Chronic Fatigue Syndrome: Lots of Speculation

Humans love to find patterns in the world. Sometimes patterns exist, sometimes they are imaginary. Sometimes you can see a pattern that may be interesting and ignore its significance. As a resident I used to say that anyone who smokes three packs of cigarettes a day has to be schizophrenic, it was meant more as a joke, when, in fact, it was later discovered that tobacco helps ameliorate the symptoms of schizophrenia. I need to pay more attention.

Part of my job is to look for patterns as a key to the patients diagnosis. Diseases and pathogens tend to (more or less) cause reproducible signs and symptoms and looking for that pattern is often the most helpful clue towards finding the diagnosis. Of course things are never as easy as one would like, as you have to consider whether you are seeing common manifestations of a common disease, uncommon manifestations of a common disease, common manifestations of a uncommon disease and, the hardest, uncommon manifestations of an uncommon disease. When I have a complex or uncertain cause, I explicitly run through that, and other, litanies so I do not miss a unusual diagnosis.

Chronic Fatigue Syndrome (CFS) has, at least to my way of thinking, two patterns. I see the occasional CFS patient in clinic and, I hope, pay attention to their disease patterns. I keep in mind I may be seeing a pattern that does not exist, but looking for disease patterns is what doctors are trained to do.

The first pattern is the patient who has been fatigued all their lives. Not much to say or do for these patients; more often than not the probable cause is psychiatric.

The second type of patient has a different, more intriguing, pattern. They are usually highly functioning people who had the abrupt onset of a ‘flu’ that never left. The have marked post-exercise fatigue and difficulty concentrating for even minor tasks. It is a striking pattern, and reasonably consistent from patient to patient. They sound, for all the world, like someone who continues to suffer from an ongoing infectious disease, yet when all the markers of infection and inflammation are evaluated, they come up normal.

The CDC criteria for CFS do not do justice in differentiating what I see as two distinct clinical presentations and perhaps is a confounding variable in evaluating CFS studies.

So do these individuals with the abrupt onset have an infection or a post-infectious disease?

People have a limited repertoire with which to respond to illness. I have thought that CFS, at least for those with the sudden onset mentioned above, have had one of any number of infections: Q fever, EBV or Ross Valley Fever, or other infections. CFS is, perhaps, the final common pathway for a variety of post-infectious diseases.

The metaphor I use is a rock in a pond. The infection, whatever it was, is the rock. The CFS state is the ripples, lasting long after the rock as disappeared. It would not be the first time an infection left behind long term clinical sequelae. As one example, Irritable Bowel Syndrome is a common, and sometimes permanent, complication after a variety of bacillary diarrhea’s, especially travelers diarrhea. Infections can interact with the host and result in permanent physiologic changes long after the pathogens have moved on.

I find it particularly intriguing that CFS patients have different sets of genes activated when compared to normal controls, although it is papers such as this that let me know how little I understand on some topics. Given the growing literature on the various genetic variations that increase or decrease our risk for infections, it will not come as a surprise if some day they discover genetic polymorphisms are responsible for CFS.

Until recently my understanding of CFS was that it is probably a post infectious syndrome, perhaps in the genetically predisposed, in at least a subset of the CFS population. While the studies show various physiologic abnormalities in CFS are not always replicated, I wonder if the results are due to the inadequacy of the CDC definition in stratifying patients.

Enter XMRV (xenotropic murine leukemia virus-related virus), a retrovirus that was first reported about a year ago and is more frequently found in CFS patients and discussed on this blog .

It has been an interesting year for XMRV.

The first report found DNA from XMRV in peripheral blood mononuclear cells (PBMCs) from 68 of 101 patients (67%) by nested PCR, as compared with 8 of 218 (3.7%) healthy controls. Interesting. Maybe an infectious etiology of CFS, which would confirm my bias, and we all like our biases confirmed. From my perspective, all diseases are infectious in origin, or at least the diseases that matter.

Then there were four subsequent studies that failed to confirm the finding of XMRV in CFS. Another dead end? Maybe, maybe not.

This month another study found XMRV DNA was more common in CFS patients than controls.

We examined 41 PBMC-derived DNA samples from 37 patients meeting accepted diagnostic criteria for CFS and found MLV-like virus gag gene sequences in 32 of 37 (86.5%) compared with only 3 of 44 (6.8%) healthy volunteer blood donors. No evidence of mouse DNA contamination was detected in the PCR assay system or the clinical samples.

Why the difference?

Previous reports of XMRV isolates from patients with CFS and with prostate cancer and from individuals in different geographic locations have described very similar nucleic acid sequences, a feature believed to be a unique characteristic of XMRVs. However, our analysis revealed three different types of MLV-related virus gag gene sequences in CFS patients. In all three groups, the sequences were more closely related to the sequences of polytropic mERVs than to XMRVs and were more distant from the sequences of ecotropic MLVs.

As I understand it, using PCR, with the wrong primers may not pick up XMRV due to variability in the virus.

Indeed, it is possible that the PCR primers used in various studies may have different sensitivity in detecting the diverse group of MLV-related virus gag gene sequences that we found in the clinical samples. The 5′ gag leader sequence of previously described XMRVs represents the most divergent segment of the XMRV genome in comparison with the genomes of the other MLVs. In particular, there is evidently a unique 15-nt deletion in the 5′ gag leader region in all of the XMRVs previously identified in patients with prostate cancer and CFS. To detect XMRVs in human samples with better sensitivity and specificity, some studies used a PCR primer spanning this unique deletion as the “XMRV-specific” primer. However, none of the viral gag gene sequences amplified from the blood samples of CFS patients and blood donors in our study has this particular deletion . As a consequence, such primers might have been insensitive in detecting the MLV-related gag gene sequences that we have identified.

As a lowly clinician I feel yet again like Mr. Gumby when presented with modern molecular biochemistry. As an old fashioned codger, I will be happier when they discover a way to grow the virus on agar.

Yet, as I am well aware, finding evidence of viral parts is humans does not mean clinical infection or causality. The classic criteria for proving the infectious etiology, Koch’s postulates, have been recognized as problematic for decades.

JC virus, Herpes simplex, and GB virus often persist or replicate asymptomatically in humans and cause no clinical disease. Association is not causation, I tell myself every day. It may turn out that XMRV causes CFS, or that XMRV is a marker of CFS and the physiologic state of CFS is permissive for XMRV replication, or XMRV may have nothing to do with CFS at all.

Still, it is an interesting finding that will hopefully shed some light on CFS. Or not.

It is an odd thing. I always say that the three most dangerous words in medicine are ‘In my experience’ , however those words mostly applied to therapy. Diagnosis in medicine is a lot less straightforward, trying to synthesize the vagaries of the history, physical, and labs into a coherent whole. Good diagnosticians are always experienced; in part because they know more, and in part because they have seen and done more. A good diagnostician is also aware of the many ways they can be fooled, and I have found the best doctors are those that are able to rapidly change their mind as new data presents itself. We all go down dead ends; the best doctors are those who do not have to collide with the brick wall at the end to know it is time to change direction.

My experience and pattern recognition suggest that some CFS patients either have or have had an infection as the cause of the disease, but I could very well be fooled.

What causes CFS? I don’t know. There are interesting hints in the presentation of some patients and perhaps XMRV will be the pathogen, or a pathogen, in CFS. The nice thing is that while it is fun to speculate, eventually the science will sort it out. Some day, if I live long enough, I may know.

Posted in: Basic Science, Science and Medicine

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27 thoughts on “Chronic Fatigue Syndrome: Lots of Speculation

  1. ZenMonkey says:

    Thanks for covering this, although as someone with the post-viral type of CFS I’m not sure the speculation is as fun for me as it may be for you. I would like to request that the word “syndrome” be added in the title of this piece. Chronic fatigue is a symptom, and not a nickname for the syndrome. Thank you.

  2. passionlessDrone says:

    Hi Mark Crislip –

    They sound, for all the world, like someone who continues to suffer from an ongoing infectious disease, yet when all the markers of infection and inflammation are evaluated, they come up normal.

    From my readings on the initial WPI paper that declared they had identified retroviral samples, they seemed to indicate that abnormal immune markers were found, though these are likely a bit different than what you are referring to.

    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

    I believe that the argument goes that at least one of the negative studies (maybe others), did not include patients with similar immunological differences. If true, this likely speaks towards two distinct syndromes, and thus, different findings, but the news cycle doesn’t seem to catch up on this.

    I have no idea if the recent PNAS paper that seems to replicate WPI used similar profiling. (Does anyone?). I’ve also read that the most recent paper found different retrovirus types. EVR @ scienceblogs had a nice piece detailing the problems with this.

    – pD

  3. TsuDhoNimh says:

    Forget the XMRV. What about the arboviruses? they are already recognized for having convalescence periods longer than most viruses.

    Scenario: Active person gets bunyavirus from bite of passing mosquito and had mild cold-like symptoms … and decides to ignore the fatigue and press on with daily activity … never really takes the time to let the body recover and drives themselves into a state of “chronic convalescence”.

  4. Ian says:

    See, this is why we need editors and journalists to write headlines. The proper headline for this story isn’t “Lot’s of Speculation”, but instead it should be “Scientists discover virus causing CFS” or better “Newly discovered virus: Are Your Children Safe?”

    Or I guess if the latest study was one of the four that were unable to replicate finding XMRV, the headline should be “Scientists dismiss virus as causing CFS”.

  5. qetzal says:

    Actually, this latest study did NOT find XMRV! What it found was “murine leukemia virus-like sequences.” In fact, phylogenetic analysis showed that these sequences do not cluster with XMRV. To quote the authors:

    [O]ur analysis revealed three different types of MLV-related virus gag gene sequences in CFS patients. In all three groups, the sequences were more closely related to the sequences of polytropic mERVs [mouse endogenous retroviruses] than to XMRVs….

    Some people (including from Alter, apparently), claim that this study vindicates the original WPI study claiming an association between XMRV and CFS, but I don’t necessarily agree. WPI found nearly the identical XMRV sequence in every positive CFS patient. Alter’s group finds at least three different sequences that are distinct from one another, and quite distinct from XMRV.

    I agree that Alter’s paper supports the idea that there may be something weird going on with CFS and retroviral sequences, but it’s still very unclear what that may be. And WPI remains the only group that’s published data claiming to find XMRV in CFS patients.

  6. Robin says:

    Thanks for showing your clinician’s viewpoint in observing patients with this illness. It’s interesting that you pick up on the discrepancy in the CDC’s case definition and the presentation of CFS. Defining patients has stymied people for years; exactly how to find a clean cohort has been controversial. The CDC’s definition has been criticized for being too broad, and, interestingly their “negative” study published in Retrovirology only included three people with the sudden onset that you describe.

    A new study from the UK just came out citing evidence of ongoing infection. They looked at the age of white blood cells rather than the traditional count and found that they were turning over quickly. Along with the presence of elevated free levels, the researchers concluded that patients suffer from chronic inflammation. (BBC article here. If true, this research suggests that maybe older methods of looking for infection are not adequate for all instances.

    A recent conference at NIH in Bethesda brought together scientists and clinicians interested in the XMRV/MLV question, and there was a great deal of interest despite the conflicting research. I suspect we’ll know the answer well within your lifetime!

  7. Maz says:


    Can we agree on:

    “Fatigue-gate: What Doctors & Big Pharma Don’t Want You To Know”

  8. windriven says:

    The link to CDC criteria for diagnosis in the sixth paragraph appears to be broken. I believe the correct link currently is:

  9. daedalus2u says:

    Doesn’t every infectious disease cause fatigue? Is there an infectious disease that does not cause fatigue? Is there any disease that does not cause fatigue?

    My understanding of the feeling of fatigue is that it is a “feature”, a feature to tell your body to rest (in quite strong terms) because you don’t have the ATP generation capacity to go about your normal activities while diverting ATP to fight what ever infection (or other disease) it is that you have.

    With this conceptualization, the problem of CFS is not with what caused the fatigue in the first place (there are a zillion things that will do that), but rather why is there a failure of the fatigue compensating pathways that get activated after the infection is cleared?

    What is it that happens in extreme and life-threatening infections, infections that cause sepsis and septic shock? There is massive production of NO from iNOS, so much that people die from hypotension because the NO level has gotten so high that guanylyl cyclase becomes too activated and the smooth muscle in the vasculature relaxes too much. That almost dying is a “feature” too, evolution has configured physiology to minimize the sum of deaths from not enough of an immune response (i.e. infection) and too much of an immune response (i.e. septic shock).

    What else can happen in septic shock? You can get multiple organ failure which comes from organs dying for the same reason that everything dies because it doesn’t have enough ATP.

    What the very high NO in septic shock does is raise the ATP levels inside every cell. That ATP comes from glycolysis because the mitochondria can’t operate at high NO levels because NO inhibits cytochrome c oxidase. That is why your physiology induces fatigue because you don’t have your mitochondria running to make enough ATP to do anything useful except lie there and have your cells turn-over their contents to get rid of any nasty bits inside of them.

    I explain all of the details in my blog, and how the mitochondria failure of sepsis (or other cases of mitochondria failure) can lead to CFS. You don’t need an infection to trigger CFS. You can get it just from immune system stimulations with vaccines. You can also get it just from trauma or surgery.

  10. ZenMonkey says:

    @daedalus: Chronic fatigue syndrome is a misnomer because fatigue is only one symptom and not even the most prominent for some people. Harping on the “fatigue” aspect just because it’s in the name of the syndrome helps no one. Although I was wondering how many comments before nitric oxide showed up; you exceeded even my expectations this time.

    @Maz & Ian: Hilarious because it’s true!

    And thank you, Mark, for changing the headline. If only we could get the writers of headlines such as those that Maz & Ian propose to do the same. (I keep trying…)

  11. Linda says:

    Marc, thanks for this well-balanced report.
    Thanks also for mentioning the problem with the Koch’s postulates in this regard.
    Good comments on the specifc problem:
    See paragraph: Assessing the Etiological Role

  12. Robin says:

    The host ate my comment so I’ll try again!

    Thanks, Dr. Crislip, for your insight as a clinician regarding this illness. It’s interesting that your observation regarding the symptom patterns these patients are at odds with the CDC. Their research definition is controversial because it’s too broad. In their “negative” XMRV study published in Retrovirology, only three patients had the sudden onset that you’ve noted clinically.

    A recent study out of the UK noted signs of persistent infection in CFS patients, in the form of increased free radicals and a higher turnover of white blood cells. BBC article here:

    Like noted, CBC are normal in CFS. If it is in fact an ongoing infection perhaps it presents differently than traditional infections.

    Earlier this week NIH hosted an XMRV conference in Bethesda. There was a great deal of interest and a lot of working going into solving the disparity of results. I think we’ll know more about this very soon, and definitely within your lifetime!

  13. Dr.Jon says:

    Adding further intrigue to this post-viral theory is the fact that there were several papers in the mid to late 90s which showed a non insignificant number of patients with CFS had markedly elevated TNF-alpha levels, which itself is known to cause depression, fatigue and the general sick feeling associated with influenza infections (or patients undergoing hepatitis treatments :))

  14. qetzal says:

    Spam filter seems to have eaten my comment from this morning as well.

    Just wanted to point out that this latest paper did NOT find XMRV in CFS patients. They found sequences that clustered most closely with mouse endogenous retroviruses.

    Apparently, a number of people (including Alter) have cited this paper as vindication of the original paper by WPI that linked XMRV to CFS. I don’t agree. WPI found nearly identical XMRV sequences in every positive patient. Alter’s group found at least three distinct sequences that were noticeably different from one another, and quite distinct from XMRV.

    AFAIK, WPI is still the only group that claims to have found XMRV in CFS patients. Alter’s findings support that something weird may be going on with CFS and retroviruses, however.

  15. ZenMonkey says:

    qetzal, yes, and a number of articles in the mainstream media also got that point wrong. I don’t consider Mikovits “vindicated” by this latest information as many of her cheerleaders do; it’s just another piece of the puzzle.

  16. SlowDescent says:

    I was struck that all the ME/CFS patients in your practice “had the abrupt onset of a ‘flu’ that never left.” I have met CFSers with sudden onset. I’m also met CFSers whose background is like mine. My ME/CFS had a gradual onset, beginning in the mid-80s with frequent migraine as well as hemiplegic body numbness and (often unbearable) inflammation of the head and limbs. Over the course of the 80s and early 90s, these symptoms became daily. More symptoms appeared, none vanished, and I finally won my family’s Dubious Achievement Award by fulfilling more than 3/4 of the Canadian criteria. I began to spend half my time in bed five years ago. I have been completely bedbound now for two.

    My rambling point is that not all genuine sufferers of ME/CFS (I was diagnosed by the infectious illness division of a hospital) have the misfortune of sudden onset. This illness has two ways of delivering its tragedy. One of them is very slowly. Drop by drop.

    I apologize if I’ve misunderstood you. And I do thank you for your column.

  17. Julia Rachel says:

    Thank you for this report Dr. Crislip. Every article and word uttered about CFS is a blessing to our patient community. I was a mean Backstroker (swimming) and competed with horses and racing cars plus ran a small farm, a non-profit, a consulting business and 2 hobby enterprises prior to be stricken with CFIDS. My son contracted CFIDS during puberty and was a star athlete in 5 sports with accolades heading into fighter pilot training and aeronautical engineering prior to being stricken. Suffice it to say, I think we both fit into your category 2 you mentioned of a “non Psychiatric” causation. Enter the words Virus and piggyback Co-infections such as HHV-6A, EBV, CMV, Lymes Diseases (Bartonella, Brucella, Borrelia) Micoplasma, Chlamydia P and C-Reactive protein testing and we can safely predict that a genetic predisposition exists then a virulent trigger hits the nail in the coffin for CFIDS patients. Now, similar to Human Luekemia t-Cell Retro-virus; XMRV is looking to contain 3+ strains and we may never know the causation. But with Dr. Jose Montoya’s Stanford published study on the correlation between 3x or greater positivity of HHV-6A and EBV combined plus 6 criteria; we have hope for treatment for millions of patients right now. Oregon is a progressive State; I spend 1/2 of my time there. I hope more Physicians think like you and walk the talk. Best Regards…Julia

  18. Jann Bellamy says:

    I’ve yet to see a SCAM practice that doesn’t pretend to be “beneficial” for chronic fatigue or CFS. The suffering of these poor patients and the lack of an effective treatment make them easy marks for snake oil salesmen. The complexity of the problem and the scientific approach to its solution contrasted with the easy claims of SCAM are an excellent argument in favor of de-licensing SCAMsters.

  19. daedalus2u says:

    Zen, yes, I am well aware that fatigue is not the only symptom of CFS. Every other symptom of CFS is also associated with the acute phase of many diseases. The only remarkable difference in CFS is that those symptoms don’t resolve over time. That suggest a problem with the physiology leading to the resolution of fatigue and other disease symptoms, not necessarily in what caused physiology to invoke fatigue and other symptoms in the first place. Under non-CFS conditions the symptoms resolve after the infection resolves. In CFS the infection has resolved but the symptoms do not. The pathways regulating those symptoms are regulated by NO.

    The extreme exercise intolerance of CFS is clearly due to insufficient ATP generation capacity caused by insufficient mitochondria. Insufficient mitochondria is clearly a problem with regulation of mitochondria number. Mitochondria have a modest lifetime (weeks to months) and so get turned over on that time scale, the same time scale that disease symptoms usually resolve over. If the pathways that regulate mitochondria number don’t produce enough mitochondria, then you will get deconditioning, exercise intolerance and eventually chronic fatigue. Nitric oxide is what regulates mitochondria biogenesis. Too low NO levels produces too few mitochondria which produces a state of elevated mitochondrial potential (to get the same basal ATP from too few mitochondria), which generates more superoxide which perpetuates a low NO state which perpetuates too few mitochondria. I discuss the specifics of low NO and CFS here.

    Robin, observing “signs of persistent infection” while being unable to find an agent causing a persistent infection suggests (to me), a problem with the physiology that causes the resolution of the “signs of a persistent infection”. If you look very carefully at the blood of CFS patients, they do have higher levels of bacteria and viruses of multiple different kinds, especially mycoplasma bacteria. They don’t have an “infection”, they have higher levels of multiple different kinds of bacteria and viruses. Usually the level of such things in blood is very low and not detectable. In CFS patients it is still very low, but measurable, higher and of statistical significance but not shown to be of clinical significance.

    My hypothesis is that the reduced clearance of bacteria and viruses is due to the low ATP level reducing the rate of turnover of cellular contents via autophagy. Everything a cell needs (except for its nuclear DNA) it can make from that DNA. Autophagy can degrade anything and everything inside a cell. If you turn-over the contents, eventually everything but what the cell puts back will be gone. The slower the cell contents are turned-over, the longer gunk will persist. The gunk isn’t causing the slow turnover, it is just the symptom of slow turnover. It is just like the gunk that builds up in all of the neurodegenerative disorders; amyloid, lipofuscin, Lewy bodies, tau. None of them are good, but the real problem is that the normal clearance pathways (i.e. autophagy) has been turned down too much.

    This XMRV result is (in my opinion) taking something that may be “statistically” significant and trying to puff it up into being “clinically” significant and “causally” significant with press releases (instead of data) and so make it into something that is “career” significant and “funding” significant. If XMRV is causally significant, there has to be physiology that couples it to the symptoms. So far, any hint of what that physiology might be is lacking. I don’t think XMRV is causally significant. I highly recommend ERV’s site for a well reasoned and thoughtful analysis of the XMRV results from the perspective of someone who is expert in the field of retroviruses.

    Jann; the reason people with CFS are so hit upon by SCAM is because the etiology of CFS is via low NO. The placebo effect works by increasing NO levels, so any disorder that is characterized by low NO will be particularly susceptible to placebo effect mediated results.

  20. Dr.Jon says:

    With low mitochondria, significant enough to cause symptoms, I would expect at least statistically significant (not grossly) elevations of lactate, which I do not think is often seen.

  21. daedalus2u says:

    It is seen when it is looked for.

    This paper pretty clearly shows reduced oxidative ATP production in muscle and increased lactate in muscle.

    If you look at this one, in figure 2, (to my eyes) clearly shows increased O2 consumption per watt of work.

    When mitochondria are run at higher potential (to get higher ATP production rates), there is more slip and less ATP per O2 molecule is produced.

    In figure 3, they show respiratory exchange ratio (RER, the ratio of CO2 produced over O2 consumed). Consistently the CFS patients show higher RER except on the last test at the highest work load where both the CFS and controls are the same. In table 2 they only show the RER at the highest work load (~1) where they both had the same value. The RER for carbohydrate oxidation is 1.0 (because no hydrogens are oxidized per carbon, for fat oxidation it is ~0.66 because fat is oxidized as C2H4 groups and for every CO2 there is an H2O produced, fat oxidation only happens directly in mitochondria). The CFS patients had a higher RER at rest and their RER saturated at 1 at a lower exercise level. RER always saturates at 1.0 because more ATP can be generated in the muscles by doing glycolysis in the muscle (which generates ATP, lactate and reducing equivalents) and oxidizing that lactate in the rest of the body (especially the brain) where the mitochondria can consume those reducing equivalents. Once you reach a RER of 1.0, you don’t have any spare mitochondrial capacity and can only increase work production by going into O2 debt, produce lactate that accumulates.

    What is interesting in this paper is that the author’s don’t believe their own data has any physiological significance and attribute the reduced output of the CFS patients to “lack of effort”. Here is their whole conclusion:

    “Conclusion: It is proposed that the reduced exercise tolerance in CFS is due to impairment in the mechanisms that constitute effort sense and/or to avoidance behaviors that result in a reluctance by these subject to exercise to full capacity.”

    This attitude is not atypical in the CFS research community. The people who think it is psychogenic interpret their data in ways that is consistent with a psychogenic hypothesis. It is unfortunate when they censor their data. In this paper they didn’t show the full range of the control subjects. The CFS subjects maxed out at 175 watts with only 3. Eight controls did 175 watts and one control even went to 250 watts.

  22. Steven R says:

    I find it funny how the solution to everything is NO. Car broke? NO will fix it according to my incredibly dense research! Pizza burnt? NO will fix that right up! Cancer? That doesnt exists, you just need more NO :P

    Seriously, its getting old. You do it ever damn time you can since the start of neurologica.

    Sorry to hear SlowDecent. Having been diagnosed with CFS, i was the sudden onset variety he talks about. Instantaneously bed ridden for a couple months, slowly got a bit better, till a bad migraine disorder developed to. In anycase, sorry to hear you have it so rough. Oddly enough, my brother was diagnosed as having fibromialga shortly after my issues, and he has swelling issues much like you describe.

  23. Kausik Datta says:

    Abbie Smith of ERV has written extensively on the XMRV studies, including the putative link with CFS. It is quite interesting – not the studies, but the holes in them. Just search for XMRV at her site.

  24. Kausik Datta says:

    Whoa! Did my comment just get gobbled up?

  25. woo-fu says:

    I was wondering if anyone could comment on the relationship, if any, among CFS, fibromyalgia and POTS (positional orthostatic tachycardia syndrome).

    I was diagnosed with CFS about five years after I was told I had orthostatic intolerance. Several years after the CFS diagnosis, I was given a diagnosis of fibromyalgia.

    Before any of that, I had a history since childhood of serious bacterial and viral infections, and I’m just wondering how these conditions might be related.

  26. ZenMonkey says:

    Steven: Isn’t it also funny how one of the hallmarks of quack medicine is a solution or treatment that “fixes” numerous unrelated medical mysteries, and how another is that only one person in all of medicine has discovered this marvelous solution?

    woo-fu: There has been no established link between CFS and fibromyalgia. However, there is a lot of speculation as to that link, and many doctors including my own (not a specialist but years of clinical experience with both) believe them to be different manifestations of the same illness. Many of the people with CFS I know also have fibro, although I do not. I can’t speak to POTS except that every doctor I see is surprised to learn there’s nothing wrong with my heart, so I’m guessing there must be some kind of correlation. Sorry not to be of more help.

  27. daedalus2u says:

    woo-fu, at the risk of offending Steven’s sensibilities, nitric oxide is what regulates vascular tone, so any dysregulation of vascular tone (especially at short time scales) is likely to involve NO. My guess is that POTS is due to low NO, that with a lower basal level there is more overshoot and instability in the control of vascular tone which shows up as POTS. It could also show up as instability in the opposite direction because it is a problem with the stability of the control system, the balance between too much and too little of something. I know that sounds like hand waving to people who don’t understand NO and control theory, but complex systems have complex dynamics and behave complexly even when they are fully and completely understood.

    All of the disorders that I associate with low NO are also (more or less) associated with reduced heart rate variability and vice versa.

    Serious infections can be a trigger for CFS, particularly intracellular infections (such as Lyme and Q-fever) and particularly when they go on for a long time or result in sepsis or septic shock.

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