I knew when I posted something positive about the use of oxygen for ME/CFS, I would hear about Dr. Cheney’s views on oxygen toxicity, just as I heard about his views on the use of Klonopin, when I said that I am opposed to any avoidable use of long term benzodiazepines (understanding full well that sometimes it can’t be avoided). I disagree with Dr. Cheney about a lot of things. Gasp! And agree with him about others. I am in the process of launching a Physician Working Group for the WPI and Dr. Cheney will of course be invited. It is wonderful that he and I can disagree and are going to work together to figure it out. There are going to be lots of other people who disagree with me, and each other, about many things. In fact, I’d say, there is absolutely zero chance for consensus in the group I’m putting together, but I am hoping for a melding of minds, nevertheless, for the betterment of patients. One thing I am sure of, we all want the same thing, to help people get well.

My understanding, from email communication with Dr. Cheney some time back, is that he is looking at one parameter, IVRT, of one organ, the heart, by echocardiogram, after administering low-flow oxygen by nasal cannula, as well as exposing patients to other substances in sequence. If I put an oxygen cannula on your face, at a time when you are under stress, and your IVRT, a measure of diastolic function gets worse, what does that mean? Hyperoxia causes vasoconstriction in normal tissues, so a compromised circulatory system might look worse at that moment. So what? I talked about and referenced all the reasons why repeated exposure to higher than normal amounts of inspired oxygen might be a good idea over the long haul, even if the treatment produces a few more free radicals than usual, for which antioxidants can be given. Free radicals are necessary for life, involved in intracellular killing by phagocytes and redox signaling. In hyperbaric wound care, high doses are needed to produce free radicals to kill bugs.

Dr. Cheney described a reaction to oxygen, in which patients become anxious or even obtunded, which I don’t understand. I administered very large doses of oxygen to chronic Lyme patients, who in hindsight had ME/CFS, and lots of patients with other diagnoses, including a couple of post-stroke COPDers with CO2 retention, and never saw anything like what he described, even in a very claustrophobic environment, the inside of a multiplace hyperbaric chamber, that looked kind of like a submarine (link to photos here and here of our chamber at New England Hyperbaric Center 1999). Nor did I ever see anything like that in many years of high volume emergency medicine practice, except in acutely decompensating chronic COPD patients.

The idea that the cells of ME/CFS patients utilize oxygen in such a different way from all other animal cells such that doses safe for other humans would somehow be dangerous for us seems ludicrous to me. I’ve gotten a bunch of confused mail about how ME/CFS patients have “high oxygen” already and more is toxic to them. CFS patients have normal oxygen saturation, O2 Sat, in the blood, meaning the carrying capacity of hemoglobin is normal. Oxygen travels from the arterial blood into cells by diffusion along a pressure gradient. The issue in ME/CFS is cellular hypoxia, meaning the interior of the cells are starved for oxygen and the mitochondria can’t generate ATP properly, due to poor mitochondrial function. So no gas in the tank. The mitochondria are the energy factories of the body and they are mucked up, still producing enough energy for life through the same chemical processes utilized by all eukaryotic cells, but with an inadequate supply of substrates necessary to generate ATP, and inadequate reduced glutathione to prevent damage by free radicals and other reactive oxygen species. Sometimes I wonder if it is more diabolical than gunked up machinery, that the virus doesn’t like oxygen and therefore causes the host not to be able to move. I presented the evidence in the literature for the use of oxygen in autism. Since I believe autism is essentially the same disease as ME/CFS acquired earlier in life, with the same mitochondrial problems, it seems logical to try mild HBOT for ME/CFS, especially in light of the very low risk of harm.

At the time that I left hyperbaric practice, I was worried about the possibility of an explosive decompression, a potentially lethal event, in a soft chamber, as they are not rated for hundreds of compression cycles. I was opposed to home treatment on that basis, not because of any inadequacy of the treatment. Since then, my understanding is that there have been more than 10,000 FDA approved soft chambers sold, and the thing I was fearing hasn’t happened. If they leak, they give at the zipper and don’t lose pressure suddenly. The only serious accidents have been related to modifications made to allow higher than rated pressures. There are risks, even to mild hyperbarics, and nobody should undertake it without training from a professional, but it’s not that hard, once you get the hang of the concepts.

Whatever is happening with respect to the length of diastole when oxygen is administered, it seems to me that we should be worrying more about the brain than the heart in light of the clinical course of most patients. The brain is very sensitive to ischemia. Whatever the oxygen saturation in the blood, ischemia can be present downstream of vascular spasm. That’s what I was addressing with some of the literature I posted. Not that we are having strokes, but that some of the cognitive issues may come from repeated localized ischemic insults, mini TIAs (transient ischemic attacks), during periods of vascular spasm. It seems rational to me to combat that with oxygen.

This is a blog, evolving opinion, not a statement of fact. I am sharing my thoughts, before even trying things in the present context, before proving anything. I am, however, putting my money where my mouth is, and I will continue to share our unfolding experiment in real time. I do this, not because I am trying to convince anyone that I am right. I could be wrong about anything. I am sharing my thinking as it happens, because we are in uncharted territory and there is so much suffering and desperation. None of us have years to waste. I have experience to tap in to and there is shockingly little information available when considering options. But at no time am I suggesting that anyone else should do what we are doing.

I posted our planned infusions, before knowing the outcome, as I’ve done all along with everything. Some of it for me is an attempt to learn from others, because patients and doctors write to share their experiences and ideas. We have done similar infusions in the past that were not noticeable or effective, concurrent with antibiotics for Lyme Disease. We did our first infusion of the formula I posted yesterday and we are working out the kinks with our doctor. Surprisingly, at least to me, we did feel it, Ali positively, me, not so positively thus far. I’ll let you know. I don’t want to start tweeting, but I put it out there last post thinking that it could only be positive or nothing, and I may want to reconsider that, though I still expect that any adverse effect would be mild and temporary. My sleep was disturbed last night and I was kind of wired today and not as stable as I have been. My guess is that it was from the Leucovorin, a folic acid derivative, the only component I haven’t been exposed to before. Deplin can cause similar adverse reactions which are dose related. I find it encouraging that the infusion was noticeable to both of us, but the formula needs tweaking.

As you might expect, I’ve been doing a lot of thinking about MCS these days, at least in the form that Ali is having it. I was speaking to the father of a patient today who is having severe light and sound sensitivity, much like the very severe patients in the UK and Norway. Ali is being triggered by smells, even natural smells like essential oils. My light bulb for today was that these problems are all very similar, all extremely heightened responses to different sensory stimuli. My first symptom was heightened and altered sense of taste. Many patients, and autistic children, have problems with touch, can’t stand tags in clothing, are hypersensitive to light touch, etc. I suspect it’s a kindling phenomenon, less than seizures, but similar, a little less than a full blown disease, as often happens in ME/CFS. Networks of neurons are being synchronized inappropriately by sensory triggers. Repeated stimulation leads to threshold reduction. I am not saying that biotoxins or petroleum products aren’t the trigger for some, but it doesn’t look to me like that’s what’s happening to Ali. It changes my thinking about how to approach it. If it’s a problem with detox and being unable to handle total toxic burden, one set of possible solutions, but if it’s being set off by smells, it’s the response that needs to be attenuated. I am not saying that we aren’t decontaminating and restructuring things so that she can avoid being triggered, which is a big task for an already over-taxed family, but it isn’t possible to be in the world and avoid smells. It is making me think about neurofeedback again. Another topic for another day…

My improvement seems to be continuing, even at altitude. I had an episode six days ago that was probably a sugar reaction, not common for me anymore. I was sick for a couple of hours followed by a kind of sleep I call “coma”. Other than that, I have been remarkably stable. The travel didn’t cost me much at all. I went out for dinner with my husband last night and realized it was the first night out I’ve had in years where I just had fun without struggling at all, after working most of the day. No faking being all right or overlooking symptoms in order to appreciate the moment.

Ali has been struggling with MCS (multiple chemical sensitivity), as a new symptom cluster. She’s had little bits of it before, but nothing like this. It was triggered by an exposure to a new cat litter about a month ago. Since then other chemicals have been triggering her, especially deodorants, perfumes, laundry products. The episodes aren’t medically scary, but involve a dramatic mood shift to blacker than black, ill-defined intolerable, sick feeling. No POTS symptoms particularly, or anything else really. The odd thing to me is that otherwise, she is doing well. Not much OI (orthostatic intolerance). Baseline mood pretty good. With avoidance of the things triggering her, she actually feels fairly well and would be thinking of getting out of the house, but for now, any outings are particularly threatening and would need to be outdoors. We are dealing with eliminating the things she needs us to from the environment.

MCS is a horribly isolating symptom. It makes a hug dangerous. It affects everyone in a household in a more direct way than other symptoms. It comes with tons of psychic overlay. Easy to disbelieve. Looks psychiatric to the uninitiated. Very, very difficult to be a canary in the coal mine.

We recently ran a bunch of labs that were not particularly illuminating, other than our Vitamin D levels are still very low despite replacement. We both still have macrocytosis from AZT, but less than before, expecting it to take 6 months overall to get back to a baseline, because that’s how long it takes to replace all of your red blood cells. Neither of us have serology suggestive of activated EBV, HHV6 or CMV. I have completely negative serology for EBV, strangely given all my years in the ER. We both had high IGF-1’s at baseline, normal now. Ali’s PCOS parameters have improved on treatment (lower LH/FSH ratio), as has my blood sugar on Actos (fasting glucose from 110 to 93, non-fasting from 140 to 110). IgG subunits were normal, my IgG and IgM borderline low. C4a’s and TGF beta-1’s were lost, again; we need to have them redrawn. We’ve been planning to send cytokine and NK cell profiles, but we don’t have baselines, so I doubt that it will tell us much we don’t know.

Our baseline labs consisted of extensive hormone testing and Richie Shoemaker’s panel, which includes all of the very few tests we’ve had that were abnormal in the past, outside of TBD (tick borne disease) testing, and a few fleeting auto-antibodies; I’ve had a mildly elevated nucleolar ANA and we’ve both had mildly elevated anti-cardiolipins. TGF beta-1 was the only test we found that was very high for both of us. When I first learned of the virus, I expected that there would be a viral load measure, but it seems all we have to monitor is downstream effects.

I’ve been receiving questions about my meds. Except for stopping AZT a couple of months ago, nothing has changed significantly since I last reported. I’ve fiddled with my hormones a little. Tried natural menopause for a little while, but it wasn’t pretty, convincing me that bioidentical HRT (hormone replacement therapy) is very important for me. Here’s my current regimen, once daily unless otherwise specified:
Viread 300mg 
Isentress 400mg twice
Cozaar 100mg
Actos 15 mg twice
Deplin 7.5mg
B12 5000 units chewable
Armour thyroid 30mg for years, now 15mg
Estradiol cream 5mg
Testosterone cream 2mg
Prometrium 200mg
Selegilene .5mg cream
Low dose aspirin
Sublingual Zofran 4mg prn nausea
Topical D3 10,000 units, now increasing and adding oral
Meriva SR, undenatured whey protein, L carnitine, glutamine, ALA, Vitamin C, CoQ-10, irregularly
Specific Carbohydrate Diet yogurt, super-fermented to reduce lactose, included here because I think it is a valuable treatment in the setting of inflammatory bowel problems: Making SCD Yogurt

We are both planning to step it up again with supplements, including some we haven’t tried before. It’s a big subject. I will post about this soon.

In consultation with our family doctor, Ali and I are about to start weekly intravenous pushes consisting of a modified Meyers’ cocktail and glutathione. Here is the formula we are planning to use:
Vitamin B complex – 100
Dexpanthenol 250mg
Hydroxocobalamin 5000mcg
Pyridoxine HCL 100mg
Leucovorin (folinic acid) 10mg
Vitamin C 500mg
Magnesium Chloride 800mg
Second Push
Glutathione 2000mg

We have also decided to rent a mild hyperbaric chamber (aka soft chamber, altitude sickness or Gamow bag) and supplement with an oxygen concentrator via mask. This safe technology delivers up to 90% FiO2 (fraction inspired oxygen) at 1.3 ATA (atmospheres of pressure), by non-rebreather mask, with a 10 L/min oxygen concentrator. I’ve been meaning to write a post about oxygen for some time. Because of the observation that CFS patients have redox problems (elevated free radicals), some practitioners think that the use of even low dose oxygen, which produces free radicals during administration, is toxic in this setting. I even heard from a patient that they had been afraid to take oxygen when they were in the ER for chest pain. This seems to be completely incorrect thinking to me. Regardless of the downstream difficulties, oxygen is essential and you have to feed the stream, especially in the face of tissue hypoxia and vascular instability, a hallmark of the disease, causing local ischemia. There are too many anecdotal reports of benefit from low flow oxygen, without added pressure, during downswings, to ignore. It is a very simple, safe thing to try. Supplemental oxygen has helped me through some bad moments. I saw too many benefits from HBOT (hyperbaric oxygen therapy) in practice with related chronic conditions, including autism and chronic Lyme Disease, to dismiss it now.

• Normobaric hyperoxia therapy for traumatic brain injury and stroke: a review. Kumaria 
• Normobaric hyperoxia–induced improvement in cerebral metabolism and reduction in intracranial pressure in patients with severe head injury: a prospective historical cohort-matched study. Tolias
• A prospective, randomized clinical trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury. Rockswold  
• Oxygen therapy in acute ischemic stroke – experimental efficacy and molecular mechanisms. Poli

Administering oxygen is one of the most powerful supportive interventions that we have. Repeated doses of hyperoxia has a salutary effect on the injured brain, whether the injury is ischemic, demyelinating or traumatic. Used therapeutically, repeated exposure to oxygen under pressure is antiinflammatory and antimicrobial. HBOT produces revascularization of ischemic tissues and may encourage mitochondrial biogenesis. Oxygen is regulated like a drug, the argument being that if the dose is high enough, it can kill you, although so can too much water. High dose oxygen can cause CNS hyperexcitability (seizures) in susceptible people. HBOT is “approved” for 13 indications that are treated in hospitals. Approved means reimburseable. Hospital hyperbaricists can be pretty territorial, but using it beyond the approved conditions is legal off-label use of a drug, like using antiretrovirals approved for HIV to treat a different retrovirus, and like the majority of prescriptions written. HBOT probably has broad applicability and nobody wants to pay for it. The technology isn’t patentable, so it hasn’t been studied and optimal dosing for various applications is largely unknown. 

The following papers provide important clues for ME/CFS. The last link will take you to slides of Dr. Rossignol’s lecture for the Autism One conference, this coming week.

• Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis. Rossignol/Frye
• The effects of hyperbaric oxygen therapy on oxidative stress, inflammation, and symptoms in children with autism: an open-label pilot study. Rossignol/Mumper 
• Hyperbaric treatment for children with autism: a multicenter, randomized, double-blind, controlled trial. Rossignol/Mumper 
• Hyperbaric oxygen therapy might improve certain pathophysiological findings in autism. Rossignol 
• Oxygen-induced mitochondrial biogenesis in the rat hippocampus. Gutsaeva/Piantadosi 
• Hyperbaric oxygen therapy may improve symptoms in autistic children.
• Dr. Rossignol’s slides 

Dr. Rossignol’s work seems to me to be hitting on all cylinders. He is beginning to explain why clinically there is an independent pressure effect, since the pO2 (partial pressure of oxygen) for the treatment he is using (FiO2 24% 1.3 ATA) can be reproduced with normobaric oxygen delivered by mask. He is also working on the methylation block question, and his work is suggesting that rather than, or in addition to, a conversion defect, it is yet another (in a long list) of receptor insensitivities, eg insulin, LH, Vitamin D and leptin, overrepresented in ME/CFS patients. This is beginning to get to the heart of the methylation defect. It should be remembered, that methylation is important for retroviral latency.

There are two related neuroimmune diseases with which we already have significant HBOT experience:
   Autism. I personally had wonderful experiences treating autism with low pressure HBOT. Autistic children have many of the same metabolic problems that ME/CFS patients do, including the mitochondrial defect. They have similar brain vulnerabilities as well. I treated children who demonstrated remarkable cognitive gains and improved sensory processing over a very short period of time.
   MS. In the UK there is a network of charity chambers, salvaged military chambers that aren’t rated to go to the depth required to treat wounds or acute carbon monoxide poisoning. At the time I closed my chamber, they had done more than a million treatments over a couple of decades. Their experience is completely uncontrolled. But it’s not that much fun, and people don’t keep doing it for years and years if they aren’t pretty sure it’s helping. There were a couple of studies that indicated benefit, but a negative Cochrane report shut down serious study. Also there’s a medical society, called the UHMS, controlled by the insurers, that exists to be sure nobody gets HBOT for anything but a short list of reimburseable conditions. They also want to make sure that nobody gets treated in anything but a hard chamber, declaring on their website that HBOT requires 1.4 ATA when soft chambers are only rated to go to 1.3 ATA. Rather transparent I would say.

Here is a potpourri of literature that in my opinion collectively support the use of HBOT as part of a coherent treatment strategy for ME/CFS:

• Hyperbaric oxygen therapy in Thai autistic children.
• Hyperbaric oxygen therapy improves spatial learning and memory in a rat model of chronic traumatic brain injury. Harch
• Evaluation of hyperbaric oxygen treatment of neuropsychiatric disorders following traumatic brain injury. Shi
• Chronic hyperbaric oxygen treatment elicits an anti-oxidant response and attenuates atherosclerosis in apoE knockout mice. Kudchodkar
• Hyperbaric oxygen treatment attenuates the pro-inflammatory and immune responses in apolipoprotein E knockout mice. Kudchodkar
• HIV: reactive oxygen species, enveloped viruses and hyperbaric oxygen. Baugh
• Hyperbaric oxygen treatment induces antioxidant gene expression. Godman
• Involvement of the mitochondrial ATP-sensitive potassium channel in the neuroprotective effect of hyperbaric oxygenation after cerebral ischemia. Lou
• Oxygen therapy in stroke: past, present, and future. Singhal
• Effect of large dose hyperbaric oxygenation therapy on prognosis and oxidative stress of acute permanent cerebral ischemic stroke in rats. Xue
• Hyperbaric oxygen preconditioning induces neuroprotection against ischemia in transient not permanent middle cerebral artery occlusion rat model. Xiong
• Optimal dosing as a necessary condition for the efficacy of hyperbaric oxygen therapy in acute ischemic stroke: a critical review. Rogatsky
• Effect of hyperbaric oxygen on the expression of proteins Bcl-2 and Bax in the gerbil hippocampus CA1 following forebrain ischemia reperfusion. Zhou
• Neuroprotection by hyperbaric oxygenation after experimental focal cerebral ischemia monitored by MRI. Schäbitz
• Integrated brain restoration after ischemic stroke–medical management, risk factors, nutrients, and other interventions for managing inflammation and enhancing brain plasticity. Kidd
• Effects of hyperbaric oxygen exposure on experimental hepatic ischemia reperfusion injury: relationship between its timing and neutrophil sequestration. Kihara
• Hyperbaric oxygen therapy for reduction of secondary brain damage in head injury: an animal model of brain contusion. Palzur
• Low pressure hyperbaric oxygen therapy and SPECT brain imaging in the treatment of blast-induced chronic traumatic brain injury (post-concussion syndrome) and post traumatic stress disorder: a case report. Harch
• Hyperbaric oxygen in the treatment of patients with cerebral stroke, brain trauma, and neurologic disease. Al-Waili
• Effects of hyperbaric oxygenation therapy on cerebral metabolism and intracranial pressure in severely brain injured patients. Rockswold
• Effects of hyperbaric oxygen therapy on facial nerve regeneration. Vilela
• Hyperbaric oxygen limits infarct size in ischemic rabbit myocardium in vivo. Sterlin

We know that changing the environment, internally, externally, in this way or that, has made the difference for some people. We also know that there are many people who stay relatively well, at least well enough to function, doing nothing at all, except living their lives within the limits of their disease. I speak to many patients who have had essentially no medical care for years who describe what for ME/CFS is a pretty good course, stable with periods of very mild symptoms only. That makes it unwise to choose a therapy that might do significant harm. Or at least, save the heroics for the sickest patients. It is ironic that using extra oxygen is more questionable than prescribing dangerous drugs for symptom relief. There was a time when prescribing B12 shots was tantamount to quackery, but how many ME/CFS patients have been helped by B12 shots? Lots. When I was in practice, I was struck by how controversial it was to prescribe oxygen for an autistic child, but SSRI’s, tricyclics, benzodiazepines, speed, whatever pharmaceutical was acceptable. I was also struck by how much some patients improved just by stopping medications. When things are going south, always consider what you can stop. I can’t know of course if this next leg of the journey will help us or not, but I’m pretty sure that it won’t hurt, except in the pocketbook. I’ll keep you posted.

I returned from Hawaii to requests to post these powerful statements of our efforts to get help and to help ourselves:

• The WPI’s response to the Singh study. link
• Angel Mac’s notes from her wonderful, authentic CFSAC testimony. link
• Mindy Kitei’s moving testimony before the CFSAC. YouTube
• Demonstration before the Department of Health and Human Services. YouTube   link to Rivka’s write-up
• Updated healKick social networking for young adults. link

I got called on my description of myself as being at 90% by a number of people. I was foolish to attempt to quantify it. I certainly didn’t mean that I felt recovered to 90% of my baseline when I got sick in 1995; I meant that I was feeling pretty close to what I might expect of this body now, which has definitely been through the mill. I am still doing very well since returning home, even after the red eye and missing a night of sleep. I expected to feel the altitude by now and I do feel a little weaker, but I don’t feel particularly sick. More like I’ve been sick for a long time and need rehab. I can get up at will and do what I need to. I’m not short of breath, though I haven’t exerted myself like I did in Hawaii. Still sleeping well. No real physical suffering at all. Ali however continues to struggle. Nothing fair about this disease.

The Singh paper was yet another study where an apparently decent scientist proved beyond a shadow of a doubt that she couldn’t find XMRV in anyone. Or at least that she couldn’t find a VP62 plasmid clone in any CFS patients or controls. But since she did not use a human isolate as a positive control, her results are meaningless. She also proved again that a test derived from monkey antibodies to a VP62 clone doesn’t detect anything in humans. What she didn’t prove is that XMRV and other similar viruses are not infecting humans and she certainly didn’t prove anything that doctors or patients should care about with respect to their treatment decisions. That she would presume to comment is outrageous.

It hurts more because she seemed to be our friend. I met her in Reno last August. She was very excited by our responses to antiretrovirals, chosen because of her in vitro drug testing paper. Interesting that she was able to find XMRV in human tissue when she was studying prostate cancer in 2009 (XMRV is present in malignant prostatic epithelium and is associated with prostate cancer, especially high-grade tumors. Schlaberg/Singh). Odd that she so recently applied for a broad patent with respect to the virus. Then she stabs the WPI, a collaborator, in the back. Very peculiar behavior. My best guess? Follow the money.

In my opinion, the scientific community is still asking the wrong questions. It is important to validate the original work of course, but that is a very small part of what needs to happen. Given that it is obvious from the pathology that we are dealing with one or more previously unrecognized retroviruses, most likely simple animal retroviruses that jumped to humans in some way, the correct question is, which virus or viruses? Not how do we make this one go away so we can all go back on coffee break, rather than recognize the public health disaster in front of our noses. Pretty poor performance, even for government work.

Since the science is progressing glacially, it is not possible for me to evaluate what antiretrovirals are doing for me now, having taken Viread and Isentress for more than 14 months. However, I am approaching 90% of function this week, still in Hawaii. I have been out every day, most of the day, for 12 days. I went snorkeling (a little). I have walked up some steep hills. I have had no PEM. Only very brief episodes of feeling sick, which are not severe and pass quickly. I am eating, sleeping, dreaming normally. I am not short of breath at rest, or even with reasonable exertion. I am very deconditioned, but feel like I can start a measured program to get back in shape. I am choosing upright and the usual energy calculation that runs through my head when I think about whether to get up or not isn’t happening.

I do think it likely that this latest improvement has something to do with the change in altitude; I became polycythemic when I moved to Santa Fe, which is at 7500 feet. I could exercise and was never short of breath without appropriate exertion before that. It will be interesting to see how I do when I go home this week. It may be that going back up will be good too, due to epo which is anti-inflammatory. Athletes know that going up and down is the hot ticket. I’ve been thinking about transitioning to the islands since I left in 1981, but never seemed to be able to make it happen. Our son is finishing up the 11th grade, doing really well, and we are committed to keeping our home in Santa Fe at least until he graduates. But life is full of possibilities again beyond the bed and the couch. My life has improved immeasurably from the positive XMRV culture I received from VIP Dx a year ago January.

Sleep architecture is an important indicator of severity of illness in ME/CFS, certainly for me, but for many others as well. I had been sleeping better for some time before this trip, so the improvement I’m experiencing isn’t all from palm trees and tropical air. It is hard for me, currently beating the odds (knock on wood), to believe that antiretrovirals are hurting me. Though it is possible that I have improved further from going off AZT, I still believe that it helped me in the beginning. It should be remembered that an efficacious treatment paradigm may turn out to be completely different from what has evolved for HIV. It may be possible to take antiretrovirals for a time to knock it back, clean out reservoirs, in conjunction with other things that are conducive to proviral latency. Even inhibiting replication, provirus is sitting there silent, or waving in the breeze. Our knowledge of HIV suggests there are things we can do to encourage latency. Our observation of the disease over decades has taught us that the balance can be tipped in our favor in various ways. Working with the internal and external environments is crucial for recovery.

As for Dr. Singh’s desire to practice clinical medicine? I guess she thinks this patient should not be allowed to continue his meds. From my email this morning:

I tested positive for XMRV. I have been taking zidovudine, tenofovir, and raltegravir for just over 5 months. I started over a 2 1/2 month period and I was on all three by January. Since the end of January, I have experienced very short periods of unmistakable clarity and no symptoms (much more pronounced compared to any period of reduced symptoms that I may have experienced in the past twelve years that I have been ill).

I wish I could report that Ali is doing as well as I am. She didn’t change noticeably one way or the other from stopping AZT. She is in no way as sick as she was when we started this journey. She is stable, but still just below the surface. She has been having some MCS symptoms recently. We are going to step it up again, considering mild HBOT, Meyer’s cocktail/glutathione IV’s and possibly Nexavir. Ali has inflammatory skin stuff and Nexavir is indicated for skin problems; always good if a therapeutic option addresses more than one problem. She only needs a small additional increment of improvement to be able to get a life again. She is hoping to experience Hawaii too. Neither of us would stop the things that have helped, Actos, Deplin, B12, vitamin D, bioidentical hormones. Nor do we have any inclination to stop antiretrovirals, certainly not on Dr. Singh’s say so. We have done too well on them so far to rock that boat. We need to keep building on our gains.

Dear Dr. Deckoff-Jones:

I would like to respond to the questions about EBV. Before I had read about retroviruses, I focused on EBV and CLL, because there were a couple or reports of EBV being found in about 25% of CLL patients. Just looking at serology is problematic as almost everyone has had an EBV infection and antibody testing is always positive. My plasma was negative for EBV DNA. A concentrate of my lymphocytes was tested at the Mayo Clinic and was also negative for EBV proteins and nucleic acid sequences.

To anonymous commenter “anciendaze”: The point is that this specific virus (similar only to the Rauscher murine leukemia virus) was found only in malignant cells and not in normal cells. If one reads the articles, one will see that other viruses were looked at but only the Rauscher virus worked in the assays. Conversely, in breast cancer, Spiegelman found evidence of the mouse mammary tumor virus not the Rauscher virus and this work has been confirmed by multiple other labs, including very recently by Pogo and Holland. I have attached this reference (Particles Containing RNA-Instructed DNA Polymerase and Virus-Related RNA in Human Breast Cancers. Axel/Spiegelman).

I too have read the article in which the term “rumor” viruses was first coined. That term speaks to the negativity and timidity that often accompanies a new way of looking at things. One must have an open mind, which is called for by the scientific method and not ignore data; otherwise one is guilty of holding back progress that could help thousands and thousands of patients.

Sol Spiegelman was highly respected and was awarded a Lasker prize for his work with nucleic acids. This is often a prelude to the Nobel prize. Robert Gallo respected his work enough to pursue it. Unfortunately Spiegelman died relatively young and his laboratory closed. Robert Gallo moved on to HIV. Nothing further happened with MLRVs and thirty years was lost until the Cleveland Clinic and WPI published their studies. We, that is we cancer patients, and we CFS patients, lost thirty years and don’t want to lose any more time needlessly. Much work remains and must start now.

Michael Snyderman, MD

Some of the responses to Dr. Snyderman’s letter indicated that my introduction was misinterpreted by a few people, so I’d like to clarify. I didn’t say that Dr. Snyderman would be dead by now if he’d not taken arv’s. I said that he would never have gotten a chance to try them if he’d waited for the science to run it’s course, to be given permission to do what he did. His numbers, and  ALC doubling time, suggested that he should be dead about a year from now. The evidence he presented suggest that he has impacted the expected course of the disease, but it is too soon to know if his life has been prolonged. He had no prior treatment for his CLL, because he didn’t like the cost/benefit ratio.

Several people requested references for Dr. Snyderman’s statement that the “supporting data actually goes back to the 1970s. Three different research labs including Robert Gallo’s the co-discoverer of HIV found MLRVs in many different types of lymphoma and leukemia.” Here are references he sent:

• RNA in Human Leukemic Cells Related to the RNA of a Mouse Leukemia Virus. Hehlmann/Spiegelman 
• RNA in Human Leukemic Cells Related to the RNA of a Mouse Leukemia Virus. Hehlmann/Spiegelman 
• Human sarcomas contain RNA related to the RNA of a mouse leukemia virus. Kufe/Spiegelman 
• Burkitt’s Tumors Contain Particles Encapsulating RNA-Instructed DNA Polymerase and High Molecular Weight Virus-Related RNA. Kufe/Spiegelman 
• Sequences Present in Both Human Leukemic Cell Nuclear DNA and Rauscher Leukemia Virus. Baxt
• Rauscher-leukemia-virus-related sequences in human DNA: Presence insome tissuesofsome patients with hematopoietic neoplasias and absence in DNA from other tissues. Aulakh/Gallo

I’d like to thank Dr. Hodgson for his considered comments, however I disagree with them in a fundamental way. If you don’t have HIV, you don’t get AIDS.  Period, end of discussion.  The retrovirus is the only meaningful biomarker. There are predictable lab abnormalities once things start to go south, like CD4 depletion, but the presence of the virus is what matters. Similarly, abnormalities of NK cell number and function may occur down the road in ME/CFS, but normal results in no way rule out the disease. Likewise there are cytokine/chemokine abnormalities, but no single signature pattern that defines the disease to the exclusion of other patterns. It would be a serious mistake and disservice to patients everywhere to define the disease narrowly based on either lab tests or symptom combinations. That would be like saying that AIDS patients with pneumocystis pneumonia have the disease, but patients with Kaposi’s sarcoma don’t.

A complicating factor may well be the presence of more than one virus. It seems likely that different combinations of virus(es), genes, types of injury are responsible for the different presentations. It is crucial that the problem be defined in the broadest possible way. There are likely an enormous number of infected people who are a little sick, or not sick at all. These are the people who should be getting the most attention, not excluded from consideration because their NK cell and cytokine profiles are normal. And then there are the uninfected…

I haven’t posted in ten days, and I was on such a roll for a while that I’m getting mail asking if I’m OK. Actually, I seem to be on a slow uphill course again. My sleep is especially improved lately, sleeping all night and even dreaming. The truth is, I’m in Hawaii. I needed to come here for personal reasons, but my husband and I have managed to squeeze in some vacation, our first since New Year’s 2003, when we were all still healthy, even me, relatively speaking. It’s been three years since I’ve been to sea level. I live in Santa Fe, at 7500 feet of elevation. I am much less short of breath with exertion here and hiked in a half a mile to a waterfall yesterday, with no PEM. I am sitting on a stunning beach as I write this. I have even been able to swim a little. My husband is snorkeling. I get little pangs of sadness that I can’t do it with him like I used to, but I am so happy that he can. It is amazing to me that I am here. I lived here when I was a young doctor and always imagined that I would return. I thought my life was over, but it is starting again. Who knows? Maybe the best is yet to come.

Aloha nui loa this beautiful May Day. A hui hou.

A lot of the dissension here feels like the squabbling of a lively, dysfunctional family, with lots of crazy relatives:). Lately, there’s been some progress in being more respectful of one another. But this being the internet, there are strangers in our midst, trying to find chinks in our nonexistent armor. That’s fine, for we are here to look at the truth. The naysayers are an opportunity to sharpen our thinking and confront rumor head-on.

I decided to blog because I couldn’t stand all the suffering in isolation. Even as a doctor, when my family got sick and started seeing Lyme doctors, there was a feeling that there were people that knew something that I didn’t, a way in which the information wasn’t freely given. I now think that happens because of everyone’s unwillingness to admit what they don’t know, even to themselves.

My only serious concern about my outspokenness on the internet has been the recent comments that my being controversial might somehow hurt the WPI. For this reason, in part, I have elected to be a consultant for the WPI, as an independent contractor, rather than an employee. I’ll take this opportunity, in advance of an announcement on the WPI website, to say that the opening of the clinic will not take place in May as hoped, primarily because of financial constraints. Our plans remain unchanged however, and I am hopeful of opening before the end of the year.

So let’s take advantage of our devil’s advocate, John, who has questioned both the science and integrity of the main protagonists at the WPI. With permission, I’d like to tell you what I’ve learned about the institute and the people involved. In particular, I’d like to address the oft heard thread that runs something like this: the Whittemores are richer than God, so why don’t they just cough up another few million dollars to save us?

Here is the reality. At a time when money was not as big an issue as it is now, the Whittemores, and other concerned patients, joined with Redlabs, owned by Dr. De Meirleir in Belgium, to start VIP Dx. This happened at great personal expense because a clinical research lab was needed to save their daughter, and others. The “and others” make the Whittemores special. They didn’t just have the money. Lots of people have the money. They thought about the problem and applied the money in a way that no one else had done before. It wasn’t about money, but the embodiment of parental love. This all happened well before there was a research lab. XMRV as a cause of CFS wasn’t even a twinkle in anyone’s eye.

Everyone knows that Harvey and Annette spent many millions, and raised millions more, to fund an institute so that everyone would be helped. They brought together the necessary ingredients in the form of Mikovits and Lombardi. Having heard the story from each of them and others, it was a synthesis of talent, skill and luck, as genius always is. The WPI scientists support and promote each other’s contributions, a rare thing in the world of science. Also unheard of, everybody passed up any intellectual property rights in favor of the institute. Any interest in eventual profit from the use of the WPI’s intellectual property by VIP Dx was passed to the institute when it was founded.

When the Science paper was published, a lab called Cooperative Diagnostics, owned by a scientist named Satterfield, brought an unvalidated test to market for XMRV, even though they had never found it in a human being. Their test was a PCR for a VP62 plasmid. Recently, in an interview with Cort Johnson, Dr. Satterfield admitted that they never did find it in anyone. More of the “I can’t find it, so it isn’t there” insanity. I thought it pretty strange that he isn’t ashamed of having charged people a bunch of money for a test, even though he knew that he had never found XMRV in an actual patient. How can you disprove an association, if you can’t find it all?

Dr. Satterfield’s attempt to jump into the market, forced VIP Dx to bring a test to market, even though there had been no intention to do so until further research was done. But the prospect that there would be a flood of negative test results that needed to be immediately challenged forced their hand. At that time, it seemed likely that the major commercial labs would be testing soon, so it was considered a band aid for the short term.

The first 10 people who write to me that have a receipt for a negative test from Cooperative Diagnostics will be tested at VIP Dx for free. Email: jdeckoffjones@gmail.com. Also, if anyone received a positive test from Cooperative Diagnostics, I’d like to hear from you.

So testing for XMRV is a gold mine, right? Wrong. VIP Dx hasn’t even begun to pay back the original founders, nor can it cover all of its current existing expenses. It pays WPI a royalty (calculated as the net profit for administering the test) that puts it further in the red. Some of the founders donated their holdings or had their holdings placed in trust for the benefit of WPI. And Harvey, who manages the lab, has never been paid a dime. Never. The lab exists to unravel the mystery of our illnesses, as it was intended from the beginning. Here’s the truth. VIP Dx has lost almost a million dollars since inception. Not accountants fiddling with red ink, but real losses. I have seen the actual numbers. Anyone want to donate to the cause?

I can tell you that in planning the clinic, VIP Dx is just as important as the WPI translational research lab. Integral parts of a unique whole. Dr. Lombardi will make available any testing that our doctors decide we need. He is looking into the tests I have asked for, so that they will be available when we open. They recently moved into their new state of the art facility next to the clinic, a tremendous undertaking. All testing done in the clinic will go into our database, so contributes to our overall understanding of the illness and how to approach it.

So why don’t the Whittemores give some more money? Because they don’t have it at the moment. If they did, they would. In my opinion, everyone who has spent a few dollars on an XMRV test from VIP Dx is contributing to the greater good. The sooner we start to think about the illness as related to XMRV, or another related but unspecified human gamma retrovirus, the better; it will affect those we tell. Personally, I’ve had good luck explaining my illness to the uninitiated as “a newly discovered retrovirus like HIV that isn’t fatal”. We are in much better shape now, with our decisions informed by this understanding, than we were before. Understanding is everything to me. For that reason, no matter how it all turns out, I owe my hugely improved quality of life to the Science paper. I’m still sick, but living in the light.

As for Dr. Mikovits being right or wrong? She questions herself every day, as any real scientist would. Clearly, she (and the WPI) were unprepared for the thousands of desperate patients who turned to her, all needing immediate help. She is a deeply compassionate person and has trouble telling patients that the science is going to take time. She bleeds for us. A consummate scientist, not a politician, she is under unimaginable pressure, caught in the center of the perfect storm. We all owe her a debt of gratitude for what she has already given.

Finally, I have spent time in the labs of both Drs. Mikovits and Lombardi, in two different places many miles apart. They can both grow the virus. Not from everyone, but in a significant percentage of patients. I wonder how they keep contaminating only some of the samples. To John. I will address your objections 1-8, 9, 10, 11….99, 100, etc. in a future post. But it is my belief that if you use the methods, materials, and processes outlined in the Lombardi paper, in an appropriate sample, you will find XMRV. Other labs besides these two can find it. We know that there are plenty of people out there who can design and complete a PCR study looking for XMRV and not find VP62. They know, and we know, that they are looking for the wrong XMRV and using the wrong methods, materials, and processes. It is that simple.

Any intelligent fool can make things bigger and more complex… It takes a touch of genius – and a lot of courage to move in the opposite direction.
~ Albert Einstein

I speak to a lot of doctors. It is common to hear that they do a bunch of elaborate tests that let them “individualize” treatment. They feel they have identified The Defect, and can address it, in this way or that. There will be an overly intellectualized theory, but mostly, the strategy involves replacing a substrate, using a little known intermediary, or overwhelming a block in a metabolic pathway. That strategy can make the difference, though it often doesn’t, because no matter how far you take it, you don’t know enough. I know a woman who was housebound for a decade who was able to return to work after she started B12 shots. But for every one of her, there are an awful lot of people for whom B12 made no noticeable difference at all. To make matters worse, an intervention might not work, but “work” at another time for a given patient. For every case of something definite that brought about a remission, I hear about a few spontaneous ones, even after many years, where there was nothing that could be identified as making the difference. One of the most tantalizing things, and you hear it regularly, is that something worked for a few days, and there was a taste of almost normal. That implies reversibility.

The blog has a tracker that shows the most recent readers on a map of the world. There is often someone tuning in from Tromsø Norway, at the top of the world. It is interesting to note that MS is more prevalent in northerm latitudes. The very extreme form of ME, which seems to be more common in Norway in particular, reminds me of an adult form of autism in a sicker body, with PEM and pain thrown in. ASD looks different because it occurs in the developing brain, but the obvious commonality of symptoms is there. Extreme sensory overstimulation. Can’t stand light and sound. Problems with touch. Problems communicating. Concurrent GI dysfunction.

We haven’t heard from the Gulf War Illness community here yet, but it seems to me, it is the same illness. I had more of a GWI, than typical CFS, presentation. If it’d been a couple of years earlier and I’d been a soldier returning from war, instead of a post-partum ER doctor, GWI would have been my diagnosis. I had olfactory hallucinations, or flashbacks, of the worst burn case of my career. I now think of them as 1rst cranial nerve discharges, rare and without emotional content at this late date, but it seemed pretty classic PTSD at the time. My psychiatrist called it “vicarious PTSD” from the ER. Do you believe it? He didn’t even let me own my own trauma. I said it felt like the flu. I used the word malaise. Psychiatrists have done me a lot of harm. But I shouldn’t single them out; it’s just somehow more personal. But the rest of my doctors and dentists, in hindsight, mostly chose the stupidest thing too, because of profound misunderstanding of the illness and disbelief. And speaking their language didn’t help at all.

Being unable to depend upon the stability of the ground beneath me has been a tough, but effective, teacher. I don’t sweat the small stuff anymore. Acceptance is my mantra. My uninsulated wiring and limited physical ability require a simplification of thought and action that in the end boils down to common sense, something I didn’t always have. I have learned to ride over the bad moments and find great joy in the good ones. It is all very close to the surface. I spoke to a woman last week who referred to herself as “an idiot savant”. That struck a chord in me. We have all had to learn to live with diminished capacity. For me, functioning requires first surrendering to the illness. If there is a silver lining, it’s easy access to my own truth. I don’t over-think things or worry much any more. It already happened. It’s become about what I can do, instead of what I can’t.

P.S. My email has gotten away from me, as it is very heavy. The survey has taken a lot of attention. If you emailed me about something important to you and I missed it, please resend. Once in a while, if I think about a question too much, it doesn’t get answered. Sometimes I have nothing to say and don’t answer because I think it might come to me. I read every word and am sustained by hearing that it is helping in some way. Your emails make me think and care. I try to cover recurring themes here.

At this juncture, with the science in an embryonic state, I am in favor of the most inclusive definition. The only problem with non-HIV AIDS is that “Deficiency” isn’t exactly right, though the disease can clearly progress to an immune deficiency, just not a devastating one like endstage HIV. Dysregulation would be a better word. However “Acquired Immune Deficiency Syndrome” unrelated to HIV, is close enough for government work, and the name evokes what it should. Before the causative agent of Hepatitis C was identified, it was clear that there was another infectious virus that caused hepatitis that had a different clinical course than either Hep A or B. This is exactly analogous to that. We will eventually have a laboratory profile that is inclusive of all the cohorts, or maybe I should say, factions.

Neuromyasthenia isn’t a bad name. It takes into account the full history of the phenomenon, but the overemphasis on muscle is inappropriate for many and it leaves out the immune problems. It also brings “the vapors” to mind for me for some reason. I haven’t heard a perfect name. Another new acronym won’t take at this time, even if accurate, because everything is in such a state of flux. It will all be easier when the causative agents are identified. For now, non-HIV AIDS explains it in very few syllables. Even a doctor should get it.

AIDS has case surveillance criteria that include “AIDS-defining conditions”. Revised Surveillance Case Definitions for HIV Infection 2008. If you are HIV positive, whether you get PCP or Kaposi’s Sarcoma, it is still AIDS. Whether you have HIV dementia or not, it is still AIDS. It is the same for us, whether you have HHV-6, Lyme Disease, CLL or ASD.

I don’t like any of the existing case definitions, though most full-blown cases are caught by the Canadian Criteria. Using us, as examples; I didn’t have a viral onset and I don’t have sore throats, fever, adenopathy. I got sick post-partum with various neurological symptoms which were all transient. I was always hyperimmune. I worked in the ER for 16 years; I was exposed to everything and never caught anything. I’ve had an influenza a few times, including Swine Flu, which was no big deal, but that’s it for viral illnesses, other than childhood illnesses, all of which I had naturally before my early teens. However, I had persistent Babesiosis despite lots of treatment, so that’s pretty immune deficient. I have never met CDC criteria. I meet Canadian Criteria (6/6), but didn’t for the first decade of my illness. As for ME? I didn’t have PEM for over a dozen years, though it’s bad now, and I still don’t have problems with cognition or memory. I have sensory deficits. I have a positive Babinski and Rhomberg. I have mini-clubbing that started before my first crash. I have low titers of autoimmune markers, sometimes. I am XMRV positive. I’ve had negative nerve conduction studies. I have been given many diagnoses over the years including chronic Lyme Disease, fibromyalgia, Crohn’s, PTSD, dysautonomia, arrhythmias, peripheral neuropathy, Raynauds, atypical migraines, intestinal migraines, pain syndrome of unclear etiology, most recently CFS. I have recurrent hypertensive crises. I have a sleep disorder from being an ER doctor, predating my illness by many years, but it’s much worse now. I am probably an Ehlers Danlos variant. I have become more flexible with each major exacerbation of my illness. My wingspan is greater than height, though I am short. Ritchie Shoemaker says my genes are “poison”, but Ali “drank” the lesser of the poisons. What do you think I have?

Ali is more classic CFS, though she also had an onset that was related to a major hormonal shift, and her illness responded to oral antibiotics for years. She does not meet CDC criteria. She does meet Candian criteria, except when she doesn’t. No sore throat, fever, nodes. She catches viral illnesses very lightly; barely registered Swine Flu. She has had inflammatory skin stuff since she was little, predating illness. She has a history of treatment resistant Lyme Disease, atypical migraine, a mild cerebral vasculitis and leukocytoclastic vasculitis twice from PICC lines. She has POTS. She has a little brain fog that comes and goes, but is really sharp mostly. Little sleep issues, but not bad. She has PEM, but didn’t always. She has a little MCS. Not much pain. She is XMRV positive. Do you think we have different diseases from each other? From you?

There is aggressive prostate cancer, Parkinson’s Disease, Multiple Myeloma, ASD and Marfan’s Syndrome in our family, which is in no way an outlier. The surveys we are receiving look compelling for demonstrating both the genetic and infectious pieces, as well as associated conditions. Thank you to everyone participating. These informal responses are helping us to determine the right questions and how to proceed. Please keep them coming, even if you are an isolated case. Our intention is to proceed with a formal study. There will be a secondary mailing to fill in the blanks and provide consent for publication. If you’ve sent in a survey, please stay tuned over the next few months for additional requests for information, and if you change your email address, let me know.

It is completely outrageous that the epidemiology has not been formally studied by our government agencies over the last decades, while so many people were getting sick. How did they let this happen? How come the Center For Disease Control has never even looked? An obviously infectious disease spreading through the population for decades. Whole families affected. But they buried their heads in the sand, because it wasn’t straight forward. It was easier to think the patients were lazy, crazy and faking. After all, they were an unusually labile bunch, hard to deal with, quite hysterical sometimes, and so fixated on their symptoms, which any good doctor could tell, couldn’t be a real disease. No wonder the people responsible can’t let it in. Imagine realizing that you were one of the people who allowed an incurable infectious virus to invade a second and third generation, ruining the lives of millions of people. No way to contain it anymore. The health of the species affected on an evolutionary scale. Just because you were wrong. That could make for some serious denial.

So, we will study the family piece ourselves. With talented, sick volunteers. Without funding. For free.

God loves to help him who strives to help himself.
Aeschylus ~500 BC