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

Recovery post-XMRV

I have a lot to say today and too little energy with which to say it, having just lost ten days of life force to red tape and worry about complying with arbitrary and capricious rules. Between states with differing regulations, plus the DEA which has yet a different set of regulations, I feel like I need a law degree to practice medicine. The system is broken and it is incredibly hard to take care of patients appropriately. When I complained about it recently to a doctor friend in an email, he replied, “My tombstone should read: He died of red tape.” It was always bad, but now nobody even pretends it has anything to do with caring for patients.

My recent month long intensive in Hawaii, treating two young women with ME/CFS and many years of disability, has further convinced me that the therapies I am using are able to tip the balance in favor of a slow climb to wellerness. For the most part, the things I’m doing are not enough alone, but together these therapies are synergistic and additive with continued use. Everything I am doing, and why, is documented and referenced on this blog. The search function in the header works well. The patients are fragile and a lot of tinkering is necessary.

In a nutshell, high dose pulsed oxygen (normobaric and mild hyperbaric) to improve inflammation and mitochondrial function, bioavailable folic acid derivatives for improved methylation (Deplin and folinic acid), sublingual or chewable methyl B-12, Vit D3 replacement, infusions of a modified Meyer’s cocktail including taurine, glutathione by IV push and neurofeedback. Most significantly, I see improvement from weaning inessential drugs, replacing synthetics with bioidenticals, and using herbal treatments instead of pharmaceuticals. In particular, medical Cannabis, if tolerated, for patients who live in a legal state, is a more effective and much safer alternative for chronic pain than opiod drugs, which damage the gut and cause central sensitization over time.

I consider diet to be a cornerstone of treatment. Food as medicine. I advocate a modified SCD diet, allowing whole grain rice, for patients with neuroimmune illnesses that almost always include a GI component in the symptom complex. I encourage SCD yogurt as a probiotic, superfemented to be lactose free and have a high live bacteria count. I also advocate eating organic, and no processed or GMO foods. In particular, avoid the excitotoxins, aspartame and MSG. Here is an important YouTube, by Dr. Terry Wahls, in remission from a wheel chair through dietary intervention alone:

I received some flak for saying that I’m a lumper, not a splitter, with respect to segregating subsets of patients, except for research. From the point of view of clinical medicine, breaking it down into separate cohorts doesn’t help me at all. It is all neuro-immune illness. The therapeutic options are extremely limited. The same things are worth trying in other cohorts also. Many, if not most, of the therapies that are being used in the ASD community are applicable to us. ME is on a continuum with MS and ALS. GWI and chronic Lyme Disease wind up clinically indistinguishable from ME. Fibromyalgia is a subset, not a separate illness. Again, the same treatments are applicable for the same reasons, even if the illnesses look a bit different.

The first thing that happens when there is a response to therapy is improved resilience. A push that would have caused a long crash, doesn’t, but brings minor payback only. At first most everything still feels crappy all the time, though some things have improved. Then some moments that aren’t so crappy creep in. Then some actual good moments. Crappy always comes back though, and when it does, it feels like falling back into the black hole. But it passes much more quickly than before. Improvement needs to be judged in fairly large increments of time, at least 6 months to be sure. One of the young women I treated last month posted this on her FaceBook a few days ago, “I had a good day today; I don’t think I’ve said that in 8 years :)”. That, after only a month of nearly risk free treatment. A long way from a cure, but relief is relief.

Here are some new noteworthy references with respect to oxygen therapy:

I had the pleasure of hearing Dr. Mikovits on Sue Vogan’s radio show, In Short Order, finally able to speak openly in public. The interview is archived here. I thought she was very clear and brave as she answered all the hard questions. XMRV is not a human pathogen. There could be other retroviruses as yet undetected. The mistakes made will inform future research. I personally felt abandoned after the Lipkin paper, subsequent interview by Dr. Lipkin and the press conference, but I am encouraged to hear that he and Dr. Ruscetti are still working on our behalf. They don’t know what the positive serologies mean.  It is tragic that she can’t go back and find out what went wrong so that everyone can learn from it, but much has been learned nevertheless. The only thing she said that I took exception with was that there is no evidence that XMRV has ever infected an animal. Persistent infection has been demonstrated in Macaques after parenteral introduction of virus, exposures similar to what has been happening regularly throughout the history of injected biologicals, dating back to vaccinations with the exudate of cow pox lesions, which certainly contained bovine leukemia viruses, similar to HTLV, and are artificially transferrable to other non-bovine species:

And take a look at this one: Long-Term Infection and Vertical Transmission of a Gammaretrovirus in a Foreign Host Species

So it isn’t XMRV. Other cell lines express other infectious animal retroviruses. Live attenuated vaccines are grown in animal cells that express exogenous retroviruses. Other vaccines contain DNA fragments. Here is the government’s list of vaccine excipients: Vaccine Excipient & Media Summary by vaccine and by excipient. That’s now. The early vaccines were attenuated in live animals. Mouse brains injected into people.

But, say it isn’t an exogenous retrovirus. Why then might antiretrovirals have an effect, in addition to the obvious elephant in the room? The drugs might be preventing transcription of activated HERV’s: Association of human endogenous retroviruses with multiple sclerosis and possible interactions with herpes viruses.

The hypothesis that human endogenous retroviruses (HERVs) play a role in autoimmune diseases is subject to increasing attention. HERVs represent both putative susceptibility genes and putative pathogenic viruses in the immune-mediated neurological disease multiple sclerosis (MS). Gammaretroviral HERV sequences are found in reverse transcriptase-positive virions produced by cultured mononuclear cells from MS patients, and they have been isolated from MS samples of plasma, serum and CSF, and characterised to some extent at the nucleotide, protein/enzyme, virion and immunogenic level. Two types of sequences, HERV-H and HERV-W, have been reported. No known HERV-H or HERV-W copy contains complete ORFs in all prerequisite genes, although several copies have coding potential, and several such sequences are specifically activated in MS, apparently resulting in the production of complete, competent virions. Increased antibody reactivity to specific Gammaretroviral HERV epitopes is found in MS serum and CSF, and cell-mediated immune responses have also been reported. Further, HERV-encoded proteins can have neuropathogenic effects. The activating factor(s) in the process resulting in protein or virion production may be members of the Herpesviridae. Several herpes viruses, such as HSV-1, VZV, EBV and HHV-6, have been associated with MS pathogenesis, and retroviruses and herpes viruses have complex interactions. The current understanding of HERVs, and specifically the investigations of HERV activation and expression in MS are the major subjects of this review, which also proposes to synergise the herpes and HERV findings, and presents several possible pathogenic mechanisms for HERVs in MS.

Or antiretrovirals, reverse transcriptase and integrase inhibitors, might be inhibiting retroposons:

What makes jumping genes jump? Demethylation.

Reverse transcriptase inhibitors presumably inhibit other viruses besides retroviruses if reverses transcription is required in the replicative process. Viread is used to treat chronic hepatitis B, for example. Hepatitis B is a DNA virus that replicates through an RNA intermediate and uses reverse transcription.

Telomerase is a reverse transcriptase. Therefore, arguably RTI’s might cause faster aging, but might tip the balance away from developing cancer. The more you think about it all, the more you realize that, like all drugs, antiretrovirals are blunt swords with many possible mechanisms of effect, all of which says that clinical trials are in order. One would think that the manufacturers would be interested in new indications for their drugs.

My own illness could be explained by a post polio syndrome caused by an attenuated virus, but it doesn’t fit my daughter. Does an enterovirus explain the vertical transmission seen in our families or a response to  antiretrovirals? Does anyone reading know the answer to those questions? Many of us remember the sugar cube that held the first oral polio vaccine. Polio virus can persist: Transmissibility and persistence of oral polio vaccine viruses: implications for the global poliomyelitis eradication initiative.

Protein from helper viruses and recombination events can rescue defective virus. Innumerable chances have occurred: Science Fiction or Fact? 35 years ago, when I was in medical school, autism and MS were rare. Autoimmunity has skyrocketed beyond belief, as has cancer.

Here’s an unsettling paper. Chemical Induction of Endogenous Retrovirus Particles from the Vero Cell Line of African Green Monkeys. Vero cells are present in the DTaP-Hep B-IPV, Poliovirus inactivated and Rotavirus vaccines. AzaC, one of the chemicals used in this paper is a demethylator. Other methods used in the lab to activate ERV’s and amplify retroviruses in tissue culture are radiation and steroid hormones, bringing to mind the myriad ways in which our environment is contaminated, contributing to the cluster fuck for the genetically susceptible and overexposed. Let’s wrap up today with this article which I haven’t finished yet, but it looks to be well researched: What Is Coming Through That Needle? The Problem of Pathogenic Vaccine Contamination.

 Today’s song: Burn One Down

Now You See It, Now You Don’t

The Lipkin study buries XMRV once and for all, completely leaving aside the question of an infectious chimera out and about that contaminates a clean lab in a matter of days and is capable of infecting monkeys. But it wasn’t in the blood of the patients or controls in this study. That much is clear, forgetting the unscientific claim that this study, or any study, is definitive of anything. Science is self-correcting, as Dr. Lipkin reminded us, but only if the game isn’t rigged. This is a repeat performance of the definitive study that showed that the MMR doesn’t cause autism, which also side-stepped the bigger question. The use of the word definitive tells us we are dealing with politics, not science. Sleight of hand.

The paper didn’t even try to speculate as to the one positive finding, that 6% of the study group, patients and controls, cross reacted with a test designed to detect SFFV, a nasty murine retrovirus. Whatever it is they are picking up with this serology test, “modified slightly” from the one once used at the WPI, the various PCR’s used in this study, optimized to detect XMRV and a piece of a “generic” pMLV, couldn’t detect it. But that doesn’t mean it isn’t there.

A young friend emailed after watching the press conference asking that I blog because my blogs are hopeful. I’m not sure how to spin this as hopeful other than XMRV got us into national news as having a real disease. It’s good that there are people studying us, even if they are abandoning the hypothesis of best fit. So, as my friend asked, do we still have retroviruses? The answer is everybody has retroviruses. 8% of the human genome consists of retroviral sequences. It is becoming accepted that these sequences are capable of causing trouble in some people, whether they produce fully replicative virus or not. SFFV is a replication-defective virus that causes disease in mice: The spleen focus-forming virus (SFFV) envelope gene, when introduced into mice in the absence of other SFFV genes, induces acute erythroleukemia. S Ruscetti

The Lipkin study in no way disproves the hypothesis that simple animal retroviruses, alpha, beta and gamma, parenterally introduced, in the form of vaccines and from other sources, e.g. hybridomas, xenografts, etc., have recombined and rescued defective endogenous retroviruses, and/or created new and as yet unrecognized exogenous retroviruses. The existence of XMRV, is supportive of this theory. There have been so many chances for it to happen, in addition to the possibility that it happened naturally. This means that we each may have something a little different. Which is why they can’t find “it”.

Personally, as a defender of Dr. Mikovits during this entire mess, I appreciated Dr. Lipkin for openly defending her struggle against the Whittemores. The scientist who put the nail in XMRV’s coffin. Dr.’s Mikovits, Ruscetti and Alter completed the difficult task of acknowledging they’d been mistaken. Our disease has finally been deemed “serious and life threatening” to enable fast tracking of drugs, should there be any drugs worth fast tracking, which seems unlikely if nobody is studying the root cause of the disease, only looking at downstream effects.

I’m not even going to question the study design, patient selection, specimen handling, that the patients chose their own controls, etc. I accept at face value that Dr. Lipkin put together a convincing study in order to put the final nail in the coffin about XMRV. No surprise there. I assumed the study would be negative. But I expected the authors to have the intellectual integrity to state that ruling out XMRV does not rule out retroviruses. Instead they allowed the press to distort in predictable ways. I therefore must conclude that Dr. Lipkin plays for the home team. His task was to kill it and reassimilate the renegade scientists into the group. To make sure that nobody does any clinical trials of arv’s, the paper suggests that the patient community has been saved from that terrible fate by this definitive paper. Mikovits’ name right there with Coffin’s. Task accomplished. But even Coffin said that it might be another retrovirus. Smart people allowing distortion and partial truths. It looks to me like we’ve been thrown back on the trash heap. From the Wall Street Journal. Viruses not to blame for chronic fatigue syndrome after all. Thank you Mr. WSJ editor for that headline, suitable for a tabloid.

Why do I still believe retroviruses are involved in causation in the face of so much evidence against XMRV? Even though we don’t have XMRV or active replicating virus with some certain degree of sequence homology to a piece of a “generic” pMLV, retroviral causation has not been ruled out. It is still the best explanation for all of the observed phenomena. It works as a clinical model to explain the symptoms and put treatments in context. It even explains the obvious but still unstudied epidemiology. Dr. Mikovits was trying to sequence what she believed were positive cultures that were negative for XMRV. She sent out letters to that effect to patients.

Then there is the response to antiretrovirals. Dr. Snyderman has presented amazing data, that most of the scientists involved in this story have seen and ignored. He has not been cured, but his leukemic cells and his cells capable of making cytokines have decreased with treatment. Cancer treated like a chronic disease, like diabetes or AIDS. I don’t think they are stupid, so they don’t want to know. Why not?

If the response of longstanding ME/CFS patients to limited arv’s (RTI’s and II’s alone) had been more robust, we wouldn’t even be having this discussion. It wasn’t. There were early responses that were encouraging, but with no way to follow, after a while, you’re left not knowing what is happening. Meaning we don’t know how to use the drugs, not that they have no value. Maybe they should be pulsed or given low dose for N chain termination. Maybe a protease inhibitor is necessary for full effect. Dr. Snyderman is documenting an ongoing response to Kaletra. The best case we heard about anecdotally was a teenager, hadn’t been sick long, responded fully and the drugs were stopped at 6 months, remaining well as far as I know. It is beyond sad that this case was not published. While new teenagers get sick with an “untreatable” disease, they are denied a trial of very safe existing drugs. It could have been studied for a lot less than the 2 million dollars spent to prove it isn’t XMRV.

I have tried to discontinue Viread on three occasions, since our drug co-pays are a problem, and I haven’t been able to do it. I get sicker within days and feel better quickly after restarting. Can I prove it? No of course not. The disease is a relapsing remitting illness all on it’s own. However, I didn’t have trouble stopping AZT or Isentress. I have been under enormous stress since June, with one thing after another, one of those times in life when the waves just keep coming, too close together for recovery. I am a little worse than I was, but only a little. I’ve even been able to ride the tandem a couple of times recently, only 5 miles on the flat, but no PEM after. Ali continues to do extremely well on Viread and Isentress. She has considered stopping arv’s, but has decided not to rock the boat at this time, since improvement seems to be continuing very, very slowly. The possible downside besides financial? I don’t know of any for Ali. I’ve aged a lot in the last couple of years, though it is on time, coming after a late menopause, so I can’t really blame Viread for that. I heard from a patient yesterday who did well on AZT, Viread and Isentress for a year, but then went back to baseline for another year with some new symptoms that could have been drug related, though hard to know. As I said, we don’t know how to use these drugs. We have no way to monitor. That doesn’t mean they have no value.

But Dr. Lipkin told Dr. Racaniello:

I know some in the community –the scientific community—feel that this was not money well spent, but the fact is, I think that we have obviated a lot of, you know, missteps that might have followed with clinical trials and such for antiretrovirals. And in addition, we have been able to establish a sample bank that will be helpful for years to come. And we’ve been able to hold, I think, the attention of the community.

So Dr. Snyderman, Ali and I are missteps…

From the 3rd paragraph of the paper:

Since the index publications, clinics have been established for the treatment of ME/CFS with antiretroviral drugs…

This is a complete fabrication. Where are these clinics?

It is completely incorrect, and unscientific, to conclude anything from the Lipkin study other than they didn’t find XMRV or a particular pMLV sequence. That’s a long way from no viruses or even no retroviruses in CFS. How is it that 2 million dollars was spent to tell us what we already knew a year ago? No reproducible assay. 2 million dollars and all that effort to prove what isn’t. For three years, we’ve been waiting for the scientific community to run with the ball. Now it is pretty clear, the ball has been dropped, while they huddle to congratulate each other on a job well done. The status quo is restored.


Today’s song: Who’ll Stop The Rain by Creedence Clearwater Revival


In cancer science, many “discoveries” don’t hold up, by Sharon Begley, a disheartening story, published today. Without integrity, there can be no science. This is probably how we got sick in the first place, though in the early years, it was more likely scientists doing whatever popped into their heads willy nilly, like Victor Frankenstein, with no framework for evaluating the possible consequences. With statistics like the one presented in Ms. Begley’s report, it seems folly to expect “science” to save us now. The system is completely broken.

The same problem with integrity in reporting results extends to doctors. This problem is particularly rampant amongst LLMDs, who continue to make exorbitant amounts of money harming patients, extolling the virtues of “sophisticated” combinations of antibiotics for “seronegative Lyme”. Not that Lyme Disease isn’t real, but it can’t be eradicated in the way they are trying to do it. Problems with a generalized lack of scientific integrity aside, here is the first paper I’ve ever read that adds something to the clinical picture.

Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection by Embers et al.

They infected monkeys with Bb and found that treated or untreated, the monkeys demonstrated persistence of the organism and inflammatory changes. Therefore trying to eradicate Lyme with endless courses of antibiotics is not the most sensible course of action, acknowledging the exception of a small subset who do relatively well on old fashioned acne treatment. Antibiotics are a double edged sword at best, particularly in the setting of preexisting dysbiosis.

My hat is off to these researchers for their fine study, sensible discussion and clear attempt to give physicians in practice something to work with. A marker!

In some cases, patients who have been treated for Lyme disease experience persistent symptoms. The assertion that further antibiotic treatment is warranted in these cases is a matter of contention and considerable debate [33,34,35,36]. Our results indicate that disseminated spirochetes of two different B. burgdorferi strains can persist in the primate host following high dose, or long- lasting antibiotic therapy. In terms of disease, only objective signs of disease post-therapy may be measurable in an animal model. While we did not find gross signs of disease postmortem, in Experiment 1 we did identify heart sections with inflammatory infiltrates in three of the treated animals. In addition, several animals, both treated and untreated showed sections of heart and meninges that were positive by immunofluorescence for B. burgdorferi. At the molecular level, B. burgdorferi DNA would indicate the presence of organisms, live or dead. The detection of RNA, however, should indicate that those present are metabolically active and thus alive. In Experiment 1, spirochetal DNA and RNA were detected in the tissues of a few animals, independent of treatment. This may reflect a low spirochetal burden, lack of flaB transcription [37], and/or seclusion in untested tissues.

And this:

The most pressing question in terms of human disease is whether or not spirochetes remain pathogenic after antimicrobial therapy. Similarly, do spirochetes persist long-term, or are they eventually cleared by the host? Clearly, the phenotype of persistent organisms needs to be elucidated. These studies support the use of the C6 test for diagnosis and measurement post-treatment; however, the absolute quantification of antibody levels may be essential in determining treatment efficacy for PTLDS patients, as low levels (yet above baseline) may indicate presence of residual spirochetes or antigen. Finally, the use of variable and pulse-dosing regimens of antibiotics may improve efficacy [43] and this warrants testing in an appropriate model.

That pretty much says it all I think. My daughter and I were an inappropriate model for a doctor testing various pulse-dosing regimens by trial and error on sick people, instead of monkeys. Saving a few isn’t an excuse for worsening the tenuous condition of the others, while claiming cure of a huge percentage, with no data, especially since the “treatment” takes years to evaluate. Treatment worse than the disease. Russian roulette. From my email yesterday:

I  want to very much thank you for steering me away from ILADS doctors! As I said, I went ahead and did a trial of antibiotics to “provoke” Igenex testing, just to settle the question for myself, and I ended up with acute pancreatitis (I do not drink alcohol; it was the antibiotics), and then an immune fatigued body so sick I was hospitalized twice with pneumonia after catching a flu (my husband says he was worried I was near death — I had pneumonia for six weeks).

After all this (and what would have been thousands of dollars in testing if I weren’t billed at the Medicare rate by Igenex and if the testing hadn’t been covered for me  by insurance), my labs for Lyme AND coinfections were flat negative (except for band 41 and mycoplasma). The ILADS doctor nonetheless encouraged me, based on this, to travel to another specialist and get a port, so we could provoke and continue treatment with even stronger drugs — and said I mostly certainly had “seronegative lyme” no matter what because of my symptoms of ME and tourette’s syndrome. I am glad my insurance and Medicare covered most of this. I am also lucky to not have died or had permanent effects (other than a collection of snake oil). Your words of warning were what kept me from damaging my body and taking the seductive and expensive hope.

The 5000 year old mummified corpse recently unthawed and autopsied had Lyme Disease. Iceman Autopsy. Although he was old enough to be developing atherosclerosis, he died of trauma. He had significant health problems, but at least he wasn’t infected with something created in a lab. They’ve sequenced the entire genome of a person dead 5000 years, not that that doesn’t have value, but when are they going to get around to us?

And hot off the presses from MedScape:

March 29, 2012 — The prevalence of autism spectrum disorders (ASDs) has increased by 78% since 2002, a new report from the Centers for Disease Control and Prevention (CDC) shows. However, the exact reason for this increase is unclear.

Overall, the report’s data, derived from the Autism and Developmental Disabilities Monitoring (ADDM) surveillance network, show that in 2008, 1 in 88 children aged 8 years — 1 in 54 boys and 1 in 252 girls — had an ASD diagnosis by age 8, a significant jump from the current estimate of 1 in 110.

Their conclusion? It must be because of better diagnosis, reporting and access to services! Oh that’s a relief. We can all relax now. In the meantime, our little team continues to make slow progress, with no paid help to complete an IRB approved Family Study. I don’t think Dr. Snyderman and I ever thanked everyone publicly for taking the time and energy to participate in the Informal Family Study last year. We learned a lot. The problem was the extremely labor intensive data entry, incomplete data sets, and no controls, but it made it clear that there is much to be learned. We are working slowly to bring it to reality. We are all in different parts of the country, with different primary responsibilities, but we will get it done. Stay tuned.

Much aloha.

Today’s song: Sounds of Silence by Simon and Garfunkle

Link if embedded video is not streaming well:

The Sound of Silence – Madison Square Garden, NYC – 2009