have been seen in private medical practices, and their diagnosis of CFS is based upon prolonged disabling fatigue and the presence of cognitive deficits and reproducible immunological abnormalities. These included but were not limited to perturbations of the 2-5A synthetase/RNase L antiviral pathway, low natural killer cell cytotoxicity (as measured by standard diagnostic assays), and elevated cytokines particularly interleukin-6 and interleukin-8. In addition to these immunological abnormalities, the patients characteristically demonstrated impaired exercise performance with extremely low VO2 max measured on stress testing. The patients had been seen over a prolonged period of time and multiple longitudinal observations of the clinical and laboratory abnormalities had been documented.”

    Here is the UK study patient selection:

    “All patients had undergone medical screening to exclude detectable organic illness, including a minimum of physical examination, urinalysis, full blood count, urea and electrolytes, thyroid function tests, liver function tests, 9 a.m. cortisol and ESR. Patients were interviewed using a semi-structured interview for CFS [9] to determine whether they met international consensus criteria for CFS. All subjects met the CDC criteria [10]; patients with the Fukuda-specified exclusionary psychiatric disorders, or somatisation disorder (as per DSM-IV), were not included.”

    Does anyone really think we should be comparing these populations?

    Take a look at some of the comments for the latest paper and you’ll see that there are a lot of people that have problems with the negative papers; mostly in terms of population selection.;jsessionid=99E0D771BD8214B92139D2D5F0466CD1

    I’ve also seen some folks complaining about the PCR in use @ WPI, but in a battle between virologists versus psychiatrists I’m choosing the former.

    – pD

  5. micheleinmichigan says:

    I’m in way over my head here, but I don’t understand why it appears that the Peterson found the XMRV at a low level even the healthy population control (around 6% I think) and the the UK studies appear to have found no verifiable XMRV. Shouldn’t it have just shown up at typical levels of the control groups? Am I just misreading? Are they using different testing for XMRV?

    I guess I was under the impression that when you tried to reproduce the result of a study you used the same criteria and tests, just with another population or sample size. Am I way of base?

  6. daedalus2u says:

    Abbie Smith over at Erv on science blogs has a number of posts on this subject, her specialty being retroviruses. She knows the techniques being used by the researchers and I find her analysis to be compelling.

    From my understanding of CFS, I think any association of viral detection is likely to be an artifact and not the cause. I see CFS as being due to insufficient mitochondria, leading to insufficient ATP generation capacity. There is enough ATP for basal metabolism, but not enough to increase metabolic activity above basal levels. When individuals with CFS try to increase their metabolic rate, they can’t and can cause injury if they try too hard. Too few mitochondria is the same mechanism for exercise intolerance in people who are out of shape. The number of mitochondria is regulated (as is everything important in physiology). When you exercise the number goes up, when you don’t exercise the number goes down. When you have CFS the number goes way down.

    It isn’t exercise per se that changes the number of mitochondria, it is the mitochondria number control system which has as one of its inputs how much exercise is being done, which it extrapolates into how many mitochondria it should make. Exactly how the mitochondria number control system works is not well understood. Obviously it is very complicated to regulate the mitochondria number in each cell, in each type of cell, in each tissue compartment under all circumstances.

    An important signaling compound in the mitochondria number control system is nitric oxide. NO triggers mitochondria biogenesis, so low NO will cause a lower mitochondria number.

    Finding bacteria and viruses in the blood of patients with CFS is pretty common. My interpretation is that these are an effect of the CFS, not the cause. CFS is characterized by insufficient ATP reserves. ATP is used by every cell to do virtually everything that the cells do. That includes immune cells. If there is insufficient ATP (as in CFS), then physiology is going to invoke steps to conserve ATP. These steps include being lethargic, they likely also include a turning down of the immune system. If the immune system is turned down to conserve ATP, then bacteria and viruses in the blood will have a longer lifetime and blood samples will show higher loads of bacteria and viruses.

    If the problem in CFS is due to insufficient mitochondria, then anti-retroviral drugs may make it worse and potentially a lot worse. The highly active anti-retroviral drugs used to treat HIV interfere with the synthesis of mitochondrial DNA. This impedes mitochondria biogenesis and is a major cause of intolerance to HAART and the liver failure sometimes associated with it. If CFS patients are already having problems making enough mitochondria, anything that makes that more difficult is going to make their CFS worse and not better. There are some antibiotics that work by interfering with protein synthesis by bacteria. Mitochondria use the same type of protein synthesis pathways as do bacteria, and mitochondria protein synthesis is inhibited by many of those same antibiotics too. Those antibiotics will likely make CFS worse also.

  7. rork says:

    Nice post by Hall. I hate uncertainty, especially about relatively simple matters, but that’s the only honest thing to say sometimes.

    One would wish that the two UK labs would have asked the US lab for a set of positive control sera, and sent them a plate of their samples as well. Is that old-fashioned?

    The other paper (Groom, Retrovirology 2010, link in Hall’s post), which found 0 of 299 samples positive using PCR, did not sound like a bunch of psychologists to me, though I did not check the authors out in detail.

  8. Harriet Hall says:

    Draal said

    “but then if the virus were the cause of CFS, there wouldn’t be any CFS in the UK. ”
    You have assumed that there is only one cause of CFS. Is that true?”

    I have no idea whether CFS has one cause or many. I’m not convinced that all those identified as having CFS have the same condition. I’m not even convinced that CFS is a meaningful diagnosis. I’m not assuming anything. Some other people are assuming that the virus is the cause of CFS, and I’m just pointing out that the facts don’t fit with that assumption.

  9. qetzal says:


    You may be right about the population differences. It sounds like WPI’s patients were a highly selected subset of CFS sufferers. Of course, if that’s the primary difference, it suggests that for most people diagnosed according to just the Fukuda or CDC criteria, XMRV probably is not related.

    As rork points out however, it’s wrong to say that the two negative studies were undertaken by psychologists. Both the PLoS ONE paper and the Retrovirology paper clearly state who conceived and designed and performed the experiments. They’re all virologists and the like.

    I know there’s been a huge outcry about psychiatrist Simon Wessely, co-author of the PLoS ONE paper, who apparently argues that most or all CFS is psychogenic. But calling this a battle between virologists and psychiatrists is both wrong and unfair.

  10. Fifi says:

    Dr Hall – “CFS is still a controversial diagnosis. Some observers have implicated psychological factors and somatization. Sufferers are on the defensive, wanting to validate CFS as a real physical entity. The finding of a virus was just what they were hoping for. They want to believe in it, and their emotions have clouded their judgment.”

    I think you get to the heart of it here – CFS is still a controversial diagnosis and treatments for it are still really about managing symptoms. And nobody likes the “it’s all in your head” diagnosis when they genuinely feel physically crappy (be it due to depression, chronic pain or CFS). Besides, anything “in our head” is biological, it’s just a chicken/egg question (and if it can be best treated via the mind and interaction or purely via biological actions, or a combination of both). It may well end up having both biological and psychological components (it’s not like the brain/mind aren’t part of biology after all).

    Obviously the virologists are going to be looking for a viral cause and the psychologists are going to be looking for psychological causes – all specialists do this so claiming one has a professional bias the other doesn’t is just silly. Having a prejudice against psychology or psychiatry is simply having a bias oneself. Besides, viruses can trigger or cause psychological conditions so there is possibly an interconnection on that level.

  11. biguglyjim says:

    Okay, I am not a doctor at all, and am probably about to look stupid. Consider this a noob asking because he doesn’t understand and seeks clarity. :)

    If we’re looking at two sets of people who have all been accurately diagnosed with CFS and we see that in one population there are no instances of XMRV and in the other there are some instances in the control and more instances in the test group, wouldn’t that more strongly suggest that the CFS makes infection to those exposed with XMRV more likely? Sort of a causal-the-other-way relationship?

    I’m basing this on the fact that controls showed the virus, which would suggest at least to me that XMRV was in the wild at the time. The fact that CFS sufferers were significantly more likely in this study to have XMRV draws a connection, but the fact that the other population had no XMRV suggests that it simply wasn’t in the wild.

  12. superdave says:

    Any pro XMRV comment that accuses the negative studies of being biased can have the exact same arguments thrown at the positive study. These kinds of accusations are silly and meaningless. At very least there is enough data to say to won’t have enough data, so lets wait for it.

  13. superdave says:

    typo…i meant don’t not won’t

  14. Harriet Hall says:

    biguglyjim asks “wouldn’t that more strongly suggest that the CFS makes infection to those exposed with XMRV more likely?”

    Yes, that’s another hypothesis. I mentioned it above; perhaps you missed it. I wrote “it could be that XMRV is an incidental finding secondary to the immune dysfunction in CFS/ME.”

  15. biguglyjim says:

    Whoops, you’re right. :) Noob is one thing, blind noob is another.

  16. ZenMonkey says:

    superdave, that is a great comment that exactly sums up the situation. I wasn’t at all surprised to see the very negative response to this column on the CFIDS Association’s wall (where I also reposted your comment), since that “advocacy” group is only encouraging patient interest in XMRV.

  17. geo says:

    While I thought this article was fair (although could give the misleading impression that those CFS patients paying for XMRV tests are anything more than a tiny minority), you only have to read Wallace Sampson’s writings on CFS on this site to see why some CFS patients no longer have much respect for some of those who claim to speak in the name of science.

    Sampson seems happy to treat all those suffering from unexplained fatigue as if they must be hysterical – and if they disagree with him they only have themselves to blame for their illness as they’re being so contrary. No wonder so many are eager to embrace anything that would help them escape from such science-based-quackery.

    I have no idea if CFS has one cause or many, is primarily psychological or physical; but I do know that CFS patients have been badly treat by the medical community and that the deep uncertainties that surround the illness have led to people following their own prejudices rather than restricting themselves to beliefs supported by the available evidence.

    Both patients and doctors have slipped into wish-thinking and quackery – but the greater power of the medical profession makes their distortions of thought the most worrying.

  18. Robin says:

    Harriet, I commend you. Thank you pointing out that that more research is needed. The science of how to detect XMRV is not resolved and thus it’s premature to speculate about its potential role in CFS. We do know that other studies have found XMRV in Europe and Japan, so the absence of XMRV in the UK points toward methodology issues. (The UK studies did not follow the American study’s protocol.) So, what is needed is consistent and reliable method of finding XMRV.

    Thankfully, the Health and Human Services department has a working group on XMRV specifically to resolve the issue of reliable testing and THEN to look into the possibility of its effect on human health.

    You need not tell me my judgment is clouded. I am a CFS patient and interested in scientific truth whatever it may be. You might be surprised that people I know with CFS — former lawyers, web developers, entertainers, engineers, scientists, doctors, etc. — feel the same and want good solid science.

    @geo — the available “evidence” about CFS is slim and beset with controversy, and funding for research is scarce. The NIH pays only $3million for research on a disease that keeps thousands out of work in the US, costs the government millions of dollars in lost income, property, and investment taxes, and the economy billions. There is a lot of preliminary data and small studies for CFS which deserve further funding; if more substantial research emerged the quackery would fade.

    I have often wished the cause of CFS was something as simple as somatization. There is nothing shameful about mental illness or somatic complaints and I would prefer to have something treatable — there is no prejudice here.

  19. Harriet Hall says:


    I think you have mischaracterized Dr. Sampson’s position. I urge you to go back and read again what he actually said:

    I was particularly intrigued by the first comment on that thread by Dr. Crislip who thinks he is seeing a subset of CFS patients who have a post-viral syndrome. We may be lumping post-viral patients in with others who have a somatization disorder or other conditions.

    The CSF diagnosis is controversial. Dr. Sampson describes the confusion created by the lack of an objective diagnostic test, the inconsistency of physical and laboratory findings, and the many other names given to this condition in the past. He does not say these patients are hysterical. The only time he used that word was when he mentioned that Freud was responsible for popularizing the diagnosis of hysteria in patients with symptoms similar to CFS. Nowhere does he suggest that patients are to be blamed for their illness. And it is unfair to call his reasoned opinion “science-based quackery.”

  20. micheleinmichigan says:

    Dr. Hall, When I read Dr. Sampson’s post originally, I found it to be quite dismissive, in fact it sounds like he is suggesting that he knows that it is a form of somatization where the patients can’t really be helped due to their defensiveness and lack of introspection and it’s just kinda odd that anti-depressants don’t work. And really just because you say something diplomatically in medicalize, does not mean that the message doesn’t come across. I found the article lacking in true curiosity to the causes or possible treatments CFS.

    I am in no way trying to condemn Dr. S. I haven’t read enough of his work to make any judgment. Even great batter’s strike out sometimes.

    I don’t have any stake on the CFS table. But I have to believe that the attitude that I read in that article does seem to drive frustrated patients into the arms of Woo.

    There are many doctor’s who just don’t feel comfortable telling their patient. “I don’t know, we don’t have enough evidence. These are the safe things we could try to see if they may help. What do you want to do?”

    I found Dr C. follow up comment more insightful.

  21. geo says:

    @ Harriet Hall:

    Have you read his other posts on CFS? (Although the post you linked to was certainly a good start).

    The only possible clarification I would make is that I chose the word ‘hysterical’ simply because I like the sound of it. I didn’t realise Sampson had used it at all – but I still think it was fair to use it in summarising his understanding of the condition.

    (I’ve just found another reference to hysteria and CFS from Dr Wallace: “Forms of somatization today, such as MCS, CFS, most fibromyalgia, are the partly socially determined symptom complexes of what 100 years ago took the form of conversion (hysterical paralysis, blindness, etc..”)

    If you’ve read his other writings on CFS and still think my description was unfair, I’d be happy to look for more quotes. If you read his other writings on CFS and then decide I was right, I do wish you’d take the time to condemn him as thoroughly as you would were he not your colleague.

  22. Fifi says:

    I also found Dr Crislip’s approach more insightful and curious. I certainly don’t discount somatization but, like placebos, it’s easy to be overly simplistic about somatization. It also can very easily have an unconscious “blame the patient” or “desperate for a diagnosis, any diagnosis” aspect when the more appropriate approach would be what michele suggests regarding saying “we/I don’t know”. Also, if it isn’t somatization then defensiveness and lack of introspection – ie. not accepting the diagnosis of somatization and not making the connection between one’s pain and emotional/psychological issues – is actually not an unhealthy response to being told your pain is a result of somatization. It’s only denial if what you’re denying is actually true.

    From what I understand, the best we can do for people suffering with CFS at the moment is provide pain management. If it’s done in a multidisciplinary setting this usually includes some form of cognitive therapy and mindfullness training and is done in such a way that it’s not denying the patient’s physical experience but may help them have insight into how their mind and body interact.

  23. Harriet Hall says:

    The evidence base for CFS is shaky. Over the course of history, people with similar symptoms have been given a wide variety of diagnoses. And there are many other controversial current diagnoses that overlap with CFS. CFS may well be a historically transient construct rather than a scientifically valid diagnosis. Dr. Sampson stuck his neck out and stated a strong opinion. Others are so politically correct that they would never dare challenge the current wisdom even if they think it is wrong. I will stick my neck out too and predict that the diagnosis of CFS will no longer be in the medical textbooks a century from now.

    There is an intermediate position. We can tell patients their symptoms fit the current diagnostic criteria for CFS, but we really don’t know what that means. While waiting for science to come up with better explanations and possibly cures, we can work with them to improve their quality of life. Psychological issues can make the symptoms of any illness worse and deserve to be addressed in all patients.

    I think Dr. Sampson would agree with that approach, but his post was not about what to do with the patient in the office. It was about how we define diseases and how those definitions change over time.

    We don’t understand what somatization is either. Who’s to say it doesn’t have a physical or chemical basis? A few decades ago we ascribed ulcers to stress and emotional factors and today we treat them with antibiotics. Medical practice responds to scientific evidence. The evidence for CFS just isn’t there yet.

  24. geo says:

    I think my understanding of Dr Sampson’s position fits far more closely with what he has written than your own. He seems rather less willing to embrace the uncertainty you suggest here:

    “To those who still must argue that CFS and related disorders are diseases and not somatiform illnesses, and to patients who deny their problems’ origins, allow me to drop the fomalities of physician behavior and to speak in language used here.
    You are wrong. Stop looking for information that fits your conceptions, and try to learn what is happening to you; how your life – the only one you may have – may slip away under a pall of unhappiness and contrariness, while disallowing entry to sources that may help you the most. There is hope if defenses relent, and none if they are maintained. ”

    Quacks are often willing to stick their necks out and make unsupported claims. I don’t see anything terribly noble about this, especially with a case like CFS where patients are already widely maligned and the claims made by Dr Sampson would serve to further reinforce the prejudices of others.

    The fact that doctors felt willing to tell those with stomach ulcers that they needed to deal with their emotional problems rather than expect medical help seems to fit in rather well with Dr Sampson’s approach towards CFS. The evidence wasn’t there for stomach ulcers. The evidence isn’t there to support the claims made by Dr Sampson.

  25. Robin says:

    @Geo. You are correct that the evidence doesn’t support Sampson’s theory. Cognitive behavior therapy, treatment aimed at reducing fatigue through psychology, often targeting patients’ “abnormal illness belief” is barely more effective than placebo and questionable in the long run.

    From cochrane review:

    “The [CBT] review included 15 studies, with a total of 1043 CFS participants. The review showed that people attending for CBT were more likely to have reduced fatigue symptoms at the end of treatment than people who received usual care or were on a waiting list for therapy, with 40% of people in the CBT group showing clinical improvement, in contrast with 26% in usual care. At follow-up, 1-7 months after treatment ended, people who had completed their course of CBT continued to have lower fatigue levels, but when including people who had dropped out of treatment, there was no difference between CBT and usual care.”

  26. Harriet Hall says:


    The fact that CBT didn’t work for CFS does not necessarily tell us anything about the cause of CFS.


    The evidence isn’t there for either CFS or somatization. Dr. Sampson is sticking his neck out to offer an opinion based on his past experience and general knowledge of medicine. If evidence is found that contradicts that opinion, I’m sure he will follow the evidence, just as well all did when we learned about Helicobacter and ulcers.

  27. Fifi says:

    Robin – The conclusion of the Cochrane Review was actually that more studies needed to be done…

    “Physical functioning, depression, anxiety and psychological distress symptoms were also more reduced when compared with other psychological therapies. However at follow-up, the results were inconsistent and the studies did not fit well together, making it difficult to draw any conclusions. Very few studies reported on the acceptability of CBT and no studies examined side effects. Only two studies compared the effectiveness of CBT against other treatments, both exercise therapy, and just one study compared a combination of CBT and other treatments with usual care. More studies should be carried out to establish whether CBT is more helpful than other treatments for CFS, and whether CBT in combination with other treatments is more helpful than single treatment approaches.”

  28. Fifi says:

    And even if CBT was shown to be effective for pain management for CFS, it wouldn’t prove that it was a somatic and not viral or due to another primary cause. What it would prove is that CBT is an effective pain management strategy for CFS.

  29. geo says:

    @ Harriet Hall:

    How very brave of Dr Sampson to ‘stick his neck out’ and assert that a group of patients are psychologically disordered, despite him not having the evidence to support his claim. He will not be oppressed by this ‘politically correct’ belief that it is wrong to dismiss a group of people as crazy without having compelling evidence – oh no. He has his own personal experiences and a general knowledge of medicine: whatever he believes is fit to be presented as Science Based Medicine.

    He’s certainly following a noble tradition of doctors who felt capable of doing the same. When the evidence became overwhelming they had to accept that black people were not more closely related to monkeys than whites, that the decisions of gays and lesbians should be treated with equal respect… that people with stomach ulcers did not just need to relax. They’d stuck their neck outs to promote their own beliefs as if they were science based, to explore their prejudiced paradigms – but it never seems to be the doctors who are left to hang.

    “based on his past experience and general knowledge of medicine”? Come off it. You must know that this is not good enough. You must know that this is a recipe for quackery.

    I remember reading an article here arguing against post-modernist critiques of science as a social enterprise – it’s the evidence that matters, not whether the claims are being made from within the ‘in group’. Shame about the follow through: if a Hindu monk had made the same claims as Dr Sampson, with the same evidence, they’d have been rightfully laughed off.

  30. Harriet Hall says:


    Please! Dr. Sampson has not “dismissed CFS patients as crazy.”

    When there is no evidence, opinions are really all we have.
    We have to form some kind of working hypothesis in order to treat patients. Sometimes we are wrong, and when the evidence is found to show we are wrong (as with ulcers), we change our minds.

  31. geo says:

    Harriet Hall:

    Maybe you do not think that so baldly asserting that those who fit the diagnosis of CFS should be treated as mentally disturbed is dismissive. Whether this word applies or not is not terribly important; that Dr Sampson’s position is unsupported by the evidence, likely further legitimise the prejudices felt against an already maligned group of patients, and supported by Science Based Medicine, is.

    If there is no evidence, prejudices are all we really have. This is when you should turn to homeopathy: if you feel the need to develop stories in your head about the nature of an illness and then treat patients accordingly, rely on sugar-pills. Dressing up your own instinctive beliefs as being Science Based Medicine, and promoting them as such, is a disservice to patients and to science. If you’re going to be a quack, at least try to be a harmless quack.

  32. Harriet Hall says:


    There is a difference between an instinctive, unreasoned prejudice and an opinion based on an understanding of history, of the vagaries of defining a diagnosis, and of the realities of psychological disorders like somatization.

    The second paragraph of your comment is offensive. “Developing stories in your head” is what we do when we form a tentative hypothesis and it is a prerequisite to treating any illness where our knowledge is insufficient. Dr. Sampson is not a quack. He expressed an opinion in an area where there is no acceptable scientific evidence. He did not promote his beliefs as being Science Based Medicine.

    Dr. Sampson is entitled to his opinions and was courageous to express them clearly in a forum where he was sure to be opposed. You are entitled to your opinion that CFS can not be explained by psychological factors, but you have no clear evidence to support your opinion either. Dr. Sampson explained why he formed his opinion; you did not. Time will tell whose opinion is right.

  33. geo says:


    I’m afraid you are getting confused. It is not my opinion that CFS cannot be explained by psychological factors – as you point out, the evidence is not there to support such a conclusion. I clearly stated that I did not know if CFS is primarily psychological or physical, so I’m afraid that I’m unable to reply to some of your post.

    There is a difference between unreasoned prejudice and opinions based upon personal experience and knowledge – but the distinction is not as clear as you may like to believe. Those involved in research that is now discarded as racist perversions of science often did not realise that their work was driven by bigotry at the time. I’m happy to admit that Dr Sampson is no more of a quack than they were, if those are the standards you think are acceptable.

    I do not believe that an honest reading of Dr Sampson’s writing allows you to claim he was putting forward a ‘tentative hypothesis’. He was rather more forthright than that. The quote above makes that perfectly clear, and there are many more if you want me to dig them up again. I’m sure you can find them yourself.

    Dr Sampson is entitled to his opinion. So is everyone else, racist, prophet and child. There is nothing necessarily courageous about expressing your opinions in a forum where you know you will be opposed. There’s nothing courageous about my explaining why I think Dr Sampson is a quack – but I want to know why his colleagues think otherwise (people seem so instinctively tribalist I never expected to able to convince you I was right, but I was hoping you might be able to show me I was wrong. The fact you were reduced to “based on his past experience and general knowledge of medicine” was not a good sign).

  34. ZenMonkey says:

    Yet another desperate attempt by Suzanne Vernon to justify the latest negative XMRV study:

    “There are going to be numerous technical, biologic and epidemiologic challenges associated with linking XMRV to CFS and other diseases including prostate cancer.”

    One challenge not remotely addressed is that there may be no link. But far be it from the CFIDS Association to provide anything like level-headed patient advocacy.

  35. manixter says:

    So sampson is a bad guy because he expressed an opinion? That Geo claims to not disagree with? But Harriet is being “tribalist” because she won’t condemn him?

    When there seems to be no evidence that there is a physical cause for CFS, and there seems to be no evidence that there is NOT a psychological cause for CFS, why does the slightest implication that CFS might be psychological seems to cause such a firestorm?

    Why can’t it be “all in your head”? That’s where your brain lives, dummy…

    (apologies to other commenters not engaging in a “you take that back” flamewar with the author)

  36. geo says:

    Have either of Dr Sampson’s defenders actually taken the time to read what he’s written?

    I already provided this quote:

    “To those who still must argue that CFS and related disorders are diseases and not somatiform illnesses, and to patients who deny their problems’ origins, allow me to drop the fomalities of physician behavior and to speak in language used here.
    You are wrong. Stop looking for information that fits your conceptions, and try to learn what is happening to you; how your life – the only one you may have – may slip away under a pall of unhappiness and contrariness, while disallowing entry to sources that may help you the most. There is hope if defenses relent, and none if they are maintained. ”

    You’d characterise that as ‘the slightest implication the CFS might be psychological’?

    Do you understand the difference between acknowledging that the uncertainty surrounding CFS is such that we cannot even say if it is a primarily psychological or physical illness, of one cause or many – and what Dr Sampson has written?

    There are many things which could possibly be true – but to assert them as if they were facts, based only on the evidence available to us, would be quackery, and should be condemned.

  37. sheryl lee says:

    Coupla things:

    I’ve had CFS for 23 years, mostly symptom-free, but reactivated when I trained for and ran a marathon, and then had a prolonged period of insane project stress at my job.

    My father and I experienced “viral onset” at the same time in 1987, when I was visiting him for a period of two weeks (and, no — we didn’t have sex).

    I find daedalus2u’s hypothesis about mitochondria and ATP quite plausible, based on my experiences with the symptoms (particularly shortness of breath, despite normal oxygen levels in my blood).

    Despite the fact that I consider the argument for somatic cause laughable, I nevertheless fit the childhood “CFS personality”. I suspect the cause is to be found there, many years before actual onset. Perhaps something to do with diet.

  38. Prometheus says:

    I find it interesting that there are so many people who think that saying CFS is a “somatiform disorder” is being dismissive of their symptoms. Aren’t we in the 21st century? Or is there still a lingering prejudice that so-called “mental illness” isn’t really as serious – isn’t as real – as a “purely physical” disorder?

    There is a great difference between saying that someone has somatiform disorder and saying they are “making it up”. Just as depression and anxiety are real (and can be as deadly as coronary aretery disease), so is somatiform disorder – the pain and disability are no less “real” because the site of the disorder is the brain rather than the heart or intestines.

    A large part of the problem with CFS is that it has no known pathology and no objective, self-consistent diagnostic criteria. In that respect, it shares a great deal with the so-call “mental illnesses”. Has the fact that depression is “all in the head” prevented research or useful treatments? Has it for schizophrenia or bipolar disorder?

    The finding of XMRV in CFS patients is intriguing, but those findings need to be independently verified before we can say that it is “the” (or “a”) cause of CFS. And there also needs to be a biologically plausible explanation for why there are thousands of people without CFS who also harbour XMRV. These are not insurmountable obstacles, but they haven’t been overcome, yet.

    Other studies looking for XMRV in patients with CFS have failed to find the virus: van Kuppeveld et al (2010) [32 CFS patients and 43 neighbourhood matched controls], Groom et al (2010) [170 CFS patients; 395 controls] and Erlwein et al (2010) [186 CFS patients].

    Although the authors of these three studies generously acknowledged the possibility that XMRV-related CFS was limited to the US, this seems a far stretch, given the length of time CFS has been around. The other possibility is that Lombardi et al (2009) made a mistake. Further research in the US will be needed to determine which scenario is correct.


  39. sheryl lee says:

    This is interesting:

    Given that CFS was once called Epstein Barr Syndrome, it makes me wonder if the CFS “personality” (childhood malaise, low energy, depression) is related to EBV infection, with onset of CFS later on.

  40. Prometheus says:

    The study cited by Sheryl Lee finds a correlation between Epstein Barr Virus (EBV) infection and multiple sclerosis (MS).

    EBV is also known as human herpes virus 4 (HHV-4). EBV infections can manifest as malaise, fatigue, swollen lymph nodes, and enlargement of the liver and spleen. This is a common infection – known as “infectious mononucleosis” when it affects adolescents and young adults – with about 95% of adults having antibodies to EBV.

    EBV is also implicated in Burkitt’s lymphoma and nasopharyngeal carcinoma. There are even some people who think it might be a factor in CFS, but that connection remains unsupported.

    One thing distinctive about EBV is that it “immortalizes” B-lymphocytes. It is also very easy to detect in the blood. If CFS was the result of chronic EBV infection, that would be relatively straightforward to determine.


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