“This is a court of law, young man, not a court of justice.”
~ Oliver Wendell Holmes, Jr.
The WPI’s lawsuit against it’s former chief scientist continues to cut its swath of destruction through the heart of the ME/CFS community. Dr. Judy was forced to declare bankruptcy yesterday. She has already spent her retirement on lawyers and now she will lose one, if not both, of her two small condominiums, which one still to be determined by a bankruptcy trustee. And most importantly, she isn’t working on our behalf…
Here’s a letter posted this morning on the Messages of Support for Dr. Judy Mikovits FaceBook page (there are several such pages with hundreds of members):
It is beyond me that in this day and age this injustice is allowed. I am not a naive person but I had hoped that the 21st Century would bring a greater justice and compassion to the world.
How can these corrupt people be able to ruin, mentally, physically and personally an innocent and truly good individual?
I am deeply sad.
Me too. It is beyond crazy. A travesty of justice. A misuse of the system. The WPI, a non-profit, spent large amounts of money on lawyers to write hundreds of pages of legal documents, to destroy what was in fact their only resource. To what end? They knew there was nothing to get monetarily. An apology? What a joke. Even if they were right, which they aren’t, what would someone interested in the greater good have done when confronted with the problems that Annette Whittemore was confronted with?
In a nutshell, this is where the case stands. The first judge ruled against Dr. Mikovits in a default judgement because she wouldn’t give up her personal email which contained confidential information on many study participants. Then he recused himself to make sure there was no appearance of impropriety, since he had received significant campaign contributions from Harvey Whittemore, who is under indictment for making illegal political contributions and lying to the FBI, not to mention his other business problems: Ex-business partners: Whittemores owe more than $24M. Of course, Harvey claims to have nothing to do with the WPI. So a new judge was appointed. One would have thought that the opportunity would have been seized to right the wrong and run the case as it should have been run in the first place, but no, the judge decided to continue where the old judge left off, leaving the judgement in place, with a “prove up” hearing scheduled for today, to determine an amount, thus forcing the bankruptcy.
The WPI wants Dr. Mikovits to pay for their loss of donations compared to before she was fired. As if they didn’t cause it all with their own actions!! They didn’t have a fund raiser this year because who would be there? They want back her entire 5 years of salary, during which she was desperately trying to, and in fact did, help their daughter. Plus, they want the entire cost of the research program from inception. Oh, and the punitive multiplier for her “bad behavior” since she was fired! And they want their legal fees, so they don’t have to defraud the community and the NIH to pay their lawyers. Of course Dr. Mikovits has no money…
In July 2011 she told Harvey Whittemore of the potential contamination, she says, and expected that the VIP Dx lab would cease testing patients for the XMRV virus. “I just kept saying, stop it, stop it, stop it. We have to sort this out,” Mikovits says. According to Mikovits, the testing did not stop. And after a tense summer, she was fired in September.
Let’s not forget what this is really about, not some imaginary IP in some old notebooks, but the thousands of bogus tests that were sold, some after they knew they were bogus, some paid for by Medicare?
The fall out from it all? The WPI’s legacy, from an advocate of 20 years, posted to FaceBook last night and republished with permission.
My Opinion: We’ve been ized
~by John Herd
The Whittemores overly self-mesmerized
Their grandiosity so fantasized
Just because of money legitimized?
They expected to be idealized
Constructive input demonized
As sound advocates often minimalized
While many amongst us patronized
And those with differing views were ostracized
Stupid actions authorized
Moral integrity compromised
“For the sake of patients” bastardized
Sound PR strategies brutalized
With so much about WPI fictionalized
In fake news coverage televised
Fabrications on the Internet digitalized
Research assets cannibalized
Clinically unvalidated test commercialized
Protecting scientific data criminalized
While Judy Mikovits sat in jail demoralized
Judicial corruption legalized
Their lavish travel and living publicized
Questionable scientific integrity sanitized
As their research director was victimized
The whole view of CFS jeopardized
By the WPI saga being so scandalized
An insult to patients already traumatized
From misinformed views of the illness so hypothesized
All WPI’s books should be scrutinized
With all their records analyzed
If they’ve not yet been sterilized
And financial assets vaporized
From the CFS world they should be exorcised
Because they added to our being even more stigmatized
Let’s face it, we’ve been sodomized
But oh how nicely Annette is accessorized
Today’s song: Which Side Are You On? Performed by Natalie Merchant
And a modern version of this classic protest song by Ani Difranco
The arrogance continues with the latest “contribution” from our government at work:
Curr Opin Virol. 2012 Jul 17. [Epub ahead of print]
Recombinant origin, contamination, and de-discovery of XMRV.
Delviks-Frankenberry K, Cingöz O, Coffin JM, Pathak VK.
Viral Mutation Section, NCI, HIV DRP, Frederick National Laboratory for Cancer Research, Frederick, MD, United States.
The discovery and de-discovery of the xenotropic murine leukemia virus-related virus (XMRV) has been a tumultuous roller-coaster ride for scientists and patients. The initial associations of XMRV with chronic fatigue syndrome and prostate cancer, while providing much hope and optimism, have now been discredited and/or retracted following overwhelming evidence that (1) numerous patient cohorts from around the world areXMRV-negative, (2) the initial reports of XMRV-positive patients were due to contamination with mouse DNA, XMRV plasmid DNA, or virus from the 22Rv1 cell line and (3) XMRV is a laboratory-derived virus generated in the mid 1990s through recombination during passage of a prostate tumor xenograft in immuno-compromised mice. While these developments are disappointing to scientists and patients, they provide a valuable road map of potential pitfalls to the would-be microbe hunters.
Game. Set. Match. Everyone can take a sigh of relief. The human race is safe, as they’ve said all along. Scientists in a power postition at the NIH have closed their minds to retroviruses other than HIV and HTLV contributing to human disease. Is this really a scientific assessment of all the available data? Or a ploy to keep the blinders on a while longer? Baffle ’em with bullshit.
There’s a giant elephant in the room. Several elephants actually. What if there’s more than this one virus that they acknowledge they created in the early 90’s? It seems likely that it’s happened more than once, given how many chances there have been to recombine and infect human cells? But they only infect human cells in tissue culture they say, not in vivo because we have restriction factors.
Here’s an experiment with human lymphoid tissue concluding we are safe:
Susceptibility of Human Lymphoid Tissue Cultured ex vivo to Xenotropic Murine Leukemia Virus-Related Virus (XMRV) Infection. Curriu et al.
Background: Xenotropic murine leukemia virus-related virus (XMRV) was generated after a recombination event between two endogenous murine leukemia viruses during the production of a prostate cancer cell line. Although the associations of the XMRV infection with human diseases appear unlikely, the XMRV is a retrovirus of undefined pathogenic potential, able to replicate in human cells in vitro. Since recent studies using animal models for infection have yielded conflicting results, we set out an ex vivo model for XMRV infection of human tonsillar tissue to determine whether XMRV produced by 22Rv1 cells is able to replicate in human lymphoid organs. Tonsil blocks were infected and infection kinetics and its pathogenic effects were monitored
Results: XMRV, though restricted by APOBEC, enters and integrates into the tissue cells. The infection did not result in changes of T or B-cells, immune activation, nor inflammatory chemokines. Infectious viruses could be recovered from supernatants of infected tonsils by reinfecting DERSE XMRV indicator cell line, although these supernatants could not establish a new infection in fresh tonsil culture, indicating that in our model, the viral replication is controlled by innate antiviral restriction factors.
Conclusions: Overall, the replication-competent retrovirus XMRV, present in a high number of laboratories, is able to infect human lymphoid tissue and produce infectious viruses, even though they were unable to establish a new infection in fresh tonsillar tissue. Hereby, laboratories working with cell lines producing XMRV should have knowledge and understanding of the potential biological biohazardous risks of this virus.
So maybe they’ll take a few extra biohazard precautions for themselves, since they are working directly with these lab anomalies, but nothing to worry about for the general public. Never mind the millions of human canaries illuminating the destructive path we are on. Never mind that this could explain the observed increase in neuroimmune diseases, autoimmunity and cancer. Never mind that we’ve been mainlining attenuated viruses cultured in animal cells which express exogenous retroviruses for eighty years now. Never mind that these viruses cause similar diseases in other mammals to that which we are observing in humans. Never mind all the clinical evidence that several large patient cohorts, ME/CFS, ASD, GWI, chronic Lyme Disease, PANDAS, RRMS are related and contagious diseases. Leave it in the realm of genetic weaknesses for now. Better to be an ostrich for a while longer since the cat is so out of the bag. Let’s remain in denial for as long as we possibly can, which I guess will be until Quest has a DNA sequencing test that insurance will pay for. They are allowed to be literal and have limited vision in the name of science.
Comparing PreXMRV-2 gag sequence diversity in laboratory and wild mice using deep sequencing. Mayer et al.
It has recently been reported that the xenotropic murine leukemia virus-related virus (XMRV) derives from a laboratory recombinant. However, sequences with characteristics of the 5′ half of XMRV (termed PreXMRV-2) have been identified in several laboratory mouse genomes and cell lines suggesting parts of the XMRV genome exist as naturally occurring retroviruses in mice. We compare here PreXMRV-2 gag sequence diversity in mice to that of reported XMRV-like sequences by testing a panel of wild mouse and common inbred laboratory mouse strain genomic DNAs and by using high throughput amplicon sequencing. Sequences with features typical of previously reported PreXMRV-2 sequences, among them a 24 nt deletion, were repeatedly identified in different wild mice and inbred mouse strains within a high background of non-XMRV-like sequences. However, Sanger sequencing of clones from amplicons failed to retrieve such sequences effectively. Phylogenetic analysis suggests that PreXMRV-2 gag sequences from mice, cell lines and patient samples belong to the same evolutionarily young clade and that such sequences are diverse and widespread within Mus musculus domesticus and laboratory mice derived from this species. No evidence of PreXMRV-2 like gag sequences could be obtained outside of the M. musculus lineage. The results suggest that accurate determination of presence, absence and relationships of specific murine retroviral strains benefit greatly from deep sequencing analysis.
Meaning that most of the work that has been done so far has been a meaningless waste of time, energy and money… More from this paper:
… in both the Sanger sequencing and high- throughput datasets, PreXMRV-2 like gag sequences were not majority sequences in any mouse DNA sample, even when account- ing for possible clonal artifacts due to PCR or emulsion PCR before GS FLX deep sequencing preferentially amplifying one sequence over another in a complex mixture. Thus, and also in the light of an often unknown sequence heterogeneity provided by mouse ERVs, we feel that high-throughput sequencing should generally be applied when attempting to detect relatively rare sequences such as PreXMRV-2 from complex retroviral mixtures. High-throughput sequencing is a common strategy used for identifying rare human immunodeficiency virus 1 variants and may need to be employed more broadly.
Here’s a paper that shows that mixing XMRV with Maloney MuLV produces a more dangerous virus. Simple animal retroviruses recombine and one can “rescue” another by providing missing pieces that evolution has silenced with mutations to protect us.
Moloney murine leukemia virus glyco-gag facilitates xenotropic murine leukemia virus-related virus replication through human APOBEC3-independent mechanism. Nitta et al.
One of the unique features of gammaretroviruses is that they contain an additional extended form of Gag, glyco-gag, which initiates in the leader sequence. MuLV glyco-gag, gPr80Gag, promotes retrovirus replication and disease progression. Although virtually all infectious MuLVs encode glyco-gag, XMRV (xenotropic murine leukemia virus-related virus) lacks the classical gPr80Gag sequence. We examined XMRV to determine if its leader sequence contains glyco-gag activity, whether the presence of conventional gPr80Gag affects replication of XMRV, and we describe the evolution of glyco-gag-deficient MuLVs in Mus.
We introduced several mutations disrupting two putative but noncanonical glyco-gag proteins in the leader sequence region in XMRV and found that those mutations did not affect virus
release nor susceptibility to the antiviral activity of hA3G (human APOBEC3G). A chimeric XMRV encoding the Moloney MuLV (M-MuLV) leader sequence (MXMRV) demonstrated that M-MuLV glyco-gag facilitated MXMRV release and increased infectivity. Infectivity assays with several cell lines showed that glyco-gag increases XMRV infectivity in all cell lines tested, but the level of this increase varies in different cell lines. Because MuLV glyco- gag counteracts mouse APOBEC3, we investigated whether M-MuLV glyco-gag enhances XMRV infection by counteracting human APOBEC3. Comparison of hAPOBEC3 isoforms expressed in different cell lines indicated that hA3B was the most likely candidate for a restrictive hA3. However over-expression of hA3B showed no enhanced restriction of infection by XMRV compared to MXMRV. Endogenous MuLVs in the sequenced mouse genome were screened for canonical glyco-gag, which was identified in two clades of xenotropic MuLVs (X-MuLVs) and ecotropic MuLVs, but not in other X-MuLVs or in any polytropic MuLVs.
M-MuLV glyco-gag facilitates XMRV replication, and the leader sequence region in XMRV does not encode proteins equivalent to M-MuLV glyco-gag. The fact that the ability of glyco- gag to enhance XMRV infection varies in different cell lines suggests a glyco-gag sensitive restrictive factor that further reduces XMRV infectivity. The M-MuLV glyco-gag enhancement for XMRV replication is through a hAPOBEC3 independent mechanism. The absence of glyco-gag in MuLVs carried by western European mice suggests that loss of this sequence is a relatively recent event with limited subspecies distribution.
While the decades long coffee break continues at the CDC, I’m trying to be well enough to work, in order to care for members of the most medically underserved population I’ve ever taken care of, including medical school in the Bronx and 10 years in the ED at Santa Clara Valley Medical Center, the county hospital in San Jose, CA, where the patients are a composite of third world misery. Those patients had nothing on this group in terms of lack of informed care; almost every patient I have has received abysmal care, due to ignorance and a lack of compassion because they have an invisible disease. Benign neglect is as good as it gets.
The last blog was the least controversial I’ve ever written judging from the comments. I have received many expressions of concern for Andrew that the ball was dropped. I would like to reassure everyone that I forwarded my findings and recommendations to Andrew’s doctor in Northern Ireland. Andrew has been seen twice since he returned home and is reportedly much better than before his trip. So the most important thing happened. Taking it all at face value, Andrew improved with oxygen and Deplin. He received about 30 hours of oxygen. In hyperbaric practice, I used to do a series of 40 hours and expect it to last for at least several months if the response was robust. I only hope that if it fades, he will be able to access more oxygen and L-methylfolate, available over the counter, as explained in my last blog.
I tremendously appreciate all of the expressions of support from friends around the world. I did hear back channel from a few people who were upset that I said that some ME/CFS patients are difficult from a physician’s perspective. I almost didn’t leave it in after I wrote it, but decided to, because it is important grist for the mill. There are several perversions that have befallen us, by virtue of being seen as lazy, crazy and faking. One is the need to refute that therapy could be useful for us in some way, since it is being forced down throats by the same people who say there is no physical basis. Therapy with people trying to talk you out of what is real isn’t very useful, but in the context of being believed, it might do a lot of good. Same goes for exercise. It is the context that is the problem. Another perversion is the need to be good if we ever want to be seen as sick or worthy of help. Well, Alzheimer’s Disease doesn’t make most patients particularly nice, but the disease still gets studied, and not only by psychiatrists. Neuroinflammation has behaviorial consequences, just as cardiac inflammation produces palpitations and GI inflammation causes diarrhea. It is a lack of compassion on the part of the medical profession to blame this on the patients. It could never have happened except that the disease doesn’t cause true dementia even when very long standing. It happened because doctors blame patients for what they fear and don’t understand, pure and simple.
The need to reaffirm one’s illness all the time leads to a further distortion, oft repeated in the patient group, the view that ME/CFS is the worst disease in the world. This is far from the truth, but the degree of injustice makes for a need to catastrophize, that word used all the time to accuse us of making too much of our little nuisance complaints.
All chronic illness is superimposed on preexisting personality. When it comes to inflammation of the brain, dysfunction impacts thought content. My experiences treating brain injury and developmental disorders with EEG biofeedback and oxygen taught me that strong emotions are not unlike other types of paroxysmal brain activity and similar therapeutic interventions are effective across the board for patients living with unstable brain states. People with a lot of fear who get this disease are prone to recurrent or persistent panic states. PTSD is another manifestation of cortisol exacerbated neuroinflammation which shows up often in the patient group. It is organic. Difficult brain states make for tricky management from a doctor’s point of view. The word encephalomyelitis means inflammation of the brain and spinal cord. Of course there are behavioral consequences.
The truth is that it is not the worst disease in the world by any stretch of the imagination. It has the potential to become a living hell due to ignorance of what it is or what to do about it. The safest things we have at our disposal are oxygen, improved methylation, stress reduction and various antiinflammatory strategies, including addressing insulin problems and doing whatever possible to heal the leaky gut, a key factor. My early practice experience with a small number of patients is that these strategies are effective for reducing the degree of suffering.
Speaking of gut inflammation, our family is working on our diet. Patients who have tried everything for many years are often resistant to changing diet. It is so much more work than just about any other therapeutic intervention you can come up with. Physical work is a problem for the patient group and eating well is more work. Also the results of dietary interventions are usually slow. Food is gratification when everything else goes to hell. But you are what you eat. I advocate a whole foods, unprocessed, organic, if possible, diet that restricts sugar. Wash any sprayed produce carefully. Avoid chemicals, especially the excitotoxins MSG and aspartame. I tell my patients to read ingredient lists and don’t buy it if there are things in it that you don’t know what a handful of it looks like. The average American consumes pounds of chemicals a year. Whether there is a retrovirus or not, the disease doesn’t kill directly, life can go on for a very long time and the quality of life of human beings is dependent upon what they put in their mouths.
A member of my husband’s family brought my attention to a film called Forks Over Knives, available on instant Netflix. It proposes a vegan diet as the way to health. I was a vegan for a few years when I was young, and whether it is or isn’t a healthy lifestyle, the premise put forth in Diet For A Small Planet in 1971, which seemed true to me way back when, is still a good argument for not eating animals, but ethical considerations and attempts to save the planet aside, the movie doesn’t draw the correct conclusions from it’s own observations in my opinion, or at least it doesn’t prove it’s premise. It is just as likely that the avoidance of the sugar, chemicals, hormones and antibiotics involved in the eating of meat and processed foods in our culture is at the bottom of the adverse health consequences of our modern diet, not meat in and of itself. Still the movie is worth watching if you are thinking about food, and the review found here: “Forks Over Knives”: Is the Science Legit? is also worth a look.
I had a Crohn’s diagnosis at one point and spent a summer on TPN (total parenteral nutrition) before being saved by a surgeon. Afterwards, the diet that facilitated healing most was the SCD or Specific Carbohydrate Diet. It is based on the premise that the inflamed gut is harmed by exposure to disaccharides and polysaccharides, contributing to dysbiosis. It allows some simple sugars. It eliminates grains and dairy products, except for hard cheese and SCD yogurt, superfermented for 24 hours to break down the lactose. SCD yogurt is an excellent probiotic, unless you are cassein sensitive. The list of SCD legal/illegal foods is here. My family is cheating with brown and wild rice. It’s tough for me to keep weight on and I am grateful to my daughters for supporting this now, since I have a hard time doing the right things for myself. It has much to do with the many years of ritual abuse involved in becoming and being a doctor. I was trained to overlook the needs of my own body and carry on no matter what, relying on magical thinking to keep going:). It isn’t working too well for me now. A bit late in the game for repatterning, but I guess it’s never too late to learn, or at least I hope not.
It has been a long time since anything went right with respect to the fiasco at the WPI, but this evening, the tide appears to be turning. The terrible injustice that was done to Dr. Mikovits has been righted at long last with the dismissal of the charges against her. I guess somebody’s enthusiasm for jailing scientists is waning with the growing fishy smell coming from the direction of the accusers.
Writing this, I see people celebrating on FaceBook, friends of Judy’s from all over the world. As we held our collective breath, we can exhale again. Our most dedicated scientist and loyal friend is free once more; may her brave and genuine heart find its way back to the work so cruelly taken from her. And from us. The justice system is meting out a little justice for a change, even while the people who did this continue to suck up a significant percentage of all the dollars the US government spends on our disease, apparently so they can pay for all their lawyers.
So now the Emperor walked under his high canopy in the midst of the procession, through the streets of his capital; and all the people standing by, and those at the windows, cried out, “Oh! How beautiful are our Emperor’s new clothes! What a magnificent train there is to the mantle; and how gracefully the scarf hangs!” in short, no one would allow that he could not see these much-admired clothes; because, in doing so, he would have declared himself either a simpleton or unfit for his office.
~ Hans Christian Andersen
The moment of clarity has passed. Science isn’t going to save us. No cavalry coming over the hill any time soon. Back to business as usual. Even as the public display of insanity continues in Reno, the discussion of the WPI’s “bad patch” is dying down. New science into a possible viral etiology for ME/CFS has all but died down, awaiting the results of the Lipkin study. It’s hard to expect much when it seems likely they aren’t looking for the right thing, but nevertheless, I still hope against hope they will find something of significance. The backlash has already started, with recent papers about reward deficiency states and perception of pain. The most innovative scientific minds willing to think about us at all are applying their attention to the genetic piece, a factor for sure, but not the root cause, still a downstream effect.
In the midst of losing the interest of the scientific community, the run for Rituxan is on. As a bit of a stalker magnet for the more extreme elements of the ME/CFS community, I got slammed after my last blog by some who like this approach. It is ironic that my opinion about this particular choice is interpreted by some as my wanting to limit access to treatment, given that I was a guinea pig for the last round of uncontrolled human drug trials. And before that, antibiotics for chronic Lyme. This option seems like the most dangerous by far to me over the long haul: hurling bazookas at the immune system will cause increasing dysfunction over time. Though the risk from the infusion itself goes down with repeated administrations, the infectious disease doctors will continue to be busy mopping up the mess caused by this approach to the disease. We are not talking a round of chemo here, but treatment that will presumably be needed for life.
Even so, no one can judge the degree of suffering of another, or what may or may not be the best course of action for anyone else at a given moment. It seems just like Lyme Disease to me. Any disagreement with their doctors’ approach is unacceptable, because those doctors are at least validating the illness. Thank God someone is willing to prescribe the big guns for our disease, no matter how misguided. An approved major pharmaceutical intervention means we have a real disease, instead of an ill-defined syndrome. I agree, it’s better; I just don’t like the risks associated with this treatment.
Big Pharma, an Emperor with no clothes if there ever was one, has waged a war on human disease that is an obviously failed experiment. The newspapers are reporting that more people die of adverse reactions to drugs than automobile fatalities. Our government’s complicity with the devil has left the entire medical establishment in an unsustainable position. You can’t run a society where everyone expects to be maintained on expensive drugs for life. The whole concept is misguided anyway. Take statins for example, which come up in my practice, because even completely unsuitable patients are subjected to the statin knee jerk reflex, though it seems particularly inadvisable in a group of patients already suffering from chronic myalgias. How did the statin brainstorm happen? Twenty five or so years back, somebody got the bright idea that since people who live to very old age sometimes have low cholesterol, we should give everyone who wants to live a long time these drugs to lower their cholesterol to some artificially predetermined number to prevent heart disease. A logical fallacy if there ever was one. It’s taken all this time for doctors to realize that maybe it wasn’t such a good idea after all. They knew it could cause Polymyalgia rheumatica way back when, so essentially healthy people wound up on steroids long term from this particular experiment. Now it turns out statins increase the risk of diabetes. And they cause cognitive decline in the elderly. Brilliant. Would you hire these critical thinkers to make an important decision for you with respect to your long term health and well being? In the meantime, Lipitor has made more money than any drug in history. Over 12 billion dollars. No evidence that it prevents primary cardiovascular disease. No improvement in quality of life. Lots of maimed people. An aside: although red rice yeast lowers cholesterol with fewer side effects than statin drugs, it contains naturally occurring lovastatin and can cause the same side effects as the drugs, though it is less likely to do so.
Nobody hopes more than I do that somebody pulls some existing drug that didn’t make it to market for something else off the shelf for us, or fast tracks an orphan drug, in the next few years, but I don’t see it happening. No one cares. No one cared enough to test the already existing possibilities for us when it made sense to do so, at one particular point in time. The round of experiments in vivo that did happen, and the very few of us still taking antiretrovirals, should have been enough to raise the question of why they may be useful for neuroimmune illnesses, but apparently, it wasn’t to be. The question is dead as far as the scientific community is concerned. All conveniently chalked up to the failings of one scientist, per Dr. Racaniello’s final analysis, which he figured out with the assistance of his good buddies Trine Tsouderos and ERV (you’d think he’d be ashamed to admit that publicly, but I guess not).
When does it stop being the human genome and become a rescuable virus that can make other people sick? How many deletions do you have to put back to call it retrovirology instead of genomics? Take the next step. What are the most likely sources of animal viruses and pieces of viruses (not just murine) that could be rescuing defective remnants of past infections long quelled by the sands of time, causing some people to spit out enough viral product to cause disease, and others, exogenous virus that can infect other people? Because it isn’t simple, in the sense that it doesn’t fit the one virus, one disease paradigm, it, or much more likely they, have been missed for decades. Also it was assumed that exogenous retroviruses known to be present in tissue culture, and known to be able to infect human cells in the lab, weren’t a problem for people, even parenterally introduced, since most human cells have retroviral restriction factors. I am not a virologist, but I can read, and retrovirology is an extension of genomics, and visa versa, meeting in the middle of each field.
Here is a paper from 1987. The Four Classes of Endogenous Murine Leukemia Virus: Structural Relationships and Potential for Recombination. The authors, John Coffin and Jonathan Stoye, went after Dr. Mikovits very publicly on multiple occasions. Coffin said publicly that she would be “burned at the stake”. I’m sure that’s what he wanted. After all, when this all comes clear, he will have to admit that almost the entire human race is infected with retroviruses that he chose not to worry about. Not surprisingly, he doesn’t want to think about that possibility now. Max Planck said science changes one funeral at a time. Highlights from this paper:
The modified polytropic proviruses can serve as env donors in some recombinants. Two viruses derived by recombination with the Friend strain of MLV have been sequenced and appear to have acquired env genes from different proviral classes.
It thus appears that different ecotropic viruses can recombine with different endogenous sequences. It is possible that viral sequences themselves directly determine whether recombination can take place… Endogenous sequences expressed in a differentiation specific fashion would thus provide distinct opportunities for recombination to occur.
In light of this relationship it seems reasonable to speculate that evolution of the ecotropic virus endogenous to inbred strains of mice might have involved a recombination between a nonecotropic virus of the type present in the mouse genome with another virus which has not been fixed in laboratory strains of mice. Thus, the recombinations which occur in highly leukemic strains of mice might in fact be reciprocal to an event that occurred many years ago.
Dr. Michael Snyderman, who has CLL (chronic lymphocytic leukemia) and CFS, and for whom we have the only hard data showing a response to antiretrovirals, was culture negative for XMRV, but had positive serology. Here is a link to Dr. Snyderman’s last guest post. We don’t know if MMTV-like virus infection can cross react with a serology test that picks up MLVs. Andrew Mason believes he has isolated a beta retrovirus associated with primary biliary cirrhosis and an anti-mitochondrial antibody. I have presented his work and lots of other evidence on this blog in the past that supports a retroviral etiology for certain neuroimmune diseases, as well as case reports of responses to antiretrovirals.
Since gamma retroviruses (and other simple animal retroviruses) replicate mostly by mitosis, unlike HIV, in hindsight, we shouldn’t have expected anything other than slow improvement, since stopping viral replication doesn’t fix the problem (n.b. there was one rapid complete response, anecdotally, in a young patient who hadn’t been sick for long). Infected cells need to be replaced by apoptosis, which the virus tries to prevent, hence the clonality that Dr. Snyderman is studying.
We have no marker of disease. When I started antiretrovirals, I naively expected to have viral load measures in a year or so, to benefit from all the work that had already been done for HIV disease. But now there is nothing to follow but patient report. Instead of going back to the drawing board to figure out what it is, everybody went home, since XMRV was created in a lab. However, that lab contaminant spreads through a clean lab in a few days, infecting human cells. It also establishes a persistent infection in macaques. Dr. Snyderman has real trackable numbers. His CFS symptoms have waxed and waned with his remissions and relapses. He will try to publish as a clinical case study in a medical journal, but no one will notice. Just like the occasional case reports that have shown antiretrovirals to be effective for MS and Sjogren’s Syndrome (both of which show up frequently in the families of CFS patients).
In what follows, any time you read “XMRV”, think instead, “similar simple animal retrovirus”…
Here are three blogs I wrote when I was figuring out the vaccine/biotechnology piece. My understanding is deeper now, but I still think the basic thesis is correct. I’ve made some scientists angry (preferable to being ignored), but nobody has yet told me why my hypothesis is wrong, or offered a better explanation for the clinical observations; what else explains all of the observed phenomena? If you haven’t read them, there’s some interesting stuff in these posts about the history of vaccinations that you may not know.
Now in the 21rst century we have “humanized” monoclonal antibodies produced from hybridomas, derived from antigenically stimulated B cells from sick mice that are known to be producing infectious virus; these B cells are then “fused” with immortalized human myeloma cells. We inject the antibodies produced, and the sludge?, into people, e.g. high risk babies to prevent RSV. Then there is xenotransplantation. And on and on. And what about the lab workers, since they are working with exogenous adventitious retroviruses that easily spread throughout the lab uncontrolled by the usual precautions?
MedScape is throwing out numbers like 20% of the population has a rheumatic disease (not to mention 1/88 children are autistic, 1/54 boys under 8, up 78% over a few years time, and it is probably already higher now). It is very difficult to absorb how serious it is and how much of it could have been prevented. I was taught, in medical school in the ’70s, to do a review of systems, so that I didn’t miss anything, expecting it to be negative for most people. Almost nobody it seems has a negative review of systems any more, even children. The mothers of ASD children know when their kids got sick, even if their doctors and the scientists studying the problem are too dumb to believe them. The state of the art can’t deal with the uncertainty involved in studying something that isn’t one thing. Why do you think more than 1/3 of Gulf War veterans have GWI or CFS or whatever you want to call it, (since they are clinically indistinguishable from ME), and their children have an unusually high rate of autism? It was, and is, in the vaccines, folks. And there were chemical and infectious exposures involved in the Gulf also, creating a perfect storm.
Something is terribly wrong and this hypothesis covers it. It explains the increase in neuroimmune and autoimmune diseases, as well as cancer- increases, and the emergence of new diseases. The diseases in question didn’t exist or were very rare in the early 20th century. Very little common sense being applied to the situation. Upcoming meeting: 2ND INTERNATIONAL SYMPOSIUM ON VACCINES: 8th International Congress on Autoimmunity at the Palacio de Exposiciones y Congresos de Granada in Grenada, Spain on May 9th.
There are still readers coming to this blog from public and private institutions of higher learning. Not as many as when Dr. Mikovits was fired, sued and arrested, but quite a few still visit and new ones are finding it. There is no “translation” happening between the clinic and the lab. Sadly, the internet is all we’ve got. Anyone who knows something about the science in question, please tell me why I’m wrong. I want to be wrong. It’s difficult to find the energy to continue to think about the science in a vacuum, with little hope now that understanding the frontiers of the science will have clinical utility any time soon.
Does the “normal” human genome contain murine sequences? Avian sequences?
What processes other than retroviral replication might be impacted by a reverse transcriptase inhibitor?
Meanwhile, Ali and I continue to do amazingly well. Not every minute, but we are having many wonderful minutes. Ali just finished her first semester at U Mass Lowell online and her first college grade was an A. She is planning to increase to a full program for the summer. She has friends and is currently in a relationship. She is starting to go out, just for fun, without any major MCS set backs. She has been making and going to her own health care appointments and dealing with the other odious tasks of life. She has been regularly cooking inspired meals for the family. She has begun to do calisthenics, without weights and walk a little, without significant PEM.
I was in Hawaii for two months, so Ali didn’t have any infusions during that time. She had an adverse reaction to a glutathione push early in the year that had soured me a bit on IV’s, and I didn’t use any for K (guest blog by her mom a few back), since we were getting good improvement without it, but Ali wanted one when I got home and she responded to her usual modified Meyer’s, no glut, with a burst of energy that has so far lasted a week.
I had a huge push to get home. I went to a big local party in North Kohala, spent the next day packing up the house so it would be together when I return, then took the red eye home. I hit the ground running and left four days later for a six day RV trip in Arizona, where my husband was entered in a mountain bike race. We went to some amazing places, Prescott, Sedona, Petrified Forest National Park. I hiked every day of the trip, including the hard part of a hike, described as “strenuous” by the park service.
Petrified Forest National Park May Day, 2012
I have been able to throw myself off the proverbial cliff and fly for a day or two for quite some time; all the while payback has been reducing in severity and duration, but this is the first time I’ve been able to keep it up. I’ve had a little PEM here and there, to let me know I was up against my limit, but at a hard half mile hike, with rock clambering, I am much beyond where I was six months ago when we went to New Orleans and I wasn’t up to walking around the Tulane campus, even though I really wanted to. The only things I’m doing consistently is taking Viread, using a little oxygen here and there, Cozaar, aspirin, hormones. I need to take my own advice and be more consistent with oxygen and do some neurofeedback. I’m on minimal supplements, D3, B12, Deplin, ubiquinone, others sporadically.
However, not to paint too rosy a picture, I’ve had some progression of my radicular sensory neuropathies, upper and lower extremities. I had one episode of numbness in the distribution of an upper extremity dermatome, with very brief motor involvement, that threatened to push me over into an RRMS (relapsing remitting multiple sclerosis) diagnosis, to go with all my other almost diagnoses, but it hasn’t recurred, and I am unwilling to go another round with the experts to be told I don’t fit neatly into any of their diagnostic categories. I already know that they don’t know. Why subject myself to ridicule and uninformed care, for something they can’t do anything about anyway. Been there, done that.
The treatments we are using, and I am using in practice, all have global effects. They interact synergistically to tip the balance in favor of the patient instead of the disease, without doing further harm. Reverse transcriptase inhibitors may be in that class, even though they are unstudied in this context. Antibiotics used intelligently may have a place as well for some patients, though determining who and when to treat, and for how long, is tantamount to being a witch doctor casting the bones.
The point is no longer that we suffered. The point is that we aren’t suffering much now and others are, needlessly. I have almost died twice due to misunderstanding of my illness. I met David Bell in Aug 2010 and told him I was going back to work after being bed and couch bound for over 5 years; he told me he’d never seen it happen at that stage of the illness and it has happened. My reason for being now is to keep others from making the mistakes I made. And to move it along if at all possible. Suffering is inevitable, but unnecessary suffering is evil. There is ample evidence for an infectious etiology, at least in some families, if anyone would bother to look. We will try. Somehow we will complete our family survey, without funding. The technology exists to answer the question, but no one cares. The disease is treatable. More importantly, it is preventable! But it appears that it will remain invisible for now, until somebody has the patent for The Test, individual DNA sequencing, readily available from your local commercial lab, which will unravel each patient’s mystery, proving ME/CFS, chronic Lyme, ASD, PANDAS, GWI, RRMS are not one thing, but variations on a theme. Then, in a decade or two, some genius will look at the data and say Ah ha!
Believing I had written my least controversial blog ever, I am confronted yet again with how unconventional it is for a doctor to share their evolving thoughts publicly. If freely sharing information is revolutionary, what revolution are we talking about here? A departure from the science of evidence based medicine? Evidence based medicine is based on purposely flawed studies designed by drug companies to “prove” that their drugs should be prescribed. Drug companies make wild claims all the time, about drugs that have never had the test of time.
If Rituxan works for ME/CFS, that’s 4 million people in the US alone who need a drug that can cost upwards of $20,000 per round of treatment, including the high level of care needed to administer safely; it probably will need to be given twice a year, must be continued forever and carries a significant risk with each infusion. For fun, that would be $80 trillion dollars per year for us all to get treated. The drug is apparently much cheaper in the UK; it is going out of patent in 2015, so it will be cheaper in the US as well, but that also means there will be no funds to study it for us. The point is, it is not a sustainable model, this drug or another expensive palliative treatment. Nor would antiretrovirals have been had they worked very well. Too many people. And it’s not just this cohort, but several huge cohorts. Wouldn’t it make more sense at this point to figure out why so many people are getting sick with immunological diseases, rather than blindly killing everybody’s B cells? With monoclonal antibodies, produced from hybridomas, a fusion of mouse and human, technology that came from the very techniques that probably got us into this mess in the first place? It sounds like science fiction, but unfortunately it isn’t.
Look at this nightmare: Risk of autism among younger siblings of a child with autism much greater than previously reported. They say they are going to monitor future siblings now that they know their risk is about 18%, so they can offer early intervention to these incredibly high risk children. What intervention do they have in mind? CBT (ABA or Applied Behavior Analysis) to help them adapt to their brain injuries? How about considering the obvious and not vaccinating these particular children. That would be a rational approach, wouldn’t it? Let’s not challenge the immune systems of these particular children in this way, since they are at risk, and some of their siblings had problems with vaccinations? A little common sense? We have an obvious epidemic on our hands. We need to get everyone’s head out of the sand. How can society possibly take care of all these disabled children when they become adults?
It is the same for children of ME/CFS patients in my opinion. Though we don’t yet have the numbers, the informal survey from last year showed similarly alarming rates of CFS in offspring of CFS sufferers, as well as increased risk of autism, beyond even the alarming rates being acknowledged currently in the general population. These children should not be vaccinated in my opinion, or at the very least should be selectively vaccinated, with fewer total vaccines, fewer shots at one time and spread over a longer period of time. Common sense, except that we aren’t allowed to apply common sense when it comes to the vaccination program, because it is a sacred cow. We still intend to complete a formal family study. We are all working as hard as we can at our individual endeavors, but know how important this is. The incredible burden of disease that some families are dealing with needs to be brought into the light.
I encourage you to watch The Greater Good, a new documentary about childhood vaccines, the damage they are doing and the over the top blindness of our government’s approach to the problem. A special court to deal with the injuries. You can buy the DVD here. Please also visit and consider The Canary Party. Although it grew from concern about autism, it is about us too. The ME/CFS community desperately needs cross-pollination from the ASD community, politically and medically. They are related diseases and there is strength in numbers. Sharing between physicians could be rewarding for both groups. I still hope to do just that. I’ve launched a private forum to begin the dialog with the intention of sharing anything interesting or productive that comes out of it. All the participants are really busy, but want to share.
In the case of Rituxan, there is vast experience already, not for this indication, but a lot of experience for other indications. Enough that infectious disease doctors will tell you that it falls on them to treat the mess from JC virus reactivation, a fatal leukoencephalopathy, and cases of sepsis caused directly by the drug. That’s if the infusion doesn’t kill you, which granted, it usually doesn’t. I have a patient who is probably the perfect candidate for Rituxan, because she has the test results that would get it paid for, but her decision has been to wait, because the immunological abnormalities and variations in the patient group make it impossible at this time to select patients optimally. Meaning no way to know who will respond or precisely how to use the drug, until some patients have been the guinea pigs. There will be hits, as we saw from the Norwegian trial, assuming that we all have the same thing, which we probably don’t, but the biggest problem with Rituxan is that there will be deaths also.
Here are the black box warnings; all but tumor lysis syndrome apply to us:
Why do the gentle therapies bear the burden of proof? Because they don’t make money for the drug companies and the medical establishment? While doctors administer drugs that can kill with impunity, not even knowing precisely why they’re doing it, or what the long term consequences of it are, I’m expected to justify my “voodoo” with proof, and it doesn’t matter how many convincing references I come up with. Since it isn’t a drug, it couldn’t have value.
I’m not trying to convince anyone to do anything. Everyone gets to make their own decisions. I am a medical libertarian. I’m not selling anything here. I started this blog before I was working. I have enough patients for what I can manage in my current state of health. I work in a very unusual, personal, hands on way and I am not right for everyone. In any case, I can only handle a very small number of active patients, especially if the intensive therapies that I’ve been writing about here are involved, so I am not writing to bring in business. I write for the same reason I wrote before I was in practice, trying to make a difference and save people from making the mistakes I made.
My writing is peppered with the anger that has been engendered by my patients’ histories, histories sent to me by email, and my family’s own history. Although I have returned to practice, I still identify most strongly with the patient group, not the doctor group. I hear from every well known CFS and Lyme doctors’ patients and it isn’t pretty. However, it is unfair to have your career contribution judged because of a few angry patients. Angry patients come with the territory and I acknowledge the inherent bias in who I hear from. I’m sure my being back in the same boat will make me more considerate of their constraints and decisions. In any case, not so much for the doctors, for some really do deserve the antipathy, but out of concern for the patients who respect them, I will refrain from gratuitous comments that divide us even further than we already are. I am getting a little tired of feeling like Don Quixote. I am not trying to convince anybody of anything and I could be wrong about anything. I am sharing my ideas, knowledge and experience, in case it helps someone. If it isn’t for you, that’s fine.
I am still hearing reports of benefit and reports of harm from various preparations of GcMAF’s and MAF yogurts. It does seem as if the opinions of the doctors managing these patients is now start low, go slow, always a good idea with ME/CFS patients, unless you are concerned about encouraging resistance of a microorganism. It isn’t clear how to tell when to stop or how to maintain an early effect. And I’m still disturbed by its being a completely unregulated blood product. Does anyone know if the newer MAF yogurts are derived from human blood?
I have always and still do tell patients that it is a bad idea to be in the first round of a drug trial. Let another million people take it first. I got called out by someone I respect for lumping Ampligen and Rituxan together and that is fair criticism. Ampligen has been around for a long time and it doesn’t kill people. Also I don’t know who is and isn’t making what money on either drug. My comment about doctors making money selling dangerous drugs was a general one, not aimed at anyone in particular, and certainly not limited to our disease. There are a very few CFS doctors who do manage to take Medicare or have been known to give away care and I acknowledge them for it. That is quite a feat with this patient group and the current system. At any rate, Ampligen costs a lot, and doesn’t seem like it works so well for many, or even most.
I would like to state for the record that I am not an angry person in my personal life. I have worked through much of my personal anger about how badly we were treated, mistreated actually, over the years. In fact, I am very happy now much of the time. I am laying down smile lines these days, not frown lines. Since you can’t see me, I want my readers to know that. My anger now is most often protective of my patients and friends. I would give anything if I could be proud of my colleagues more often, fully acknowledging that there is bias in the sample I am hearing from. Happy customers are less likely to write letters.
There is no cure and there isn’t going to be a cure, most likely. It is going to be about palliative care, at least for the foreseeable future. Hopefully it will also be about prevention, sooner rather than later, so we don’t have to feel so helpless watching while our friends’ children go down. Once you give up the idea of one drug to fix it, it becomes easier to see the wisdom of using multiple adjunctive therapies synergistically, all of which support the possibility of healing over the long haul, without harm.
My opinions about drugs aside, they are sometimes the best course of action and I still think that future treatment may include antiretrovirals, reverse transcriptase inhibitors in particular. The results of the uncontrolled patient experimentation that happened left a few of us on long term treatment that we think is helping; nobody was seriously harmed that I am aware of. The drugs in question are low risk. I have been reading and considering other reasons why RTI’s might be a good idea besides inhibiting exogenous retroviruses. It is a fascinating subject, taking us to the frontier of what is currently known about the human genome. Future blog fodder. The take home message from this blog is that I believe I can get to the same place with the therapies I am using, along with common sense primary care, without the risk, compared to any single treatment currently available. And I predict that my patients will do better over the long haul than allowing themselves to be used as human guinea pigs for the testing of dangerous drugs. Time will tell. However, it will always be only anecdote, not evidence based medicine. If my patients, friends and family are suffering less, it will have to do.
Let me start by answering some FAQ’s I’m getting with respect to neurofeedback.
Does it have to be the Othmer’s system? There are quite a few choices of systems on the market. I am out of date, because I am just starting to reconnect with old friends in the neurofeedback community, or should I say communities. The Othmer’s new system, Cygnet, does what the others do, plus it is able work at the “ultra low frequencies” that Sue is using in her clinic. They also have a tight network of practitioners who share clinical experiences on a private listserve and consult with Sue about particular patients if needed. It allows me, for example to start a patient here and have them follow-up with someone close to them at home who has the same equipment and uses the same protocol, though, as I said before, it is not a one size fits all protocol. Unfortunately. Judgement is required. It’s getting closer and closer though. It’s fun to think about a future with wireless electrodes and one size fits all neurofeedback that anyone can do anywhere, on their iPhone.
BrainMaster used to give the most for the least money. A quick look at their website and it looks like they still do. I also had a little experience with Roshi and LENS, but I consider them to be in a different category, because they use stim to entrain the brain. It is a powerful technique, but I don’t have enough experience with it personally to write about it or advise strangers to try it. There are many testimonials out there for those techniques, however. They fall into the category of things that could help so many people, but will never be studied, because it doesn’t fit into the dominant paradigm and there isn’t enough money to be made, unless people start saying no to drugs.
Can it hurt you? In the hands of the wrong therapist, yes. As I said in the last post, it can further destabilize initially until a protocol that works for that person is found. For a stable epileptic, tolerating meds, it may not be a good idea. For someone on the brink of harming themselves or others, it may not be a good idea, unless done in a controlled setting. For someone who has not tried meds, or wants off of them? For almost anyone with a neuropsychiatric disorder (and for those of you that haven’t read the DSM IV, that’s most of the entire human race), it’s worth a try.
I do think it’s worthy of comment here. There are people who say they are bothered by WiFi and on first glance, it sounds crazy, but one of things the internet and cell phones have done (also flourescent lights) is create an environment where we are constantly bombarded with electromagnetic frequencies which may entrain the brain to some extent towards poorer function and thus cause symptoms.
Now, oxygen reports and answers to some questions. I have heard from two more people reading the blog who experienced a flare of symptoms (herx) from the doses of normobaric oxygen I am using in my practice. I no longer think a herx is a good thing, but a potentially damaging cytokine storm, though I did see people push through it and improve with very high dose HBOT in my last practice. I now think that if that were to happen in my practice, I would back off, to maybe a half an hour every other day, see if that is helpful and go up from there. I would assume that those people would herx with hyperbaric also and it is possible that they could improve enough with lower dose oxygen that they would later tolerate the addition of pressure. All speculative for now. Anyone trying oxygen, please keep me informed. My practice is tiny and this is how I learn, how we are all learning for now.
I’ve gotten some questions which indicate that some don’t know the difference between a concentrator and a chamber. A concentrator puts oxygen directly into the room, through a tube, which is delivered to the patient in one of several ways- a cannula that goes in the nose, a simple mask, with holes in the side, or non-rebreather mask that has an oxygen reservoir that holds 100% oxygen and has one way valves to prevent inspiration of ambient air and to allow exhalation of exhalation gases. Oxygen can be brought to the home in tanks or in the form of a concentrator, that takes the oxygen out of the air. Tanks are quieter, but at the flows I’m using, need to be replaced frequently. Concentrators are noisy, but more portable and never run out. Concentrators can be portable or ultra-portable, but portables only give 2-4L/min (liters of flow per minute) and are used with a cannula (delivering 24-27% oxygen, instead of the 21% in air). A standard concentrator usually goes to 5 or 6L/min and can be used with a simple mask (delivering up to 35 or 40% oxygen). Some concentrators go to 10L/min and then can be used with a non-rebreather mask (delivering >60% oxygen depending upon fit). A non-rebreather mask should not be used without enough flow to inflate the bag.
Non rebreather mask
A chamber is a way to raise the ambient pressure of the patient above that in the room (normobaric pressure). Chambers can be monoplace, the patient goes into a 100% oxygen environment, or multiplace, multiple people go in together and oxygen is delivered by Scott mask or by hood, a bubble around the head with an airtight neckdam (latex or neoprene) to which oxygen is delivered with high enough flow to blow out the exhaled gases. Hard chambers go to pressures, or “depths”, of up to 3 ATA. Hyperbaric technology came from the need to treat divers with the bends. A huge amount of work has been done by the Navy and the commercial diving industry that has helped to elucidate the physiology of exposure to pressure and hyperoxia.
Sea level is defined as 1 ATA (measure of atmospheric pressure equivalent to 760mm Hg). 2 ATA is equivalent to the pressure at 33 FSW (feet of sea water), the way divers think of pressure. Depth and pressure can be measured in many ways; some common conversions are 1 atmosphere (atm or ATA) = 33 feet of seawater (fsw) = 10 meters of sea water (msw) = 14.7 pounds per square inch (psi) = 1.01 bar. The protocol generally used for treating brain injury is 1.3-1.5 ATA with 24-100% oxygen.
There is ongoing debate in the hyperbaric community as to whether the addition of pressure adds anything to a treatment that you could deliver without it. For example, there have been studies done showing that autistic kids respond to very mild hyperbaric treatments, 1.3 ATA and 24% O2. PaO2 = partial pressure of oxygen in arterial blood is between 75 mmHg and 100 mmHg at sea level (765 mmHg) on room air. A 1.3 ATA treatment with an FiO2 (fraction of inspired oxygen) of 24% will produce a paO2, or partial pressure of oxygen in the plasma of around 300mm Hg; you can get that with a mask and a concentrator, without a chamber (400mm Hg +). But my guess is, yes, it’s better with pressure. And our trail blazer K’s experience, a few blogs back, suggests that will turn out to be the case. A few references below re: possible independent pressure effects.
The breakthrough for hyperbaric treatment that allows it to be safe and simple enough for home use has actually happened since I left my last practice, in the form of the soft chamber. Gamow bags were developed to treat mountain climbers who develop altitude sickness. For this purpose, they are used without oxygen, simply adding pressure to increase the pO2 a little, and this works. It works by compressing the air so that the lung tissue is exposed to a greater number of O2 molecules in the same volume. In the early ’00’s I was worried about the possibility of an explosive decompression, which can be fatal, because the soft chambers sold are not rated for hundreds of duty cycles. But in practice, over quite a number of years now in home settings, it hasn’t happened. They do develop leaks on occasion, but slowly, and then they can be repaired. I see on the internet, there are quite a few newer companies selling cheap chambers, also some from China. I’d advise refraining from a bargain without a track record. To help with cost, I’ve heard of groups who live near each other sharing a chamber.
Soft chamber inflated
The chambers can be used with or without oxygen, though it says right on them that they are not supposed to be used with oxygen. Nevertheless, they provide a port to hook up your concentrator:). Oxygen should not be delivered directly into the open chamber, but through a mask, just as with a concentrator alone.
Oxygen saturation in blood, or O2 Sat, is measurable by pulse oximetry on the finger and expressed as a percentage. It tells you how much oxygen is getting through the lung into the blood. Since we don’t have trouble saturating hemoglobin, this number is often cited as the reason that we don’t need oxygen. However, it is possible to hyperoxygenate the plasma and we do have cellular hypoxia, meaning not enough oxygen is making it into the cell, or mitochondria (and/or it isn’t being metabolized properly). My guess is that there is an issue with oxygen getting across the mitochondrial membrane. Viral product from activated virus in mtDNA? Elevated anticardiolipin antibodies (and other autoimmune markers) are seen fairly commonly in the patient group. Cardiolipins are located on the inside of the mitochondrial membrane. Oxygen gets into the mitochondria by diffusion across a pressure gradient. Without enough oxygen, the cell can’t make ATP. If you raise the diffusion pressure, more goes in.
Relative contraindications to hyperbarics are seizure disorder, inability to clear ears for pressurization, though this should be able to be handled in almost all cases, without barotrauma, but takes patience on the part of the chamber operator, as well as good communication with the patient. Severe COPD with CO2 retention, is another relative contraindication, although in practice CO2 narcosis only happens in the setting of acute decompensation. Asthma is a concern, because wheezing can cause air trapping and a wheezing patient shouldn’t be decompressed as trapped gases will expand and cause barotrauma. Asthmatic patients should be pretreated. Hereditary spherocytosis because of red cell fragility. Pregnancy and cancer are considered relative contraindications because of the unknown, although there are hints that HBOT may in fact be helpful for cancer. Certain prior ear surgeries are a concern and should be discussed with an otolaryngologist. Also some eye problems should be carefully considered. Hyperbarics may accelerate the maturation of existing cataracts, though if this is true, it takes a lot; HBOT does not cause cataracts de novo, according to the literature. An exam by an ophthalmologist is a good idea prior to embarking on hyperbaric treatment. There have been cases of optic neuritis that worsened with hyperbaric treatments. Implanted devices should be checked prior to treatment with the manufacturer as to whether they are hyperbaric safe. The only absolute contraindictions to hyperbarics are the presence of an untreated pneumothorax (collapsed lung) and recent prior or concurrent treatment with doxyrubicin, cisplatinum, Sulfamylon or disulfiram (Antabuse).
Hyperbaric safety amounts to common sense. Don’t create sparks in the chamber as oxygen is an accelerant. It sounds like a simple thing, but there have been some terrible accidents, all due to human error. Only cotton should be worn in the chamber. Reading material is permitted, but not newsprint. Always make sure you have nothing in your pockets when entering a chamber.
There is a review on MedScape (here’s the link for those who can get in) from 2010 that lays out the party line, which is that only patients with certain very circumscribed indications should do it, but when you look into it further, it’s pretty clear that that is all about what insurance will and won’t pay for. Hospitals charge exorbitant per session prices and will only treat the indications that insurance covers. It is a global treatment. It affects every cell in the body and its potential uses are very broad. Risks low. The article also says that soft chambers are becoming popular (gasp) and that they can go to 1.5 or 1.7 ATA. DO NOT TRY THIS AT HOME. The soft chambers come with a pressure relief valve that prevents going above 1.3 ATA (aka 4 PSI). These can be disabled to allow higher pressures. The only accident I have heard about through the rumor mill involved someone who altered a chamber to go to 1.5 ATA. It doesn’t sound like much of a difference, but I’m sure there is an engineer out there reading who can put it in perspective for us. Amusingly, the Undersea and Hyperbaric Medicine Society defines a hyperbaric treatment as above 1.5 ATA.
A little interesting history of hyperbarics from the MedScape article:
Hyperbaric oxygen therapy (HBOT) is breathing 100% oxygen while under increased atmospheric pressure. HBOT is a treatment that can be traced back to the 1600s. The first well-known chamber was built and run by a British clergyman named Henshaw. He built a structure called the domicilium that was used to treat a multitude of diseases.The chamber was pressurized with air or unpressurized using bellows. The idea of treating patients under increased pressure was continued by the French surgeon Fontaine, who built a pressurized, mobile operating room in 1879.Dr. Orville Cunningham, a professor of anesthesia, ran what was known as the “Steel Ball Hospital.” The structure, erected in 1928, was 6 stories high and 64 feet in diameter. The hospital could reach 3 atmospheres of pressure.The hospital was closed in 1930 because of the lack of scientific evidence indicating that such treatment alleviated disease. It was deconstructed during World War II for scrap.
The military continued work with hyperbaric oxygen. The work of Paul Bert, who demonstrated the toxic effects of oxygen (producing grand mal seizures), as well as the work of J. Lorrain-Smith, who demonstrated pulmonary oxygen toxicity, were used with Navy divers. Exposure times to oxygen at different depths of water (and, hence, different levels of pressure) were quantified and tested based on time to convulsions.
This last work mentioned may be the source of the fear of oxygen. However, the Navy worked out the doses long ago. They have been using Nitrox, or oxygen enriched air, to prevent the complications of prolonged and repeated exposure to nitrogen bubbles produced during depressurization. Over time, hundreds of dives on air cause cognitive decline and joint disease. If you are diving with a mask in a multiplace or soft chamber, please make sure to wear your oxygen on the way up. There is huge experience from the diving industry that oxygen enriched air exposure, during exercise, is safe over many, many exposures. And that’s with pressure.
From this same MedScape article, which was written by detractors of alternative uses of HBOT:
Additionally, evidence is growing that HBOT alters the levels of proinflammatory mediators and may blunt the inflammatory cascade. More studies are needed to further elucidate this complex interaction.
And possibly pertinent to our patient group, although frank congestive heart failure is not typical of our illness…
As HBOT is known to decrease heart rate while maintaining stroke volume, it has the potential to decrease cardiac output. At the same time, through systemic vasoconstriction, HBOT increases afterload. This combined effect can exacerbate congestive heart failure in patients with severe disease; however, clinically significant worsening of congestive heart failure is rare.
I am weaning patients off fentanyl patches with oxygen concentrators and getting mail from all over the world from very sick people about how much it is helping them and thanking me. Oxygen is the best thing I’ve got to offer, not all by itself, but in synergy with other things. Of course not everyone benefits, but lots of people do and no one is harmed if used sensibly. If I could only do one thing for the sickest people, it would be to give them a concentrator to try daily for a while and during their worst moments. CFS doctors have bad mouthed oxygen for decades due to a logical fallacy, that because there is already oxidative stress, and oxygen produces temporary oxidative stress, during administration, that that is all it does, so therefore it is bad for us. As a result, patients have had to suffer more than necessary for a very long time. But no worries, soon those same doctors, who said oxygen was too dangerous to try, will be able to make lots of money giving everybody Ampligen and Rituxan.
Numerous in vivo and in vitro studies confirm that HBOT induces neurogenesis however, underlying mechanisms remain unknown. Activation of several signaling pathways and transcription factors have been suggested to play an important role in HBOT induced neurogenesis, including Wnt, hypoxia-inducible factors (HIFs) and cAMP response element-binding (CREB)…
On HBOT and oxidative stress: HBOT enhances the production of reactive oxygen species (ROS) and causes oxidative stress in body tissues. Excessive accumulation of oxidative stress may contribute to neurodegenerative processes and cell death in the brain, as seen in diseases like Alzheimer’s disease (AD) and Parkinson’s disease (PD). Since HBOT-induced oxidative stress is directly proportional to both exposure pressure and duration, the benefits of HBOT, may outweigh the side effects due to the phenomenon of hormesis. Hormesis is a process that results in a functional improvement of cellular stress resistance, survival, and longevity in response to sub-lethal levels of stress. We suggest that this process might be beneficial in the treatment of oxidative stress associated neurodegenerative diseases like AD and PD.
Our data suggest that HBOT significantly ameliorates mitochondrial dysfunction in the motor cortex and spinal cord and greatly delays the onset of the disease in an animal model of motor neuron disease.
This prospective open-label pilot study in children with autism indicates, as measured by changes in plasma GSSG, that HBOT ranging from 1.3 to 1.5 atm and 24% to 100% oxygen was not significantly associated with increased intracellular oxidative stress. The use of therapies to raise glutathione levels and lower oxidative stress before beginning HBOT in individuals with autism appears prudent. Among children with high initial CRP, hyperbaric therapy led to a large improvement in CRP levels; this suggests that inflammation in these children improved with treatment. Improvements in clinical outcomes as measured by several scales were observed at both 1.3 atm and 1.5 atm.
Here are some interesting random recent references:
Conclusions: HBOT lowered markers of inflammation and oxidative stress and ameliorated IBD (inflammatory bowel disease) in both human and animal studies. Most treated patients were refractory to standard medical treatments. Additional studies are warranted to investigate the effects of HBOT on biomarkers of oxidative stress and inflammation as well as clinical outcomes in individuals with IBD.
These data show that HBOT alleviates CCI-induced neuropathic pain and inhibits endoneuronal TNF-α production, but not IL-1β in CCI-induced neuropathic pain. Reduced TNF-α production may, at least in part, contribute to the beneficial effect of HBOT.
Thus, HBOT may present an option for the management of PSH (paroxysmal sympathetic activity) in addition to pharmacologic therapy. Potential mechanisms for these effects are discussed.
But whatever the mechanism, the proof is in the pudding. Relief is relief. Patients know it if they feel it. If it doesn’t make them feel better they can turn it off. The patients tell you what they need, if you listen. They tell you they have air hunger and are short of breath. Well, not at all surprisingly, oxygen can relieve it. The disease is characterized by diffuse vascular spasm. Even insurance companies will pay for oxygen for migraines. Unless you have CFS. Then you get nothing.
Our chamber, early 2000, Great Barrington, MA, and my husband, Anthony, at the console.
Today’s song: Black Muddy River
Erratum: De novo cataract development following a standard course of hyperbaric oxygen therapy. A recent paper reporting a case of de novo cataract formation after 48 HBOT sessions at 2.5 ATA for 90 minutes for chronic refractory osteomyelitis, an enormous dose compared to the doses discussed in this blog (high dose normobaric and mild hyperbaric treatments, all <1.5 ATA with 100% O2). There is a huge amount of wound care that has been done over many, many years now at the doses this patient was treated with and this case was considered reportable as a cautionary statement to suggest that it can occasionally happen at doses less than previously thought. As I said above, it is a good idea to get an eye exam prior to embarking on oxygen treatment and discuss any contraindications you might have. More importantly, if you try it and it works, you might want to involve your ophthalmologist in the decision to continue long term, especially if you have any pre-existing eye conditions.
As soon as Siegfried’s post went up, I was questioned on FaceBook as to how I could promote something as unscientific as neurofeedback. There is science to support its use, but my personal answer to that question is, let’s not get blinded by science. I’m a clinician. Neurofeedback helps sometimes, maybe even oftentimes in some hands, when nothing else has. And here’s some interesting science as well.
Medicine is an art. Healing, different from curing, happens in the context of relationship. There are many factors at play. I mostly treated untreatable things in my last practice, and now again. I try things that aren’t dangerous, relatively speaking, discard the things that don’t work and keep the things that do, and I look for synergy. When a patient is successful at turning their illness around, it is generally because of a constellation of things. There are always many uncontrollable variables in clinical practice. Science doesn’t do well with multi-factorial treatments. Sometimes anecdote is the best thing we have to go on.
Here are a few cases from my last practice that come immediately to mind. Cases I treated with neurofeedback, on now obsolete equipment.
6 year old boy with greater than 100 seizures a day. Idiopathic onset of grand mal seizures 6 months prior. On 3 anticonvulsant drugs, having many small breakthrough seizures, without loss of postural tone or incontinence, but followed by a period of post-ictal confusion. Very disruptive to his life and that of his family members. The child was a well behaved, very smart, well functioning kid prior to onset of epilepsy. On presentation, his EEG showed generalized slow wave activity with intermittent paroxysmal bursts, also generalized.
We did a few sessions and he responded with fewer seizures, but he lived over an hour from me, could come for treatment only a couple of times per week, and would slide between sessions. After a dozen or so sessions, it was clear that neurofeedback helped him. His mother learned to run his sessions and bought a machine that she used to treat him at home under my direction. He was seizure free in 3 months and drug free in 6 months. Now 14, he continues to train on that same obsolete system, 21 minutes a day. He is an A student and has avoided years of brain deadening drugs. The only time he has seized is when he tried to wean from the neurofeedback and wound up back on drugs for a few months. Is he cured? No, his epilepsy is controlled with neurofeedback, something that helps brain function, without hurting anything.
Here’s another: Anna’s Story. Her doctors wanted to remove part of her brain.
I remember a 12 year old boy with NLD, on the autistic spectrum. He had wonderful, proactive parents. He had such severe dysgraphia that he needed a scribe at school. He was too clumbsy for sports. He had no friends. He had an obsessive interest in movies, knew all the names of everyone involved in many, many movies. After, maybe 9 months of neurofeedback, about twice a week?, don’t remember exactly, his handwriting was legible, he was on the basketball team at school, had had a sleep over date at a friend’s house and was writing a movie column for the school paper. I eventually did some hyperbaric with him, but for him, it was the neurofeedback that had the power. Have no long-term follow-up on him. He was a lovely boy. I’d love to know what kind of a man he grew into. I recall that his father had fibromyalgia.
I treated a yoga instructor with life long full blown panic attacks. Appeared out of the blue, without content. They went away after the first treatment. She finished 20 treatments, for luck, but the first treatment appeared to fix them. I had maybe 6 months or a year of follow-up and they didn’t reappear. Like a restart of a computer. This was an extremely rare case and I treated people who weren’t helped at all. But hey, no harm, no foul.
Obviously, these are very memorable cases, but I treated hundreds of people and it is useful, as an adjunctive therapy, for many conditions, especially conditions that involve unstable brain states. I found it especially effective for all kinds of anxiety disorders and it often significantly reduced the need for medication in short order. I used to advise committing to 10 sessions. If it is helping, continue. If nothing has happened by then, quit. The worst reaction is no reaction. I also used to say, if I can move you in the wrong direction, I can move you in the right direction. The diagnoses I worried about with respect to moving someone even temporarily in the wrong direction were epilepsy, depression with suicidal ideation and serious anger management problems. For these conditions, I advise a very experienced therapist.
The history of neurofeedback has a wonderful, serendipitous story behind it. Barry Sterman, PhD at UCLA, a psychologist and sleep researcher, did Pavlov type experiments with cats, where they had to push levers to get food. He monitored their EEGs during testing. Cats have an unusual rhythm that shows up at about 14 Hz, a burst of high amplitude activity, a little higher than the alpha rhythm. The SMR, or sensori-motor rhythm, is associated with stalking behavior in cats, a state of watchful waiting, not resting, but active and in the moment. He decided to use that rhythm as a training device, because it was easy to see and count. He was able to teach the cats to produce these bursts of EEG activity at will to get food. Some time later, he was hired by the Air Force to figure out how much rocket fuel their pilots could be exposed to before they had seizures. He tested on cats, because he had them. After doing the experiments, the data showed two clear groups, with respect to seizure threshold. Barry then realized that the cats with the higher seizure thresholds were the ones that had previous SMR reward training. He went on to try it with people. I am telling this story from memory, so Barry, forgive me if I butchered it.
Various people also started realizing that there was some advantage to down training, or inhibiting, slow waves, for performance enhancement in ADD kids. A lot of work has been done on this. However it is much easier to give children speed than to do this non-invasive treatment that takes time and effort. In fact, neurofeedback costs less than psychostimulants over time, but the drugs have big money behind them to prove that a normal variant is a disease, and to label large numbers of children with it. Ritalin is a performance enhancer for anyone that can tolerate the side effects. If you want your perfectly normal B student to get B+’s, just add some Ritalin. And when they get old enough, they can make extra money selling it to their friends. Or you could try some neurofeedback. Except that it isn’t scientific. Don’t get me going… However, brain damage, MBD, as it was known when I went to medical school, from a structural injury or persistent inflammation, is another story entirely. Neurofeedback helps here too, when no amount of Ritalin will change it.
Here’s how it works. You put electrodes on the scalp, in various locations, depending on what part of the brain you want to exercise or challenge. The electrodes don’t put anything into the patient, but they measure the EEG, the electrical activity produced by the brain and measurable on the scalp. First the area gets prepped with a mildly abrasive substance, the electrode is applied with paste between it and the scalp to reduce the impedance, or how much opposition there is to measuring the signal. The EEG is amplified and fed into a computer where software breaks the signal down into frequency bands, generally 0-40 Hz. One hertz or Hz is one cycle per second of a wave form. The Othmer’s new work is looking at a very slow signal, close to zero. It is pioneering work, and as such, is being met with resistance in the more conventional neurofeedback community, since it is so unscientific, meaning clinically driven.
The signal is converted by the neurofeedback system into a graphic representation of the information gleaned from the EKG. If the brainwaves change, the picture changes. The graphic reinforces increases in the reward band and tries to inhibit slow wave excursions. The visual feedback can be anything you want, including a movie. Different people respond to different graphics. Auditory feedback used to be beeps, but blessedly, the new software uses music instead of beeps, getting louder to reinforce whatever the therapist has chosen to reinforce. There is also tactile feedback in the form of a vibrating teddy bear, like holding a purring cat.
Unfortunately, clinical results with neurofeedback are highly system and operator dependent. A choice must be made at the start of each session about where and at what frequency to train. Reinforcing the wrong thing over time can even make things worse, though in eight years of practice, I never produced a new symptom that persisted. If the treatment is wrong, it sends the patient in the wrong direction, but generally somewhere familiar, and then the protocol can be changed to address symptoms. Usually, a protocol is found that can be repeated going forward. When that is the case, home training becomes a good option for some people.
Experience has taught that certain locations produce predictable effects in groups of people with common symptoms. Sue Othmer, in particular, has a coherent model for choosing training sites and optimal frequencies to reward that accomodate entire spectrums of neuropsychiatric illness. Without drugs. The downsides? Cost and time.
There are fractious groups within the neurofeedback community. Some are wedded to the more scientific approach of measuring the QEEG, or quantitative analysis of the EEG signal at multiple sites and subjecting the data to comparisons with various normative databases. A number of people have tried to define neuropsychiatric disorders and brain injury according to deviations from statistical norms. Then the idea is to fix those abnormalities. I did QEEG in my last practice and it’s fascinating, but I was never impressed that I was able to fix the QEEG with neurofeedback, even in the face of huge clinical improvements, so in the end, I decided it wasn’t worth the trouble or expense, generally speaking; if there is a structural abnormality, then a QEEG may be helpful, mostly to tell you where not to train. Anecdotally, I had better luck “fixing” the EEG with HBOT than neurofeedback.
My metaphor to explain why neurofeedback works is that it is like a reset, or mini shock treatment, all of the effort on up-training and down-training particular features in the EEG notwithstanding. If you tug on the EEG, cause a perturbation in the system, the brain will take over and order things in a more functional fashion. It has nothing to do with learning, or even training really, though that word is often used, for want of a better word. Here is a baby performing the task. Understanding is not required.
This is a YouTube video of a teenager currently in treatment with Sue Othmer. It is a small introduction, a glimpse into her approach. Many providers do neurofeedback in the context of psychotherapy, but therapy is not needed for efficacy. As a physician, it wasn’t that different from prescribing drugs, except that it worked better.
When I became disabled the first time, in early 1996, I was completely at a loss. I had had insidious onset of sensory neurological symptoms associated with autonomic and vascular instability, as well as anxiety and symptoms of PTSD for a year. I thought I might have MS, but whatever the diagnosis of my then mystery illness, I knew enough to know that conventional medicine had nothing to offer me. Instead I turned to biofeedback. I went to a conference in ?, can’t even remember where anymore, but I met Sue and Siegfried Othmer in an auditorium, after hearing them lecture. I gave Sue a little history and she hooked me up. I did maybe 20 minutes on her machine, went back to my hotel room and had the first good night’s sleep I’d had in years. I bought a system the next morning, then $14,000 (they are much less now). I took their training course, trained myself, then a few friends and was so impressed with the results that I went into practice with it, still in recovery myself. I used their system for 8 years in practice. Their new system and training protocol seem even stronger to me so far this time around, space age compared to my old system. Sue Othmer is a master clinician and anyone within shouting distance should certainly consider training with her. Siegfried has been a mentor to me for many years now. I am excited to introduce him to you. There is too little cross-pollination between the ME/CFS group and other communities. Please note: caregivers can benefit as much as patients. Neurofeedback is peak performance training, starting from wherever you are. So, without further ado, here’s Siegfried…
The question has been asked on this blog: “What is Neurofeedback?” And Jamie has asked me to answer it with reference to neuroimmune diseases. Neurofeedback is basically a biofeedback technique that utilizes the EEG as an index to our internal states. Biofeedback commonly uses measures of peripheral physiology, such as hand temperature, sweat gland activity, muscle tension, and heart rate. The objective is the same: it is to train the central nervous system toward better regulation of its internal states. Using the EEG, we get a little closer to the central processor, although we get a bit further away from what we can readily relate to.
Neurofeedback has been explored over the last forty years in connection with conditions such as epilepsy and Attention Deficit Hyperactivity Disorder. But over the last twenty years, it has come to cover the whole domain of mental function. So it has potential relevance to the management of CFS, fibromyalgia and Lyme disease as well. The argument goes as follows: With the emergence of brain imaging over the last fifteen years we have discovered that the quality of brain function depends upon the organization of the brain in its resting condition. Now this resting state is in fact a very active state, but still it can be readily distinguished from states in which the brain is externally engaged. Further we have found that the common mental dysfunctions are associated with disruptions in the functioning of these resting state networks.
Consider the example of a severe emotional trauma, one that results in persistent PTSD. There has been no blow to the head; no loss of neural integrity; no physical injury to the central nervous system. And yet the resulting dysfunction can be profound and lasting, as we well know from the experience of our veterans. What has changed in these nervous systems? In our new model, one would say that the nervous system lives perpetually in such an agitated state that it has lost access to its resting states. Or in slightly different language, resting state activity is now disturbed, perhaps permanently in the absence of intervention. The same occurs when the stressors to which the CNS is subjected are internal rather than external. That’s where CFS and Lyme disease comes into the story. Just as in the case of emotional trauma there is no need for ongoing insults to maintain the state of dysfunction, the same holds true for organic insults to the system. Once brain regulation has been profoundly disturbed even by a single event, the brain may not find its way back to wholesome organization. And if the insult is ongoing, then of course matters are all the worse. If the neuroimmune disease had a direct impact on the integrity of our neural systems, then again matters are all the worse. But they are not without recourse.
Before we go on, the take-home message from the above is that even if no disease marker survives, the brain dysfunction may nevertheless persist. This is the downside of brain plasticity! The brain can consolidate dysfunction just as readily as it can consolidate function. This brain dysfunction must be targeted directly because effectively it lives a life of its own. And neurofeedback is the best means to do that. What is involved in the neurofeedback as it has evolved at our hands is that we simply allow the nervous system to see itself in action. That is literally all there is to it. We do have to be quite selective in what we show the brain, but in view of what I have already told you, it wouldn’t be hard for you to figure out what that is: We have to focus the brain’s attention on its own resting state activity! Once we ‘shine a light’ on that activity, the brain can find its way back toward better-organized resting states. Progressively, step by careful step, we get the brain functioning better again.
The journey may not be smooth if the trainee is coming with a raft of symptoms. So a knowledgeable clinician has to steer the journey in a way that maximizes the person’s functional status at every moment. The rule is simple: if the person feels better as the training goes forward, then we are doing the right thing. If the person starts feeling worse in any way, we need to change course. So the brain itself is telling us what it needs by way of information about itself—figuratively it is telling us where to point the flashlight in the dark.
The metaphor has its limits. We are the only ones who are in the dark with respect to the signal on the screen. The brain is not in the dark. In fact the whole process only works because the brain recognizes its relationship to that signal. And once it realizes the connection, it ‘takes responsibility’ for that signal. That is what our brains do. This is no different from your brain taking charge of the steering wheel of the car while you have decided to think about other things than keeping the car properly in the lane. The signal on the screen is part of a control loop that the brain must manage… because that is just what brains are organized to do.
The implications of the above are that anyone with a neuroimmune illness dealing with persistent symptoms is well-advised to try neurofeedback to see how much function can be restored. This works even if there are serious ongoing organic issues. We are up against the same problem with the autistic spectrum, where there are lots of ongoing organic issues but we can still substantially enhance the level of function with neurofeedback. But if there are ongoing organic insults to the system, then one may well need to keep the training going at some level in order to maintain function.
There are other kinds of neurofeedback besides what I have discussed. The brain will react to all kinds of information about itself. But ours is presently the only neurofeedback method that trains the brain’s resting state activity so directly, and that appears to be the most efficient training method for a variety of very challenging conditions, including PTSD, the autism spectrum, and the other conditions where resting state functional organization is so profoundly compromised.
Siegfried Othmer, Ph.D.
Chief Scientist, The EEG Institute
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.
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 , and/or seclusion in untested tissues.
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  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.
Today’s song: Sounds of Silence by Simon and Garfunkle
What follows was written by Val, the mother of the patient I mentioned in the last blog. I am posting it, at risk of being criticized for self-promoting, because it says some very important things about how to get better. That doesn’t mean you have to come see me. Everything I am doing is public information, simple and safe. I want to thank K from the bottom of my heart for her generosity in sharing her experiences. Here’s Val…
Well, I’m the Mom of the young patient Jamie just treated for the month-long intensive. I’ve been intending to blog about “treatment with Dr. Jamie” since we flew to Hawaii last September to see her, but now I’m feeling an urgency to share the experiences, and I have my daughter’s permission to talk about all of it.
Before I go into the details, the most important thing I want to say here is that if you have a child or young adult with the MEICC or fibromyalgia or OI/POTs diagnostic symptoms, don’t mess around with your GP or family/primary care doc or even the docs you find who at least “believe” this isn’t psychiatric. Go see Jamie or find a doc who will work with her, if you can possibly afford it. Her shit works. We don’t know if it can stave off the worst of the debilitation that this disease devolves into, but if she’d been able to practice and I’d had sense enough to get my daughter to Hawaii to see her 10 years ago when she first got sick, I strongly believe my daughter would have been saved from years of misery. And, in the end, we certainly paid more on useless Dr.s, treatments and supplements during that 10 years of fruitless searching than we would ever have paid if we could have just gone to see Jamie in the first place. That’s my main message. The rest is details.
My daughter, K, had symptoms from birth. She had major colic that prevented her from sleeping for more than 2 hours at a time from birth to about age 4. Constipation was a huge issue, including fissures from age 4 onward. No celiac, no detectable allergies, no Crone’s diagnosis, just on-going poop misery. Sleep has always been impossible. In kindergarten, she was diagnosed as having ADD without the HD. Tutoring taught her to read during first grade and she’s always tested ‘way above average on scholastic aptitude tests since, accompanied by – lol – Harvard-level grades and excessive success on other achievement measures, blah blah, until she started getting really sick in middle school. (For those who aren’t ME/CFS-knowledgeable, high achievement used to be a hallmark “symptom” that was seen as contributing to the psychiatric evolution of this “stress-related” disease.)
At age 10, she needed an emergency appendectomy. The surgeon was drunk and didn’t close the one artery that feeds the area. Consequently, she needed another emergency surgery about 8 hours later as well as a massive blood transfusion from stranger blood. Who knows what was in it, right?
She recovered from the surgery, but suddenly developed migraines out of nowhere 1.5 years later, about the time of the onset of puberty. And I should also mention that we put all our kids through the remainder of the “required” vaccine regimen we’d avoided until then, when she was about 12 years old.
Migraines and dizziness started at age 12. At 13, the migraines were bad enough that she started missing a lot of school. By the end of 8th grade US, she’d developed a “status migrainus” that lasted for over a month (with total misery, puking, etc.) and which wasn’t touched by any existing migraine meds, amitriptyline, or any other meds except tramadol injections. Our PCP finally decided to admit her to the hospital at the end of 8th grade to monitor her while he administered ergotamine, an old-fashioned migraine med with potentially scary side effects, for 3 days and other meds (including morphine), and that finally kicked it.
She was OK over the summer and into the next school year. But at the end of October, she developed horrible pain in her neck and upper back, as well as more dizziness and continuing migraines, and OI symptoms, too. Our doc finally diagnosed her with “fibromyalgia.”
She just got worse from there. It was as if this disease systematically attacked every bodily system in succession. There may be a consistent order to the progression, but I’m not aware that anyone has studied and documented it. She learned to avoid the migraines, but the pain became ascendant, which continues to the present. Her gastro symptoms got much worse and she gained 40 pounds for no reason, then developed intractable nausea and lost 60 pounds for no reason. All of her hormones went out of whack. Hypothyroid, no androgens, no DHEA, blah blah. Total fail on blood pressure regulation, totally frightening unpredictable fainting events. And then the cognitive symptoms arose and she stopped being able to get online to do college courses, let alone for social reasons. I’m sure I’m forgetting some symptoms that went haywire, too, but these were the worst. She’d become completely bedbound by age 18, but by about age 22-23, she was also completely unable to even handle computer time.
We saw many, many docs and alternative-type healers. About age 17, she bailed out on the alternative types and said she wouldn’t try any further treatments that weren’t documented in at least one peer-reviewed paper published in a mainstream journal. (I kinda don’t blame her. She had a jello cake for her 16th birthday while she was doing the low-carb diet.) She liked acupuncture for the pain, but the analgesic effects only lasted a few hours.
So, we succumbed to mainstream medicine and she ended up with 8 daily meds and some 20 others for “as needed” symptoms. This stabilized her, but at what a miserable level. She had no brain, no energy, still had massive pain, and still no hope. Like everyone else, we were watching the HGRV research closely, as well as Jamie’s and Ali’s progress on the ARVs, but weren’t committed to this hypothesis until we saw more evidence. It’s still the causal hypothesis that makes the most sense to me, and there are MAJOR clinical reasons to go there, but we just weren’t there yet.
What pushed us over the edge to make the investment in going to see Jamie in Hawaii was a stupid cow of a nurse in our pain-management’s doc’s practice here in DC. We’d moved K’s care from our small town doc in PA to a pain-management specialist in DC a few years ago. We’d agreed with our PCP up in PA to try long-acting opiates to control the pain about the time K was 17 and we were otherwise trying to see if she could live alone with a nurse’s aide for about 5 years. But it turned out that she just needed much more care than an aide could provide, so she moved here to DC, where I work during the week, to live with me about 3 years ago.
The doc down here in DC had newer ideas than our PCP up in PA, but all his tricks also stopped working and he wanted K to go up on her opiate doses, which she already knew was a path to nowhere. We somehow ended up in his office talking to his nurse, instead of him. She was new to a pain practice, had attended a 1-day seminar on drug abuse, and absolutely flipped out about all the different meds K was prescribed. All by herself, this nurse decided that their practice couldn’t continue prescribing for K unless she saw a psychiatrist specializing in ADDICTIONS, because, obviously, my daughter is a drug-seeking junkie dope fiend trying to manipulate their practice into what? Giving her enough drugs to sell on the street? Which we’ve obviously been doing for the past 10 years, right? And then, when we met with the doc, he went on and on about how special K’s case is, how we shouldn’t have ever seen his nurse (umm, why didn’t his office staff know this?), how grateful we should be that he’d deal with K’s many and complex needs (like that’s our fault, right?), and he never once apologized for the massive insults to our integrity that his ignorant cow nurse inflicted on both of us.
I was beside myself with panic and fury. The last thing K needed was to see an addiction PSYCHIATRIST, who knew nothing about ME/CFS/FM except probably the crap that the CDC publishes on their website, would try to make HER responsible for her disease again, chalk it all up to drug addiction, and otherwise visit another set of attacks on her self-esteem with no path forward to getting better. I emailed Jamie because I already knew her as another Mom of a kid with this disease who I knew had gone through similar insults and stupidity. And when we talked (bless her, her immediate friend response was “call me”), it was just obvious that she was in a place to take on K, including all the drug-fiend complications, and might have wild new ideas, based in research, that seemed to be working for her and Ali and could maybe work for K.
As my facebook friends know, K and I flew to Hawaii to see Jamie last September. It was a HUGE effort for K and she was a mess because of it. But before Jamie did any kind of treatment, just getting together with her and talking over all the crap we’d been through was healing in itself. I loved it that I didn’t have to explain anything we’d tried. Jamie already knew about all of them and just nodded. K loved it because Jamie treated her just like I do – with the tenderness and care of a Mom – but with the massively more important set of skills of a Dr. , and, amazingly, one who knows how much a random touch can hurt, let alone standing up against a wall for 5 minutes. As we all know from her blog, Jamie is a firebrand on our behalf, god bless her! But, in person with a patient, she couldn’t possibly be more gentle, nurturing and sweet, let alone smart.
So, she changed K’s meds all around and is still in hot pursuit of treating K’s hormones. One of the most effective things she did was prescribe the high-flow oxygen. Since K started using it, her pain levels have decreased and she’s just stopped fainting. Once we finally got it together to have the oxygen tanks delivered here in Nov or so (it took a while to deal with my insurance), K has fainted only a couple of times, rather than the 3-4 or more times/week previously. And her overall pain levels are massively down.
Jamie also encouraged us to believe K’s personal experience that the opiates had simply lost their effectiveness. We all discussed what K’s Dr. here was saying, which was that she could go up in her dose levels for immediate pain relief, but agreed that it would only work for a while until she built up a tolerance to the new dose level. Jamie said K could go off the opiates and not feel any more pain than currently, but would achieve the secondary gains of not being labeled as a dope fiend and not having to worry about withdrawal if something happened that she couldn’t get her patches or pills for any reason. So, K started slowly weaning herself off the opiates after that Sept visit and it turned out Jamie was right – the pain was the same, the high-flow oxygen helped it as well as the OI/POTS symptoms, and…on the very positive side, we all rediscovered K’s massive brain.
Jamie also took her off Lexapro and got her started on Deplin last fall for depression. Last year (winter of 2010), K was a hopeless emotional mess. Some of you on MECFSforums know how scared I was about how depressed and borderline suicidal she was feeling. The combination of Jamie, the pain-relieving, anti-fainting and brain-improving effects of the oxygen, and the Deplin have absolutely turned the mood problem around. Since Sept, as every month went by, K laughed more, talked more, read more current events, and has absolutely recovered her passion for politics. She was once going to become a lawyer and run for political office…
The Month in Hawaii
The main purpose of spending the past month in Hawaii was to get K off as many of her current meds as possible. Jamie wanted her to be in the hyperbaric chamber and do neurofeedback, on top of the continuing high-flow oxygen, while she detoxed. It just really worked. Getting off that damned pain patch turned out to be nothing – 2 days of mild discomfort. And K was able to cut her daily oxycodone pain pills down by 2/3rds and completely dumped one of the benzodiazepines she’d been using for sleep.
We all got overconfident because this was going so well and K decided to stop her Lyrica cold-turkey. Considering it’s supposedly non-habit-forming and others have done well stopping it cold, we expected she’d be fine. Wrong. She was miserable and it taught us, as getting off the opiates had, that Rome was neither built nor fell in a day and we had to deal with this one slowly, too. Once she re-started it, she was again great, so the lesson learned is that K needs to go off it as slowly as she went down on her opiate doses. And now she’s doing fine with the smaller dose decreases every few weeks instead.
But, get this – while K was dropping meds and doses left and right, and should have been miserable, she was doing unbelievably well. I think we only cancelled 2 appointments over the entire month because she was feeling too bad to go vs. the 3-4 re-schedules we’ve often had to do for Dr. and dentist and other appointments over the past 10 years. And, other re-schedules were simply because K wanted a day at the beach instead of sweating it out in the hyperbaric chamber (it gets really hot in there) and we all agreed sun and water would be more healing. For a bedbound person, it was astounding to see her snorkel and swim with such joy, go out for dinner, watch her chasing scary bugs around the place we were staying, talk and laugh and engage, and overall enjoy life in a way we haven’t seen and she hasn’t experienced in years and years.
We travelled 16 hours to get back to DC last night. It was awful for all of us. K isn’t doing cartwheels today, but she’s also not curled up in PENE fetal position. In fact, she’s voraciously catching up on all the political TV coverage we couldn’t watch in Hawaii.
Hell, we don’t know. I’m pretty sure that if we only stopped here with oxygen, hyperbaric and Deplin, all these gains would fade over the next 2 years. Jamie has more tricks up her sleeve to get K’s hormones normalized, work on her blood sugar, and fine-tune this and that. And those things will surely lead to more progress.
But, what’s the disease-causing mechanism we’re fighting here? The treatments so far are basic healthcare and tweaks based on Jamie’s clinical intuition (oh, gee, we get dizzy and have pain – maybe our tissues aren’t getting enough oxygen!). But Jamie and Ali are continuing to improve on ARVs. Dr. Snyderman’s results are also incredible. If K continues to improve and stabilizes at a better level than she’s experienced since she first started getting sick, is there any reason to NOT try ARVs? I don’t think so. Jamie isn’t talking about this, but I am. Stay tuned.
And, in the meantime, parents, get your sick kids to Hawaii immediately. Do what Jamie offers now – it could make the difference between graduating from high school or college vs. having to do all that delayed or not at all. Save your sick kids some misery. The benefits may not last. We’ll see. But, these have been the ONLY treatments over the past 13 years that have had any clear, unequivocal positive results. Seriously, if you can’t get to Hawaii, get your Dr. to read her blog, join the forum, and consult with her. If only she’d been in practice when K began getting so sick…