A New Decade of ME Research: The 11th Invest in ME International ME Conference 2016
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Article: Light on ME/CFS I: Bad Reception: A Key to ME Uncovered? The Light Gene Expression Studies

Discussion in 'Phoenix Rising Articles' started by Phoenix Rising Team, Jul 15, 2011.

  1. Michelle

    Michelle Decennial ME/CFS patient

    Portland, OR

    I'm on Neurontin at the moment (and was on it 6 years ago) for severe nerve pain and have also been on Lyrica. I went off both and may have to go off Neurontin again because they (have) gradually stopped being effective. The only side effect I've ever had has been an increase in appetite. Not only have they reduced my pain, but they reduced my fatigue (when I first went on Neurontin it was like the Elixir of the Gods). While on Lyrica, it reduced my sensory overload symptoms (I could actually manage being around groups of people without feeling weak and icky within a few minutes due to the sensory stimulation involved) as well as the profound facial flushing I get with the most trivial exertion (thus also reducing my migraine headaches) in addition to reducing pain and fatigue. I'm also not alone in that as I've known a number of other ME/CFS patients who have found varying degrees of success with these two drugs with little or no side effects.

    I say this not to invalidate your and other PWME's experience with these drugs (I've had my own freak reaction to another anticonvulsant called Tegretol) but to note that these drugs are warranted and can be really effective for some PWME -- including people who may be reading this thread. To say it's never warranted is simply not true. Indeed to say anything is ALWAYS or NEVER warranted in PWME not only ignores the heterogeneous nature of this disease but of human beings in general as each unique person has his or her unique body chemistry.

    Given the lack of treatments for this disease and the profound suffering it causes (I'm bedbound and housebound; ME for me is like having the flu, a hangover, jet lag and being burned from the inside out all at the same time all the time -- not to mention has been life threatening when I ended up with blood clots in both lungs), it makes sense to me why physicians are desperate to prescribe -- and for us to try -- any treatment with some science behind it that suggests it might be useful (money is indeed a factor too). Unfortunately at the moment it's a crap shoot for doctors. The only way they know if a medication is going to work is for us to swallow it. Medieval? Absolutely.

    Which is why I find this research from the Drs Light promising as there may be a way for doctors to know in advance which of us is going to respond poorly or well to these medications. And, of course, it may also explain why ME/CFS is such a heterogeneous disorder.

    It's also interesting as it may explain why the drugs stopped working after providing 3 weeks (Lyrica) to 5 months (Neurotin) of sweet, blessed relief. At the moment, this second trial of Neurontin at it's highest dose is working -- barely. If I keep my activity level below my anaerobic heart rate, I'm okay -- for the moment. I'm hoping that managing my activity level better this time around with Neurontin will be more effective.
  2. Annikki


    Hi, I'm busy working on proving it is worth testing interstitial cystitis patients for XMRV. Much of what I'm finding which is pointing to IC being XMRV related is similar to the ideas Dr. Light has had on both fibromyaligia. The idea that Dr. Light has had on fibro is that the muscle fatigue of fibromyalgia stems from the purinergic receptor malfunction. Dr. Light said that there are purinergic receptors which monitor ATP consumption and that these purinergic receptors send pain signals based on ATP to save muscle wear.

    I'm finding something similiar with IC:
    Studies have shown that when bladder epithelial cells are stretched they release ATP. In the bladders of people with interstitial cystitis, more extracellular ATP is released than in control patients.

    Quote: (BMJ August 8th, 2009: 339:337-342)
    (IC bladder uroepithelial cells released significantly higher concentrations of ATP (adenosine triphosphate) than control biopsies suggesting that ATP plays an important role in this syndrome. An investigation of cultured bladder epithelial cells showed that such cells have an abnormal, much higher concentration of ATP. This higher concentration of ATP decreases the ability of the bladder wall to conduct (channel) potassium ions which again indicates impaired potassium ion conduction is part of the pathology of interstitial cystitis.

    Studies on ME/CFS have shown deficient ion channelopathy to be part of the pathology of ME/CFS. Some studies about ME/CFS and potassium conduction attribute this flaw to abnormal mitochondrial gene expression.

    The BMJ article cited says studies on IC showing ATP increase and changes in potassium conduction as also resulting from abnormal gene expression.

    I suggest the issue of ATP, potassium ion channelopathy as being the result of XMRV. Idiosyncratic production of ATP and its components such as purinergic receptors, ATP- binding cassettes (ABCs) and or ABC transporters is well documented in many other autoimmune diseases and can be fully attributed to the source of most IC symptoms.

    I hypothesize these abnormalities are the result the presence of XMRV in interstitial cystitis, and occur through many different mechanisms, including viral mimicry and others.

    The hypothesis that XMRV likely cause of significantly high release of ATP in bladder urothelial cells is supported by observed defects in ATP-binding cassette transporters, where XMRV viral mimicry of proteins is likely to have occurred..

    About ATP Binding Cassettes
    ATP-binding cassette transporters are members of a protein superfamily that is one of the largest and oldest proteins.
    ABC transporters are transmembrane proteins that utilize the energy of adenosine triphosphate (ATP) hydrolysis to carry out certain biological processes including the translocation of various substrates across membranes and non-transport related processes such as translation of RNA and DNA repair. ABCs transport a wide variety of substrates across extra and intracellular membranes, including metabolic products, lipids and sterols, and drugs. Proteins are classified as ABC transporters based on the sequence and organization of their ATP-binding cassette (ABC) domain(s). ABC transporters are involved in tumor resistance, cystic fibrosis, bacterial multi drug resistance and a range of other inherited human diseases.

    One of these diseases is Pseudoxanthoma Elasticum (PXE), a hereditary connective tissue disease in which proteoglycans have altered properties. In pseudoxanthoma elasticum there are abnormalities which show some relevance to interstitial cystitis. Both diseases show a relationship with sulfated glycosaminoglycans. The only difference is that in PXE, an inherited genetic defect in an ATP-binding cassette transporter identified as ABCC6/MRP6

    The idea that ABCC6/MRP6 is the cause of PXE was tested in 2003 in Italy.
    Proteoglycan metabolism in PXE was studied by Francesca Maccari, Dealba Gheduzzi and Nicola Vopi at the University of Modena, in Modena, Italy.

    In this study, the researchers measured sulfated glycosaminoglycans in the urine of people with PXE, people carrying the disease and healthy controls. Sulfated glycosaminoglycans are what compose the mucosal lining of the human bladder, known as the GAG layer. The GAG layer is deficient in IC patients because the bladder epithelial cells which secrete GAG become compromised and cease to serve their function.

    The glycosaminoglycans this study on PXE tested for were chondriotin sulfate disaccharide and heparan sulfate disaccharide. Note also that to treat interstitial cystitis, heparin sulfate is instilled into the bladder to augment the defective GAG layer. In Canada and elsewhere outside the U.S., chondriotin sulfate has been used with even better results than heparin sulfate as a bladder instillation, to help IC patients in those places.

    In PXE 34% less of the polysaccharides were detected in the urine of PXE individuals, than controls or unaffected carriers of the genetic defect.

    It is worth noting that the commonality between IC and PXE patients may extend beyond glycosaminoglycans being abnormally low. On the revealing of the genome for XMRV, a comparison of what human proteins the XMRV retrovirus mimics finds a link between the virus and ABC transporters.

    A retrovirus is different from normal viruses. Normal viruses only have their DNA transcribed into RNA in the host, and the RNA is then translated into a protein. A retrovirus functions in a different way, which more adeptly inserts its genome into human DNA. Retroviruses have their RNA reverse-transcribed into DNA, which is then integrated into the hosts genome and then undergoes the usual transcription and translation processes to express the genes carried by the virus.

    How this relates to the issue of XMRV and autoimmune diseases, its speculated that XMRV creates proteins which mimic those in the human body. The idea is that the fake DNA created by the virus initiates a response from the human immune system. Some believe that the human immune system becomes confused from the retroviral proteins which mimic its own proteins. This leads to the unending attack from the body on its own tissue.

    There is an ATP-binding cassette associated with the viral mimicry of XMRV infection. It is called ABCC9:

    It is known as EAW96452.1. This is an ATP-binding cassette of the subfamily C (CFTR/MRP), member 9, isoform ABCC9. XMRV GAG- PRO-POL was found to mimic the natural properties of this ABC.

    Note that ABCC6 in PXE where altered levels of glycosaminoglycans is very closely related to ABCC9. Both of these ATP-binding cassettes are of the subfamily MRP.

    However, a link between this possibly compromised ATP binding cassette know as ABCC9 and interstitial cystitis goes further than its proximity in nature to ABCC6.
    Here is what the genome mapping project says about ABCC9

    ABC proteins transport various molecules across extra and intra cellular membranes. ABC genes are divided into seven distinct subfamilies (ABC1, MDR/TAP, MRP, ALD, OABP, GCN20, White). This protein is a member of the MRP subfamily which is involved in multi-drug resistance. This protein is thought to form ATP sensitive potassium channels in cardiac, skeletal and vascular and non-vascular smooth muscle. Protein structure suggests a role as the drug-binding channel modulating subunit of the extra pancreatic ATP-sensitive potassium channels. Mutations in this gene are associated in cardiomyopathy dilated type 10. Alternative splicing results in multiple transcript variants.

    Now we go back to the idea the BMJ article expressed; the idea that come IC pain comes from inability for the bladder epithelial cells in IC patients to channel potassium ions. Also issues involving dysfunctional bladder smooth muscle activity parallel a possible defect in ABCC9 as a causative agent in IC symptoms. Bladder spasms and pelvic floor muscle issues become clearer when the idea of viral mimicry of ABCC9, or other ABCs.

    Potassium channeling function by ABCC9 also alludes to the co-morbidity of mitral valve prolapse in interstitial cystitis patients. This too is another trait common to both IC and CFS/ME. Furthermore, defective cassette binders have been linked to the lack of energy proliferation in the bodies of CFS patients. Potassium channeling has also been linked to the pain of fibromyalgia.

    The studies of Dr. Light bind the idea that a defect in receptors in the muscle fiber of fibromyalgia patientsreceptors which detect levels of ATP used or not used by the body which is part of the role which ABCs and or ATP sensors like purinergic receptors play in the pathology of that disease.

    This makes good enough sense to me. Looking at the many studies which show the prevalence of extracellular ATP in both human and feline IC patients, and furthermore, studies which demonstrate a clear link between extracellular ATP and pain in the human bladders, I have a good feeling about the stability of my hypothesis.

    Studies regarding extracellular ATP causing pain in human bladders go far beyond IC research. There was a study performed in Sweden demonstrating that extracellular ATP and the purinergic receptors P2Y are responsible for the inflammatory response in human bladders exposed to the E coli bacteria. Or to put in simple terms, ATP and purinergic receptors which bind to ATP are responsible for the pain and inflammation in the common urinary tract infection.

    Bladder stretching itself also causes the bladder epithelial cells to excrete ATP. Studies have ranged from hypothesizing that extracellular ATP serves a role as a signaling mechanism in the human body, where its release upon stretching the human bladder generates the feeling and urge to go. I blame the inability of ABC transporters to serve their role in transporting substrates through intra and extracellular membranes as being part of why some substances irritate IC bladders and cause no sensation of pain in people with normal bladder tissue.

    I attribute the experience of interstitial cystitis as being largely dependent upon defective ATP-binding cassette behavior.

    I suggest exercise works as an IC therapy because it uses up the extracellular ATP.

    I will show proof for my argument in referring to a study which show that extracellular ATP is responsible for other IC anomalies, including the defect where tryptophan in IC patients is broken down into kynurenine over serotonin and melatonin. The indoleamine 2,3, dioxygenase pathway is the formal name for the modification of tryptophan into various other chemicals.

    There is a study proving that extracellular ATP effects the maturation of human dendritic cells (immune cells), affecting the indoleamine pathway.

    Extracellular adenosine triphosphate affects the maturation of human dendritic cells, mainly by inhibiting T-helper (Th 1) cytokines, promoting Th2 cytokines and modulating the expression of costimulatory molecules. In this study we report that adenosine triphosphate can induce immunosuppression through its own action on DCs, defining a new role for extracellular nucleotides. Microarray analysis of ATP-stimulated human DCs revealed an inter alia a drastic up-regulation of 2 genes encoding mediators involved in immunosuppression: thrombospondin-1 and indoleamine 2,3 dioxygenase.

    Hypothesis 2

    It is possible that bladder stretching in interstitial cystitis is the result of when the bladder is distended, abnormal ATP release and possibly more abnormalities enable the glycosaminoglycans heparin sulfate to allow viruses, bacteria or mycoplasma to penetrate the blood brain barrier.

    It is known that bladder stretching causes cells to release ATP. This is one way physical changes alone can alter bladder surface biochemistry.

    Furthermore, the amounts of extracellular ATP becomes more prevalent upon mechanical stretch can be reduced by chemicals already present in the bladder. In a study by Sun Y and Chai TC at the Division of Urology at the University of Maryland School of Medicine, both heparin sulfate and dimethyl sulphoxide (DMSO) reduce the higher levels of stretch activated ATP release in the bladders of people with interstitial cystitis.

    The idea supported by the results of this study is that bladder epithelial cells (bladder urothelial cells or BUCs) are able to detect levels of ATP and rely upon ATP as a chemical messenger of sorts.

    Here are links to ATP and IC correlations:
  3. MishMash


    I will accept that some PWME have positive reactions from these drugs. It is indeed a crap shoot. Unfortunately, at the craps table in Vegas you get to decide when to roll the dice and when to walk away. The doctors push these drugs very hard and there is a financial incentive to do so. New, naive, or less experienced PWMEs usually just take the word of the doc that there is no potential downside. Also, the docs should know that Lyrica and Neurontin weren't intended for long-term use. They weren't intended for years-long usage, any more than prescription sleeping pills or painkillers. As you experienced the affect wears off after several months; usually the case if the meds haven't driven you to near madness.
  4. oceanblue

    oceanblue Guest

    That was good of you to pass on my post to Alan and please thank him for addressing my concerns. And like you, I was impressed by how many other studies are in the pipeline.

    His points go a long way to allay my concerns over deconditioning. I was particularly struck by this:
    If gene expression goes down in healthy controls at max exertion then the same genes going up in patients (even if the exercise proved to be maximal rather than moderate) becomes hugely significant.

    However, I'm confused as to how these latest findings of decreased expression in controls at max exertion fit with the original basis for the experiment - which was that these same genes went UP in controls on strenuous exercise, and that was why they were chosen. I suspect I've missed something important here.

    I completely understand why Alan doesn't want to do more exercise experiments because of the stress the existing exercise protocol places on patients, and agree that they'll never find healthy 'matched' controls that are as deconditioned as housebound/bedbound patients.

    That said, what makes the current study so compelling is that it focuses on one of the main symptoms for most people: post-exertional malaise ie people reacting very badly to relatively minor execise - and shows gene expression mirroring a key symptom in response to a challenge. And this suggests that the pathology involved could be central to CFS rather than some secondary effect.

    For that reason I'd like to see many more of these kinds of studies, but with modifications to make them less stressful. That's why I was keen on an exercise challenge that was related to the patient's status, with a much lower level of exercise for iller patients (effectively compensating for the inevitable deconditioning of these patients by lowering the exercise target). This could overcome the problem of overstressing patients, as well as meeting the stated aim of 'closer similarity to the natural exercise experiences reported to exacerbate CFS symptoms in patients daily lives'.

    Clearly the Lights have completed their exercise-challenge studies of CFS patients. I hope other groups will recognise the importance of their work and we'll see replication studies before long.
  5. Cort

    Cort Phoenix Rising Founder

    Fascinating Marco! We're quite similar in some ways - I think I have more issues with pain and less IBS and OI and temperature dysregulation...I sound a bit more sensory (MCS) and I think you sound a bit more autonomic. I wonder if you would fit in the alpha 2a group?
  6. Cort

    Cort Phoenix Rising Founder

    I'm actually not clear on what basis the genes were chosen. I had the idea that these genes have been shown to be upregulated in fatigue and pain animal models but am not clear.
  7. oceanblue

    oceanblue Guest

    This is from the 2009 pilot study:
  8. valentinelynx

    valentinelynx Senior Member

    More ? on Propranolol & comment on drugs for FMS

    Thanks, Cort, that was very helpful. I am left wondering, though, especially since he said something about an "experience with propranolol," if they have observed a positive effect of this or other beta blockers on CFS patients with autonomic nervous system problems like OI or POTS, or are just theorizing?

    Re: Neurontin & Lyrica. In my pain fellowship, I observed quite a few patients benefitting from these meds for neuropathic pain, such as caused by herpes zoster (shingles), post-herpetic neuralgia, diabetes or nerve impingements like sciatica. However, they are not without side effects, and any physician who says otherwise is very, very wrong. The side effect profile of these drugs is, in my opinion, more of a problem than that of the opioids. Most people find they cause profound drowsiness at first, many get severe dizziness, some get really loopy. That's why you have to start at a very low dose and work up slowly, over weeks to an effective level. Severe peripheral edema (swelling of the legs) is fairly common, and unfortunately this is more common in patients with diabetes, people who are most likely to need the drugs for diabetic neuropathy. I have never been impressed with the data from the studies showing benefit from these drugs, or for Cymbalta and Savella for fibromyalgia. The drugs have been shown to either give about half of patients about a 20% improvement in pain, or about 20% a 50% improvement in pain, over a short period of time. This is a terrible overgeneralization, but really, the data is underwhelming. Both Cymbalta and Savella are SNRIs, drugs that can cause a horrendous "abstinence" syndrome. Savella can cause hypertension in a fair number of people.

    The drugs companies are making it look like they have found wonder drugs for fibromyalgia, and physicians are convinced by these campaigns that all FM patients should be on these drugs (and quit whining?). Personally, I don't think any of them are any more exciting than the old tricyclics (amitriptyline, desipramine), which provide similar benefits with similar mechanisms at far lower cost, and perhaps even slightly less side effects at the very low doses that should be used.

    BTW, not sure where the idea that gabapentin (Neurontin) and pregabalin (Lyrica) were not meant for long term use would come from. Both drugs were originally intended to be used as anti-seizure medications, as booster adjuncts to other, more effective drugs. As such, they would be expected to be used indefinitely.

    I feel I should reiterate that Neurontin and Lyrica are really great drugs for some indications, particularly nerve pain of the weird burning, electrical, shooting variety. Theoretically FM pain might be neuropathic, but experientially it is quite different from these other types of neuropathic pain. These drugs also have some anti-anxiety effects as well as promoting sleep, so it's unclear where the benefit comes from in those it helps.

    I think the main point of this extended diatribe is that I really don't want people to feel they have failed somehow by not responding to the FM "wonder drugs." Most people don't, or not much, or not for long.
  9. Marco

    Marco Grrrrrrr!

    Near Cognac, France
    Possibly Cort.

    Although i'd be surprised if we neatly fit into any of these discrete catergories.

    For example, my exercise intolerance started when doing above shoulder exercises in Ju Jitsu class (I fainted). For a few years afterwards i did tend to get very dizzy on standing but not any more. Despite that I still can't tolerate aerobic exercise.

    On the other hand the number and severity of food and chemical sensitivities have increased over time and I have other symptoms (never get colds or flu's etc) which would suggest immune issues.

    One last thing. My GP prescribed a beta blocker for the temperature regulation problems and it was one of the worst reactions I ever had to medication. Absolutely freezing and feeling I was about to die (and I'm not prone to exaggeration). Having said that it was probably the standard dosage which could have overshot the target so to speak. I didn't try them again.
  10. bertiedog

    bertiedog Senior Member

    South East England, UK
    Well I for one benefit hugely both from 20 mg Propananol and 1/2 tab Florinef daily. It has virtually got rid of the severe POTs I used to suffer. The only time it might be a problem is first thing in the morning or if standing for over 10 minutes in a queue.

    They are wonderful drugs for me but I only need very small doses.
  11. Cort

    Cort Phoenix Rising Founder

    I have heard this about beta blockers before and I can understand yours and mishmash's concerns. They seem to be the most Jekyll and Hyde type drugs; they can be either devastating or very helpful depending on who you are. Obviously the medical profession needs to learn more about who to prescribe them to. Perhaps the Lights work will eventually help in that area.
  12. Cort

    Cort Phoenix Rising Founder

    Right - not wonder drugs yet - which Kathleen Light kind of alluded to when she talked about creating drugs that match the gene signatures most present in CFS. I know somebody who does so much better on cymbalta - which really surprised me since I hadn't heard that much good on it - but really tanked on Lyrica. It's really a crap shoot at this point, isn't it? If the Lights can figure out Lyrica really helps that will be a big help. Still, there's a long way to go with these drugs.

    Wyller also did a case study of a young patient who did so well on propanolol that he was able after a year of missing school and being in a wheelchair to return to school and lead a mostly normal life. He was one of hte lucky ones who happened to fit that drug really well.

    Attached Files:

  13. August59

    August59 Daughters High School Graduation

    Upstate SC, USA
    I know it has probably been said already, buy if they could collaborate with Pacific Research Lab it would seem to help gather a lot of usable information at a quick pace.
  14. BEG

    BEG Senior Member

    Southeast US
    They are vasodilators. Since most all of us have low blood volume and cardiac impedancy, we want those veins open to allow our blood to flow easily. This is my layman interpretaion. When I googled "mechanism of bystolic (my beta-blocker)," I actually read the following:

    Nebivolol also possesses novel vasoactive factors. It provides vasodilation by releasing endothelial nitric oxide. The vasodilation properties result in an overall positive hemodynamic side-effect profile, including cold extremities and a reduction in exercise intolerance

    A reduction in execise intolerance are words we don't hear everyday.

    Note* I was answering LaurelW's question which seems to be located elsewhere. I'm so confused.
  15. omegaman


    What kind of ME/CFS patient has never had deconditioning? With PEM being the hallmark of ME I can't see how it is possible not to be deconditioned unless you are one of those rare individuals like Michelle Akers was and could get a medical team to help you and push yourself beyond the bounds of most humans endurance.

    My question was ignored but I will ask again. Are the Lights going to publish a comparison in there Gene expression work between ME/CFS and MDD. MDD is often misdiagnosed as CFS especially using Fukuda and by many Primary Care doctors. To establish and publish a differential study between these two groups using their techniques would give tthere work a big boost.

    They chose to compare and publish with an MS group yet the overlap in incorrect diagonis between MDD and CFS is probably much greater. So an imprtant step would be to publish a comparison of these two groups using stringent criteria and multiple sites for collecting samples like the Lipkin study is doing.

    If they could do this then I might start donating to there work directly
  16. LaurelW

    LaurelW Senior Member

    All the Lights' patients were chosen by Dr. Bateman, who would definitely not send them someone who had MDD and not CFS.
  17. Cort

    Cort Phoenix Rising Founder

    Sorry about that. I don't believe they are. They did look at whether depression in CFS effected results in the first study and I don't think it did. It is pretty common to include a MDD control group in studies and that group almost invariably turns out to be different from the ME/CFS patients - that is my recollection anyway. It could be that they consider that question pretty much resolved or they don't have a good MDD group at hand or I don't know.

    Dr. Light said that if the fatigued prostate cancer group turns out to have significantly different results (as it appears now) they may use that group as a control group. They have also looked at fibromyalgia, of course, and multiple sclerosis patients and each has been different. They are also giving healthy controls extensive and varied exercise tests - really pushing them hard - and seeing what turns up. He never mentioned anything about MDD - so my guess is that they are not part of the current protocols.
  18. Cort

    Cort Phoenix Rising Founder

    That is a very good point come to think of it - she really is known to be a really excellent diagnostician and if anybody would know she would. There were some MDD patients in the healthy control group of the first study by the way.
  19. eric_s

    eric_s Senior Member

    Switzerland/Spain (Valencia)
    I think at least in the first phase many patients continue to go to work or school, so you could test these. There are people on this forum too, who go to work. If they've never stopped working so far, i guess they would not be deconditioned or at least not more than a healthy control with a similar lifestyle.
  20. biophile

    biophile Places I'd rather be.

    What about stress and anxiety controls?

    I agree this direction of research is very interesting and potentially groundbreaking. I haven't looked into it as much as oceanblue but he made some good points and suggestions for making the research more solid in the future. It is especially encouraging if most patients met Canadian criteria. However I would like to see more comparative cohorts studied if possible, not just major depression but those with (primary) chronic anxiety disorders and (primary) sleep disorders, and possibly "burnout" and "overtraining" if it is possible. Their exploration of other diseases like MS and prostate cancer is useful too. I watched the 2011 NIH presentation of this study and Light seemed surprised that the ME/CFS profile is unique rather than generic to fatigue and pain.

    Whatever the findings in these tests, the CBT/GET biopsychosocialists will be eager to relegate the abnormalities to functional mind-body disruptions. It needs to be established beyond doubt that these abnormalities cannot be dismissed as the consequences of psychological stress, "deconditioning", or a result of sleep deprivation etc. Unfortunately it is possible that there will be some overlap because both psychological and physiological stressors involve some but not all the same systems. Light understands this, so finding the cause of these abnormalities is crucial, because acceptance of causation is going to be a bitter struggle, this "mind-body problem" will haunt us to the very end.

    I always suspected that if the sympathetic nervous system is overactive in CFS it is because the body is compensating for symptoms and impairments and underlying pathology stressing the system (which Light believes is in part due to an infected and/or damaged dorsal root ganglia contributing to excessive signaling).

    I have shown a few people those coloured graphs and they were impressed and concerned. A picture really can be worth 1000 words.

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