Although the personal questions in the comments of the last blog were asked very rudely, I will try to answer them anyway. I have represented myself as an open book, and I truly am, even though it gets me in trouble, as witnessed by the tone of the questions. Most of this has been said before, but things have changed, and perhaps it needs to be said again, from our current vantage point. So, I’ll give it a go.
I am not trying to persuade anyone to take anything. I share my reasoning, with references, within the limits of my writing ability. I intentionally report before I know the outcome so that it won’t be seen as my pushing a particular protocol. I am in the same boat as everyone else. I don’t know what to do to fix it. I don’t believe that anyone else does either. Arv’s are only one of the treatments I have written about here. I am sharing my thoughts and experiences in real time.
This is a blog. Opinion. If you read it carefully, there are inconsistencies. I even reserve the right to change my opinion from time to time. I try to summarize occasionally, but yes, a “casual” reader might come away with something I didn’t intend. I am not sure what to do about that. I cannot recapitulate the entire blog each time I write. It is an ongoing discussion, not “the truth” at a moment in time. Almost everybody gets that, I think.
I am endlessly surprised that my opinions are so controversial and can evoke such ire. Most of it seems common sense to me. It is incredible, and very telling, that there are actually people that want to restrict my freedom of speech! Why does anyone care if others find my musings useful? I am not telling anyone else what to think. I have said repeatedly that I could be wrong about anything. If I were to say nothing until everything is scientifically validated and I was positive, I would never say anything at all. I am learning as I go, as is everyone. For some peculiar reason, I seem to need to write, and some people find it helpful. The blog is the best I can do, with the limited energy and time I have left, and I am grateful for it. When Ali suggested I write a blog, I didn’t know what a blog was:). The patients who comment and write are very sophisticated and opinionated all on their own, not needing me to tell them what to think. They ask for my thoughts so they can put the information into their own equations, not take it as some kind of truth written in stone. The reflex to restrict what I say so that the poor gullible patients won’t hear it is patronizing. And to the conventional physicians who might be reading, why the sudden concern for our well being? There are many useless things that you are willing to prescribe that are much more dangerous than arv’s.
I have never claimed to be anywhere near “well” and I have said all along that there were confounders with respect to our treatment with arv’s. As noted in the comments, gamma retroviruses replicate by clonal expansion, so we need specific drugs, but transcription of viral proteins and the assembly of new viral particles may be involved in pathogenesis, if the hypothesis is correct. I am endlessly reevaluating everything with new information as it becomes available. I am not in fact a “true believer”. I would love to hear any alternative hypothesis that fits close to as well. Anything at all that might suggest a direction to turn for efficacious treatment. I am dismayed that we are back to having an idiopathic immune disorder, albeit repackaged to sound like good news. Redefining it as a syndrome, yet again.
There is no way to know if arv’s are helping us at this time, as I have said several times. I expected viral load measures and other ways to monitor that didn’t pan out. I did monitor several likely parameters which showed trends, but not convincingly enough to be useful. There are specimens sitting at the WPI that might contain valuable information. I certainly hoped it would be less ambiguous than it turned out to be. But there are others that experienced what we did, apparent cause and effect improvement from starting arv’s (often after an initial mild symptom flare). Some of them have written on this blog. I am NOT saying anyone should take arv’s, and never have, only that they shouldn’t be forbidden. The main problem I have recommending it as an option now, is that because it isn’t being studied, anyone starting will likely find themselves where we are, not knowing what to do for the long haul, and no help coming anytime soon. I actually think it is probably mostly a moot point now; the forces against have essentially won, shut it down for all practical purposes. The important thing isn’t really even arv’s, which at best only help incompletely, but our inability to get any help at all due to the attitude displayed in the reaction we have seen to the idea.
There are many drugs that are used because they work, even though the mechanism is unknown. One would think that for a debilitating disease which affects millions of people, for which there is no meaningful treatment, somebody would want to find out if that might be the case here. The usual way that happens is somebody has a good case, publishes it and then it gets studied. I have reported our experience. The burden of proof is not on me. What if it was a serendipitous discovery for the wrong reasons? The reaction of the medical community to trying arv’s is irrational, as the reactions of the medical community often are, especially when it comes to anything to do with this disease. The reaction of the scientific community is a joke, with no basis for an opinion at all; practicing medicine without a license, understanding nothing of the disease about which they are so opinionated.
Take a look at this paper: Zidovudine in primary Sjögren’s syndrome. Steinfeld. Rheumatology (Oxford). 1999 Sep;38(9):814-7. Did everyone get up in arms about this small clinical trial? Were the authors discredited for trying it? It doesn’t look like anyone followed up on it.
I have shared many personal details here, both physical and emotional. I have been very forthcoming, approaching undressing in public at times, so it is strange to be accused of “hiding”. The problem is that my sharing a list of symptoms that are “better” than before isn’t terribly illuminating, since some things are better or gone and some things aren’t. I even have a couple of new things. Like most ME/CFS patients, my condition changes from day to day and tweeting my moment to moment condition would benefit no one. However, I will try to define the big things.
The most tangible thing that happened to me, seemingly from arv’s, was the near resolution of my chronic malaise. I had it much of the time for 15 years. It went away shortly after starting AZT/Isentress and I almost never have it now. So 90% of the time before, 10% or less now. That alone was life changing for me.
My down periods used to last for 5 days to a week at a time, and now, rarely more than part of a day. The worst moments happen less often.
When I started arv’s, I never slept more than two hours without awakening, and I didn’t dream at all. I now often sleep all night with one or two awakenings and I dream normally. My day to day wellness is linked to the quality of my sleep in a chicken or egg fashion, so this improvement is key.
Painless migraines (scintillating scotoma without headache) and hypertensive crises are much reduced in frequency.
Another “big thing” that happened: I experienced a definite decrease in my peripheral neuropathy pain at one point early into arv’s. However, trying to explain one’s pain to anyone else is an exercise in futility. The pain I have now is worse than pain that almost drove me insane at the beginning of my illness, but my coping skills are very different. Still when the reduction happened, it seemed definite. I am not pain free, but my pain is quite tolerable and does not require pain medicine. Others have also reported less pain on arv’s. Again, I am reporting, not selling. For everyone who thinks they were helped, somebody else thinks they weren’t, but the risks of trying it are pretty minimal with proper monitoring.
I acknowledge that it is possible that all these things happened in spite of, and not because of, arv’s.
A big disappointment for me has been that the abnormal response to big time stressors remains, though it may be attenuated. Impossible to tell.
As for my daily functioning? I am able to work long days, most days, electronically (phone, Skype, email). I don’t have brain fog, but do sometimes have more symptoms after mental exertion. I am limited physically, more so in Santa Fe than Hawaii. I can climb a couple of flights of stairs with some dyspnea, more if needed, if I go slowly. I can usually walk several blocks, but might have some mild PEM if I overdo it, though my exercise tolerance is very variable. I don’t need handicap parking. I have no difficulty lifting groceries, etc. Resistance exercise is easier than anything aerobic. Swimming is easier than walking. Standing still is the hardest. The most physically challenging thing I have to do is negotiating airports and I use the airport wheelchair service for that. Gentle yoga is helpful. Pretty much all of the above is better than before I started arv’s, though as a commenter said, and, as I have said all along, other things happened too, before, during and after. Also my illness historically follows my state of mind (knowing full well how unPC it is to say that out loud). I am also much more tolerant of symptoms than I used to be, and not a very compliant patient, more confounders.
I can only work part-time face to face, a couple of hours at a time, but I’m OK for many successive days. I could fake it for longer hours than that, but don’t want to do that. My patients travel a long way to see me, and I want it to be useful and special. I am seeing new patients for 4-5 hours on two different days, which is working out well for all concerned. It is a unique, collaborative endeavor. Sick doctor and sick patient. I am limited, but can function fairly reliably, though there are days when it’s tough; however, there are more days when it isn’t.
When I started arv’s, I was unable to speak on the phone, because of auditory processing disturbance. I also had to lie down most of the day, only sitting or standing for a very short time, and I now sit up most of the day. Standing is more difficult some days than others, but there is never a time when I can’t if I need to; that was not always true.
So huge functional change in the last 20 months on arv’s, but improvement started about 6 months before that, with cessation of Lyme and symptom-based treatment. From housebound to functional, but not at all “well”. I have written about the reasons why I abandoned the use of rating scales to evaluate our experiment and don’t want to rehash it again. It is sad that it’s all we have. I am collecting them on my patients, but don’t expect them to be as useful as patients’ subjective reports. Yes, I do believe what my patients tell me.
My illness certainly isn’t gone, though it has lifted, lessened, but it is a relapsing, remitting illness all on its own, making it extremely difficult to assess cause and effect. I have said this over and over again. I am fully aware that many ineffective or harmful treatments have been perpetuated because of this feature of the illness (see my prior blog entries about Lyme Disease treatment). Whenever anyone gets better, they think it’s because of whatever they were doing at the time. I received an email recently from a patient who was housebound for fourteen years and suddenly improved enough to get a life, having changed nothing. I was of course influenced by the fact that there were two of us sharing the same experience; Ali and I had similar experiences with respect to the timing of improvement, though she had no side effects and I did experience a flare of symptoms initially. And for the record, neither of us has a history of placebo responses.
Ali went uphill during her first 6 months or so on arv’s, but had more therapeutic interventions concurrently than I did. The goal was always to get her better, not demonstrate something scientific to others. Her treatments did not prevent her crash when she tried to engage life again a year ago. She is doing well again now, but it is impossible to say if this level of wellness is the same, above or below her last remission. The “crash” didn’t become as serious as prior crashes have been for her. The important thing to her now, I think, is that she is better at this moment, and seems still to be slowly improving. Will it last? She is savoring it while it does.
My baseline was better prior to the events of early July than it is now, though I am not “crashed”. I have been under a great deal of stress, though I am hoping things will calm down a little now, so I can regain what I have lost. There is no way to know if I tolerated the crisis better than I would have without arv’s. I suffered the kinds of losses and persistent stress that have historically set me back in a major way. I stopped Isentress a while back, and am worse. Cause and effect? Who knows, but I don’t want to stay on monotherapy and am afraid to stop Viread, since a couple of patients who were forced to go off have lost gains. I may go back on Isentress. Also thinking about Lexiva (see Li on the sidebar).
I have received several demands for an apology from me to Dr. Peterson. As I said when I mentioned his name for the first time, I have never met him. Making enemies was never my intention, just the inevitable consequence of stating one’s opinions openly and publicly in such a contentious arena. My frustration feels overwhelming sometimes and it comes out in my writing. I hear from patients that love Dr. Peterson, and that does make a difference to me, but it still seems inconceivable that he abandoned the pursuit of a retroviral etiology when he jettisoned the WPI, knowing what he knows about the science and the disease. His teaming up with Konstance Knox to sink the WPI still seems really sleazy to me and his claim that it was to protect patients disingenuous. He could not have known there were problems with the VIP Dx test, or questions of contamination, at the time that he left, so how could he have been “right”. His agenda appears to go beyond figuring out how to treat the disease and help patients. I am not saying that I know precisely what that agenda is. It would seem that everyone who was involved with the WPI was hurt, likely including Dr. Peterson. I only wish that he hadn’t thrown the baby out with the bath water.
I regret any pain that I have caused, but some truths are painful. For me, it is painful to acknowledge how few friends there are worth having in the medical or scientific communities. My referral list for mainland doctors is a very short list. When I think back over the people I have mentioned by name in an angry or personal way, it is a select few that had it coming. My lack of professional decorum, or whatever you want to call it, comes from outrage, and mostly justified. I challenge anyone who has been sick with this disease for any length of time to write their truth and not say some angry things. My writing is also full of hope for the future. It’s just that it is the hope of learning to live well with the disease, rather than to truly vanquish it any time soon.
I really think many have too much confidence in “science”, especially retrovirology, which seems to have an unusual number of landmines scattered across its landscape. Even if Dr. Lipkin were to say tomorrow that he agrees that there are gamma retroviruses infecting ME/CFS patients, it will be a long time before that translates into specific treatment. Compassionate use of existing drugs should be tried and available, especially for the sickest patients. There are possibilities besides arv’s. Lenolidamide? Pentoxyfyllin? Nexavir? Existing drugs. What others? I recently heard of a big time response to Copaxone. Is anyone looking in a systematic way? Really looking? Why does it feel almost subversive to talk about it? The idea that these patients should, or can, wait is indecent. Again, I am not trying to convince anyone to do anything other than consider my ideas. I continue to write because some find it helpful, and I have made many friends, but I have made enemies too, and that gives me pause. I do grow weary of the personal attacks, on top of everything else that has happened recently. I need to focus on my patients, but want to continue to reach out to readers; there is so little information with respect to how and what to consider for treatment in the here and now. Five or ten more years is too late for many of us.
OK. Now I have some actual work to do:).
Aloha,
Jamie
Today’s song: Can’t Find My Way Home
>John Coffin saw all the originally data from Lombardi et al. also had the slide in question for the best part of 6 months and was in the audience where the use of AZA on PCR negative patients in Lombardi et al. was discussed 2 years ago.
Hiding the identity of patients is an ethical issue and is standard practice
So why did Coffin and Pathak fail to name the RT-PCR assay, which is a more sensitive assay then the standard PCR used on the early xenografts, in their paper Paprotka et al.?
>And is there any relationship to one having had mononucleosis 20 years earlier before CFIDS onset? Or having had a partner who had cancer?
Or having had horrible cases of the flu for several winters from literally Jan. 1 – May 1, dragging around after the 2 weeks of intense illness.
Or several relatives on one side of the family who had cancer? And allergies?
Wonder how all of this is related, if it is.
I hope someone is trying to figure this out.
>Dan Petersons's slides from the Oct 29 CFSAC 2009. John Coffin was in the audience and spoke after.
"10/33 Protein expression in Decitibine (5Aza2DC) treated PBMC"
XMRV Association with CFS – Part 4
http://www.hhs.gov/advcomcfs/meetings/presentations/xmrv_cfs.html
>This is for Jason.
Although Meniere's is probably initiated by an infection, perhaps most likely viral, the attacks themselves might be perpetuated by food allergy. You might be one of the lucky ones who could lessen or eliminate attacks by figuring out if this is the case for you, and which foods might trigger it.
Chronic inflammation, even if initiated by infection, often has flares and "remissions" or periods of stability–therefore you have to look to the environment, and for Meniere's, food, to see what triggers a flare.
Here is a google search:
http://www.google.com/search?q=meniere%27s+food+allergy&ie=utf-8&oe=utf-8&aq=t&rls=org.mozilla:en-US:official&client=firefox-a
Good luck, Jason.
Jill Neimark
>It looks as though the original gel was mislabeled by a lab tech corrected then sent to science
You will have to ask john Coffin as the peer reviewer why the published gels and the gels as sent were described differently.
>@Anon October 12, 2011 8:08 PM
my whole family is sick from either cancer or a neuroimmune disease. These illnesses hit at various stages of our lives. gammaretroviruses were known to cause cancer and neuroimmune illness in mice. It's been said that MLV's act more like HTLV1 then HIV. Not everyone with HTLV1 end ups with illness. I believe there is a 5% change of developing lymphoma. So in the case of MLV's not everyone will get sick, or sick at the same time, or with the same illness. That's how I've understood it to mean. My family was very unlucky.
>if this membrane slide was a rescan from a source material by a mole, you could stick any label you like on the same blot presumably.
Oh and, Lack of meta data in that actually kills any claim to having produced a verifiable slide in the first place (meta data isn't a cast iron guarantee either, but it being missing makes it worse).
>"Well here is something that is no joke. My father is sick with Parkinson's, his wife has MS, my mother has Breast cancer, another brother Graves disease, My sister and I have ME/fibromyalgia, and I've lost one brother to leukemia. My only healthy brother has been showing symptoms of unexplained illness for the last 5 months. I work in the area of health. Eight of my co-workers have unexplained illness. One of them has MS. They have worked around me for 12 years. There is no previous history of any of the illnesses I listed in my family. I have tested postitve for HGRV. What a coincidence all this is!"
While I'm truly sorry that there has been so much illness in your family, what in the world does this prove except that people get sick?
As for your coworkers getting sick, is the building ventilated properly, or is it sealed? Is it next to some chemical factory or coal plant, or has it been investigated for mold, or sick building issues, etc., etc.?
What any of this has to do with your testing positive for a "HGRV" (or was it XMRV?), just doesn't make any sense at all.
IHMO.
>And so the interminable soap-operatic Lombardi et al. saga continues to plod along….
interesting about the CFSAC Oct. 2009 slide materials.
From the link Anonymous@October 13, 2011 3:46 AM posted above, the first slide in the ppt file "peterson_1009_pt4.pptx" titled "Evidence for the presence of XMRV in 33 PCR Negative US CFS Patients" contains the following bullet points: 1) "19/33 Antibodies in the plasma", 2) "30/33
Transmissable virus in the plasma" 3) "10/33 Protein expression in Decitibine (5Aza2DC) treated PBMC" and 4) "Thus, since the submission to Science we determined 99 of 101 US patients show evidence of XMRV infection." So "99 of 101" CFS patients found positive by October 2009 in Lombardi et al. follow up work? 33/33 PCR-negative patients actually showing evidence of viral infection by at least one of three assays, including "protein expression in
Decitibine (5AZA2DC) treated PBMC"?
So how come this triumph was not the lead story by the WPI and the Lombardi et al. authors from October 2009 onwards? That's an astounding 98% correlation in the CFS Patient group. Was this data ever actually published anywhere? Was it ever written up and submitted after the FDA presentation by Dr. Peterson et al? But instead all that got consistently reported was the 68/101 positive by the (most likely contaminated) PCR assay? Something must
have happened that kept them from brandishing and trumpeting forth the 99/101 result that was presented in that Oct. 2009 slide. Privately, did cooler heads prevail (both at NIH and within WPI?)
From the last bullet point from that slide, this data was seemingly acquired after the initial publication in Science: "Thus, since the submission to Science we determined 99 of 101 US patients show evidence of XMRV infection" so perhaps the reviewers at that time probably did not knowingly have before them the 5-AZA data nor the 99/101 positive correlation (the Western blot slide called into dispute by ERV's blog post, which labelling was it bearing at that time?).
But shouldn't Coffin and any other virologists in the audience at that time have raised a public alarum at the use of 5-AZA in the assay? (It wasn't until after ERV's "Slide-gate" post that commenters were going on about possible 5-AZA subterfuge.) And I wonder if the WPI ever got around to doing the necessary control experiment, namely normal (or non-CFS control) PBMC + 5-AZA? And, after having shown that testing negative by PCR was not sufficient to rule out infection, did they re-test any of the 218 normal non-CSF controls by any of the three additional methods to see if there were more
silent/non-PCR detectable infection in any of that control group? Any positive results from the "healthy PCR-negative non-CFS patient group" would've really freaked out the NIH. (The fact that Lombardi et al. reported 8/218 or 3.7% of non-healthy CFS controls PCR-positive was enough to launch the BWG studies.)
This whole thing is making less and less sense.
I am so glad I'm not a virologist. You guys sure do make an awful lot of extra unnecessary work for yourselves.
October 13, 2011 11:56 PM
>HGRVs look like they can be aerosolised.
>grandmother with Atypical MS, Aunt with Atypical MS.
me (MS symptoms but DX of Fibromyalgia and Multi-Chemical-Sensitivty( which seems to have exploded after a Tettanus jab).
eldest daughter many cfs symptoms, youngest daughter dyspraxic(25hrs per week LSA) and some cfs sysmptoms.
I also have step children with neuro/pain symptoms.
I beleive there has been a slow burning contagious infection running through my family for decades likely generations.
I don't know wether the common denominator is a retro virus that is contagious, somethink in medical interventions such as vaccines/tetanus jabs.
Whatever it is, it has affected my children at a much younger age than myslef.
What ever it is it continues to progress into different systems within my body, ovaries, bladder, bowel, intestines, gut, kidneys, muscles, lungs, joints, glands, brain. My immune system is constantly under the impression its fighting something.
Oh and my other half of twenty years, after a few years of my being ill, worried silently that I might have aids, even tho I've neither been promiscuous, or messed with drugs and needles.
Perhaps some of us think a retro-virus fits because its the closest we've come to something that adds-up.
Oh and don't forget many of us posting on this blog would not be able to be in study cohorts, due to disabilty and
exclusionary tests that show we have a current infection or are on pain meds, or anti-depressants (which are virtually forced on us).
Once we have the diagnosis of FM cfs ME, we are excluded from normal testing procedures becasue all new symptoms are assigned to cfs FM ME.
I hope the USA will not be mislead by the bogus british clap trap, and understand why the patients and carers fight tough, and why they seem crazy angry.
The history makes it obvious that biomedical information about this disease is not what any of our governments wanted to encourage or hear about.
thank you to everyone participating here.
>@AnonymousNonRetrovirologist
Dr Peterson's slide showing use of AZA highlights how not all assays in Lombardi et al. were used on all patients. When they were used again those are the additional results. So they are the same assays.
Using the same experents on more of the 101 is not a part of the published Lombardi paper, so not hard to see why that is not the focus. Coffin knew though.
Coffin has always known as the peer reviewer that AZA was used, so Science have too. They wanted the labelling that way. The editors and Coffin accepted the paper without mention of that chemical as they agreed it was not germane.
>'And I wonder if the WPI ever got around to doing the necessary control experiment, namely normal (or non-CFS control) PBMC + 5-AZA? And, after having shown that testing negative by PCR was not sufficient to rule out infection, did they re-test any of the 218 normal non-CSF controls by any of the three additional methods to see if there were more
silent/non-PCR detectable infection in any of that control group? Any positive results from the "healthy PCR-negative non-CFS patient group" would've really freaked out the NIH. (The fact that Lombardi et al. reported 8/218 or 3.7% of non-healthy CFS controls PCR-positive was enough to launch the BWG studies.) "
The study was blinded. You are only looking at the results from one western blot that was put into the paper as per the peer review process and the requirements of Science.
>Hey Jamie
hope everything is OKish with you, we're all rooting for ya.