Where To Now?

Life is full of misery, loneliness, and suffering – and it’s all over much too soon.
~ Woody Allen

Humor and music get me through, so here is tonight’s song:
Where to now St. Peter by Elton John

Every time I write a blog I feel like it might be my last. How could I have anything left to say? Then the next one appears in my head, generally pretty much fully formed, and I need to write it. It’s a strange process to reveal one’s personal journey so publicly. But your letters have made it well worth putting up with the unpleasantness and infighting. The feedback that my writing has helped someone’s isolation, or helped medically in some way, means everything to me. One of the worst things about getting sick for me was being unable to be of service.

Writing this blog has required a willingness to be wrong. As I’ve said repeatedly, I could be wrong about anything, though it seems unlikely that I’m wrong about everything. If I am, I figure I can still become Jamie Jones and move someplace where there is no internet:). There must be somewhere on earth one could still go and live completely unplugged:). There are inconsistencies inherent in blogging, writing on different days from different moods. When I sit down to write, I try to center myself so I can find what is true for me at that moment. It isn’t about building a flawless argument over time. It is a moving target. I have made being honest more important than being perfectly consistent, but there isn’t much I’ve written that I’d retract. I’m not as angry now as I was when I wrote certain things, so I might be gentler if I wrote some of it today, but not so different in substance.

I received a lot of mail today concerned that I sounded depressed and hopeless yesterday. I am neither. I am sad and, unfortunately, somewhat sicker than I was a couple of months ago. And really tired of this fight, because absence of proof is not proof of absence and we’ve got something serious, most likely of retroviral origin. Something I now have to treat, with or without all the answers. Like all of us, I hope that the BWG and Lipkin are positive studies. But if they aren’t, it doesn’t change a thing for me, except for the timeframe in which I can reasonably expect help and change. As Karina so eloquently said in the comments of the last post:

I have accepted that I have to live with this disease and I will most probably die from it too. As ridiculous as it sounds accepting that is somehow giving me some peace of mind.
I am no longer trying to reach for the stars but try to reach for the possible.
I worry less…..
But I still worry for our children
and for our children we must continue to fight…. 

I took a big emotional hit in early July, and my declines are always a month or two after a major physical or emotional stressor, so right on time. I am sorry that arv’s didn’t protect me. Until now, it has seemed to me that I was more resilient than expected. But I am not depressed and I certainly still have hope. My coping mechanism is always to look for meaning in my predicament. However, I am getting real about what I can expect, personally and professionally. Baby steps. I’ve put a lot of energy into understanding the unfolding science. The heady days of discovery seem to have wound down to this period of uncertainty. My focus has turned to the clinical now. I have a limited bag of tricks at my disposal, but not an empty one. I don’t feel in any way powerless. The patients I’m seeing have some maneuvering room and we will work with what we have.

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82 thoughts on “Where To Now?

  1. >XMRV is a polytropic and xenotropic hybrid. The CDC now say it is also ecotropic. Lo et al. discovered polytropic,modified polytropic, and xenotropic sequences. How is that different? If you doubt it read Towers latest paper.

    The new WPI sequences in the GenBank are polytropic and modified polytropic.

    Lombardi et al. used an assay which had already been shown capable of detecting HGRVs. They then dropped the annealing temperature to increase sensitivity. Lo also dropped his annealing temperatures, but wisely used multiple primers, but used different outer primers to Lombardi, so he missed more of the X variants. Still like I said, he did find xenotropic gag sequences.

  2. >I guess you mean the study "Phylogenetic analysis of MLV sequences from longitudinally sampled Chronic Fatigue Syndrome patients suggests PCR contamination rather than viral evolution" (http://jvi.asm.org/cgi/content/abstract/JVI.00827-11v1), which as is clear from the title and abstract does not support the idea that the MLV-like sequences detected by Lo et al. are genuine human pathogens. I can't comment further, as I do not have access to the full study.

    Most now consider the Lombardi et al. and Lo et. al studies to be separate findings, including Harvey Alter. Lo is keeping a low profile (no pun intended).

  3. >No. Alter does not consider the findings to be different and no one else has said they are different. Only that they would like them not to be looked at together. On what scientific basis, they won't say. They did find the same variants.

    The Towers paper applied a model of virology that is not suitable for retroviruses. If he had applied it to the human retoviruses HTLV, that would now not exist, even though it kills people.

    From the Towers paper.

    "CFS type 1 infected patients are derived from three strongly supported and distinct regions of the tree, namely, the polytropic, modified polytropic and xenotropic clades."

    "Another 2010 (MLV_001_2010) sequence is robustly placed within the xenotropic clade,"

    Towers makes if very clear that the Lo sequences do not match any mouse virus.

  4. >I just changed the settings on the blog to require some form of registration before posting a comment. Please identify yourselves in some way. A handle is fine. Nobody can follow what's being said with all the anonymous comments. The thoughts don't hang together because we can't tell who is saying what. It would also be useful to know the background of the person commenting. I hope this doesn't cut down too much on ease of sharing your thoughts, but I think we will all learn more this way.

    Thank you all,

  5. >Is Towers not saying that the viruses identified in CFS patient samples are from 3 distinctly different regions of the phylogenetic tree and not variants of the same virus?

    Excerpt from Phoenix Rising website report from NIH SOK Workshop:
    "A Talk with Dr. Alter – in a personal conversation Dr. Alter stated he is now personally leaning to the idea that XMRV was accidentally created in a lab. Two things, in particular, seem to have struck him, the fact that the 22RV1 cell line was created using mice (he hadn’t realized that) and the lack of genetic variability in the samples to date. He no longer appears to believe the MLV sequences that he and Dr. Lo found are part of a larger XMRV family; instead he believes that they are probably separate entities."

    John Coffin has also said a number of times on record that they are different viruses.

    UK ME/CFS Patient
    XMRV+ by VIPdx (Serology)
    XMRV- by Imperial College London (PCR, Culture & Serology)

  6. >@Ed.

    Lo found sequences of different variants, some were xenotropic. What is XMRV Ed? Think about it.

    I'm sorry but that statement about Alter is not true.

    Coffin has never said they are different viruses, and has no proof that they are.

  7. >For 26 years, doctors have been hinting to ME/CFS patients that a pill to control the many pathogens in their bodies is just on the horizon.

    And for 26 years, every single pill offered has been a failure at helping any more than a tiny percentage of ME/CFS patients to feel anything more than slightly better.

    Meanwhile, every single ME/CFS patient who has followed Erik’s instructions to the letter has improved markedly.

    Yesterday, I heard from another person (prominent on ME/CFS boards) who has spent many years doggedly trying every treatment discussed.

    Finally, after witnessing improvements of others and reading Ritchie Shoemaker’s “Surviving Mold,” she got an ERMI test on her house. When it came up as problematic, she bought some new camping gear and tried sleeping in a tent in her backyard. (She lives in a place where I did reasonably okay, when I visited.)

    She got a good deal of improvement immediately and so decided to try camping in some spots that I suggested were particularly good. She writes: “I did great in the mountains. Now I’m at a friend’s house, in (a big city). Not good here. Didn’t like the air at all. Wish we had stayed in the rainy forest but we were tired of being wet! So far I haven’t found a building I can tolerate. I’m impatient to get home, in order to take care of everything I have to do before the weather turns too cold.”

    (Of course, there really ARE buildings out there that extreme responders can tolerate. Sometimes it does take some searching though.)

    I’ve now had dozens of people share with me stories of feeling better or worse in particular locations, and even more ask me for suggestions on good places to go. Paul Beith and I therefore put together a board for people to share their experiences.


    My own experiences traveling in my RV to hundreds of places in 23 states over the past two and a half years are a start. Especially if folks have different experiences than mine, please share them.

    Hopefully this, along with the compilation of Erik’s writings on how to do extreme avoidance (along with other topics), will give people the tools they need to get started if they so choose.

    Nobody’s obliged to do any sort of avoidance, of course. It’s certainly not an easy way to go.

It does work though.


    Lisa Petrison, Ph.D.

    lisapetrison at yahoo

  8. >Dr. Jamie,

    My drumbeat may begin to sound dull and repetitive, but I will repeat my sentiments–not because I think you NEED to hear them but because I want to reiterate them. I appreciate the fact that you have decided to walk out this epic tightrope of a life sans safety nets. Thank you for posting your thoughts, feelings, desires and disappointments with us. This reality, this time in life resonates with the same kind of emotional residue of a Gabriel García Márquez novel–inexplicably splendid and horrible…simultaneously. Although I appreciate this blog, your blog, for adding a wealth of information to the storehouse of my mind, I appreciate far more the space that has been created. Almost every blog has some desperate, pressing question or a story of resilience, grace and courage. People are finding their voices and of all the places in the world…they are sharing their narratives and lives with you. Even pesky posters and those who carry dull axes that need perpetual grinding…this is their place. I think that says volumes.

  9. >@448c82ee-cc37-11e0-9256-000f20980440 (not the sort of identification Dr Jamie is asking for I think)

    If you are going to accuse Cort Johnson of lying, then I think you need provide some back-up, as to how you could know that conversation with Dr Alter did not take place.

    Also, are you a patient, scientist involved in XMRV research or interested bystander?

    As for what XMRV is. It's either a virus that is infecting me and many others and maybe making us sick, or it's a virus created in a lab in a prostate cancer cell line during the 90's and contaminating labs. The BWG & Lipkin studies will answer that question.

  10. >@Ed

    You may wish to read what Jamie actually said and take the time to realise that is what the system did.

    If you are going to accuse Alter of lying then I think you will need to provide some back-up. Others were at that conference and spoke to him. You can see his real thoughts on video at the conference. He has said that he stands by the comments he made then.

    The answer I was hoping that you may be able to give is that XMRV is a xenotropic and polytropic hybrid. According to the CDC it is now also ecotropic. Alter and Lo found sequences, some were xenotropic, some polytropic and some modified polytropic. That means they did find the same virus. If you are going to dispute this please provide scientific evidence. I know there is non.

    The BWG is already on shaky ground because they have allowed the CDC to change all their assays after detecting the virus.

    The Lipkin study is also on shaky ground. It is not putting prostate cancer under the microscope even when we know the ME studies so far have looked at blood, when it is known the main reservoir of the virus is not the blood. When there are now 3 positive ME papers published and many more appearing at conference. When we know that Lo et al. detected the same thing Lombardi et al. did. The patients to be included are coming from clinicians who always have mixed cohorts. The labs are not also being forced to use each others methods to prove that others are able to detect the virus. What if the WPI only gets negatives?

    The XMRV variant VP62 cannot have been created in a lab 1993 to 1996. The virus was first being detected in 1989, XMRV is also ecotropic and the two viruses Coffin wants to blame are not, and one of those viruses has not been proven to even exist at this time. The recombinant event is also hypothetical and like i said so is one of the viruses. The cell line was also not in the labs of the WPI/NCI or Lo et al, and cannot account for all strains and variants.

  11. >@Muckle

    Jamie clearly states "It would also be useful to know the background of the person commenting".

    Like the wise and experienced scientist Dr Alter is, he is not committed either way and will let the science decide. I suspect that is not the case with you, as you are already making excuses for the BWG and Lipkin studies. When it comes to patient selection, even in the worst case scenario you'd have to expect at least a 3rd of patients to match the profile of those from the Lombardi and Lo studies. If the WPI get all negatives, then that is surely an indication of contamination in previous results, as of course 3.7% of controls tested positive. And they will again be using multiple methods of detection. Also, the political situation with prostate cancer is completely different, as the vast majority of PCa patients have probably never heard or XMRV and there are no calls for the use anti-retroviral drugs. However, those arguing for contamination say it equally applies to PCa.

    I'm not qualified to get into a detailed scientific debate with you about the nature and origin of XMRV, as my background is in finance. Part of me hopes you're right, as it could lead to better treatment and another part of me hopes your're wrong, as I don't particularly like the idea of having a retrovirus. Either way, I remain confident that like so many others I will recover from this illness, and still find ways to enjoy life until I do. If you are a patient, then you may want to consider remaining open-minded to all outcomes, as life with ME/CFS can be isolating and challenging enough, without having to also cope with brooding over the injustice of a perceived cover-up. I think the NIH are bending over backwards to allow the WPI to prove they are right.

    You mention there are 3 published positive ME studies. Can I ask which the 3rd is, as I'm not aware of it?

  12. >@Ed

    I have a masters degree in neuroscience and I specialise in the action of neural networks and the formation of mental representations.

    Thank you for admitting Alter's position.

    You think that altering the design of a study after it has commenced is reasonable and that a multi laboratory study, funded by the NIH, should not test both tissue and blood in the two patient populations where the virus has been detected, even though blood is not the natural reservoir of the virus. That it should not be a replication of the proven methods and some of the failed. Why is it ok for the CDC to switch assays in the Blood working group? Why are they only looking at ME/cfs and not prostate cancer? Why are they not getting each lab to use the others methods? Science cannot proceed this way.

    If the NIH was bending over backwards, they would not have allowed their staff to produce a propaganda video on the claims of Coffin and Paprotka, or peppered the pages of the NIH with definitive statements about the origin of one variant. It undermines those studies you think are designed to be definitive when, neither in design or the obvious political intent, they are to be definitive. There are some very serious problems with the way Paprotka et al. came to the conclusion that one variant was created in a lab accident, but to suggest that no one subsequent to that was infected is putting people's lives at risk. We do have reports that lab techs are testing positive to that variant.

    Your figure of a 3rd of people meeting CCC is speculation. If the WPI only get the people without CCC, how does that equate with it disproving that those with CCC have HGRVs? You do understand the scientific method don't you?

    Those prostate cancer patients with HGRVs are not going to be cured by cancer treatment if they don't ever address the retrovirus, if that is indeed the cause. Be aware it is know that in humans it is producing an immune response and is, after all, a retrovirus of a type known to be highly pathogenic. Those calling for this to be lab contamination have never given any scientific evidence this is the cause of the results. It is really shocking distasteful that they are using their contacts and positions to beguile innocent patients and the wider public.

    The third positive paper is Grossberg et al., 1997. The JHK virus is a xenotropic polytropic.

    I wish too that this was all wrong. But that is not what the evidence shows and denial won't help those who are sick. We need to be moving on with the science and investigating pathogenesis. The focus should be on clinical trials, not this pantomime.

  13. >Muckle:

    Is this the study you mean? I don't see a reference to ME in the abstract.

    Res Virol. 1997 May-Jun;148(3):191-206.
    A human B-lymphoblastoid cell line constitutively producing Epstein-Barr herpesvirus and JHK retrovirus.
    Grossberg SE, Kushnaryov VM, Cashdollar LW, Raisch KP, Miller G, Sun HY.
    Department of Microbiology, Medical College of Wisconsin, Milwaukee 53226, USA.
    The human B-lymphoblastoid cell line, designated JHK-3, with pre-B-cell characteristics, chronically produces two viruses, Epstein-Barr virus (EBV) and JHK virus, an apparently novel retrovirus. The JHK-3 cells are much more productive of extracellular EBV than the high-producer marmoset line B95-8. The extracellular virus of the JHK-3 EBV strain is relatively fragile, more broadly dispersed in an ultracentrifuged sucrose gradient than the B95-8 EBV and more susceptible to disruption by combined treatment with urea and dithiothreitol. By restriction fragment length polymorphism analysis, the JHK-3 EBV strain resembles the EBV strain FF-41. The JHK-3 cells also produce an incompletely characterized, relatively fragile, enveloped, icosahedral RNA virus that contains Mn(++)-dependent reverse transcriptase. JHK virions measure 85 nm in ultrathin sections, much smaller than other Retroviridae. The JHK virus exhibits a distinctive morphogenesis, most nearly resembling C-type retroviruses. The JHK-3 cell line provides a human cell model for investigating virus/virus interactions and their pathogenetic affects on host cells which chronically and simultaneously produce DNA and RNA viruses.

    PMID: 9201810 [PubMed – indexed for MEDLINE]

  14. >@Muckle

    I'm sure that someone with your intelligence and education could make an equally, if not more convincing argument against XMRV, if it was something you wanted to believe. I'll leave it to the scientists whose jobs it is to work it out.

    The way I see it, ME/CFS is being given priority over prostate cancer to try to get an answer quicker, as to whether there is an association with XMRV. Firstly because of blood transfusion risks, secondly because pressure from patient groups is higher and thirdly because there are no effective existing treatments. If the Lipkin study is a wash out then I imagine the WPI and Dr Lo will hold their hands up that mistakes have been made. If it goes the other way, like you, I hope they commence clinical trials as soon as possible.

  15. >@Ed

    If you confine your arguments to the data there is no evidence of laboratory contamination. You are choosing to believe a select few who are presenting feelings on the topic as if they were data.

    I'm not sure on what basis you think ME/CFS is being given a priority on human gammas. The Lipkin study is not designed to further scientific understanding on the virus and again could not be scientific evidence of laboratory contamination. The BWG is to screen the blood supply with assays for blood, not tissue.

    What is needed is a replication study. That would provide scientific evidence.

  16. >Jamie, I have a question for you and Dr Snyderman.

    If you follow google alerts for rituximab,you will find out tht it is being tried for all kinds of diseases including of course cancer and lymphomas.

    I wonder what Dr Snyderman (being an oncologist) thinks of the use of Rituximab and B-Cell depletion as at least a palliative to our symptoms, is it something that could be used in multi-center clinical trial anytime soon for patients with ME? (Being a chemo nurse, I am aware of the potential side
    effects and risks of the drug and suspect that the benefits of the drug excedes the.risks).


  17. >If Rituximab brings relief for even a few months it is more supporting evidence that the cause is human gammas. What we don't know is the risks long term of killing a patients B-cells. With a potentially cancer causing retrovirus at the heart of it, we may only be exposing patients to a much worse payback later on.

  18. >I have a question for the people knowledgeable about viruses who read this board.

    A key question in this illness is why our hyper-reactivity to inflammatory stimuli (not just mold toxin, but also things like mercury and naphthalene) is so high.

    My own feeling is that it's not that it's wrong for my body to have an inflammatory reaction, but that it's wrong for the inflammatory reaction not to STOP.

    What I am wondering is whether it's possible that certain pathogens may interfere with the ability of the body to make or use specific anti-inflammatory cytokines that would stop this sort of reaction from continuing into infinity.

    Does this make any sense? Is there any evidence that would suggest that might be the case?

    Thank you very much for any thoughts you might be able to provide.


    Lisa Petrison, Ph.D.

    lisapetrison at yahoo

  19. >Inflammation, virsues, stress, can all activate human gammaretroviruses. The knock on affect will be more inflammation caused by the HGRVs producing a cytokine storm.

    Jamie wrote an article on this in March:


    This paper specifically deals with some of this:

    NF-B Activation Stimulates Transcription and Replication of Retrovirus XMRV in Human B-Lineage and Prostate Carcinoma Cells

    "…suggesting that inflammation, EBV infection, and other conditions leading to NF-B activation may promote XMRV spread in humans."

  20. >Yes, of course, I do know that about inflammation causing the spread of XMRV.

    What I'd like to understand is the other component of the phenomenon — why the reactivity to inflammation-producing toxins in this disease is so high.

    For instance, when I was at my more reactive, the amount of mold that would stick to my hair and clothing after a 30-second visit to a moldy building would be enough to make me keep spiraling down into severe illness (unless I took a shower and changed clothes, in which case I would quickly recover to near 100% wellness).

    This is abnormal, of course.

    What is it about being infected with a retrovirus that would make this happen?

    Taking antivirals and antibiotics has decreased this reactivity somewhat, for me and for others. So clearly it's being driven by pathogens.

    What are some plausible mechanisms for what might make it happen? The idea that the viruses cause some anti-inflammatory cytokine to not be present is the most consistent with my experience of the phenomenon, but I don't know if viruses could do that.

    If we could figure out the mechanism, maybe there would be ways to fix it.

    Thanks for your response.

    Best, Lisa

  21. >Dear Kati,

    I am not in favor of using rituximab. The MLVs can and probably do infect many types of cells: epithelial cells, microglial cells, T-cells as well as B-cells. Temporarily depleting B-cells would have no beneficial effect on these other and potentially just as important areas of infection. In oncology rituximab by itself rarely has significant or long lasting value as a single agent against lymphoid malignancies.

    In addition rituximab is very immunosuppressive and that doesn't sound like a good thing to me when we are fighting a viral infection. As you know, patients who take rituximab have an increased risk of various life-threatening infections.

    I have decided that I will not take rituximab for myself.

    Michael Snyderman

  22. >@Lisa

    Having ME means that you have high levels of proinflammatory cytokines. These cause many of your symptoms. Environmental toxins, such as mould, will further raise cytokine levels even higher, making your symptoms worse.

    If you apply this to the retroviral hypothesis, it is easy to see how this can get out of control. Because the toxins raising you cytokines will activate the virus and which in turn will increase your inflammation.

    Every assault which can active the virus can further increase the levels of the virus and the cytokine level. Thus, each assault will make you much sicker, unless you can prevent these everyday assaults, which is going to be very difficult. You would also still be left with the damage the virus has already caused.

  23. >Muckle –

    Everything you say is how I'm thinking about the topic. There's just one more weirdness that I don't get.

    At some points, when I was first moving toward recovery, I didn't feel 100% well even in super-good places. I felt a lot better than when I was living in the moldy house, but certainly not normal ever. This seems totally consistent with what you're saying — I was sick from "within," all the time, and adding inflammatory environmental toxin mades things worse.

    Now, if I'm in a super-good place, I do feel 100% normal. Like I've never been sick at all.

    The problem is that just a tiny bit of exposure to inflammatory toxin can make me totally sick again. I'm talking — the amount of toxin on an item that's been in a really bad place for a short period of time, and then washed.

    This is ridiculous.

    I'm thinking this absurd level of reactivity must be caused by the retrovirus. But what exactly is it that a retrovirus does to my body (in terms of the mechanism) to make me feel great unless I'm in contact with such a tiny amount of that sort of toxin — at which point I go back to having classic ME/CFS again?

    I don't think it's due to XMRV multiplying, because it happens too fast (within minutes). How soon after getting an inflammatory hit do you think that XMRV could multiply/activate enough to have a bigger effect?

    Thanks very much for putting some thought into this. I really appreciate it. :)

    Best, Lisa

  24. >@Lisa.

    It will probably be the damage already caused. In simplest terms everything will be functioning on the edge of where it should. A small change will tip you over. At that point it is not the virus directly, but the result of the virus having already caused damage to your body.

  25. >@Michael Snyderman, thank you for your answer.

    Somehow I think that in the currentmXMRV climate we're in, it would be easier to convice a physician to prescribe Rituximab (and get it administered, of course) than to pres rie antiretrovirals.

    i am not scared of trying the most cytotoxic treatments, I would be ready to be a guinea pig. However physicians here don't test for NK cells, do not do viral titers, and are not open to anything that is out of the box. I wonder how long it will be before it changes, whether this is measurable in months, in years or decades.

    The pecking order in the medicine world usually makes it that patients' suggestions are the least accepted. You can't tell them what to do.(You can only say yes or no to their suggestions) For most of them anyways.

    thank you again. I will keep on tying because there is nothing else to do…

  26. >Muckle –

    So in theory, if medical scientists were going to put resources into addressing that damage, what direction would they be taking?

    I guess this is where stem cells come in, for instance?

    Cheney's experiments with stem cells do not seem to have been particularly successful, but that may be because most of those folks are living in such bad environments that their bodes weren't able to use them effectively.

    It would be interesting to talk to someone who has had a good experience with stem cells, in an in-depth way. If anyone reading this fits that description, would you please consider getting in touch with me? I'd like to interview you for the project I'm working on (with Dr. Keith Berndtson), about people with severe ME/CFS who have gotten to "mostly recovered" status in whatever ways.

    I wonder what other ways there might be to repair the damage?

    Thanks much for your thoughts.

    Best, Lisa

  27. >I posted on the wrong blog entry. I meant to post here.

    Maybe there's a primary ongoing viral insult in some cases. Maybe there are retroviruses of murky animal origin, strains, different species, with odd and curious and occasionally bad consequences in humans. Maybe virii are implicated but not causal in some. Other pathogens, toxic insults, epigeneics, toxic mold, etc etc.

    All are possibilities.

    Any instantaneous response that is extreme, is neurological. In such case a thorough read of everything by Ramachandran is useful:


    Sometimes the brain needs to be retrained. Jamie used to use EEG neurofeedback especially to help epileptics reduce seizures. If one could train oneself into a deeply relaxed state and learn to reach that almost instantly through neurofeedack…one might then expose oneself to the noxious item while being measured on EEG, see what goes kaflooey, and see if brain retraining can overcome it.

    A lot of work, but might be useful.

    Jill Neimark

  28. >Hi Jill,

    Thanks for mentioning neurofeedback, or EEG biofeedback. I definitely think there is a place for biofeedback in the treatment of ME/CFS. Unfortunately, as a treatment modality, neurofeedback is extremely system and operator dependent. I've been planning to write about it for some time, and will do so in the near future. Too much for a comment. Also, there are lots of oxygen questions. I'll try to answer those soon too.


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