Article: Looking Forward: Dr. Peterson on ME/CFS Research, Treatment Options and Hope for the Future

Article: Looking Forward: Dr. Peterson's ME/CFS - Hope For the Future

You can view the page at http://forums.phoenixrising.me/content.php?490-Dr.-Peterson-Talks-On-Diagnosing-Treating-XMRV-CFS-MECFS-chronic-fatigue-syndrome

 

Thanks for this, Cort!

I have for some time been wondering about the NK cell function tests. Many ME/CFS researchers/clinicians seem to be viewing them as a hot candidate for a biomarker (or even plainly: a biomarker) for ME/CFS. Why hasn't this test been accepted as a biomarker? - one wonders. Are the results not consistent enough? (I heard there was a study at the Ottawa conference with opposite results?) Is it just a matter of more studies needing to be done? Or is it not accepted for some other reason (expensive?)

Any comment on this from those of you who might know (Cort... ;-) would be great!

 

Thank you Cort. Very interesting.

What I don't understand is, if the immune abnormalities are consistent, then why there is no widely used biomarker yet?

I'm not sure if I understand Peterson's opinions about ME being primarily an immune system disorder (if I have interpreted that correctly?) - I seem to have more endocrine issues, rather than obvious immune issues. So that makes me think that something else is going on rather than a primary immune disorder - unless my pituitary gland or hypothalamus has some autoimmune thing going on, in which case it would be interesting and helpful to know why they are affected specifically.

Anyway, it's all thought provoking, thank you.

Some people Dr Peterson has been treating with AV's, have improved CNS function = Improved Endocrine function. Starts upstairs.

 

Sorry if I am being a bit slow on the uptake, but if Peterson believes no specific pathogen or even any pathogen is the root cause of M.E, then why is the drug CM001 potentially going to be of great benefit to people with m.e? Is it because if immune dysfunction is the root cause of m.e then pathogens like hhv6 can take hold and destroying hhv6 will bring significant clinical improvement to the patient if not a full cure?

Dr Peterson has seen some great results with Cidofavir over the last few years. People regaining much of their health. Yet, this is only treating opportunistic infections, not cause. I would have no problem taking CMX for life if it gave me 80+ percent of my health back. The drug sounds much safer and more effective than Vistide (IV form).

 

"The hyper-aggressive patients impugning researchers' integrity are, from his stance, only hurting the community and their own chances for help".

That's putting it politely. I think it's been obvious for some time just how much damage this small "hyper-aggressive" group has caused. Disheartening to see how many people have jumped on the conspiracy bandwagon railing against some of our best and most dedicated doctors and researchers. Baffling and absurd that anyone would believe someone like Dr Peterson would participate in attempting to squelch research for his own personal gain. Nothing could be further from the truth.

I choose to focus on the reality of how much these dedicated folks have given and continue to give to this community. Those who perpetrate lies and hostility will fade away. Truth/integrity will win out. I choose to stick with the winners.

 

Dr Peterson has seen some great results with Cidofavir over the last few years. People regaining much of their health. Yet, this is only treating opportunistic infections, not cause. I would have no problem taking CMX for life if it gave me 80+ percent of my health back. The drug sounds much safer and more effective than Vistide (IV form).

Thanks Tristen for your reply, very helpful. Yes, I too would happily take a drug for life if it gave me 80% of my health back. Do you know whether those who do well on cidofavir are those who show active hhv6 infection? Thank you.

 

Thanks Tristen for your reply, very helpful. Yes, I too would happily take a drug for life if it gave me 80% of my health back. Do you know whether those who do well on cidofavir are those who show active hhv6 infection? Thank you.

It seems there is no doubt that it's helpful for those whose primary active infection is CMV. I'm not completely sure about the other HHV's. My impression from him is that it is hitting those as well, and very likely other undiagnosed viruses. Sorry that I can't answer how much. It would be nice to hear from those who treated HHV6 with the drug. His office and clinic had people everywhere hooked to IV's getting infusions. Sometimes in the halls. Gotta be some of those folks here.

 

At last!

Someone is bothering to look at pregnancy! Having had ME for 41 years and seen two pregnancies in that time, other than very severe hyperemesis gravidarum for both, by 22 weeks I felt as though I'd been let out of a cage my ME symptoms had improved so much. I had had some relative remissions between onset (age 10) and my pregnancies, but something very different happened during that time which led me to, not total wellness but, a degree of wellness I had not seen prior to onset and certainly haven't seen since. I'd put it at about 80% well. I tried two courses of different forms of HRT to try to replicate without avail and actually with a worsening of symptoms, though admittedly I was told by one Gynae that if it had been the sex hormones which had contributed to my well being then I would have been abruptly thrown back into relapse at parturition and this did not happen. Tbh the timings of benefit seem to mirror the Rituximab studies so fantastically well that I personally think this is where a pregnancy / autoimmune study should look. (I am positive for ANA).

 

It seems there is no doubt that it's helpful for those whose primary active infection is CMV. I'm not completely sure about the other HHV's. My impression from him is that it is hitting those as well, and very likely other undiagnosed viruses. Sorry that I can't answer how much. It would be nice to hear from those who treated HHV6 with the drug. His office and clinic had people everywhere hooked to IV's getting infusions. Sometimes in the halls. Gotta be some of those folks here.

Thanks Tristen...

 

"The hyper-aggressive patients impugning researchers' integrity are, from his stance, only hurting the community and their own chances for help".

That's putting it politely. I think it's been obvious for some time just how much damage this small "hyper-aggressive" group has caused. Disheartening to see how many people have jumped on the conspiracy bandwagon railing against some of our best and most dedicated doctors and researchers. Baffling and absurd that anyone would believe someone like Dr Peterson would participate in attempting to squelch research for his own personal gain. Nothing could be further from the truth.

I couldn't agree more with these sentiments. There is a huge difference between being assertive and being aggressive/bullying. We always need to use our voice to ask for good research, compassionate and humane medical care, and a government that has our best interest at heart. We want to be recognized as the truly physically ill people that we are. We want doctors, researchers and the world in general to care about our well-being and to do everything in their power to help us.

However, we all learn when we are small that the world doesn't revolve around us. People are living their lives, going to work, socializing with friends without once ever thinking about us. Unfortunately, that is the world in which we live. Everyone has their own issues that consume most of their thoughts and energy.

One of our major goals - if not the goal - is to attract top-notch researchers into the field. Which ones of us would not want a diverse set of scientists all in one room debating and tearing down theories, building better ones and tearing them down again until they finally come up with something concrete and definitive! I want this I would pay big money for this!

So it completely blows my mind when some patients ridicule anything or anyone that doesn't fit neatly into their own current hypothesis. Since the cause and cure for ME/CFS is not known, wouldn't it be highly possible that the true answers will be something that is not yet understood by medical science today!!

Don't we need every scientist that we can get, digging at the cause of this illness and debating results with other scientists until they figure the cause and treatment?

Why are patients rude and mean-spirited to these very people that we need fighting for us. For example, just months ago, some patients were sending nasty emails to John Coffin, who said XMRV was dead but that he was not ruling out other pathogens. It's easy to see that he was right in hindsight - but there were actually patients who were not retrovirologists, virologists, or even scientists arguing that he was dead wrong and calling him every name in the book. Really??

So even before the BWG study came out and Dr. M still believed in XMRV, we as a patient population could have thanked Dr Coffin for his honest evaluation and asked if then he would at least work on finding other pathogens. We could have had a BIG ally. We could have been much further down the road with other pathogens then we are now. IMO, we continue to blow good opportunities like this because we insist that he must not want to find a cause for ME/CFS, he doesnt believe in it, or hes part of a conspiracy.

Not only does this discourage the researchers in question, but also many others who are on the side-lines that we will never know about, because they do not want the same treatment. To work against ones own well-being for the sake of screaming the loudest on a forum is ill-logical behavior that gives Wessleys camp more ammunition and makes it that much harder for the rest of us.

 

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0026358 Looks like I might get some answers soon. Norwegian study is now out And we can talk about it yippee!

 

I am sorry but I can't really agree with Dr. Peterson's assessment that CFS must be the result of immune dysfunction and not an underlying acquired trigger. Its a chicken and egg problem I know, but if you look at the epidemiology of CFS - it weighs heavily in the favor of a contagious entity that becomes chronic or some common exposure to a toxin. How else can you explain outbreaks? Its very very unlikely that a whole town full of previously healthy people of all different ages and background who are genetically unrelated all have the same underlying susceptibility to develop ME/CFS at the same time unless the susceptibility was somehow acquired. Immune dysfunction is very likely a secondary effect of a primary pathogen or toxin than it is the primary cause of the illness. Just because we haven't found it yet, doesn't mean it doesn't exist. This interview makes it sound like Dr. Peterson has given up on that idea. That seems unfortunate at a time where CFS is only starting to get the resources it needs to do the quality research required to answer these questions.

A whole town full of people's immune systems don't just one day go out of whack after functioning normally for a lifetime. Something has to be causing it.

 

Regarding HGRV research...

This has been posted elsewhere. But it highlights why, in my opinion, it would be bad to throw the baby out with the bathwater regarding XMRV. I hope they don't stop retroviral research in CFS in general just because research on one particular strain of one retrovirus seems like its not working out. It is conceivable that Mikovits et al were on the right track with the retrovirus idea.

---

http://www.ncbi.nlm.nih.gov/pubmed/6202923

J Natl Cancer Inst. 1984 Jun;72(6):1349-56.
Suppression of natural killer cell activity by Friend murine leukemia virus.
Moody DJ, Specter S, Bendinelli M, Friedman H.
Abstract
BALB/c mice infected with Friend murine leukemia virus (F-MuLV) evinced a decreased natural killer (NK) cell activity to susceptible target cells. This suppression increased as the interval between infection and assay was lengthened. The decrease in NK activity due to F-MuLV infection was partially reversible when spleen cells were pretreated with interferon before the cytolytic assay. The ability of F-MuLV-infected splenocytes to bind to target cells was unaltered, indicating that the defect was in the lytic phase of NK cytolysis. When mixed with uninfected spleen cells, F-MuLV-infected splenocytes suppressed their NK cell activity. This suppression was associated with a nylon wool-adherent cell population in the F-MuLV-infected spleens.

---

 

This experiment needs to be run again using today's micro-array technology to see if they can catch what exactly is being transmitted to the monkeys that is causing the pathology to develop. IMHO this argues against the idea of "hit and run" because they were able to take blood from humans with ME and after putting it in monkeys, the monkeys developed pathological changes similar to the humans.

In this outbreak of ME in Adelaide the punative agent could be transmitted to monkeys
Pellew RAA, Miles JAR; Med J Aust:1955:

1955:

In this outbreak of ME in Adelaide, Australia, an agent was repeatedly transmitted to monkeys; when the monkeys were killed, microscopically, infiltration of nerve roots with lymphocytes and mononuclear cells was seen and some of the nerve fibres showed patchy damage in the myelin sheaths and axon swellings consistent with neurological involvement.

In these monkeys, there were widespread changes involving the dorsal root ganglia, cervical and lumbar nerve roots and peripheral nerves. Perivascular collars of lymphocytes and plasma cells were in the cerebral cortex, brainstem and cerebellum, spinal cord and around blood vessels to nerve roots (Pellew RAA, Miles JAR; Med J Aust:1955:2:13:480-482, cited by J Gordon Parish; Postgraduate Medical Journal 1978:54:711-717 - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2425322/ ).

 

I sometimes fear that the 'state' of ME/CFS is analogous to logging all calls to the AA (the UK Automobile Association that provides a breakdown recovery service) involving cars not starting and grouping them all under 'failure to start syndrome'. Subsequently they are found to be due to no petrol; a wiring fault; faulty starter motor etc with no consistent findings and no association at all between the various faults. Alternatively it may be that there is one underlying systemic pathology that produces similar (but not always identical) symptoms regardless of the pattern of onset or eventual cause. I'm more confortable with the latter scenario.

Given the various onsets and the range of symptoms, one potential systemic avenue that I'm surprised hasn't been explored much to date is that of a sensory gating defect :

http://en.wikipedia.org/wiki/Sensory_gating

This is a fairly easy thing to test using a paired response paradigm to determine the degree to which the nervous system is able to habituate 'harmless' stimuli.

I'm aware that, in the past, Dr Goldstein has suggested sensory gating as the mechanism underlying ME/CFS but as far as I'm aware he hasn't published any experimental evidence to support this. I've only been able to find one dissertation that found a weak association between ME/CFS in adolescents and a sensory gating defect using an auditory stimulus :

http://docs.google.com/viewer?a=v&q...2-zqfV&sig=AHIEtbT6RtKcAUL1HEGgQFagTGz8pGlTkQ


On the other hand, there is a reasonably consistent literature around the role of a sensory gating deficit in Fibromyalgia. This study is interesting in that they found a significant difference between Fibro patients and controls using a painless somatic stimulus but not an auditory one :

http://docs.google.com/viewer?a=v&q...pE9pAE&sig=AHIEtbTvzqW_RVjFyK2BPmjQzQPZPk9frw


Of course, even if a sensory gating deficit is found in ME/CFS, the same question arises as it does in Fibromyalgia does the gating problem cause the condition or does it result from years of chronic illness?

Interesingly, Substance P (the pain related neurotransmitter/neuromodulator), which is sometimes found to be raised in ME/CFS which might be expected if pain signals are not properly attenuated, downregulates NK cell toxicity which of course might open up a route for opportunistic infections.

Additionally, it appears that norepinephrine provides the inhibitory signal that attenuates and thus habituates sensory input and if I recall correctly, Broderick's systems approach found that the adrenergic arm of the HPA axis is 'disassociated' in ME/CFS patients.

I'd be interested if anyone has come across any other similar studies in ME/CFS?

Really interesting Marco! A Nijs recently concluded the central sensitization is present in CFS. I think the studies showing increased pain sensitivity after exercise - now pretty well established I think, are fascinating. I think this fits in with sensory gating? The Lights believe infections in the dorsal root ganglia may effect sensory processing and Clauw believes sensory processing problems are key in FM - and really with all the problems with outside stimuli, chemical sensitivity and the many symptoms present in these disorders, I think it fits really well.

Eur J Clin Invest. 2011 Jul 2. doi: 10.1111/j.1365-2362.2011.02575.x. [Epub ahead of print]
In the mind or in the brain? Scientific evidence for central sensitisation in chronic fatigue syndrome.
Nijs J, Meeus M, Van Oosterwijck J, Ickmans K, Moorkens G, Hans G, De Clerck LS.

Various studies showed generalised hyperalgesia in CFS for a variety of sensory stimuli, including electrical stimulation, mechanical pressure, heat and histamine. Various tissues are affected by generalised hyperalgesia: the skin, muscle tissue and the lungs. Generalised hyperalgesia in CFS is augmented, rather than decreased, following various types of stressors like exercise and noxious heat pain. Endogenous inhibition is not activated in response to exercise and activation of diffuse noxious inhibitory controls following noxious heat application to the skin is delayed.

Conclusions? The observation of central sensitisation in CFS is in line with our current understanding of CFS. The presence of central sensitisation in CFS corroborates with the presence of several psychological influences on the illness, the presence of infectious agents and immune dysfunctions and the dysfunctional hypothalamus-pituitary-adrenal axis as seen in these severely debilitated patients.

 

The problem with low NK cell activity, diagnostically, is that it is also associated with depression.

I didn't know that! Hah! I do remember that NK cell activity is highly effected by stress. Well, we do know that CFS is not depression - they've looked at that exhaustively....

 

Cort, your interview with Peterson and the new info is really fantastic. Good work.

Thanks - it was fascinating sitting down him. Thanks to Corrine for getting me in there - she was quite persistent

 

Sorry if I am being a bit slow on the uptake, but if Peterson believes no specific pathogen or even any pathogen is the root cause of M.E, then why is the drug CM001 potentially going to be of great benefit to people with m.e? Is it because if immune dysfunction is the root cause of m.e then pathogens like hhv6 can take hold and destroying hhv6 will bring significant clinical improvement to the patient if not a full cure?

Good question....hmmmm. I think you may be right that something like natural killer cell sets the stage for these problems.. - he did attribute one patients decline probably to his NK cells functioning getting wiped out. Why NK cell dysfunction is low is one of the key questions - and the Peterson/Bond group, the CDC and the Klimas/Fletcher group is looking at that.

I think he thinks the central problem is sickness behavior; that is something like a cytokine cascade in the central nervous system AND I think he probably thinks that it can be caused by herpesviruses. Herpesviruses are so intriguing because they fit the Light theory of CFS as well - since they actually maintain their latency in the dorsal root ganglia (these bundles of sensory nerves outside in the body).

 

Thanks for this, Cort!

I have for some time been wondering about the NK cell function tests. Many ME/CFS researchers/clinicians seem to be viewing them as a hot candidate for a biomarker (or even plainly: a biomarker) for ME/CFS. Why hasn't this test been accepted as a biomarker? - one wonders. Are the results not consistent enough? (I heard there was a study at the Ottawa conference with opposite results?) Is it just a matter of more studies needing to be done? Or is it not accepted for some other reason (expensive?)

Any comment on this from those of you who might know (Cort... ;-) would be great!

I think NK cell function tests are emerging as a biomarker. I'm not sure why its taking so long but there is more and more interest - even the CDC is doing studies on them. My guess is that NK cells are relatively new to the medical profession, they aren't considered the heavy hitters of the immune response and it takes a long time to do anything definitive in CFS given the low funding. There was a study that did have opposite results at Ottawa but that was the first one that I had seen and there was quite a talk about it and what went wrong at the conference. Dr. Klimas and Fletcher had several ideas.

 

Dr Peterson has seen some great results with Cidofavir over the last few years. People regaining much of their health. Yet, this is only treating opportunistic infections, not cause. I would have no problem taking CMX for life if it gave me 80+ percent of my health back. The drug sounds much safer and more effective than Vistide (IV form).

He's VERY excited about this drug. Hopefully it will be much more effective - gets in there deeper - and much easier to handle than other herpesvirus drugs. Dr. Dantini also mentioned another herpesvirus drug under development by another pharmaceutical company. I think Corinne is going to start the drug in the next couple of months; I'm sure we'll hear how she's doing.

 

At last!

Someone is bothering to look at pregnancy! Having had ME for 41 years and seen two pregnancies in that time, other than very severe hyperemesis gravidarum for both, by 22 weeks I felt as though I'd been let out of a cage my ME symptoms had improved so much. I had had some relative remissions between onset (age 10) and my pregnancies, but something very different happened during that time which led me to, not total wellness but, a degree of wellness I had not seen prior to onset and certainly haven't seen since. I'd put it at about 80% well. I tried two courses of different forms of HRT to try to replicate without avail and actually with a worsening of symptoms, though admittedly I was told by one Gynae that if it had been the sex hormones which had contributed to my well being then I would have been abruptly thrown back into relapse at parturition and this did not happen. Tbh the timings of benefit seem to mirror the Rituximab studies so fantastically well that I personally think this is where a pregnancy / autoimmune study should look. (I am positive for ANA).

Well the CDC, believe it or not, is quite interested in this as well - and why? Because they have a female researcher (Boneva) who wonders why so many women have CFS. She found that very high rates of increased bleed, early menopause, endometriosis and hysterectomies in CFS. There is some study evidence suggesting problems with estrogen. Clearly something is going on in this area.