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The Gupta Program and XMRV: discussion

Discussion in 'XMRV Testing, Treatment and Transmission' started by gracenote, Oct 30, 2009.

  1. gracenote

    gracenote All shall be well . . .

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    Gupta has distributed a statement on XMRV and his program (October 29, 2009). I would love to open this up for discussion / comment from anyone who cares to venture into these waters.

    I have not tried this program but I know some of you have.

    Below is the full text of his email communication with permission to repost and forward. (I'm sorry I couldn't find a web link to this.)

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    HOW XMRV RETROVIRUS FINDINGS MAY FIT WITH THE AMYGDALA HYPERAROUSAL MODEL FOR ME/CFS (draft)

    Background

    Recently scientists from the Whittemore Peterson Institute (WPI) led by Dr Mikovits, claim to have discovered a retroviral link to ME/CFS (1). This pioneering research has identified a retrovirus called XMRV, shown to be active in two-thirds of patients (published), and antibodies for the virus were present in 95% of patient (unpublished research). The samples were taken from outbreaks of ME/CFS in the 80s and 90s.

    Mikovits' team said further research must now determine whether XMRV directly causes CFS, is just a passenger virus in the suppressed immune systems of sufferers, or a pathogen that acts in concert with other viruses that have been implicated in the disorder by previous research.

    The purpose of this paper is to hypothesise how these findings may fit with the Amygdala Hyperarousal Model for ME/CFS (2).

    Three Potential Hypotheses

    Overall there are three broad hypotheses that we can infer from the findings so far, as per Mikovits statement:

    1. The XMRV virus directly causes the symptoms of ME/CFS
    2. The XMRV virus indirectly causes ME/CFS by suppressing the immune system in concert with other pathogens, allowing opportunistic viral and bacterial infections to flourish causing the symptoms of ME/CFS
    3. The XMRV virus is simply a passive opportunistic infection which establishes itself due to general suppression and dysfunction of the immune system from another source. (This general immune dysfunction may be caused by autonomic dysfunction as a result of amygdala hyperarousal).

    Evaluation

    There are two broad aspects to the immune system, TH1 and TH2. TH1 involves Natural Killer (NK) cells whose job it is to identify and destroy viruses. The TH2 side of the immune system involves, amongst other things, antibodies which respond to threats. There is evidence in the literature that patients with ME/CFS are TH2 biased, i.e. the TH2 aspect of the immune system is over-activated, causing suppression of the TH1 side and high levels of inflammatory cytokines; patients have lower Natural Killer (NK) cell immunity. This bias may mean that opportunistic viruses and bacterial infections can no longer be kept at bay effectively by the TH1 side of the system.

    RNase L conducts a function of holding the virus at bay until NK cells are available to eradicate the pathogen, however even the RNase Ls ability to perform this function can be compromised over time if TH2 dominates for too long. RNase L dysfunction was also reported in the prostate cancer cases of XMRV, although later research has not found a genetic link. In ME/CFS, any suspected Rnase L deficiency many simply be due to chronic TH2 dominance. If TH2 dominates for too long, it can be hypothesised that viruses such as HHV-6, Epstein Barr Virus (EBV), CMV and Parvovirus B19 can flourish, as well as bacterial infections such as mycoplasma and chlamydia pneumonia.

    It has been established that the majority of neurodegenerative disease, fatiguing illnesses and neurobehavioral disease patients have chronic bacterial and viral infections. (3). In fact the WPI research claimed to have found higher levels of XMRA in atypical MS and Autism.

    The XMRV virus may simply represent one of many viral and bacterial infections present in the blood of ME/CFS patients, and that many of these previous infections (including EBV) had been previously prematurely suspected as the root cause of ME/CFS. There have been many previous studies which have shown similar results to those found for XMRV. As an example, a 2002 study found that out of 261 patients with ME/CFS, 68.6% of patients had active mycoplasma bacterial infection present compared to 5.6% of controls, a similar result to that found for XMRV (4). A 2003 study found that 30.5% of CFS patients had active HHV-6 virus present, but only 9% of controls (5). For Chlamydia pneumoniae it was 7.8% of CFS patients compared to 1% of controls (5). For Parvovirus B19, it was detected in 40% of CFS patients but only 15% of controls (6).

    What was interesting in the 2003 (5) study was that having one particular infection did not predict the likelihood of having another infection. This may indicate that the infections themselves are not cumulatively affecting the strength of the immune system to fight off opportunistic infections, but that a general immune deficiency is allowing particular types of infections to establish themselves in a pattern unique to each patient.

    According to the WPI research, 4% of healthy controls had active XMRV virus in their blood (versus 67% of ME/CFS patients), which is similar to the levels of active mycoplasma infection in healthy controls. Therefore presence of active XMRV does not necessarily predict ME/CFS, and would not support the first hypothesis. If 4% of the US population were found to have active XMRV pathogen in their blood, this would amount to over 10 million people. Yet there is no evidence that XMRV causes cancer where it is active, or that it has any effect on health. It is merely a suspected link in 23% of prostate cancer cases where it is found in 1% of surrounding tissue, with no causal link established at this stage; one hypothesis is that its presence is simply linked to immune deficiency. Once again, the XMRV virus was found in 6% of benign biopsies showing that its presence may be widespread in the general USA population. Further research however is critical.

    It may be that XMRV may be a localised virus to the USA, especially since a recent report from Germany (7) found that out of 589 biopsies carried out on prostate cancer cases, not a single patient showed any evidence of XMRV. They conclude that One possible reason for this could be a geographically restricted incidence of XMRV infections. (7) The WPI research was carried out on documented ME/CFS outbreaks which represent a very small percentage of ME/CFS cases.

    If 95% of ME/CFS patients show antibodies to XMRV (yet unpublished data from Mikovits team), yet only 67% show active virus, this could indicate that a third of ME/CFS patients no longer had the active XMRV virus, yet still were suffering from ME/CFS. If this is confirmed to be true, then the first hypothesis would seem redundant, and XMRV could only be the root cause of ME/CFS if the second hypothesis were correct, i.e. that XMRV had adversely affected the long term performance of the immune system. Alternatively the presence of antibodies could imply that the virus is still active in more that 67% of patients, but had not been picked up through previous methods. It would also be interesting to know the percentage of healthy controls that tested positive for XMRV antibodies which has not been revealed.

    One way the link within the second hypothesis could be established, is to test whether the presence of active XMRV predicted higher levels of other opportunistic viruses and bacterial infections. According to the second hypothesis, presence of active XMRV should predict suppression of the immune system and further opportunistic pathogens. However, as previously mentioned, there is little evidence that having one opportunistic pathogen in ME/CFS predicts the likelihood of having another, therefore cumulative immune deficiency caused by XMRV attack is unlikely, otherwise previous studies would have highlighted this finding in the blood of ME/CFS patients. This once again seems to tentatively support the third hypothesis, in that XMRV may simply be a passive opportunistic virus similar to other herpes viruses such as HHV-6 and EBV. Even if presence of XMRV did predict the likelihood of secondary infection, it would still be difficult to infer causality.

    The Amygdala Hyperarousal Model and XMRV

    The Amygdala Hyperarousal model states that ME/CFS and Fibromyalgia may be caused by a conditioned trauma in the amygdala following an acute viral, bacterial or physical insult, combined with psycho-social distress. Once the classical and operant conditioning has occurred, the amygdala in association with the insula, become hyper-sensitive to signals from both the body and external stimuli, and magnify both the extent and frequency of the incoming stimuli in the sensory thalamus and cortex. This then produces the ME/CFS vicious circle, where an unconscious sensitivity reaction to symptoms causes chronic stimulation of the HPA axis, immune reactivation/dysfunction, chronic sympathetic stimulation leading to autonomic dysfunction, mental and physical exhaustion, allergies, compromised detoxification, mitochondria dysfunction, oxidative stress and a host of other distressing symptoms and secondary complications. And these are exactly the symptoms that the amygdala, the insula, a
    nd associated limbic structures are trained to monitor and respond to, perpetuating a vicious circle.

    The Amygdala model predicts that there is likely to be TH2 dominance over TH1 due to overstimulation of the sympathetic nervous system. This has already been extensively documented in many studies of sympathetic overactivity due to acute stress and anxiety (8, 9, 10). Although an ME/CFS patient may not necessarily mentally experience acute stress or anxiety, the model predicts that the physiological aspects of the stress response are chronically engaged, thereby causing disruption in various systems of the body including the immune system. TH2 will dominate over TH1, causing a likely increase in opportunistic viral and bacterial pathogens such as XMRV, as well as an increase in allergic responses due to TH2 over-sensitivity, as well as increased propensity to produce antibodies. There is extensive evidence of increased chemical and physical sensitivities in patients. The parasympathetic system is suppressed, compromising digestive and detoxifying processes in the body.

    Once the sympathetic autonomic system is conditioned to be chronically activated, it is very difficult for autonomic and Th1/Th2 balance to be restored. Opportunistic viruses and bacterial infections flourish, in themselves causing further symptoms in addition to the ones caused directly by amygdala hyperarousal.

    In the field of Psychoneuroimmunology, many studies have shown that excessive sympathetic activity can have an immuno-suppressive effect on the body via Neuropeptide Y release, thereby pointing to another pathway by which excessive sympathetic stimulation may compromise immune function. A study by Fletcher et al (11) seems to model this effect in ME/CFS patients. ME/CFS patients tend to show low natural killer cell cytotoxicity, (NKCC), and it is known that Neuropeptide Y (NPY) suppresses NKCC. NPY is concentrated in the sympathetic nerve endings, and following stress, is released together with adrenaline and noradrenalin. Fletcher et als study tested the hypothesis that elevation of NPY occurs in ME/CFS and that the elevation of NPY is associated with severity of clinical symptoms. They found that NPY was significantly associated with severity of clinical symptoms, and that NPY could be a potential bio-marker for ME/CFS. This shows a direct link between levels of symptoms
    , and sympathetic overactivity where the most likely culprit is amygdala hyperarousal.

    The WPI team are working on the hypothesis that many of the symptoms of ME/CFS may be caused by XMRV attacking the cells of the immune system, thereby compromising immunity. However, there is potentially another culprit for reduced immunity as discussed: chronic sympathetic activity. This has already been shown to suppress general immunity and especially TH1 function, whilst at the same time causing TH2 dominance, inappropriately stimulating allergic responses in the immune system. (8,9,10)

    There is a possibility that XMRV somehow directly affects TH1 function, and simultaneously directly affects the autonomic nervous system, however there is no evidence of this and further research is required.

    What is most interesting about the XMRV announcement is that the team also found higher levels of XMRV in people with Autism and atypical Multiple Sclerosis (as yet unpublished). A study by Nicholson et al (12) looked at the presence of co-infections in ME/CFS patients versus patients with Autism Spectrum Disorders. The study found that both groups had higher incidence of multiple, systemic bacterial and viral infections compared to controls, but interestingly, both ME/CFS and Autism patients had very similar levels of active infections when compared to one another. Autism is a disorder where sustained amygdala hyperarousal is accepted as a model for partly explaining the disorder (13), so once again there is tentative support for the amygdalas role in ME/CFS.

    This is a very important finding because of the differences and commonalities between ME/CFS and Autism. We would not necessarily expect any commonalities with respect to infections as the conditions seem to have a very different neurobiological basis. However, the common factor may be sustained amygdala hyperarousal, but due to very different causes. The sustained amygdala hyperarousal in Autism may develop in early childhood due to socio-biological reasons, whereas sustained amygdala hyperarousal in ME/CFS may develop as a result of several co-curring acute factors triggering a conditioned trauma in the amygdala later in life. Both conditions then result in a unique pattern of chronic sympathetic stimulation, but for very different reasons, causing similar levels and types of opportunistic viral and bacterial infections. It is likely that the level of hyperarousal in ME/CFS is much more severe and dwarfs that of Autism, but both conditions exhibit enough of a chronic long t
    erm sympathetic response to result in opportunistic infections.

    Several recent studies have reported abnormalities in amygdala volume in Autism. (14,15). Furthermore, most studies in Autism show abnormal processing by the brain and the amygdala in response to emotional stimuli, and continual background amygdala hyperarousal is once again suspected (13). Further research is required to test any abnormalities in the function of the amygdala in patients with ME/CFS, which may not show up on standard brain scans. It would be interesting to understand the levels of active XMRV virus and antibodies in Autism.

    Finally there are a host of physical changes in the brains and bodies of ME/CFS patients which have been well documented and which are consistent with the concept of chronic autonomic dysfunction. These findings cannot be ignored as a result of the XMRV announcement, but need to fit within an integrated hypothesis.

    There are many patients who do recover from ME/CFS and Fibromyalgia over time, and yet may not have taken any kind of anti-viral medication. This may indicate that changes that a patient themselves initiate, may be enough to strengthen the immune system, bring the body back to homeostasis, and eradicate opportunistic infections such as the suspected XMRV.

    How Amygdala Retraining Might Reduce XMRV and other Opportunistic Pathogen Levels

    Amygdala retraining aims to reduce the stimulation of the sympathetic nervous system by creating a projecting neurone from the prefrontal cortex to the amygdala to control its over-zealous reactions. This in turn would reduce the sympathetic overload, allowing TH1/Th2 ratios to gradually return to normal, allowing the bodys own immune system to fight off opportunistic infections such as the suspected XMRV. Symptoms from amygdala hyperarousal (including changes in the brain), and symptoms from opportunistic infections would then subside, as well as any allergic effects of TH2 dominance.

    Amygdala retraining aims to bring homeostasis back to the body after a period of imbalance, where the balance between the sympathetic and parasympathetic systems returns to normal, as does the TH1/TH2 balance.

    Conclusion

    The WPI findings are indeed a step forward in ME/CFS research, and are significant findings. However, further research is required to validate the idea that XMRV is a contributing factor in the pathogenesis of ME/CFS, versus being simply another passive co-curring infection such as mycoplasma, HHV-6 and EBV.

    Amygdala retraining aims to reduce the levels of opportunistic infections such as the suspected XMRV virus by strengthening the immune system through balancing the TH1/TH2 ratio and bringing the body back to homeostasis.

    Future Research
    Further research is required to answer the following questions:
    - What was the percentage of healthy controls that tested positive for XMRV antibodies? (The 3.7% figure seems to be referring to the percentage of healthy controls which tested positive for XRMV virus DNA rather than antibodies in unpublished research)
    - What percentage of people with Autism display evidence of active virus or antibodies?
    - What percentage of patients with other neurodegenerative disease, fatiguing illnesses and neurobehavioral disease show evidence of XMRV?
    - Can the studies be replicated effectively across the ME/CFS population?
    - Can the studies be replicated in different parts of the world?
    - Why are controls which have active XMRV not displaying obvious pathology?

    References

    (1) Mikovits JA et al. Detection of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome. Science. 2009 Oct 8
    (2) Gupta, A. Unconscious Amygdalar Fear Conditioning in a Subset of Chronic Fatigue Syndrome Patients. Medical Hypotheses Volume 59, Issue 6, 12 November 2002, Pages 727-735
    (3) Nicolson, G.L. Chronic Infections in Neurodegenerative and Neurobehavioral Diseases. Lab Medicine 2008; 39 (5): 291-299
    (4) Nijs J et al. High prevalence of Mycoplasma infections among European chronic fatigue syndrome patients. Examination of four Mycoplasma species in blood of chronic fatigue syndrome patients. FEMS Immunol Med Microbiol. 2002 Nov 15;34(3):209-14
    (5) Nicolson GL et al. Multiple co-infections (Mycoplasma, Chlamydia, human herpes virus-6) in blood of chronic fatigue syndrome patients: association with signs and symptoms. APMIS. 2003 May;111(5):557-66.
    (6) Frmont M et al. Detection of herpesviruses and parvovirus B19 in gastric and intestinal mucosa of chronic fatigue syndrome patients. In Vivo. 2009 Mar-Apr;23(2):209-13
    (7) Hohn 0 et al. Lack of evidence for xenotropic murine leukemia virus-related virus (XMRV) in German prostate cancer patients. Retrovirology. 2009 Oct 16;6(1):92. [Epub ahead of print]
    (8) Hashizume H et al. Anxiety accelerates T-helper 2-tilted immune responses in patients with atopic dermatitis. Br J Dermatol. 2005 Jun;152(6):1161-4
    (9) Ermolao A et al. Relationship between stress hormones and immune response during high altitude exposure in women. J Endocrinol Invest. 2009 May 21. [Epub ahead of print]
    (10) Hglund CO et al. Changes in immune regulation in response to examination stress in atopic and healthy individuals. Clin Exp Allergy. 2006 Aug;36(8):969-71.
    (11) Fletcher AM et al. Neuropeptide Y (NPY): Correlates with Symptom Severity in Chronic Fatigue Syndrome. Abstract of presentation to IACFS/ME Conference, Mar 2009, Reno, Nevada
    (12) Nicolson G. et al. (2009) Similarities of CFS and Autism Spectrum Disorders: Comparison of Blood Co-Infections. (Source: Abstract of presentation to IACFS/ME Conference, Mar 2009, Reno, Nevada. By Nicolson GL, Nicolson NL, Haier J. The Institute for Molecular Medicine, Huntington Beach, California, USA; Department of Surgery, University Hospital, Munster, Germany.
    (13) Kleinhans NM et al. Reduced neural habituation in the amygdala and social impairments in autism spectrum disorders. Am J Psychiatry. 2009 Apr;166(4):467-75
    (14) Schumann CM et al. Amygdala Enlargement in Toddlers with Autism Related to Severity of Social and Communication Impairments. Biol Psychiatry. 2009 Sep 1 [Epub ahead of print]
    (15) Mosconi MW et al. Longitudinal study of amygdala volume and joint attention in 2- to 4-year-old children with autism. Arch Gen Psychiatry. 2009 May;66(5):509-16.

    Gupta Programme

    No.1 Harley Street
    London, Greater London
    W1G 9QD
    GB
  2. Advocate

    Advocate Senior Member

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    I'm reposting my previous message, which didn't show up.

    I just wanted to say that I believe Gupta's statement is full of misinformation.
  3. susan

    susan Senior Member

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    Because I personally know 2 people recover from being bed bound from his programme, I take on board his view of the disease too, along with others.
  4. zoe.a.m.

    zoe.a.m. Senior Member

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    I received this by email

    I don't doubt that many are improving using his program, though at last count, I had not heard of anyone--even after a couple of years--getting past the hallmark symptom: post-exertional fatigue.

    Again, as with a few CFS docs/experts with protocols, cures, programs, I don't care for their statement that retroviruses are as ubiquitous (sorry for hauling out the Reeves' terminology!) as viruses. They function in very different ways.

    I have no doubt that CFS/ME is about impaired immune function, but Ashok goes a bit far in how he relates everything back to the amygdala theory. I really felt like this statement was a stretch to pull all of the new research in under his umbrella. It simply didn't resonate as truthful to me.

    For the record, I wish programs like his were available for the treatment of all chronic illnesses! I don't see/hear evidence that it is a cure. I consider it detrimental for CFS/ME to be the one biological illness for which there is no medical treatment offered along with a program such as this one. Because Ashok promotes/markets this as a cure, I feel it needs to be held to that standard.

    I also believe he's misrepresenting psychoneuroimmunology to some degree in that he seems to suggest it is the pathogenesis. I noticed his list of references is psychiatry based. This isn't totally unexpected as autism is considered a developmental/psychology/psychiatry issue, but it hardly speaks to more recent research (which was around long before the WPI's).
  5. Alice Band

    Alice Band PWME - ME by Ramsay

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    The whole things is barking mad

    I've written detailed critiques of him before and this is no different

    The only people I know who have benefited from his help have been those with "Reeves disease"
  6. August59

    August59 Daughters High School Graduation

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    He is desperate. I can only imagine the limited amount of sales he had are now even smaller with this discovery and it is taking a lot of bread off of his table. I'm not knocking his treatment because I can see it being a very good therapy, but not a cure.
  7. lebowski

    lebowski

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    what about aids

    he only needs to say that "antiretrovirals can turn th1/th2 balance " to add AİDS to his amygdala theory ..

    antiretrovirals decrease neuropeptide-y this normalise th1/th2 and u dont have aids anymore therefore ur hiv load is down ..

    a bad event 30 years ago made ur whole body have a shock like reaction 15 years ago and it couldnt find its balance still after 15 years ..

    xmrv xand theory does not have a proof yet but strong evidence to its case .. but this theory is totally fiction .. y is it more valuable than the ufo abduction theory i cant understand ..
  8. Snowcat

    Snowcat

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    Advocate or Alice, can you say more about - or point to - your criticisms of him? This is the first I've seen of this theory.

    Thanks.
  9. usedtobeperkytina

    usedtobeperkytina Senior Member

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    first

    This is my first post. You may know me from another forum.

    I think somehow central nervous system is part of the dysfunction that is in our disease. The question is whether the XMRV can cause a central nervous system dysfunction (including over-stimulated sympathetic system) or if the central nervous system sets the stage for XMRV to do more damage to us than those with the virus that don't get sick. (Not assuming that the 4% won't later get sick.)

    I know I showed the hypotension problems as young as five. A time of sudden stress and my blood pressure would drop. I would faint and often have a seizure in the middle of my faint.

    But I didn't get CFS until I was 40. That would lead me to believe my central nervous system problem predates the XMRV.

    But, could the virus have been there the whole time, waiting for androgens and cortisol to "turn it on" as I was under tremendous stress and was in perimenopause?

    Mikovitz connects XMRV activity to cortisol and androgens turning it on.

    So I don't know. I do know that it is too early to draw definite conclusions.

    I do agree though, the central nervous system must fit into this. But that does not exclude XMRV being the main cause.

    Tina
  10. kurt

    kurt Senior Member

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    almost a brilliant paper, keep trying Ashok

    Nice reasoning Tina, I agree completely. Gupta's hypothesis may or may not be correct but his treatments help many people. That is data that can not be ignored. The idea that we have some type of CNS dysfunction would help explain why Gupta's interventions work for many people with CFS.

    As for your question, whether XMRV can cause CNS dysfunction, I believe the answer is a resounding YES IT CAN. I am studying XMRV and its effects, and found a research study that shows that one of the areas of DNA that this retrovirus disrupts is a communication mechanism used in neuroendocrine cells. These are critical cells in the sympathetic nervous system, they are the 'middle-man' between neural signals and hormonal release. There are other effects of XMRV, many people are focusing on the immune problems it may cause, but this neuroendocrine problem really caught my eye, and it lines up perfectly with Gupta. He should have done more homework before writing this article, because he almost made a brilliant connection... someone will in time I think figure this out. More is coming...

    --Kurt
  11. zoe.a.m.

    zoe.a.m. Senior Member

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    I look forward to hearing more about your research Kurt. Is any of this information pertaining to the neuroendocrine disruption available to the public? You mention a study; can you point me in the right direction? Thanks!
  12. myco

    myco Guest

    I wonder how many have "recovered" with Gupta's program. I ordered the DVD last year while I was in the middle of antibiotic therapy. I have since recovered my "post exertional fatigue" with antibiotics for Borrelia, Babesia, Mycoplasma, and Bartonella, so I can say that I fortunately never got a chance to watch his series. Oh well, at least I'm back in the gym.
  13. zoe.a.m.

    zoe.a.m. Senior Member

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    question for Myco

    Not the best place to post this question, but how were tested for Borrelia, Babesia, Mycoplasma and Bartonella? I'd really appreciate any insights you've got. How far into your illness were you when you received treatment?

    I envy you the gym!!
  14. myco

    myco Guest

    I won't hijack this thread but you can read more about my illness on the Lyme/XMRV thread. I was a few years in before I received treatment. But I did have some minor symptoms since 95' to give you an idea.
  15. Zona

    Zona

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    Don't Throw out the baby...

    In my case I have no question about CNS. I had pesticide poisoning (first dx)
    which affects the CNS. My son also has CFS. He didn't develop CFS until he was 16, which has nine years after we were exposed to the pesticide. However, I was exposed more than the rest of the family, including him. He and I are the only ones who have CFS. Why didn't they get it, or why did he? IMHO it has partly to do with the fact that he had a wierd virus a year after the pesticide incidents which the other kids didn't get and shortly there after I did too (though I believe they were different viruses, if indeed they were viruses at all). He as about seven at the time. Somehow I believe that was part of the setup for him getting CFS/FM later.

    As i have said before in this forum, I've been ill for 30 yrs now. I have a friend who's had CFS/FM for 28 years too. She is Dr Lapp, was Dr Cheney's patient. We've watched all kinds of theories and findings come and go and she's run the gamit of treatments from natural ones to being an antiviral guinea pig. While neither of us see Gupta as the end all cure we both see that it could well be one of the long missing peices and worth investigating. It makes sense.

    And as another friend says "Don't throw the baby out with the bath!"...
  16. dannybex

    dannybex Senior Member

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    I agree...

    XMRV may play a huge role, but other co-factors (which are different in everyone) also have to be considered...which is why this disease is so difficult to recover from. Pesticide, mold exposure, heavy metals, etc., probably all have to be addressed, XMRV or not.

    Note that the Whittemore's daughter got sick when she was 11-12, saw many doctors, didn't improve until she started homeopathy, felt well enough to enroll in the university, but then relapsed severely after vaccinations. Was there XMRV in the vaccinations, or mercury?

    Of course, I don't know.

    But regarding XMRV, Gupta's theory may help explain part of the puzzle. Mikovitz said that one of the three things that "turns on" the retrovirus, is STRESS hormones.

    If we can work on lowering those by whatever means, then perhaps it will help some people.

    d.

    p.s. I do know one person who was sick for about 12 years or maybe more, who had both PEM and could not sit up in a chair for more than 10 minutes or so without passing out (can't remember the name of that dysfunction). She went to all the top docs, tried a multitude of treatments, but it wasn't until 2 1/2 years ago when she slowly started doing Eden's "Energy Medicine" exercises -- which she started in bed because she was so disabled -- and then Gupta's CD's -- that she finally recovered to about 70%.
  17. kurt

    kurt Senior Member

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    Hi Zoe, I can point to one study, but also this is a conclusion I am drawing from everything I am learning about XMRV and how it works in prostate cancer. Much prostate cancer research implicates the neuroendocrine cells in the prostate. A 'smoking gun' article in a neuroendocrine view of XMRV may be the following:

    http://jvi.asm.org/cgi/content/full/82/20/9964

    Title: "Integration Site Preference of Xenotropic Murine Leukemia Virus-Related Virus, a New Human Retrovirus Associated with Prostate Cancer"

    This article discusses the DNA insertion point of XMRV, and it concludes with the following (from the abstract) "These results are consistent with a model in which XMRV may contribute to tumorigenicity via a paracrine mechanism."

    Paracrine mechanisms are communication mechanisms between neighbor cells within an organ or gland. The prostate has neuroendocrine cells in it, cells that receive (or send) a signal from (or to) the nervous system and then as a result release (or receive) hormones or other substances. So in that way it is similar to other systems in the body that contain neuroendocrine cells, such as the adrenals and pituitary. Anyway, according to this study, in prostate cancer the paracrine (communication) mechanism of those neuroendocrine cells appears to be disrupted by XMRV. Basically the retrovirus blasts away the paracrine coding area of the cell's DNA when it infects. So the cell loses some inter-organ communication capacity. In other words, if I am interpreting this correctly, the XMRV infected neuroendocrine cell becomes blind to its neighbor neuroendocrine cells. In prostate cancer this causes eventual loss of functions for the neuroendocrine cells. Obviously in CFS the effect is a bit different, the virus is affecting other cells somewhere else in the body. But this XMRV coding to disrupt the paracrine mechanism would be maintained in CFS.

    This leads to the possibility that XMRV may be affecting neuroendocrine cells in other systems in CFS, perhaps also damaging their paracrine mechanism DNA.

    At one time I was seeing an Endocrinologist for my CFS, and his tests showing off-cycle cortisol spikes (typical for Stage I CFS) led him to the conclusion that I had a cortisol-producing tumor. A full body scan revealed no tumors, but maybe he actually had discovered a viral-damaged paracrine mechanism in my adrenals causing dysregulation. I hope the serious researchers are pursuing this type of reasoning and are studying the prostate cancer mechanism and its links to CFS.

    --Kurt
  18. zoe.a.m.

    zoe.a.m. Senior Member

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    Thank you Kurt

    I apologize up front for asking any questions whose answers might seem obvious to you given that you obviously have a background in these matters.

    First, the XMRV associated with CFS is not the same virus as the prostate cancer XMRV if I understood Dr. Peterson's speech on the Whittemore Peterson Institute's study. I'm not sure that this matters all that much, other than certainly the 2 types might likely express themselves differently to some degree. I don't doubt that whatever CFS is, it's linked entirely to cellular communication. Your explanation did leave me wondering about what exactly it means to the body for, say, the adrenals to become dysregulated as a result of XMRV. Certainly I would think that the adrenals would link in to the entire HPA axis and more, and at that point, the hormonal and glandular systems might dysregulate in a way that is comparable to how cells become cancerous (i.e. toll receptor malfunction). In this context, I fully believe that XMRV can explain what has so far seemed, to many clinicians, to be a mass of unrelated symptoms. I can't say that I understand the full complexity of retroviruses (specifically), but I don't see the other system abnormalities as difficult to relate to a retrovirus.

    The real question remains (other than how/does XMRV play a large part in CFS) is how best to treat the damage done to these mechanisms if the virus has already created the damage and can't be controlled in every person with current/new meds?

    I think you are lucky to have seen an endocrinologist who would look so deeply into your CFS. This seems to be very unusual! In what way were your cortisol levels measured? I am in complete agreement that we can only hope that researchers are looking very closely at the implications of the mechanisms you describe. Sometimes the subtleties are lost, but I hope that will not be the case.

    But to bring this back to Gupta for a second; do you see Gupta's program as being a cure (or as close as one might get) for this type of dysregulation? I wrote to him with some questions about how his program addressed the pathophysiology of CFS as I disagree with his statement that CFS does not cause "organic changes" in patients but still praising his overall concept and work; unfortunately, the response I received was a general response to all "skeptics." I find this unsatisfying as CFS patients do appear to suffer very real organic changes that shorten their lifespan significantly.

    I have a great deal of respect for mindfulness as it relates to working with illness, but I don't feel confident that it is stronger than a retrovirus (or something similarly 'real'). As with cancer where imagery and guided meditation can be helpful, certainly many positive, upbeat and mindful patients cannot beat the cancer. So, while attitude and modifying automatic reactions are important, they are not indicative of who will defeat disease. It's far more complex. I couldn't really tell from your post if you are excited that Gupta is making some of these connections in his paper, or if you think his program is the best treatment for these problems.

    Thanks for your response!
  19. kurt

    kurt Senior Member

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    Good questions Zoe, if I have any insights they are from corresponding with retroviral researchers and even they are only one half step ahead, there is still a lot of data to uncover.

    OK, first, the Peterson comment, if you read the 'supporting online material' from the Science article, you will find out that in an 8,000 base genome there are only a handful of differences between the WPI XMRV and the prostate cancer XMRV, and those differences are in areas that typically vary anyway, so for most practical purposes they are the same.

    As far as the neuroendocrine dysregulation from XMRV, that was a hypothesis on my part based on the study I cited, which suggests an inter-cellular communication mechanism is broken by XMRV. Basically the neuroendocrine cells still can communicate with the brain and produce hormones, but they no longer can 'text' each other. So you don't have any more 'flash mob' effects. I don't know another good way to explain this, sorry if the cell phone analogy does not work. Anyway, the result would be imbalances between signals and responses in the neuroendocrine system, and the hypothalamus and amygdala must try to make sense out of the mixed-up hormone chemistry that would result.

    I have not read anything suggesting the retrovirus could be blocking neuroendocrine cell androgen receptors as the virus appears to in prostate cancer, but suspect that if that were happening we probably would have seen strong evidence by now, after 25 years of CFS documentation.

    There are many good studies of neurological problem due to MRV in mice, and probably some will relate to CFS. Those problems include neural net damage, maybe another issue besides the neuroendocrine problems. I have not read any mouse MRV studies yet, but that is on my list of things to do...

    As far as the Gupta approach, the fact that it helps some PWC is relevant and must be explained in any causal model of CFS. And what I find compelling in the XMRV situation is his treatment recommendations may somehow compensate for a dysregulated neuroendocrine system.

    So following this line of reasoning, Gupta's method could help compensate for the damage the XMRV has caused, so although not a cure, it might be a useful rehabilitation to address the effects of XMRV on the neuroendocrine system. Ultimately antivirals are not likely to correct the damaged neuroendocrine cells, because once the retrovirus has inserted itself into the cell's DNA the damage is done. But antivirals might conceivably block further damage.

    One other item, I know from my experience as a researcher that the WPI data will be challenged. We should not get mentally set in any XMRV ideas yet, there is more to learn.
  20. zoe.a.m.

    zoe.a.m. Senior Member

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    ITA with this. I think it's very useful in terms of having opened up the flood gates concerning what biomarkers doctors have been seeing (MRIs, SPECT scans, cytokine levels, NK function) that have been relatively quiet until this finding.

    This is quite interesting, especially the concept of Gupta's method as rehabilitation. I agree that the improvements reported are compelling and need to be investigated further! I had a conversation some months ago with a woman (who works for my ND) and brought up the amygdala retraining technique and asked her for her thoughts. She said that she had had a significant head injury due to a car accident and had to re-learn to speak, write, etc. and very much believed in the possibilities of "retraining."

    If Gupta presented his program as such, and had not suggested that XMRV was likely no more important than any other bug found to be residing in CFS patients, I would be a huge supporter. It is my own hang up that I cannot get past his calling it a "cure." Also, just based on my own experience over the years and what I see/hear of other cases, I do believe physiological damage must be repaired in order to improve neurological functioning (even to the point of one being able to take full advantage of Gupta's program).

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