Hibernation Consternation

My muse left on extended vacation when the Lipkin XMRV study and subsequent press conference succeeded in discrediting retroviruses as a possible explanation for ME/CFS, with lots of important questions still left unanswered. The discussion reverted to whether or not it is a real disease and which set of diagnostic criteria are best, so there hasn’t been much to inspire me. It got pretty depressing. The IOM report was a joke: “The term ‘myalgic encephalomyelitis’ is not appropriate because there is a lack of evidence for encephalomyelitis (brain inflammation) in patients with this disease…”. Fail. I don’t know what to make of the Lipkin cytokine paper, because I take with a grain of salt results from a debunker on call for the government. XMRV wasn’t the first time: Lack of association between measles virus vaccine and autism with enteropathy: a case-control study. Nothing worth blogging about there. Certainly nothing hopeful. But recently, the Naviaux study was published and a couple of proposals posted by NIH have been making the rounds on Facebook, so I’ve had an uptick in email, some asking what I think about the paper and some telling me about successes with antiretrovirals in Europe, as well as encouragement to blog again. So, feeling very rusty, I’m going to give it a go.

My reaction to the Naviaux et al paper, Metabolic features of chronic fatigue syndrome, was dismay that the damage is so extensive and widespread. So many broken pathways. Finding a specific drug target seems very unlikely. There won’t be an answer anytime soon. They, and everyone else, including Lipkin and Hanson, are studying downstream effects, without attempting to identify the root cause. It’s a good thing that people are thinking and looking, but hibernation and dauer are not disease states and being compared to larval worms isn’t exactly the image change we need ;-). Even if they’re right and a handful of common abnormalities in this very heterogeneous group is accepted as validating real disease, my guess is that the findings will be similar in other diseases, e.g. GWI, fibromyalgia, ASD, maybe even chronic depression. GWI patients have PEM and often meet criteria for ME/CFS. As I said five years ago, I think all of these diseases of modern civilization are related and there is a family factor that confers risk to partners and offspring. There are even a few patients who believe themselves to be contagious by casual contact.

So what lies in wait to be activated by heterogeneous triggers and once activated causes immune dysfunction, neurological disease and opportunistic infections? The most likely explanation lives in the realm between retrovirology and genomics, the difference between the fields being as small as a single mutation. We have been injecting retroviruses and pieces of retroviruses into people for over a century. What are the chances that nothing bad happened from that? XMRV apparently doesn’t infect people, but injected into monkeys, it sets up a low level infection. Retroviruses recombine and rescue each other. Environmental toxins activate retroelements (HERVs and retrotransposons) which can recombine with each other or new incoming retroviral sequences and fully replicative retroviruses from vaccinations, biologics and lab workers. XMRV was created in a lab. The Paprotka paper said the odds of the recombination event that produced XMRV happening twice are infinitesimal. On the other hand, the odds of similar events having happened many times is very high I would think, since there have been so many chances. In the last few years it has been found that many cell lines produce viruses like XMRV which are capable of infecting human cells in tissue culture. Lipkin said in a press conference that 85% of Montoya’s samples contained retroviral sequences and in the XMRV study, 6% of patients and controls were positive for an antibody to SFFV, a very nasty murine retrovirus, but everybody is choosing to ignore those clues because that well is poisoned. Nobody wants to be the next Judy Mikovits. Lo and Alter both dropped it like a hot potato, returning to other research, never mind the question of how all these labs, Mikovits, Ruscetti, Silverman and Lo/Alter managed to consistently contaminate the patient samples at a higher rate than the controls.

Take a look at this paper: Are human endogenous retroviruses triggers of autoimmune diseases? Unveiling associations of three diseases and viral loci by Bjørn et al. “We speculate the possibility that recombinants or mixed viral particles are formed and that the resulting viruses stimulate the innate immune system, thereby initiating the autoimmune response.” They looked at multiple sclerosis, type 1 diabetes mellitus, and rheumatoid arthritis. It is one of several recent papers heading in this direction.

I hypothesized way back when that ME/CFS is related to MS. There are case reports of MS improving when patients take antiretrovirals, Multiple sclerosis patient walks after taking HIV drugs, and new cases of MS are rare or nonexistent in patients taking AIDS drugs, HIV and lower risk of multiple sclerosis: beginning to unravel a mystery using a record-linked database study.

Our very own Gerwyn Morris published an excellent paper on the subject of ME and MS being related diseases. Myalgic encephalomyelitis/chronic fatigue syndrome and encephalomyelitis disseminata/multiple sclerosis show remarkable levels of similarity in phenomenology and neuroimmune characteristics. I’d like to take this opportunity to acknowledge Gerwyn’s extraordinary achievement. If you search “Morris Gerwyn” on PubMed, his name appears as an author on 23 papers since 2013, usually as first author.

Lots of evidence has been published about the MS retrovirus, MSRV. Viral particles have clearly been detected, but it is less clear if these particles are ever infectious. There are several new papers reporting findings similar to this one, Two endogenous retroviral loci appear to contribute to Multiple Sclerosis.

Which brings us back to where this blog began. Are retroviruses at the bottom of ME/CFS? Might antiretrovirals be effective for ME/CFS and other diseases? Despite the thorough trashing of retroviruses in our disease and the intense ongoing fear mongering about how dangerous antiretroviral drugs are, apparently people are still trying it in Europe. The experience five years ago, when maybe a hundred people tried various regimens in a completely uncontrolled fashion, was some subjective improvement in about half, and no complete recoveries, except for one notable exception. The exception was a teenager who had only been sick for eight months. His mother wrote in the comments on this blog. He recovered fully, took the drugs for 6 months, stopped and as far as I know, didn’t relapse. I still find it upsetting that the prescribing physician was too cowardly to come forward and write a case report. How many teenagers could have been treated acutely since then? There were no injuries that I ever heard of. I was in touch with many of the doctors who were prescribing and there was lots of sharing, doctors and patients together, the only time I’ve ever seen that happen. One doctor I knew prescribed for 50 patients and concluded that it was better than placebo, but not worth the risk of prescribing it.

However encouraging the Naviaux paper may be with respect to advancing the case that ME/CFS is, in fact, a real and dreadful disease, it is discouraging with respect to finding treatment. A viable drug target seems unlikely. We are left with global strategies, hoping for synergy between therapies that don’t stand alone, same as now. But just as I was feeling dour about dauer…

The NIH compilation of responses to their request for proposals was published here. Read bottom of page 3 to top of page 4. I’m not going to mention any names for Google, because I don’t want to increase the risk of regulatory repercussions against a doctor brave enough to report successes with antiretrovirals. Also please read pages 9-12.

Then I heard from a patient in Europe who is having success with antiretrovirals after 20+ years of illness. In his own words:

I have been ill with ME since my mid-teens in 1994. Onset was in two stages. Firstly a gradual onset, whereby I was feeling increasingly more tested after the combined measleas/rubella vaccine, followed a few weeks later by the polio booster. And then secondly once that prodrome had got its hold, the downward cascade was always inevitable, and just waiting for me around the corner. 1994-2014 were harsh and brutal years. I hovered around 55% on the Bell scale and it was torture enough.

From September 2014 to July 2015 I took tenofovir 245mg. Improvement was an upward curve, albeit with some turbulence. Sometimes taking half- week, or full-week, or month-long breaks when I felt my body needed a rest from it so as to hold its own for a while. From August 2015 to September 2016 I added raltegravir to tenofovir and initially at full dose daily which sent me to sleep almost in the first few days. During this period I toggled around until I found the right balance for me. I got it right in the end around about June/July 2016 and the past two/three months have been great. My current regimen is tenofovir 245mg Tuesday through Friday, and on Tuesday and Thursday I also take raltegravir 400mg x 2. My original baseline was about 55% on the Bell scale for the twenty or so years when I was sick. I am now 95-100% and can go to the gym once weekly thanks to the antiretrovirals where I can build up quite a healthy sweat and recuperate normally. My VO2 max continues to increase substantially and my CD3-4-8 counts are x2.5 to 3 fold what they were before I started the antiretrovirals. Life is very good. I also take celebrex and multivitamin/antioxidant supplements and I am monitored closely.

This year I feel more confident about the winter than I did in 2014 on just tenofovir and than in 2015 when I was grappling with adding raltegravir. They were bad winters even though the arv’s did help me through better I guess. Winter 2016 can throw at me what it wants however. Now that I have hit the perfect treatment regimen with the antiretrovirals I am sure it will be a better winter. It was worth sticking it out and learning. I thank Dr Judy Mikovits and my physician over in Germany, along with the continued support of a rare and dedicated French doctor over there in Paris. Finally I thank two doctors over there in the UK for listening. I salute them all as men and women of true honour.

Several people wrote to ask what happened with antiretrovirals for my daughter and me. Ali and I plateaued without recovering fully. After the initial improvement, there was really no way to know what was happening. We both had a very mild flare of symptoms for the first six weeks and then a noticeable increase in energy and resilience. We started with AZT and Isentress, then switched the AZT to Viread a year later. Ali stayed on the two drugs for three years, not wanting to rock the boat, as she was doing relatively well. I stopped the Isentress after about a year and half and took Viread alone after that. We both improved during the three years we took antiretrovirals, but we were doing lots of other things documented on this blog. Since there was always the possibility that we might do better without them, eventually we decided we should find out. As it turned out, we didn’t decline when we stopped. I had some trouble coming off Viread, because my always labile blood pressure went crazy when I stopped, twice. Go figure. In the end, I weaned without any sort of noticeable decline. When we started, we were all so hopeful. Judy believed we’d be able to monitor viral load in a year, but it wasn’t to be. Our combined copays were breaking the bank and after three years, with no way to monitor and able to stop, it just didn’t make sense to continue. I would consider antiretroviral drugs again if either of us crashed completely.

My experience treating six very informed patients was similar to what other doctors have reported, 50% improved subjectively. Two had adverse reactions to Viread, including one who had responded initially; both resolved quickly when the drugs were stopped. Two patients continued long term, one on two drugs and one who opted for Viread monotherapy. I didn’t see anything dramatic enough to make me very encouraged though. I had successes with other things that were similar in scale with less risk to the patient and the doctor. However, it’s possible that tinkering with lower doses and less than every day regimens would make the drugs we have more useful for ME/CFS, even if they were designed for a virus we don’t have. Although we do not want to encourage resistance to the drugs, it’s possible that a small dose of a reverse transcriptase inhibitor would work for us. I heard from a doctor in Europe who reported complete recovery in 2011 after nine months on micro dose AZT (20-30mg/day). I don’t know how it turned out long term, but will write to him and ask.

Dr. Michael Snyderman is still doing remarkably well, still able to work in his hematology oncology practice at 75, controlling his cancer like a chronic disease, specifically like AIDS. He has been taking HAART for over 6 years, having twice passed his median survival, meaning there was less than a 25% chance that he’d still be alive by now. I will share his data here in the near future. He is still hoping to collaborate with Roswell Park Cancer Center in his hometown of Buffalo, NY to help patients who have cancer and who have a poor prognosis. The same viruses that infect cancers infect the immune system.  If cancer patients benefit as he expects they will, initiatives can be made with the neuroinflammatory disorders including ME/CFS. There is now a reliable virus detection methodology, ViroCap invented by the Wylies at Washington University and the Wylies are interested in collaborating with this research.

These are leads, the only leads we have. If drugs developed for a completely different retrovirus have some activity against a disease, think what could happen with some attention to the process that is actually occurring. The technology, next generation sequencing, already exists to begin to answer our questions, but the various software platforms that analyze the data are still in their infancy. The metabolomics studies are happening because there is a new toy. There are going to be lots of new toys in the near future. It already didn’t happen by random doctors prescribing off label. Since it wasn’t a slam dunk, it needs to be formally and properly studied.

It is possible that the metabolites that Naviaux et al have identified as a potential diagnostic panel might be useful for monitoring success with antiretrovirals. Dr. Naviaux has answered questions here, stating that he thinks the use of antibiotics and antivirals aren’t indicated and I mostly agree with him, planning to share my thoughts on treatment in a future blog.

I continued to go slowly uphill after I last blogged about ME/CFS almost two years ago, but nothing like a full recovery. I was able to work a little and I was able to ride on the back of a tandem, close to a thousand miles in two years according to Strava, half of it on dirt. Still lots of symptoms, but a life, where once there wasn’t one, plus a way to get endorphins. My recovery was slow after exercise; I felt drained the next day, but nothing like full blown PEM. I was still maintaining the fantasy that someday I would recover fully. But a year ago, while hiking, I twisted my ankle and broke my distal fibula. It was a minor fracture that should have healed without problems in 6 weeks. Instead I got RSD/CRPS (reflex sympathetic dystrophy/complex regional pain syndrome), a very challenging and painful condition. It takes most of my energy just to cope and I’ve been out of commission since it started, able to attend only to my own treatment (HBOT).

After 5 years of managing patients, I had to retire completely. I only worked with a very small number of patients, scattered all over the country, who saw me in person once a year in Hawaii or Arizona, but I got to know them very well, because most of the contact was electronic, day to day, moment to moment even, and that works well for ME/CFS patients. It was enough to learn quite a bit about the spectrum of disease, what works and what doesn’t, especially given that almost everyone I saw had been around the block and came with voluminous records, having failed treatment with the best. I’d like to share my impressions while still fresh, so intend to keep blogging, if I don’t get too beat up over this one ;-).

Today’s song from Les Misérables

The Fox Guarding The Henhouse

It’s been quite a while since I’ve had the urge to blog. Throughout the years when I was writing regularly, even when very angry, I always had a positive feeling that awareness was growing and answers would be found. However, I’ve lost that feeling in a growing realization of just how corrupt the people we need to save us actually are. I haven’t wanted to write from a place of negativity, because God knows there’s already enough bad news, but the recent CDC whistleblower scandal, dismissed by the mainstream media, has given me twitchy fingers again.

As far as I can tell from the various sources on the internet, Brian Hooker, PhD, an engineer, autism dad and board member of an organization called Focus Autism, after years of trying to exercise his Freedom of Information Act rights, managed to obtain the original data set for a study published by the CDC in 2004: Age at first measles-mumps-rubella vaccination in children with autism and school-matched control subjects: a population-based study in metropolitan Atlanta by DeStefano et al, 5 authors including one William Thompson. Apparently, late last year, Thompson contacted Hooker and in a series of conversations confessed privately to fraudulent manipulation of data to cover-up a 240% increase in autism in African American males who were given the MMR vaccine on time compared to those vaccinated later. However, the decision was made to use only children with a valid birth certificate, thus eliminating enough black children to dilute the increase to below statistical significance. Some email by Thompson expressing his concerns at the time have also come to light. All of this is very well covered on the Age Of Autism website.

Brian Hooker recently published a paper reanalyzing the original data and showing the association: Measles-mumps-rubella vaccination timing and autism among young african american boys: a reanalysis of CDC data. In a YouTube, Dr. Thompson was outed, initially with his voice disguised electronically, then a couple of days later, without the distortion, including this quote, “Oh my God, I did not believe that we did what we did, but we did. It’s all there… This is the lowest point in my career, that I went along with that paper. I have great shame now when I meet families of kids with autism, because I have been part of the problem.” 

Despite a chillingly complete black out by the mainstream media, Dr. Thompson issued a statement published on his lawyers’ website, which included this admission of guilt. “I regret that my coauthors and I omitted statistically significant information  in our 2004 article published in the journal Pediatrics. The omitted data suggested that African American males who received the MMR vaccine before age 36 months were at increased risk for autism. Decisions were made regarding which findings to report after the data were collected, and I believe that the final study protocol was not followed.” Then the predictable backpedaling. He believes vaccines have saved millions of lives, blah, blah, blah. What can he say to ameliorate his admission that he is personally responsible for publishing disinformation, a lie, when the truth could have spared how many black boys from relentless suffering? Thousands? Tens of thousands?

According to the CDC website, Coleen Boyle, the senior author of the paper in question went to work at the CDC in 1984 and now “serves as Director of the National Center on Birth Defects and Developmental Disabilities (NCBDDD)”. She was appointed to this position in 2004, the same year the DeStefano paper was published. It was on her watch, working as a visiting researcher in Boyle’s department, that Danish researcher Poul Thorsen, was financed by the CDC, in part to study the relationship between autism and vaccine exposure. 22 publications come up when PubMed is queried with his name and “autism”, two in high impact journals (Pediatrics and NEJM) purporting to prove that thimerosal and the MMR vaccine don’t cause autism. In 2011, he was indicted on 22 counts of wire fraud and money laundering for diverting over a million dollars of CDC money to his personal accounts. His papers have not been retracted. In fact, he is still publishing. Here is his listing on the Office of Inspector General’s Most Wanted Fugitives list (scroll down the page). The combined efforts of these fraudsters constitutes much of the literature on vaccine safety.

If they had been honest, how might the world be different today? Might vaccinations have been questioned in an even broader context than black boys with autism? What about the combined effect of all vaccines on innate immunity, in not just black children, but all children? What about children with ME? What about children with autoimmune diseases? 5 authors took responsibility for that paper. How many papers did they publish collectively which state unequivocally that vaccines are safe (even though the various package inserts state pretty clearly they are not)? More than half of our children have a chronic disease. Is this one of the reasons why? I say one of the reasons, because there are so many confounders, so many ways our children have been poisoned in our toxic world, in addition to vaccines. Since some unvaccinated children are autistic, does that mean that vaccines don’t cause autism? Of course not, but that is what our vaccine experts would have you believe. 

Data falsified, drug companies indemnified from consequences, media outlets proving beyond a shadow of doubt that their talking heads are shills for industry, eye witnesses of the damage done discredited as nutcases or worse. It can only be called a conspiracy.

I have no expectation that this will play out in a just manner. First there was a media black out, then Dr. Hooker’s paper was removed from the web, with a statement that it might be incorrect or endanger the public; it is back up today with a disclaimer that it is a troubled paper. CNN finally reported, concluding vaccines are absolutely safe, except in the rarest of cases, and people who decide not to vaccinate are the problem. The only other mainstream media report seems to be Time Magazine, a few days ago. It is behind a pay wall, but here is the headline and subtitle, “Whistleblower Claims CDC Covered Up Data Showing Vaccine-Autism Link: The claim, however, may just be more unsubstantiated fuel from the anti-vaccination movement.” That sounds unbiased, doesn’t it?

So there you have it, folks. Even when the evil doing is exposed, actually admitted, there is no interest. Dr. Hooker and Dr. Thompson will both be discredited in different ways. Dr. Hooker will be called a liar and not competent to evaluate the data because his degree isn’t in statistics. Dr. Thompson will be deemed unstable and his guilt delusional. Whatever it takes. The vaccine program is a sacred cow. It is thought of as the one unequivocally good thing modern medicine has accomplished. Anyone who questions that meme is an antivax crazy person. All the parents that witnessed their children regress into autism from their vaccines are too ignorant to understand what really happened.

The doctors administering the shots have been rendered comatose with explicit instructions not to worry about all the harm they are doing, since, like the drug companies, they are indemnified by the National Childhood Vaccine Injury Act of 1986. Kangaroo Court, created by necessity, because vaccines are dangerous, but designed to perpetuate the myth that they are not. If we made doctors responsible for the bad outcomes, things would change in a hurry. If every doctor had to consider the merits of each shot, what is actually in the shot and ask themselves, what is the risk to the particular child sitting in front of me right now if I do or don’t give it, what would happen then? I can feel pediatricians shuddering from here. At this moment, how many pediatricians are even aware of exactly what is in each of those shots or how they are manufactured? Do they know that some of them contain adventitious replication competent retroviruses and pieces of retroviruses, when we know only too well that retroviruses have a propensity to recombine and rescue one another? Let’s not forget the Recombinant origin of the retrovirus XMRV and its riveting sequel, Recombinant origin, contamination, and de-discovery of XMRV.

The fact that good things happened because of the vaccine program for small pox and polio in the mid 20th century does not justify what has come since. And just because good things happened, doesn’t mean bad things didn’t happen too. Millions of people were infected with SV40 for example; that mishap is acknowledged, but any possible adverse consequences denied. The retroviruses that inevitably were present in the first yellow fever and oral polio vaccines aren’t even acknowledged. Even now, when we have the technology to know what we are doing, we are still doing it. For example, we know that live attenuated virus vaccines grown in chick embryo fibroblasts contain avian leukosis virus and other retroviral nucleic acid sequences, but our CDC scientists have determined it is safe to inject these viruses and pieces of viruses into babies, in order to prevent diseases which, in fact, most individuals would be better off getting naturally. Here is a paper where they found bad stuff, but conclude it is safe anyway. Viral Nucleic Acids in Live-Attenuated Vaccines: Detection of Minority Variants and an Adventitious Virus.

Mutations and minority variants, relative to vaccine strains, not known to affect attenuation were detected in OPV, mumps virus, and varicella-zoster virus. The anticipated detection of endogenous retroviral sequences from the producer avian and primate cells was confirmed. Avian leukosis virus (ALV), previously shown to be noninfectious for humans, was present as RNA in viral particles, while simian retrovirus (SRV) was present as genetically defective DNA. Rotarix, an orally administered rotavirus vaccine, contained porcine circovirus-1 (PCV1), a highly prevalent nonpathogenic pig virus, which has not been shown to be infectious in humans. Hybridization of vaccine nucleic acids to a panmicrobial microarray confirmed the presence of endogenous retroviral and PCV1 nucleic acids. 

The “extensive proof” that avian leukosis virus (ALV) does not pose a threat to human health consists of three small studies, published from 1999 to 2003, all by the CDC and all by the same senior author, W. Heneine. Interestingly, his name also appears on the Lipkin XMRV study. His 1999 paper said,Our data indicate that the sources of RT activity in all RT-positive measles and mumps vaccines may not be similar and depend on the particular endogenous retroviral loci present in the chicken cell substrate used.”, but PCR of PBMC’s on 33 children after measles and mumps vaccines were negative, so they concluded this should “provide reassurance for current immunization policies.” In 2001, 206 recipients of the MMR were negative by PCR for 2 known avian retroviruses and had negative serology to an antibody developed specifically for the study. In 2003, studying adventitious retroviruses contaminating 3 brands of the yellow fever vaccine, they found there were 3 kinds of RT, more than expected from the 2 retroviruses they knew to be there; nevertheless, they concluded, “None of the samples were seropositive by an ALV-E-based Western blot assay or had detectable EAV or ALV-E RNA sequences by RT-PCR. YF vaccines produced by the three manufacturers all have particles containing EAV genomes and various levels of defective or nondefective ALV-E sequences. The absence of evidence of infection with ALV-E or EAV in 43 YF vaccine recipients suggests low risks for transmission of these viruses, further supporting the safety of these vaccines.” 282 cases from the millions of doses given where they couldn’t find evidence of anything shortly after inoculation, with technology that is now 15 years old? Are we comforted yet?

This work isn’t science. It is religion. There is no room for the precautionary principle here. Vaccines are good. Necessary. Period. No need to discriminate which babies might be at greater risk for complications, because we need our herd immunity. The needs of the many outweigh the needs of the few. Only it isn’t just a few anymore. That logic might make sense if the health of the species had actually improved during the period in question, but it is quite the opposite. More than half of everyone in the U.S. has a chronic disease, including our children. Our infant mortality rate is 34th in the world, despite, or perhaps because, of the fact that we give more vaccine doses before the age of 1 than the 33 countries ahead of us. Take a look at this paper: Infant mortality rates regressed against number of vaccine doses routinely given: Is there a biochemical or synergistic toxicity?

I am in no way saying that vaccines are to blame for everything, just that the vaccine program is one of a long list of high risk things we have done blindly, uncritically, while the health of our species has dramatically deteriorated. But what can we expect when the fox is guarding the henhouse?

Recovery In Neverland

Even though the last blog was the least controversial I’ve ever written, it managed to ruffle a few feathers. On the one hand, it couldn’t possibly be as simple as a diet cure and, on the other, it is too hard to implement, especially if you are sick and short of money. And what about retroviruses?

I am not cured. It is a relapsing, remitting illness and I am experiencing a remission. I am not asymptomatic, but much, much better. My husband and I have ridden our tandem 180 miles so far this month. Our rides are quickly getting longer, faster and more challenging. My husband said I have never worked harder. I don’t know if that’s because I want it more, or because I finally fixed my rubidium deficiency;-). No doubt a real doctor would say I finally decided to get off my ass;-). But anyone with real knowledge of the disease knows what a profound change has to occur for an ME patient to return to exercise after nine years.

Ali also has noticed improvement with respect to her physical abilities. She went to an hour long yoga class a few days ago with no PEM and expects to continue. She is living away from me, something neither of us thought possible just a few short years ago.

It isn’t just the diet. The diet happened to us in the context of a slow recovery over a number of years during which several treatments were contributory, all documented on this blog. Antiretrovirals, oxygen, Deplin, at one time Actos, at another modified Meyer’s cocktail IVs, metformin and Prometrium for Ali, prior dietary modifications and ever more awareness of the importance of biotoxin avoidance. I believe all of these things have helped to tip the balance towards recovery. When you are treating an incurable disease, it is necessary to look for therapeutic synergy.

As to the diet being hard, some of the biggest things aren’t too hard. A daily smoothie, big plates of organic greens, bone broth from clean grass fed animals. Buy organic. Try your local CSA (community sponsored agriculture) who sometimes deliver. Try eliminating gluten and dairy for three months. Consider nutrient density before eating something. Don’t try to change everything at once. Pick one thing and do that, then add to it. It is more expensive to eat this way. If it is too expensive, I am thinking the food is more important than supplements, on which most patients spend a lot of money. I am increasingly suspicious of things that come in pill form, including supplements.

One of the really interesting things that has happened to me on the Wahls diet is I am not tolerating B vitamins at all, finding them overactivating and sleep disrupting, after taking Deplin for years. I presume this is because I am getting what I need from my food. Can we infer from this that my methylation status has improved? Take a look at the numbers midway through this article by Dr. Wahls: Maximizing Nutrient Density for the Modern Day Hunter-Gatherer.

In addition to a relatively small number of known required nutrients, whole food contains thousands of compounds which work together in ways we do not begin to understand. Supplements supply an excess of a single nutrient. In the case of L-methylfolate, the idea is to overcome an enzyme deficiency by supplying the activated form of the nutrient folic acid to prime the pump of essential metabolic pathways. The deficiency occurs more often in the presence of certain genetic mutations, or SNPs, but remember, the problem is most often not caused by the genetic make-up of the individual, who was healthy once, but by epigenetic changes that have occurred. Also remember that methylation silences retroviruses.

I still think retroviruses are at the bottom of it, endogenous and/or exogenous. I will prevail upon Dr. Snyderman, who has lots to say on this subject, to give us an update in the near future. There is a growing body of literature to support the association of activated HERVs with various diseases. There are even a few intrepid researchers still pursuing novel retroviruses in chronic disease, working at the edge of our current understanding. Andrew Mason‘s betaretrovirus associated with primary billiary cirrhosis, clinical trials with antiretrovirals ongoing, Sidney Grossberg‘s JHK gammaretrovirus which he has identified in CFS patients, and Hervé Perron‘s MSRV, particles from HERV-W transcripts, with an immunopathogenic envelope protein, severity of illness correlates to viral load, replication competence still unknown. “Most HERVs are unable to replicate but MSRV expression associated with reverse-transcriptase activity in MS would explain reported DNA copy number increase in MS patients.” from The DNA copy number of human endogenous retrovirus-W (MSRV-type) is increased in multiple sclerosis patients and is influenced by gender and disease severity.

The possibility that animal retroviruses are the root cause of the enormous increase in chronic neuroinflammatory illnesses, autoimmunity and cancer in our modern world has not been ruled out, just because the particular sequence called XMRV has been put to bed. In fact, in figuring out where XMRV came from, created in a lab using techniques in use every day all over the world, a can of worms has been opened. How many times have similar organisms been created? How many cell lines commonly in use produce infectious virus that can spread airborne through a clean lab, as XMRV does.

Given that retroviruses recombine and rescue each other, that under certain conditions HERVs activate to produce viral product, that the environment is full of the very toxins used to amplify retroviruses in the lab and that high risk biotechnologies have offered up so many chances for new retroviruses to infect humans, it seems more likely than unlikely that it has happened, and more than once. After all, we have been injecting adventitious retroviruses into people for 80 plus years in combination with other live viruses. We think nothing of fusing human and mouse genetic material to produce monoclonal antibodies that are given to immunocompromised people. Passaging human tumor tissue through immunodeficient mice, gene vector technology, genetically modifying animals to produce human proteins for IV administration (Atryn) are all very high risk things to do. Lots and lots of chances. Hubris allowed it. Money drives it. How could the legacy of all that science be that half of everybody has a chronic illness, including children? Who wants to know that?

Injected into monkeys, XMRV causes a low level latent infection, which isn’t communicated by transfusion. However, Dr. Mikovits found other sequences in patients besides XMRV. Here is a slide from her recent lecture at Dr. Enlander’s conference showing just that.

The Exotic Biology of XMRVsfinal slide 10

Of course, she doesn’t have her notes, so all of the unpublished work she did is lost to us. Meanwhile, the WPI continues to suck up a big chunk of the government dollars spent on our disease, while their co-founder awaits jail for his felony convictions.

$450,000 of taxpayer money was spent on the specimens collected for the Lipkin study, which was negative, as expected. The good news was that Dr. Lipkin was going to use those specimens to answer some questions. I guess he couldn’t get funding. Instead those specimens have gone to Dr. Peterson, who is raising money to look for evidence of arthropod borne disease, even though the collection criteria for the specimens specifically excluded Lyme Disease. How’s that for looking under the streetlight?

Meanwhile, as a patient community, we are back to case definitions, an obfuscation if there ever was one. A case definition is an exercise in futility, because the disease isn’t one thing. ME/CFS is a garbage pail diagnosis, somewhere to put all those patients who feel awful, have non-specific immune dysfunction and secondary mitochondrial failure, with nothing else to define their illnesses. Many roads lead to Rome. The question of causation is simply too complex for our current scientific methods. The ability to analyze huge amounts of genetic material cost effectively is coming, but it isn’t here yet. It may turn out that the specific retroviral sequences involved are found in particular families or groups of people with certain environmental exposures, e.g. certain chemicals or vaccines.

With the burying of XMRV has come a resurgence of Lyme Disease as The Cause. The CDC recently admitted that they were low on the number of annual cases by a factor of ten, right on time for the release of Baxter’s new vaccine and Lyme test. The CDC’s admission is unfortunately a boon to ILADS, a renegade medical society based on an incestuous relationship with a private lab, to which they refer and then use the unvalidated results to perpetuate their mythology: Patients congratulated for “herx” reactions to antibiotics, rather than recognizing it for the damaging cytokine storm that it is. Then there’s the one about how enough antibiotics in the right combination for the right duration can eradicate it, despite all evidence to the contrary. And the one about how chronic Lyme Disease is a distinct entity from ME/CFS, despite the fact that the two groups are clinically indistinguishable without test results from this one particular cash only lab whose results no other lab can duplicate. And then, if they happen to get a negative test, which is a rare event, the most imaginative of all, seronegative Lyme can be diagnosed clinically, even in people with no risk factors. It’s a scam and a dangerous one. I saw this yesterday: Is Lyme Disease Contagious? Clues Hint That It May Be A Sexually Transmitted Disease, quoting no other than Dr. Raphael Stricker, the most published of the so called LLMDs. Here is what the Office of Research Integrity at the NIH has to say about him (link):

Raphael B. Stricker, M.D., University of California at San Francisco. An investigation conducted by the University found that Dr. Stricker falsified data for a manuscript and a PHS-supported publication reporting research on AIDS. In the manuscript, Dr. Stricker selectively suppressed data that did not support his hypothesis, and reported consistently positive data whereas only one of four experiments had produced positive results. In the publication, Dr. Stricker reported that an antibody was found in 29 of 30 homosexuals, but not found in non-homosexuals. However, Dr. Stricker”s control data, which he suppressed, showed the antibody in 33 of 65 non- homosexuals. The falsified data was used as the basis for a grant application to the National Institutes of Health. The ORI concurred in the University”s finding. Dr. Stricker executed a Voluntary Exclusion and Settlement Agreement in which he has agreed not to apply for Federal grant or contract funds and will not serve on PHS advisory committees, boards or peer review groups for a three year period beginning April 1, 1993. The publication “Target platelet antigen in homosexual men with immune thrombocytopenia” in the New England Journal of Medicine, 313: 1315-1380, 1985 has been retracted (New England Journal of Medicine, 325: 1487,1991).

ME/CFS, Chronic Lyme Disease, mold illness, MCS, fibromyalgia, GWI, all have pretty much the same symptoms. Lots of tunnel vision going on in each group. A retroviral hypothesis is the most parsimonious explanation for all of these diseases, which didn’t exist or were very rare when I went to medical school 35 years ago. Dysautonomia, now common, wasn’t seen then except rarely in advanced diabetes. A retroviral hypothesis fits for ASD also. This very brief distillation is all referenced elsewhere on this blog. However, even when one turns to the literature for answers, you have to figure that a very large proportion of it is wrong due to mistakes, contamination and fraud (lots of that going around). Why Scientific Studies Are So Often Wrong: The Streetlight Effect. So whatever cohort you fall into, which may depend more upon which doctor you go to than anything else, you get to choose between neglect by conventional doctors and expensive overtreatment by the “experts”. My advice is avoid doctors and eat your vegetables.

Tonight’s song: We Shall Overcome by Pete Seeger

Bats In The Belfry

I missed Dr. Lipkin’s dog and pony show a few days ago, but thank you to ME/CFS Forums for posting a transcript. Here again, it appears he has dismissed the only finding that actually adds to the discussion. It is just like last time when he dismissed the only positive finding in the XMRV study, that 6% of the people tested were positive for an antibody to a nasty mouse retrovirus, significance unknown. This time:

We found retroviruses in 85 percent of the samples. Again, it is very difficult at this point to know whether or not this is clinically significant, and given the previous experience with retroviruses in Chronic Fatigue I am going to be very clear in telling you, although I am reporting this at present in Prof. Montoya’s samples, neither he nor we have concluded that there is a relationship to disease. I’ll repeat that one more time. We found retroviral sequences, but their relationship, at this time, to Chronic Fatigue Syndrome is unclear and, in fact, if I were to place bets and speculate, I would say that they are not going to pan out.

In addition to this astonishingly unscientific statement, in the same week, he announced other recent findings. From the BBC News: “They found nearly 60 different types of viruses, most of which had never been seen before”, in one species of bat. He extrapolated this to suggest that there are 320,000 new viruses in mammals still to be discovered. However, he could find nothing at all in hundreds of sick humans. Presumably using the same techniques. Or is that the problem? Doesn’t it seem unlikely that there would be nothing to find in sick humans with low NK function and a propensity for opportunistic infections of all kinds? We are mammals after all. Here is the paper: A Strategy To Estimate Unknown Viral Diversity in Mammals. He wants to spend billions of dollars in an attempt to avert a pandemic, when he has several existing pandemics staring him in the face. I guess existing diseases aren’t as much fun as teaching Gwyneth Paltrow how to have a seizure. Then again, maybe we all really do need to be vaccinated for the next bat virus we might encounter.

But, he did give the nod that we are sick, not just crazy, so I guess that’s a good thing coming from such a high profile scientist. We have elevated levels of proinflammatory cytokines and chemokines. Completely nonspecific, all downstream effects, but abnormal numbers nevertheless, something measurable. In my experience however, the commercially available tests (Labcorp and ARUP via Quest) don’t show the abnormalities he describes (and which have been previously described by others), so we need more sensitive assays commercially. I’m not sure why the difficulty, but the clinical reality is that the doctors who are actually treating the patients have almost nothing to follow, except for a very few nonspecific inflammatory markers in some patients, e.g. hsCRP, C4a and TGF beta-1.

So that leaves us exactly nowhere, as usual. We are not going to be saved anytime soon by the medical model. Look how much the scientific method has accomplished for us in the last few years:-). As a doctor, I have a small bag of tricks to fight a terrible, incurable disease. However, it is an inherently unstable disease, relapsing and remitting all on its own. Look for a way to get a foot in the door. It is possible to tip the balance in favor of better health with global strategies that support the body, mind and spirit. Find synergy. Ali and I continue to be committed to the Wahls paleo diet. Less suffering for sure, after only a couple of months. Just like oxygen, methylation supplements, hormone balancing, we feel better from this intervention. Not expecting a cure, but we are both experiencing a bit more uphill movement, even though our diets were already pretty good. Please take a hard look at this diet, most likely beneficial for all neurodegenerative and inflammatory diseases.

Ali has all but moved out, her symptoms so manageable that she is mostly living with her boyfriend in Albuquerque, despite nearly new construction that once triggered her MCS so badly, she almost couldn’t be there. There was a time when I didn’t think she would ever be able to live away from me. Bittersweet…

She Blinded Me With Science (Live) by Thomas Dolby

Status Post XMRV

I have been in the doldrums, but since blogging is my hedge against powerlessness…

This is how deep in it I have been; my inner blogger didn’t even twitch for this: Partial molecular cloning of the JHK retrovirus using gammaretrovirus consensus PCR primers. Grossberg SE, …, Sun HY

 “Unlike earlier reports, in which MLV-like sequences were identified in human source material, which may have been due to murine contamination, budding retrovirions were demonstrated repeatedly by electron microscopy in uncultivated lymphocytes of the index patient that were morphologically identical in their development to the virions in the JHK-3 cells, and immunological evidence was obtained that the index patient produced IgG antibodies that bound to the budding viral particles in patient PBMCs and in the JHK-3 cells. “

It’s tough to keep writing about it when the medical and scientific communities aren’t interested. This group has been publishing about their retrovirus since 1995. Andrew Mason and Hervé Perron have been publishing about their respective retroviruses for over a decade and nobody is interested:

I haven’t heard or seen anything that makes me feel hopeful of meaningful treatment since the demise of XMRV. The only perhaps promising development was Dr. Hornig saying publicly that they have isolated a novel pathogen. Cruel to have said so without more information, but let’s hope it is true and they publish soon. Otherwise, it is pretty much the same ole, same ole.

Chronic Lyme Disease seems to be experiencing a horrifying resurgence as the explanation for what ails us. A wise doctor, one of the few, once told me that antibiotics are the surest path to worse. Wish I had listened to him. ILADS hasn’t updated their guidelines since 2006, even though lots and lots of people have been made worse by their protocols. They are stumped because in all these years they still can’t show that what they do is a good idea.

Borrelia burgdorferi is obviously one of the things that can happen to the microbiome if one is bitten by deer ticks. The problem is that it can’t be eradicated  with antibiotics once it is established and the antibiotics are harmful. Weigh these papers:

This is as positive as it gets in the literature:

Nevermind that we can’t really tell who has it or whether it is what is making them sick. They could tell that a man from 5000 years ago, found frozen in the Aps had Bb, but he died of trauma. However, they can’t really tell if we have it. The Iceman’s Genome Reveals Evidence Of Lyme Disease, Lactose Intolerance And Distant Relatives.

But what about the people who do get better from antibiotics? My daughter got several remissions in the early years. Did it even have anything to do with Lyme? Broad spectrum antibiotics kill in a broad spectrum way.

So who should get antibiotics? That is the million dollar question. I keep listening and it seems to me the people who are better off for having taken antibiotics know it pretty quickly when they go on. When it works, it works. This idea that a prolonged “herx” is a good thing is lunacy. As bad as blood letting with leeches. It is a cytokine storm, not a good thing and if it lasts a long time, it is damaging.

Two suicides in the Facebook ME/Lyme community yesterday. Both beautiful young women. This should not be happening! And the response is, we understand why they did it. How can that be? When is it going to change? Not soon. Nobody is going to save us. We have to help ourselves. The disease is treatable. Not curable, but treatable. Read the last blog. K is not an anomaly. She has come a huge distance by finding synergy in gentle therapies, none of which would have done it alone. But those therapies aren’t even on the table for discussion.

Ali and I have been on the Wahls diet for 2 weeks. Terry Wahls is a physician with secondary progressive MS who got herself out of a reclining wheelchair with diet. She was already on a paleo diet which had slowed her progression, but modified it to get reversal. Since my working hypothesis is that we have MS Light, I decided to give it a try. I already know it is helping me. My chronic nausea is almost gone and my gut function is much improved. Ali is less sure, but likes it and plans to continue. Only two weeks. We were already on a good gluten free, mostly dairy free, whole food diet. Changing diet is a process, but we have taken it to the next level. Force feeding vegetables:). 9 cups daily, or as much as we can stuff in. Lots of leaf and berry smoothies. We have eliminated grains and added sea vegetables. Working on organ meats and bone soup.

There is no one right diet for everybody. Nor do I expect it to be curative. Like everything I do, it is about quality of life. In particular, getting our food from local CSA’s and learning about the source of what we are eating is feeling really good. Learning about food is fascinating. Focusing on making each bite nutrient dense is working for me. Yes, it is a lot of prep work and yes, it is more expensive. I couldn’t have started without Ali, but now I could do it alone. I posted something about the diet on Facebook and the comments that it is impossible are heartbreaking. Why do these patients have no help?

Dr. Wahls has a book on Amazon Minding My Mitochondria in print and kindle editions. Here are her recent papers:

She is doing the work. The Wahls Foundation is working to further her research and is on Facebook. She found something that helps and she is putting it out there. Here are the videos that inspired me: 

The Doomsday Scenario

An important new paper has been published: Xenotropic MLV envelope proteins induce tumor cells to secrete factors that promote the formation of immature blood vessels. Muegai et al. The et al includes Pathak who published the paper with Coffin which identified XMRV as a virus created in the lab. From the title you might think it is about cancer and blood vessels; however, look at the last sentence of the conclusion:

… the results suggest that xenograft approaches commonly used in the study of human cancer promote the evolution of novel retroviruses with pathogenic properties.

Here is the crux of the matter:

The evidence that XMRV was generated as a consequence of studies aimed at elucidating the pathology of human disease is disturbing in that it highlights long feared dangers of use of xenograft tissues in clinical settings, including porcine valves [14,15]. Of even greater concern, the results support the idea that attempts to develop better therapeutic interventions might inadvertently promote the development of pathogenic viruses. However, the following observations refute this possibility: First, although xenotropic and polytropic MLVs have been described as far back as 1970 [16,17], as of yet there has been no validated evidence of human infection by this class of viruses. Second, despite intensive investigation of XMRV by many laboratories [1,18,19] there is no evidence that XMRV is capable of inducing transformation of cells [1,20], although there is recent evidence showing that XMRV infection of LNCaP cells resulted in modest increases in proliferation, and invasion of cells into Matrigel in vitro (Pandhare-Dash et al. [4,21]).

Are you reassured? Their first point is a basic logical fallacy. Absence of proof is not proof of absence. Nobody ever found it, so it isn’t there. Their second point says XMRV, the manmade gamma retrovirus about which we know the most, isn’t dangerous, maybe. What a relief. Yet even they are now admitting, XMRV is not the only one out there. They found a new one for this paper. So now there are at least two, and no longer such a remote possibility.

The studies described herein address these questions, and show that at least one other XMRV-like virus exists, and that the virus evolved the ability to infect human cells and to express gene products that impact tumor pathogenesis.

But no need to panic. The folks that brought you this mess, will figure it out one of these decades. Recombinant Origin of the Retrovirus XMRV, now a year old, where they argued that the chances were “vanishingly small” that XMRV wasn’t created in a lab in the mid 90’s, while studiously ignoring the fact that other similar events were in fact quite likely. So they are finally admitting that the chances aren’t so small, since there have been so many chances. Now there are two. Or is it three? This paper, identified a cell line in use at the NCI that produces another infectious XMLV: The Human Lung Adenocarcinoma Cell Line EKVX Produces an Infectious Xenotropic Murine Leukemia Virus.

Inductive logic is forbidden. No connecting the dots allowed. And who can blame them, when it has been recently demonstrated that dot connecting gets you burned at the stake in the scientific community. Have to start with what we know and carefully build step by step, hoping that the pyramid ends with something coherent. God forbid, we should decide that we have learned something new, something so big that a top down approach should be employed. It is so big in fact, it could explain why 133 million of our people and 55% of our children have chronic illnesses in the US, and why 20% of adults in the developed world have an autoimmune disease. ME/CFS is little. It is time for a revolution. It is an emergency. I wrote that same sentence in 2010 and nothing has changed.

How many young people have been felled by ME/CFS since then? I know about one teenager that was treated in 2010 with antiretroviral drugs and recovered. His mother posted on this blog anonymously at one point, but was presumably prevented from going public. Sick for 8 months, better in 6 weeks. Treated for 6 months and remained in remission off treatment, as far as I know. How did that case report not  make it into the literature? It is unconscionable. I am sick of hearing about how an N of 1 is irrelevant. An N of 1 is called a case report. If important enough, it leads to a pilot study and then a clinical trial.

This burden of chronic disease in children is our replacement for the 20% that used to die before the age of 5 of infectious diseases. So instead of dead children we have live disabled ones. What is going to happen to all these disabled children? Whether the cause turns out to be an activated HERV, or an exogenous simple animal retrovirus (alpha, beta or gamma), the use of antiretroviral drugs is a logical thing to try. It is unfortunate that the only drugs available to us were developed for a retrovirus that is phylogenetically dissimilar from the simple viruses in question here, but even so, AZT, Viread, and Isentress have had a positive effect on a number of patients with ME/CFS, incomplete and, after a while, not clearly worth it, but there is a noticeable positive response in a percentage of patients, which appears annecdotally to be greater than placebo. That should be a beacon in the fog, not a reason to make the drugs taboo. Dr. Snyderman’s cancer is stable on full HAART. Shame on both the scientific and medical communities for ignoring him.

What would happen if you gave antiretrovirals to children at the time of an autistic regression? I know your government wants you to believe that the astonishing increase in ASD, now acknowledged by CDC at about 2%, is because we got better at diagnosing it. While that is undoubtedly partially true, since it is now a common disease, it is insulting to our intelligence to reassure people on that basis. It is only 2%, so no worries; your individual chances of having an autisitic child are still low. But what are your chances if you have CFS or a first degree relative with CFS, or autism, GWI, Lyme Disease, PANDAS, RRMS? These diseases are running rampant. Certain families bear an incredible burden of illness, including early aggressive reproductive and hematologic cancers. It is frightening, even if you look at only one disease at a time, but as part of a preapocalyptic whole involving the health of the species? Terrifying. Virus, injury, genetics. Many perfect storms.

Whatever happened to vaccines being inappropriate for people with immunological abnormailities? Given that patients with various immunological problems now encompass a very significant proportion of the population, the entire vaccine program needs to be seriously reevaluated. Continuing to give ever increasing immunological challenges to a patient population with seriously declining immunological health, for diseases that are extremely unlikely to cause long term morbidity or mortality, is no longer clinically justifiable in my opinion. It is medically incorrect and unethical at this point to take the current vaccination schedules for civilians and the military at face value, especially in light of the implications from this paper, and the recent acknowledgement that GWI is not in fact limited to the veterans of Desert Storm, but still occurring.

The upcoming FDA meeting will no doubt give mention to many more dangerous treatment options than AIDS drugs. AIDS patients got the best. Lots of very clean drugs to work with that cost billions to develop. There are probably many drugs on the shelf that didn’t work well enough for HIV, but might have activity against the viruses we are dealing with. My guess is antiretrovirals will not even be on the table for discussion.

IT IS STILL HAPPENING. Every single day. New people getting sick that should be treatable. The scientific community should not be allowed to take their own sweet time about this. It is not acceptable in the midst of this pandemic for them to withhold anything clinically relevant, whilst expressly trying to prohibit the off-label use of legal, safe drugs that might help patients who are in dire straights, patients suffering beyond belief, for whom there is no meaningful treatment. But the culture is to “burn at the stake” any scientist that steps out of bounds, as we have already witnessed. Doctors too, for that matter.

Look at the tunnel vision in this paper. It is all about cancer and xenografts. No mention that gamma retroviruses cause neuroimmune diseases in vivo, as well as cancer. No mention that there are aspects of modern biotechnology that could be causing the same or worse problems than the ones described in this paper, notably hybridoma technology. And nothing about vaccines, the sacred cow, which contain foreign DNA and are parenterally introduced, given in ever increasing numbers and combinations to an ever more vulnerable population. Live attenuated vaccines are grown in cultures known to express animal retroviruses, e.g. chick embryo, mouse brain culture, monkey kidney cells. Here is a list of vaccine excipients and culture mediums used for production from Wikipedia. And that’s now. Can you imagine what the technology was like in the 50’s, 60’s and 70’s? Viruses successively passaged through mouse brains, passaged meaning brain sucked up with a big needle and injected into the next mouse, then eventually the resultant sludge was injected into or fed to people. Now we can tell what we are doing and we are still doing it. Chemical Induction of Endogenous Retrovirus Particles from the Vero Cell Line of African Green Monkeys.

The paper under discussion mentions the “plasticity” of these viruses. They recombine and rescue each other. But scientists aren’t allowed to connect the dots, even when obvious, as it should have been a couple of decades ago, since it was known by the 70’s that these viruses were there. Here, written by a couple of the scientists who have recently contributed to the distortion of the true significance of XMRV, telling us in 1995 what they feared, but did nothing about. I have posted it before and try not to repeat myself, but in light of this paper, it deserves to reappear.


The assumption that these viruses could not harm humans was made on very shakey ground; everybody was having too much fun tinkering to be stopped by a few qualms. There were a few absence of proof experiments. What hubris! Now, this is the only explanation for ALL of the observed phenomena, encompassing the environmental and genetic aspects, the variations on a theme so clear to see in the various patient cohorts. The Lipkin paper came up with positive serology in 6% of the study population, patients and controls, to a very nasty defective murine retrovirus that produces Env. That particular mystery should be a high priority by now. Why is the 6% not being studied intensively? They found positive serology in human beings to pathogenic retroviral Env in Lombardi et al, they found it in Lo et al and they found it in the Lipkin study. The 6% may be, probably is, only one of many. But no need to panic.

On the personal side, as I reported last time, I went back on Viread. I again noticed an uptick in function and ability to withstand stress 6 or 7 weeks after starting it. My blood pressure is now well controlled on additional antihypertensive medicines, in fact better controlled than at any other time in my illness. I started Isentress a couple of days ago and plan to add Kaletra very soon. Ali remains remarkably stable on Viread and Isentress for 3 years now. Her life is very full. She is productive and happy. Her most limiting symptom remains MCS.

I just returned home after a trip to Tucson seeing patients. The first 5 patients I saw were 3 women almost exactly my age and 2 men, both 48 years old and sick for almost four decades. That strikes me as a bit much for coincidence. I have noticed for years, and especially since I’ve been writing this blog, that my December 1953 birth date seems to be at the peak of a bell curve for middle aged ME/CFS women, suggesting something went out horizontally. Was it when we were born? We received the oral polio vaccine, on a sugar cube, but we wouldn’t have all been the same age when we got it, since it wasn’t released until 1961. And we know that there were outbreaks before the polio vaccine. Papers have documented certain years with peak waves of onset. All of this fits with the idea that it has happened multiple times and each time, it looks a little different, e.g. average age of onset, gender susceptibility, most prominent symptoms, thus the misconception that it is a heterogeneous problem.

Just as there were many retroviral invasions in the distant past, in this paper we have emerging evidence that it has happened again, on a grand scale, over a very short period of time. There are most likely already some viruses that are endogenized in families, since it has gone unchecked for so long. The very high incidence of PCOS in young ME/CFS women may be consistent with a retrovirus invading the germline. When I first wrote about this possibility, I thought it was irreparable, a true doomsday scenario, but it is not. Evolution will deal with it, even while our fertility is dropping at an alarming rate. Deletions will occur, possibly in not very many generations. We will learn how to stay methylated to keep our viruses quiescent. We will eventually learn to manipulate epigentic factors in our favor. But like carbon emissions, we need to stop it now. A retrovirus or pieces of a retrovirus now and again, repeated exposures to endocrine disruptors, synthetic hormones and steroids, add a little Bt toxin, a “cover your ass” CT scan and a couple of radioactive tracers for worthless imaging, courtesy of your doctor, and voila! A recipe for the disaster that is occurring, while nobody panics.

Today’s song: You Haven’t Done Nothing by Stevie Wonder

MS Light?

What’s occurred in the last 30 years is criminal, Mikovits says today. “Mothers and fathers got sick, their children got sick.” But with heightened attention, she adds, patients are likely to get help soon. Even lacking a causal pathogen, biomarkers in this patient population can be studied for clues. “We can find therapies for the CFS patient population even before we determine the exact cause,” Mikovits says.
Chasing the Shadow Virus by Hillary Johnson Discover March 2013.


As I said last time, I started Viread again, because I became dangerously hypertensive, a few weeks after stopping it. I had a significant drop in my BP, almost to normal from days 6-12, then it went up again, not quite as high as before, but very high. After much fiddling, it is now controlled, but I had to add additional antihypertensive medication. Happily, after a month back on Viread, there is a downward trend again and I’m hoping I’ll be able to wean from the extra treatment soon. This is not the first time I’ve had this problem, but it was the worst episode yet, and was related in time to stopping Viread. I have been feeling significantly better for the last week, and am also back to baseline productivity. I flared for the first few weeks I went on Viread the first time also. I am going to Tucson to see patients in a couple of weeks and when I come home, am planning to restart Isentress and then Kaletra. I really didn’t want to go back on Viread, but it does seem that I’m getting a payoff again from it. I went off because I wasn’t doing well, and things got even worse, now better back on. I am just reporting, not explaining why or how. The disease is a relapsing remitting illness all on it’s own and changes may or may not have anything to do with the last thing you did.

My reading lately has been about retrotransposons and HERVs, especially MSRV, multiple sclerosis-associated retrovirus. Here is a cutting edge, must read paper, senior author Hervé Perron, whose name appears on most of the important papers on this topic: The DNA Copy Number of Human Endogenous Retrovirus-W (MSRV-Type) Is Increased in Multiple Sclerosis Patients and Is Influenced by Gender and Disease Severity.

MSRV increases its copy number in PBMC of MS patients and particularly in women with high clinical scores. This may explain causes underlying the higher prevalence of MS in women. The association with the clinical severity calls for further investigations on MSRV load in PBMCs as a biomarker for MS.

Human endogenous retrovirus type W envelope expression in blood and brain cells provides new insights into multiple sclerosis disease.

The envelope protein from multiple sclerosis (MS) associated retroviral element (MSRV), a member of the Human Endogenous Retroviral family ‘W’ (HERV-W), induces dysimmunity and inflammation.

Env antigen was detected in a serum of 73% of patients with MS with similar prevalence in all clinical forms, and not in chronic infection, systemic lupus, most other neurological diseases and healthy donors (p<0.01). Cases with chronic inflammatory demyelinating polyneuropathy (5/8) and rare HC (4/103) were positive. RNA expression in PBMC and DNA copy numbers were significantly elevated in patients with MS versus HC (p<0.001). In patients with MS, DNA copy numbers were significantly increased in chronic progressive MS (secondary progressive MS vs relapsing-remitting MS (RRMS) p<0.001; primary progressive MS vs RRMS -<0.02). Env protein was evidenced in macrophages within MS brain lesions with particular concentrations around vascular elements.

The above paper concludes that exogenous virus production is unlikely. Particles have been identified in MS patients going back to 1989: Leptomeningeal cell line from multiple sclerosis with reverse transcriptase activity and viral particles. 

In fact, a virus was identified in MS in 1975. Look at how far they got with the technology at hand at that time: Multiple sclerosis-associated agent: transmission to animals and some properties of the agent.

In confirmation and extension of observations by Carp and his associates, brain tissue and sera from patients with multiple sclerosis (MS) were found to harbor an agent which induces a transitory depression in polymorphonuclear leukocytes (PMN) in mice as well as in rats, hamsters, and guinea pigs. All of eight MD brains contained this agent at titers as high as 10(-9)/g of brain tissue. The agent was found in MS sera at titers up to 10(-3)/ml of serum, but its presence depended to some extent on the clinical status of the patients; it was observed more frequently in sera of patients with active disease (73%) thatn in sera of patients with quiescent disease (31%). Control brain tissues or sera failed to induce PMN depression. The apparently MS-associated agent (MSAA) passed through 50-nm but not 25-nm membrane filters (Millipore Corp.) and was largely sedimented at 105,000 X g but not at 50,000 X g for 1 h. It multiplied to high titers in the central nervous tissue of the inoculated animals and could be serially transmitted from animal to animal by passage of brain homeganates. Various observations and considerations appear to preclude that MS-associated agent represents an indigenous animal virus. Although its role in MS remains to be determined, it should be considered a candidate for the etiology of this disease.

Endogenous retroviral genes, Herpesviruses and gender in Multiple Sclerosis contains electron micrographs of MSRV particles.

Particle-associated retroviral RNA and tandem RGH/HERV-W copies on human chromosome 7q: possible components of a ‘chain-reaction’ triggered by infectious agents in multiple sclerosis?

The human endogenous retrovirus link between genes and environment in multiple sclerosis and in multifactorial diseases associating neuroinflammation.

Endogenous retroviruses represent about 8% of the human genome and belong to the superfamily of transposable and retrotransposable genetic elements. Altogether, these mobile genetic elements and their numerous inactivated “junk” sequences represent nearly one half of the human DNA. Nonetheless, a significant part of this “non-conventional” genome has retained potential activity. Epigenetic control is notably involved in silencing most of these genetic elements but certain environmental factors such as viruses are known to dysregulate their expression in susceptible cells. More particularly, embryonal cells with limited gene methylation are most susceptible to uncontrolled activation of these mobile genetic elements by, e.g., viral infections. In particular, certain viruses transactivate promoters from endogenous retroviral family type W (HERV-W). HERV-W RNA was first isolated in circulating viral particles (Multiple Sclerosis-associated RetroViral element, MSRV) that have been associated with the evolution and prognosis of multiple sclerosis. HERV-W elements encode a powerful immunopathogenic envelope protein (ENV) that activates a pro-inflammatory and autoimmune cascade through interaction with Toll-like receptor 4 on immune cells. This ENV protein has repeatedly been detected in MS brain lesions and may be involved in other diseases. Epigenetic factors controlling HERV-W ENV protein expression then reveal critical. This review addresses the gene-environment epigenetic interface of such HERV-W elements and its potential involvement in disease.

Here is a paper about something that could turn into useful therapy, overlooking the significant risks associated with the administration of monoclonal antibodies and the inherent risks involved in hybridoma technology, which involves fusing human cancer with animal B cells. GNbAC1, a humanized monoclonal antibody against the envelope protein of Multiple Sclerosis-associated endogenous retrovirus: a first-in-humans randomized clinical study.

Human endogenous retrovirus (HERV) genes represent about 8% of the human genome. A member of the HERV family W, the Multiple Sclerosis-Associated Retrovirus (MSRV) gene, encodes an envelope protein (Env), which can activate a proinflammatory and autoimmune cascade through its interaction with Toll-like receptor 4. Due to its proinflammatory property and an inhibitory effect on oligodendrocyte precursor cell differentiation, the MSRV-Env protein could play a crucial role in the pathogeny of multiple sclerosis. GNbAC1 is a humanized monoclonal antibody of the immunoglobulin G4 type, which is directed against MSRV-Env. After validation of the MSRV-Env as a therapeutic target in preclinical experimental models, a clinical development program was initiated.

In these healthy male subjects, the safety and pharmacokinetic profiles of GNbAC1 appeared favorable. These findings are expected to allow for the launch of a Phase II development program for this innovative therapeutic approach in patients with multiple sclerosis. ClinicalTrials.gov identifier: NCT01699555.

However, rather than injecting antibodies to gobble up the viral envelope, given the real and theoretical problems with monoclonal antibodies, it would be better to keep Env from being produced in the first place. Maybe a protease inhibitor is the missing link. AIDS drugs didn’t work well until they had PI’s. Dr. Snyderman’s data suggests this was the case for him. I am happy to report that he remains stable at 32 months. Does a response to a PI imply exogenous virus? How far does a HERV have to get in its reproductive cycle before a PI would do some good? SFFV is a defective virus with a pathogenic envelope. If MSRV produces variable particles, some of which appear complete on EM, is it ever infectious?

Reading about MS, thinking about my own clinical presentation and putting it together with everything we have learned since XMRV entered our lives, ME/CFS may exist on a spectrum with MS, in the same way that Aspergers Syndrome is part of the autistic spectrum. Certainly, we are a variation on a theme. I have called it MS light before and I think it is a good working hypothesis for now. Up To Date’s summary on MS is here. Note the many similarities, genetics, epidemiology (including cluster outbreaks), possible problems with the Hepatitis B vaccine. It seems to me our best hope post XMRV is to ride on the coattails of MS, even though it is pathetic that we need to, given that there are at least three times as many of us.

I’m getting lots of questions about what I think of the paper published by De Meirlier et al. Plasmacytoid dendritic cells in the duodenum of individuals diagnosed with myalgic encephalomyelitis are uniquely immunoreactive to antibodies to human endogenous retroviral proteins. I am not going to evoke all the reasons why I might have a problem with this paper, whatever it says. I have moved on. Much of it is documented elsewhere on this blog.

Taking the paper at face value, problems with it are the tiny sample size, from patients that I hope had very serious GI complaints, compared to the patient population as a whole, since, presumably, they warranted a duodenal biopsy. I would like to take this opportunity to emphasize that I am completely opposed to taking any risk of harming fragile patients with unnecessary procedures in order to study the disease. There is no reason to do duodenal biopsies on garden variety ME patients, so the patients in this study should have had significant inflammatory bowel disease, not just IBS. The procedure carries a significant risk. A duodenal punch biopsy can result in death. There is lots of tissue to study without resorting to that. Fresh tissue is harvested all the time for other reasons, there is lots of material to autopsy and lots of specimens in paraffin, which is what was used in this study. My small intestine in paraffin is stored down the street at the local hospital. And plasmacytoid dendritic cells can be harvested from peripheral blood.

The simplest explanation for the findings in this paper is that there was a range of proteins consistent with a generalized activation of HERVs. Many things can transactivate HERVs including recombination events and exposure to exogenous retroviruses. Perhaps they didn’t name the HERV because they were all transactivated? This is what you might expect in someone with inflammatory bowel disease. We have no idea whether these people had a neuroimmune disease or not. The fact that they had a range of symptoms that would qualify for a clasification of CFS is neither here nor there. Endogenous retrovirus-K promoter: a landing strip for inflammatory transcription factors?

There are quite a few papers worth reading in the references, but they missed one:  Cell-free HTLV-1 infects dendritic cells leading to transmission and transformation of CD4(+) T cells.

I hope they are right. It would set us on a path to catch us up to MS, where we belong. However, the paper is so vague. Antibodies to proteins expressed by a generic HERV. This negative paper was also just published: Human Endogenous Retrovirus-K18 Superantigen Expression and Human Herpesvirus-6 and Human Herpesvirus-7 Viral Loads in Chronic Fatigue Patients. It is good news for us that this avenue of research is being pursued.

I expect the De Meirleir paper to get shot down or be ignored completely. The scientific world will probably only read it for laughs, considering the source. They didn’t find a “real” virus this time, so nobody needs to spend millions of dollars to prove it wrong. MSRV was ignored for decades, even though it is associated with a more sympathetic disease than ME/CFS. Progress with it has been glacial, revealing the non-urgent, almost lackadaisacal attitude of the biomedical world towards activated HERVs, even one that was shown to produce viral particles over 20 years ago. In any case, infectious or not, there is increasing agreement that HERV W is associated with MS and can transcribe an Env protein which is neuropathogenic.

And another related illness: HERVs expression in Autism Spectrum Disorders.

I am particularly happy to report that my friend Dr. Mikovits is doing well through it all. She has received many letters of support and asked me to let the community know that she is fine and excited about the future. She is consulting with respect to drugs and diagnostics. She continues to lecture. Currently, she is working on projects with Dr’s Ruscetti and Lipkin, and, in a translational capacity with several medical doctors, Eric Gordon, Chitra Bhakta, Derek Enlander, Paul Cheney, Michael Snyderman and myself.

This excerpt is from an email to me a couple of days ago when I asked her a few questions for this blog:

Planning for the April 25th FDA meeting…a two day meeting to get drug companies and clinical trials going..to avoid the failure of Hemispherx..we have a huge opportunity here..talk about that..tell the patient community I will go there and work to bring them the drugs that are out there as soon as possible..we as a community do not have to go back to basic research where we are decades away..we can translate what we know.. write about that …move forward..

My background is in antiviral drug mechanisms and epigenetic drug development..I am going back to my roots to focus on drug development in infectious/ inflammatory disease…I can now apply my expertise and extensive network to ME/CFS..

Dr. Lipkin said this about her in Nature, only a few months ago:

I feel very badly for Mikovits, [her co-author] Ruscetti and Harvey Alter [a hematologist at the NIH Clinical Center in Bethesda, Maryland, who led one of the CFS studies]. Mikovits in particular — she has lost everything. She can be wrong but she’s not a criminal. She has been honest in a respectful, forceful way and said that we have to conclude that we were wrong. You can imagine how difficult it must be, and I think she should be applauded. Lots of people wouldn’t have the balls to do that. She has come across as a scientist who really believes in the importance of truth.

Dr. Judy has come a long way since then, pulling herself up by her own bootstraps. I am in awe of her resilience. Handed lemons, she is making excellent lemonade. Stay tuned.

Today’s song: Titanium by David Guetta

Twists And Turns

The world will not be destroyed by those who do evil, but by those who watch them without doing anything. ~ Albert Einstein

When I started this blog, I promised to share my journey as it unfolded, before knowing the outcome. My goal was always to explore and learn, not convince anybody I’m right, since I clearly don’t know. So here’s what’s happened since I last wrote. A day after I wrote the last blog, I ran out of Cozaar (losartan), forgot I hadn’t put it in my pill case for the whole week and missed two doses. Before restarting it, I checked my blood pressure and it was 212/127. I’ve missed losartan other times in the last few years, but never with such a severe elevation and always responsive to restarting the med. But this time, my pressure stayed ridiculously high, even after adding a second drug, amlodipine, which I have used as a second drug before, but haven’t needed in several years. I have a long history of labile hypertension and a period of persistent severe hypertension was the problem that ended my Emergency Medicine career in 1996.

It happened about a year after my first symptom, following a period of unrelenting stress. The blood pressure elevation came with a feeling of doom. The numbers were often high, for most of a year, despite all the drugs my doctors threw at it. Initially my academically inclined physicians were excited by creepy medically unexplained symptoms in a colleague. They thought I had something cool, like a pheochromocytoma or carcinoid. They sent off all their esoteric tests and when it was all negative, or almost negative, they concluded that I either had a world class case of white coat hypertension or was crazy and not taking my meds. Indeed, the independent medical exam ordered by my disability carrier concluded I could return to the ER if I took my antidepressants like a good girl, despite my protestations that I wasn’t depressed and my blood pressure was very high at home too, with nary a white coat in sight, besides my own.

It is a long, sad story, filled with injustice and stupidity, mine and my doctors’. I’ve written some of it here before, but I’m mentioning it again now, because this current episode was so similar to what happened then. The hypertension occurred in the context of an abnormal stress response and autonomic dysfunction/instability. Because my dysautonomia occurs in the setting of hypertension, I don’t have POTS per se, but a variant. The autonomic nervous system wasn’t even part of the discussion back then, and here is why. The first paper in the medical literature on POTS, or orthostatic postural tachycardia syndrome, was published in 1993, only 2 years before my first symptoms and had no penetration as yet to an average work-a-day doc: Idiopathic postural orthostatic tachycardia syndrome: an attenuated form of acute pandysautonomia?

Even by 2002 when my husband developed severe dysautonomia, it was not part of the common medical lexicon, as it is beginning to be now, finally. Recognizing autonomic nervous system dysfunction as a core deficit in Gulf War Syndrome sufferers is a big step from our old concept of PTSD. So what do we think? Was it a new phenomenon? Or were all the doctors who came before me such poor physical diagnosticians that they missed it without the benefit of tilt tables?

As I have previously reported, I did not have viral onset CFS, but a very atypical onset and course, which was clinically more similar to Gulf War Illness than ME or CFIDS, as it was called then. If I’d been in the military at the time, instead of a civilian working in a trauma center, I might have landed in that bin. Now, 20 years later, it is finally starting to occur to the scientific and medical communities that the problem is in fact more extensive than the 250,000 soldiers who got sick at that one particular place and time: Report: New veterans showing Gulf War illness symptoms. Could this be a prelude to asking questions about the pathophysiological similarities observed in the various neuroimmune disease cohorts, diseases which were rare or unknown just a few decades ago? What risk factors are shared by vets with GWI-like illness, autistic children and patients with ME? Why is that question not being asked in the context of the public health emergency that it is?

So I’ve had problems with my BP all along, but nothing as severe or sustained since way back then, until now. I’m intolerant of most classes of antihypertensives, but have evolved an approach to BP spikes that works for me, basically temporizing until the episode resolves on its own, since experience has taught me that aggressive treatment will make me bottom out suddenly at some point. I’m better off accepting a mild elevation than pushing my luck, with such an unstable baseline. Hypotension is probably worse. Certainly, it feels worse. I did all the things this time that usually help, and everything else I could think of. I mentioned in the last blog that I had reduced my dose of Deplin as I was feeling sensitive to it while things were getting worse in December. I went back to my old dose of 7.5mg to see if that was the problem. Mood improved, but blood pressure didn’t. Went up to max dose on the newly added calcium channel blocker and took supplements and herbs which support vasodiliatation and relaxation. High dose Epsom salt baths. Biofeedback. Everything worked briefly, but still with regular readings above 200 systolic, plus the continuing waves of dread I was experiencing, so similar to the beginning of my illness. I was trying to figure out which 3rd drug to add soon if something didn’t give, knowing that all the choices were likely to be problematic.

Faced with only unpleasant choices, and since the problem was related, at least temporally, to discontinuing Viread, I decided to restart it. I was in no way excited or positive about it, but felt it was the least of the bad choices. Since stopping it, I had been feeling better in some important ways, with notably less nausea and possibly feeling a little stronger. So despite a strong preference for going ‘au naturelle’, and tired of being a guinea for drugs developed for patients with a different disease by drug companies with no interest in ours, and very tired of copays, I nevertheless found myself surprised to be back in a place where restarting antiretrovirals was looking like my best option. When Ali and I first started arv’s in early 2010, I believed we had a virus which had been confirmed at 3 labs, including the Cleveland Clinic and the NCI, plus published supportive in vitro testing. It made sense then, but now? I spend my energy working on natural solutions for patients. My own goal was to get off any drugs I possibly could. But the blood pressure wouldn’t give, trumping all my reasoning. I went back on…

On the 5th day back on Viread, with a resurgence of nausea worse than before I stopped, I was cursing drugs and drug companies, when my symptoms broke, like a fever. The high blood pressure let go, as did the other symptoms that came with it in a chicken or egg fashion, such as the fight or flight feeling from too much sympathetic tone. It isn’t just a number on a blood pressure monitor, but part of an entire symptom complex. Since things turned around 6 days ago, I’m doing better than before I stopped it in the first place. I have no logical explanation for that. BP is adequately controlled, at least pretty good for me. I am planning to restart Isentress in a week and I am considering lopinavir as a 3rd drug. See the last blog for Dr. Snyderman’s data demonstrating his response to lopinavir. Kaletra is currently part of a regimen undergoing a clinical trial for a beta retrovirus, similar to MMTV, in PBC (primary biliary cirrhosis), with evidence for growing, slowly, as is always the case when it comes to investigations of human retroviruses other than HIV.

Why might this recent experience of mine be interesting to other ME/CFS patients? Hypertension is not usually a finding in this patient group. However, vascular instability is. Increased sympathetic tone is. An abnormal stress response most definitely is. All of that apparently got worse and now better again, in an A – B – A fashion, taking, stopping and restarting Viread. And, distinct from my usual predicament, I could actually measure something. Numbers! BP now coming into line after 11 days back on, starting to decrease the second antihypertensive, didn’t have to start a 3rd class with intolerable side effects. I really wanted off, but I am not afraid of these drugs, so here I am again, and so far, so good.

After watching me twist in the wind for the last couple of months, Ali is planning to sit tight with respect to her antiretrovirals, enjoying her good fortune and relative stability. For those readers who are interested in her regimen for PCOS, she has decided to discontinue Actos for the long haul, even though it helps her in the here and now. She has started a slow wean, planning to increase metformin if necessary.

Having learned the hard lessons personally with respect to unvalidated tests from small labs with special interests, I came across this on Medscape and think it needs to be shared: Lyme Culture Test Causes Uproar. The link works if you have an account, but here is the first paragraph and exerpts of the article about a culture for Borrelia burgdorferi from a lab called Advanced Laboratory Services:

A new chapter in the Lyme disease controversy opened in September 2011 when Advanced Laboratory Services, Inc, announced the commercial availability of a new culture test for Borrelia burgdorferi. Some Lyme patient advocacy groups and physicians began encouraging patients to have the $595 test, but others are concerned about the early commercialization of the still-unvalidated test. This concern may result in changes to how the US Food and Drug Administration (FDA) regulates so-called “homebrew” or laboratory-developed tests (LDTs)…

Soon after Advanced Laboratory Services’ initial public announcements about the new culture test, emails and public statements attributed to Dr. Burrascano began appearing on Lyme-related Internet sites, including comments that the culture test was approximately 94% sensitive and 100% specific.

Dr. Burrascano told Medscape Medical News that the validity of the culture test was established using blood samples provided by physicians and that the identity of Borrelia was confirmed by its ability to grow in Borrelia-specific media, by its characteristic appearance on darkfield microscopy, by reacting to published Borrelia-specific polyclonal and monoclonal immunostains, by DNA polymerase chain reaction (PCR) at 2 different loci, and by direct DNA sequencing. These data are so far unpublished…

And here is the disclosure statement at the end of the article:

Dr. Burrascano has disclosed no financial interest in the laboratory, in the Borrelia culture, or in any intellectual property and receives no commissions from the tests. Dr. Burrascano is senior vice president of medical affairs and medical director for Advanced Research Corporation, a contract research organization with the same president and corporate address as Advanced Laboratory Services, Inc. Dr. Mead And Dr. Green have disclosed no relevant financial relationships.

Oy vey. Here we go again. Another unvalidated test to justify bad treatment. What’s wrong with the unvalidated tests they’ve been using all along? The ones that are almost never negative for various tick borne diseases? And this, hitting the presses coincident with the WPI promoting Dr. De Meirleir’s lecture, yet another doctor with a history of profiting from unvalidated lab tests. I think I’ll stop now, so my blood pressure stays down, and end on a positive note.

I just had the pleasure of reading Hillary Johnson’s very fine piece in the latest edition of Discover Magazine, available to non-subscribers soon in print at a newsstand near you. Her most excellent account of the XMRV saga, “Chasing The Shadow Virus” sheds journalistic light on the events that occurred and raises desperately needed awareness for our shadow illness. I was close to the events, have my own perspective and strong opinions about what happened and why; this article rings true to me, maybe because I have this same quote on my phone in a text message, “I still see the footprints of a retrovirus..” Yes, Pandora, the box is open forever. Denial is dark and powerful, but eventually, the truth will shine through.

We can discuss possible esoteric mechanisms from now until the cows come home as to why Viread stops an inflammatory process which causes my blood vessels to go into spasm: Brain Microglial Cytokines in Neurogenic Hypertension. But why not start with the most likely explanation? It is a drug which inhibits retroviral reverse transcription. Certainly it is a real possibility that it is doing what it was designed to do.


Big Yellow Taxi – Joni Mitchell

“2013 will be a year of optimism, opportunity and HOPE”

Dr. Judy’s bankruptcy was final yesterday. She has lost everything financially. Let’s hope the vengeance is now complete. Her homes are being sold and she still doesn’t have her notebooks. She isn’t working as a lab scientist because of the Whittemore’s defamation of her character, despite Dr. Lipkin’s support.

And still the WPI asks for money from the community? For what? They have not published one paper in the year and a half since Dr. Mikovits was fired. Instead they have spent a bunch of money to ensure she is completely stopped. What kind of people would do that? Why wouldn’t they want her to be able to work? To live her life? She gave them five years, trying to help their daughter, but wanted to follow the truth instead of the money, so they did everything they could to destroy her. What’s in those notebooks that they are so concerned about? There is no intellectual property, since XMRV is not a human retrovirus, but a lab contaminant, so there must be something incriminating, something that leaves them vulnerable. But they won. They have the notebooks.

From a big picture perspective, as affects the patient community, the whole misadventure was so wrong, it’s hard to count the ways. We were robbed, on many levels. From a personal perspective, it is still incomprehensible to me that the promise we felt, back when Dr. Judy was being promoted like a rock star, has turned to dust. However, she has told me repeatedly that they have taken her money, but they can never take the most important things from her. From an email last night, after reading my draft for this blog, copied here with permission:

The copies of my notebooks prove my total innocence. I did my job and beyond…their actions prevented the truth and prevented me from getting work, and not only me, my students as well…but as you say it robbed the scientific and patient communities of data paid for by federal dollars and donations to a “non-profit” institution. I could NOT LIE or ALLOW the truth to remain hidden or support those who would not tell the truth in order to take advantage of a vulnerable patient population.

Their intellectual property was unraveling when it was found that XMRV was a Silverman lab contaminant..what they are and were afraid of is that they will be held liable for the fraudulent testing.. Lombardi and the Whittemores lied for 3 years and they all had a financial interest in VIPDx. There simply cannot be intellectual property or diagnostic testing for a virus that does not exist in any natural organism!!!

From my personal perspective it is incomprehensible, that in the United States of America, all of my constitutional rights can be denied in order to cover up the truth  …They do not want me to work because they are that vindictive. They know I live for my work in cancer and neuroimmune disease and for patients everywhere. They know my work is my life ..they thought they could take my integrity..but you know what ..THEY FAILED!  Because Lipkin applauded my integrity and succeeded at showing the world what Silverman and Lombardi did to this patient population..THEY are the COWARDS and I have my honor and my integrity but most importantly of all, I have the support and confidence of the patient population, not just the CFS patients but the cancer, Chronic Lyme, Autism, MS ALS, Parkinson’s.. that is, ALL the patients to whom I have dedicated my life.

You see, my life was never about money and never will be. I am still working as a volunteer, I enjoyed coffee with two CFS patients yesterday and a cancer patient this morning, before I went with her to an appointment. I have never stopped being a patient advocate and will continue to be one in 2013. As one of my courageous friends with aggressive Parkinson’ s wrote in a Xmas card: “2012 was a year of change and loss,  faith..we all needed tremendous faith to survive 2012!! 2013 will be a year of optimism, opportunity and HOPE”.

Today’s song: I Will Not Be Broken by Bonnie Raitt


Our current predicament reminds me of the Jack Kornfield book, After The Ecstasy, The Laundry. Retroviral causation is still a possibility, but what to do after that flash of illumination? How do we circumvent the despair that comes with getting it and losing it again? I catch myself stuck in negative thinking, feeling like I have gained so much insight into the illness, but it came too late for me to do anything “important” with it. After I wrote the last blog, I felt guilty. I mean, after where we’ve been together as a community, who wants to read about watching your diet?

I returned to work still improving, but I’m not any more. In fact, following a couple of back to back bugs that my grandson brought home from his first grade class, on top of several months of prolonged stress, I’m back to pretty definitely sick. Therefore, I’ve decided to take the next 6 weeks to rehab myself, rather than dive off the cliff again next week, when I was planning to make my first trip to Tucson. Magical thinking pretty clearly isn’t going to get me through this time. I need to take my own advice. Physician heal thyself.

What do I want to do differently with this time, besides lowering my energy output for a while and being more consistent with oxygen, diet, supplements, neurofeedback, all of which I’ve done before? For some time, I’ve wanted to try EWOT or exercise with oxygen therapy. I use oxygen to prevent PEM, but I have never exercised with it on. It requires a high flow concentrator (> 8L/min) and a mask with a reservoir that will stay on, but not restrict air flow. There is literature to support the idea that elite athletes (and rats) can do more work while wearing supplemental oxygen, though results have been equivocal as to whether exercising while hyperoxic improves performance in the long run.

I have wondered if it might not also be true that our exercise capacity could be increased this way, we who are on the low end of the bell curve. There isn’t much to go on in the literature, but there are a few papers about exercising with COPD and an oldie but goodie about using periodic hyperoxia to improve exercise capacity in CHF.

And this important paper, that addresses the question of how a treatment that increases ROS in the short term, could be good for us? It suggests that periodic administration, as opposed to long term hyperoxia, enhances antioxidant defense mechanisms, essentially a training effect for the body to fight oxidative stress: Effects of exposure of rats to periodic versus continuous hyperoxia on antioxidant potentials and free radical production in relation to ultrastructural changes in myocardial cells.

Hormesis, a concept from toxicology theory, is a blend of less is more and what doesn’t kill you makes you stronger. Modulation of cellular response by the correct amount of stress encourages plasticity in biological systems. Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders. Calabrese et al. Here is an excerpt from the section “Hormesis, Mitochondria, and Neuroprotection”:

Recent findings have overturned the long-held belief that mitochondrial ROS have only a negative impact on cell function and survival. It is now clear that mitochondrial superoxide and hydrogen peroxide play important roles in a range of cellular functions, and can also activate signaling pathways that promote cell survival and disease resistance…Mitochondrial superoxide production is believed to contribute to damage of neurons in conditions ranging from chronic intermittent cerebral hypoxia to Alzheimer’s disease. However, it has been widely reported that transient exposure of neurons to low levels of superoxide that are converted into hydrogen peroxide can protect the neurons against a subsequent exposure to what would have otherwise been a lethal level of stress. This neuroprotective effect of a subtoxic increase in cellular oxidative stress has been termed “preconditioning” by neuroscientists who study stroke, but clearly falls under the broad umbrella of hormesis… [An] example of trans-cellular hormesis mediated by ROS comes from studies showing that oxidative stress can stimulate angiogenesis in the brain…

Here is another dot to connect:

  • Supplemental oxygen and muscle metabolism in mitochondrial myopathy patients.  In summary, patients with MM show impaired oxidative ATP production in their skeletal muscle, consistent with mitochondrial disease. This study has also shown that increased inspired oxygen concentration improves oxidative function in patients with mitochondrial myopathy, but not sedentary healthy individuals. It is hypothesised that the improvement in oxidative function with increased oxygen inhalation could be the result suboptimal oxygen conductance during exercise.
  • Oxygen Therapy for Mitochondrial Myopathy.  Letter to the editor, so no abstract, but here are excerpts: We report on a physician-patient with a diagnosis of undifferentiated autoimmune disease, pandysautonomia, and mitochondrial dysfunction… Her functional capacity has gradually improved, and her prednisone dose has been substantially decreased for the first time in 8 years. She can now drive around town, walk in a shopping mall, and perform some household chores. In addition, the hair that had previously disappeared from her extremities (thought to be secondary to either the autoimmune disease or medication side effect) has regrown. Prior to oxygen therapy, her soft tissues in the extremities were painful with a boggy firmness, a fibromyalgia-like finding also thought to be part of the autoimmune syndrome. This symptom has gradually, but significantly, improved through a combination of body work (osteopathy and massage) and oxygen therapy. Prior to receiving supplemental oxygen, the same type of body work had been only minimally effective… This case report suggests that supplemental oxygen can enable patients to perform higher levels of cardiopulmonary work with less lactic acid accumulation than room air alone. The use of supplemental oxygen may not only improve functional capacity and certain physiologic abnormalities but may also minimize the mitochondrial stress, which has been postulated to increase the proportion of mutant mitochondria.

I mentioned this paper recently, but it bears a closer look: Normobaric hyperoxia treatment of schizophrenia. It showed that schizophrenics improve sleeping with a nasal cannula at 4-6L/min for 7 hours at night (an uncomfortable treatment). The improvement in symptoms was confirmed by a cross-over design of the treatment and control group. The rat study of periodic vs continuous hyperoxia above suggests that the effects demonstrated in this study might be even more profound with a higher dose for a shorter time. Why would oxygen help this group of patients and what does it have to do with us? Schizophrenia is increasingly recognized as a neuroinflammatory disorder associated with HERV activation. Here is a paper suggesting even more common ground… Antibodies to retroviruses in recent onset psychosis and multi-episode schizophrenia. So, another group of patients who have antibodies that cross react with MuLV sequences, at least in the acute phase.

I wish I could share this whole paper here, because it touches on so many of the questions left in the wake of XMRV. It is well worth a careful read in its entirety: Human retroviral sequences associated with extracellular particles in autoimmune diseases: epiphenomenon or possible role in aetiopathogenesis? Perron. There has been quite a lot of work done on MSRV, a retrovirus, which lies at the interface of endogenous and exogenous retroviruses. Since ME is essentially MS light, MSRV is a good model for us, with a 10 year head start from where we stand right now. Some, but not all MS patients studied express viral particles, which may or may not be infectious. That fits the variable epidemiology seen in our families, where some patients are isolated cases, having never known anyone else with the disease, others have partners and children affected, but otherwise no evidence of being contagious, and there are even a few who believe that they have infected many people through casual contact (food sharing). The idea of recombination and copackaging of viral genomes once again brings to mind the issue of vaccines contaminated with genetic material from animal cells.

As part of the complex ‘biological life’ of such retroviruses, it also appears necessary to study copackaged ERV genomes which may account for their potential pathogenicity by e.g., recombinations or propagation of defective clone expressing pathogenic molecules, and may be at the origin of their rapid loss of infectivity by defective interference and/or ERV takeover. The complexity of retroviral genome studies in these situations, represented in this review by IDDMK in autoimmune diabetes and MSRV in multiple sclerosis, can become a major difficulty for a definite conclusion.

The multiple sclerosis-associated retrovirus and its HERV-W endogenous family: a biological interface between virology, genetics, and immunology in human physiology and disease. Dolei/Perron 

The HERV-W family is one of the most studied, after the discovery of its MSRV founder member (Perron et al. 1989, 1997b). Our haploid genome contains about 70 gag, 100 pro, and 30 env HERV- W related regions (Voisset et al. 2000), but numbers can vary (Mirsattari et al. 2001; Zawada et al.2003); in silico expression data indicate that 22 complete HERV-W subfamilies from chromosomes 1 to 3, 5 to 8, 10 to 12, 15, 19, and X are randomly expressed in various tissues (Kim et al. 2008). Presently, this family is active and generates new recombinant copies in cancer cells (Yi et al. 2004), retains characteristics of functional retroviral envelopes (An et al. 2001; Kim et al. 2008), and HERV-W transposition and retrosequence integration have been evidenced in the human genome through interactions with active LINE-1 elements (Costas, 2002; Pavlicek et al. 2002). Thus, non-Mendelian genetic rules can apply to HERV-W elements: a key feature to understanding their biology.

None of the known stably inserted HERV-W elements is replication-competent (Blond et al. 1999): a study of HERV-W intragenomic spread (Costas, 2002) confirmed that, in the few individuals used for genomewide analysis, the sequenced HERV-W elements lack intact open reading frames (ORFs) in all genes within a single copy. This finding, and the unusual short period of evolutionary time of HERV-Ws (5 million years, estimated on average integration age of different subfamilies), suggested that MSRV might be either an exogenous HERV-W, as in animal ERVs (Palmarini et al. 1996), or a nonubiquitous replication-competent member, or a partly defective but nonubiquitous copy seldom complemented within the HERV-W family (Perron et al. 1997b, 2000; Komurian-Pradel et al. 1999; Dolei, 2005; Serra et al. 2003). Today, though reasonable arguments in favor of the existence of a replication-competent HERV-W member, which might even be ‘‘exogenous,’’ have been provided (Belshaw et al. 2005; Costas, 2002; Perron et al. 1997b, 1992), the very nature of MSRV remains to be confirmed by future studies (Voisset et al. 2008).

They can follow viral load in patients and there is clinical correlation… From the same paper:

A direct parallelism was found between MSRV positivity and load (in blood, CSF, and brain samples) and MS temporal and clinical stages, as well as active/remission phases (Dolei et al. 2002); at MS onset, 50% of CSFs were MSRV positive, and positivity increased with pro- gression. Importantly, MSRV presence in CSF at MS onset was related to poor prognosis; starting from otherwise comparable conditions, after 3 and 6 years mean EDSS (expanded disability status scale), an- nual relapse rate, therapy requirement, and progres- sion to secondary-progressive MS were significantly higher (Figure 2) in patients with detectable MSRV CSF load at onset (Sotgiu et al. 2002, 2006a).

A recent study (Mameli et al. 2008) found that plasmatic MSRV load of naive patients with active MS was directly related to MS duration; longitudinal evaluation of patients during 1 year of IFNb therapy showed that MS progression index (EDSS/MS years) was reduced for the majority of patients, whose viremia became rapidly undetectable. Notably, one patient had atypically high viremia at enrolment and, after initial virus inhibition and clinical benefit, had MSRV reemergence, accompanied by strong progres- sion with therapy failure. The authors concluded that evaluation of plasmatic MSRV could be considered the first prognostic marker for the individual patient to monitor disease progression and therapy outcome (Mameli et al. 2008).

Just published: HERVs Expression in Autism Spectrum Disorders. Balestriere et al, an addition to the growing literature supporting the idea that activated HERVs are involved in autoimmunity, an appealing idea, providing an explanation of why the immune system might become confused as to what is self and what is not. The authors of this paper found increased expression of HERV-H, one of the HERV families implicated in complex chronic disease, in autistics as compared to controls. They also report expression inversely proportional to age and proportional to disease severity.

Our answers lie at the interface of retrovirology, genetics, molecular medicine  and toxicology. The further I go in my attempt to understand the problem on a biochemical level, the less optimistic I am with respect to so called “targeted therapies”. We simply aren’t smart enough and the system we are trying to influence is too complex. This is why therapies that affect the system globally are so attractive. Which brings me back to EWOT. Perhaps the poor, misunderstood Dr. Wessely could let his patients try some oxygen with their GET, now that he says he thinks they do in fact have some sort of a physical problem, in addition to being lazy, crazy and faking.

So, EWOT for ME? I ordered a couple of masks to try. Now I’ve really gone and done it. Set myself up by telling you all about it:). I will report back soon.

Today’s song: Fire And Rain by James Taylor