“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

Back To Basics

I have always found this to be a trying time of year, even before I got sick. Our family is one of blended traditions and we often wind up celebrating both Chanukah and Christmas, making the whole ordeal go on and on (bah humbug:-). My husband and I thought we had fulfilled our obligations on that front, but now we have little kids at home again. Our eldest daughter Julie, who is half native American, moved back home last year with her two children who are Pomo Indians, and our son is home from his first semester at Tulane. Talk about a mish mosh!

I am having one of those days where even my arms feel heavy. Hey, who turned up the gravity? I feel tremulous, but it doesn’t show. I would like to go to a Christmas party tonight, but I’m not sure at the moment if I’m up for it or not. I’m replaying my whole tape loop about not wanting to disappoint. It doesn’t mean I won’t feel good to go when the time comes, but it’s up in the air at this moment. I’ll use my oxygen, take an epsom salt bath, and probably get the boost I need. More bothersome than the weakness though, with which I’m accustomed to struggling, is the emotional reactivity that comes with more inflammation. I’m sure many of you can relate…

That particular symptom was one of my first. It started just a few months after the birth of my second baby at 40, and it made me feel like I was becoming a different person. For those of you that don’t know me, I had gradual onset of symptoms, no PEM and no diagnosis for a decade, followed by incorrect diagnoses. I haven’t been bothered by this particular symptom for quite a long time and reexperiencing it is sending me back to the exploration of biofeedback that began when I first became ill in 1995 and was looking for a non-pharmaceutical solution for this and other alarming symptoms. In addition to neurofeedback with Cygnet, which I use in practice, I’m enjoying trying out some of the innovations for biofeedback hometrainers and stim devices on the market now. Advancements in electronics have made for easier to use, more effective and less expensive devices. I am particularly interested in them, because most of my patients can’t access a neurfeedback therapist and I had some devices way back when that might be helpful in this context. I’ll report on this subject at some point in the near future.

The FDA committee’s rejection of Ampligen filled me with mixed emotions. As it has been clear for a long time that only a minority of patients do well on it, and as it has some significant downsides, I’m happy for the would be non-responders who will be spared yet another therapeutic failure. On the other hand, other patient groups with real diseases are allowed to try toxic treatments that have only a small chance of success. I am of course concerned about the people who need the drug being able to get it, but the tragedy for all of us is Hemispherx’s failure to figure out who to treat with their drug; thus they have contributed nothing to our understanding of the pathogensis of our disease. They have also sent a loud and clear message to other would be drug developers to avoid CFS like the plague: SHAREHOLDER ALERT: Pomerantz Law Firm Has Filed a Class Action Against Hemispherx Biopharma, Inc., and Certain Officers

The same problem with patient selection is now happening again with the early experimentation with Rituxan: patient selection is random and there are no markers to follow. If you are sick enough, want it and can pay for it, you can be a guinea pig. I predict the stats won’t be good, for the same reason that the Ampligen results weren’t. There may well be a subset of patients that would have a higher hit rate, but nobody knows which ones. For me, it’s even simpler than that. I don’t want anything to do with it, personally or professionally, if it can kill. ME/CFS is a relapsing remitting illness. MS light. The best place to start is with the safest things, try to encourage remission, which requires synergy of global strategies.

One day soon, coming to a Quest or LabCorp near you, we will have a whole genome sequencing test that insurance will pay for. Then we will finally learn something that might change our options. But until then?

Still trying to understand why oxygen works so well clinically, in the setting of patients with increased oxidative stress, I’ve been reading about “mitohormesis”. Please take a look at these papers. This is a very important concept. Oxygen has been used to good advantage in the autism community and I still believe that the diseases are related, the differences in disease expression being due to the developmental stage at onset of illness. These papers describe the mechanism by which repeated doses of increased reactive oxygen species produce cellular resistance to stress. So repeated doses of hyperoxia in patients unable to exercise might produce better mitochondrial function over time, a theoretical framework for a clinically observed phenomenon.

Since I returned to practice, I’ve been intending to turn my attention to supplement recommendations for my patients. To date, I haven’t had a protocol and my advice has been random and half-baked. The passing of Rich Van Konynenberg left a great hole in our community. I feel a great personal sense of loss, because he and I intended to share with each other and it didn’t happen, completely due to my limitations, all my small supply of energy going to my practice. Now that I am studying the subject in depth and coming across his lectures and posts on the internet, I am very upset with myself. He was a brilliant, giving man. Generous of spirit. I am learning a great deal from him now, since he shared his ideas so freely.

As my second year back in the world comes to a close, my most powerful interventions remain high dose pulsed normobaric oxygen, Deplin, B-12, organic SCD diet, hormone balancing, stopping meds if possible, eliminating environmental toxins and biofeedback. I don’t think such a program will cure anyone, but I believe it can help a lot and is almost risk free. Three and a half years ago, when Ali and I discontinued Lyme treatment, I made deals with the universe that, if Ali got better, I’d be satisfied. Acceptance is my mantra. This recent dip of mine is challenging me to use that mantra, rather than dwell on my losses which only increases suffering.

Ali is spending Christmas eve with her wonderful beau, visiting with his family in Albuquerque, experiencing their traditions, planning to bring him back here in the morning for presents and brunch. She has finished 25 of 120 credits towards her degree at U Mass Lowell with a 4.0 average. I am so grateful that she is able to lead a full life – with disability, it is true, but a happy life nevertheless. Finishing this up, I realize I don’t have it in me to go to a party tonight, then walk in the cold for Santa Fe’s Christmas walk with the kids. I don’t want to hold them up or have them worrying about me. I prefer to save my energy for tomorrow. I’m a little sad that I’m not going, but my husband doesn’t seem disappointed, so it’s all good.  It is a glass half empty vs half full moment, sitting by the fire, thinking about friends that are also alone tonight, envisioning a wonderful new year for all of us, filled with peace, love and greater wellerness. Merry Christmas.

Tonight’s song: It Came Upon A Midnight Clear


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