Dynamic Duo
It seemed like a dicey thing – a talk on chronic fatigue syndrome (ME/CFS) that seemingly had little to do with the conference. The Brain Science Conference is a small conference series which began in 1990 and has been going ever since. Its goal is basically to provide brain researchers with a diverse set of talks on their field.
The 2018 Brain Science Conference was held in beautiful Sedona, Arizona
Mixed in amongst the talks on Parkinson’s, Epilepsy, neurotoxins, pain circuits and neurodevelopment was a session simply titled “Chronic Fatigue Syndrome”. The two talks: “Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): a multisystem illness invisible in plain sight”, by Lucinda Bateman, MD; and, “Developing new technologies to unravel chronic fatigue syndrome“, by Ron Davis PhD, didn’t even pretend to make an explicit connection with brain science. I wondered how many people would show up and how the talks would be received. I readied myself for a paltry turnout but the small conference room was full.
How the Brain Science Conference had managed to insert a session on the basics of chronic fatigue syndrome (Dr. Bateman) and innovative tools for understanding it (Ron Davis) was a mystery to me, until, that is, I talked to the person sitting next to me. I’d snuck into the conference. I was camping out in Flagstaff when Janet Dafoe, Ron’s wife, informed me that Ron was going to speaking on ME/CFS that weekend in Sedona – just an hour away.
After asking if I could attend the session, Ron said he thought I could probably sneak in – so I did. Furtively sitting at a table in the corner, I looked to the right to find a woman staring at me. Who are you, she said? It turned out she was the conference organizer and she was happy to have me there. 🙂
I was certainly happy to be there. It was a treat listening to these pros.
Dr. Bateman: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): a multisystem illness invisible in plain sight
“These patients are trapped inside of a body that isn’t working”.
Dr. Bateman started by blunting stating, “I’m here to get all of you to start thinking of this illness”. She aimed to give them a talk they would remember — and she did. First, she hit them between the eyes with one of those chronic fatigue syndrome stories that could keep one up at night.
She took them back to 1979 to a young woman on a high school cross country team who had taken time off to heal from a stress fracture. Her stress fracture healed, but her body mysteriously fell apart. Instead of leaving her stronger, running left her fatigued, nauseous and prone to vomiting. By her senior year in the early 1980’s – well before chronic fatigue syndrome even had a name in the U.S. – she’d had to abandon all physical exercise.
Dr. Bateman – the head of the Bateman Horne Center in Salt Lake City gave a powerful presentation on the clinical side of ME/CFS
She struggled on and was able to complete her college degree and become a preschool teacher, but had trouble maintaining a regular work schedule. A severe respiratory illness triggered problems with insomnia that continue to this day. On one of her many attempts to figure out what the heck was happening to her, she was misdiagnosed with schizo-affective disorder.
As time went on, she got worse and worse. By the time she saw Dr. Bateman, our former runner and teacher had trouble reading and comprehending the printed word on her worst days. It took only a few simple tests to indicate that her autonomic nervous system had gone haywire. Upon standing, her heart rate zoomed from 67 to 130, while her pulse pressure (the difference between systolic and diastolic pressure) dropped from a normal 61 to a decidedly low 29.
According to Wikipedia, a pulse pressure of 25 mmHg or less signifies either congestive heart failure or cardiogenic shock. It’s usually associated with significant blood loss due to trauma (aka a significant injury). In ME/CFS, it probably just reflects extremely low blood volume. Remarkably, this woman – who could hardly stand without her system collapsing – had had a tilt table test before seeing Dr. Bateman but was told it was negative because she hadn’t passed out. A cardiopulmonary exercise test of this former runner indicated that her VO2 max was now 16 – 25% of normal.
Compression socks, midrodrine and propanolol helped, but even with these therapies she still meets the criteria for postural orthostatic tachycardia syndrome (POTS). At 37, she can manage about 4-6 hours upright – not standing upright but sitting upright. Over half her life has now been spent ill.
Dr. Bateman moved onto some key characteristics of the disease. There’s the inability to reproduce energy production after an exercise challenge – still probably the most startling study result ever found in ME/CFS. It’s a result that goes to the core of this disease. After showing that result to a guru of exercise physiology, Dr. Bateman reported he said, “If that’s true then it’s unique”. Yet, that finding has actually been demonstrated in studies containing 51 patients, 22 patients, 15 patients and six patients – but apparently not yet to the guru’s satisfaction.
Over ten years since this finding appeared, we still lack the definitive study that would prove to him and others that something has gone badly awry with energy production and exercise in ME/CFS. Why that study hasn’t been done is a mystery to me. It would also explain ME/CFS in simple, basic terms that everyone could understand.
My view is that the best way to wake up the research community to the seriousness and uniqueness of this disease would be with a large, rigorously controlled, two-day exercise study that irrevocably demonstrated the presence of a unique energy deficit in chronic fatigue syndrome (ME/CFS).
Dr. Bateman highlighted the weird sleep problems in ME/CFS – the high alpha waves at a time they should be low, and the low delta waves at a time they should be high). (ME/CFS patients brains are in sleep mode when they are awake, and in awake mode when they’re asleep.) She suggested that central sensitivity may be responsible for a lot of the sleep problems in ME/CFS.
Continuing with this theme, Dr. Bateman talked about the “wired and tired” issues, the too-exhausted-to-sleep problems and the over-signaling; i.e. the unrelenting brain activation that leaves the brain highly sensitive to any kind of stimuli and keeps it from settling down, resting and rejuvenating.
That shows in the sympathetic overdrive and the increased heart rates during sleep and the reduced heart rate variability. With the loss of HPA axis stability comes problems with circadian rhythms.
Dr. Bateman suggested that central sensitization could be responsible for many of the sleep problems in ME/CFS
Spitting out some eye-opening statistics – the disease affects from 800,000 to 2 million Americans, is responsible for $17-24 billion in economic losses yearly but is undiagnosed in 80% of patients, is not taught in medical school, and gets about $13 million in funding from the NIH — Dr. Bateman asked: how one earth does a disease this common and this serious get overlooked?
She asserted that part of the problem is just the way our medical system works. By and large, the U.S. medical system is not concerned about viruses – which triggers many people’s illnesses – and has a rudimentary understanding of the immune and endocrine system. Cellular metabolism – possibly a very big deal in ME/CFS – is hardly on its radar at all.
That said, Dr. Bateman said that she firmly believed that early diagnosis and proper early treatment could change the prognosis for many. She also believes that we know 90% of what we need to know about ME/CFS and if we could get more cross-talk across specialties going, we could figure this thing out. On that positive note, Ron Davis came in.
Ron Davis: Developing new technologies to unravel chronic fatigue syndrome
Davis provided a different tack. Describing the technologies his lab is developing that may be helpful in many diseases, he again and again used ME/CFS to demonstrate its worth.
Ron Davis asked how a major disease could get so little attention
He started out by noting that chronic fatigue syndrome (ME/CFS) is more common than HIV, Parkinson’s and multiple sclerosis, and too wondered how such a common disease could be so unknown. It’s the lowest funded of any major disease. ME/CFS receives just 0.1% of the money that goes to HIV research.
Davis was on a roll, joking and delivering pointed comments to the audience. He said his job description was “reducing noise”; i.e. finding ways to deliver vast amounts of meaningful clean data, cheaply and efficiently. Davis presented a cornucopia of new technologies his lab was working.
First up was the nanoneedle. With its 2,500 electrodes per cm measuring whatever they are measuring 200 times a second, the nanoneedle is capable of providing a billion data points in one sample. There was the test able to detect antibodies with 10,000 times more sensitivity than standard Elisa tests and the the wearable biosensors that electrically analyze very small amounts of sweat, and eventually cytokines and other immune factors. (They could determine what’s happening to people with ME/CFS as they descend into PEM). There was the miniaturized energy harvesting device which uses movement in the blood to generate energy and monitor what’s going on there. (It’s so small you can’t see it.) The way to levitate cells and so on.
It was mind-boggling stuff and then it was onto ME/CFS and Davis’s grand fishing expedition.
The Grand Fishing Expedition
Davis said that when you don’t have a clear pathophysiological pathway, you look everywhere. We have two grand fishing expeditions underway in ME/CFS; Davis’s Open Medicine Foundation study and Avindra Nath’s intramural study at the NIH. Medicine research is now so complex that the two hardly overlap. Davis is focusing on getting molecular observations and Nath is including things like metabolic chambers, growing neurons in a dish, autonomic nervous system testing and exercise.
Davis noted that most of the “fishing holes” will not pan out, but in a process of addition by subtraction, the negative results allow you to move past dead ends and onto new possibilities. The key is that you don’t step over something by pretending to know more than you know.
The Severe Patient Big Data Study contains 20 ME/CFS patients – so sick they never leave their house – and their families. Because the disease is so prominent in them, Davis believes they may provide a clearer signal. Davis listed 30 tests and gave some early results.
Thus far Davis has found more evidence of viral activity in the healthy controls.
Viruses – In a major surprise, Davis has thus far found no evidence of viral activity in the severely ill. In fact, Davis is finding less viral activity in the severely ill patients than in the healthy controls. The severely ill patients are so clean that Davis is searching for a reason why. He believes their immune systems may be so activated that they’re able to immediately repel pathogens. His search for viruses is not done yet but – he’ll go after RNA viruses next – but thus far, there’s been no cheese down the viral tunne!
Toxins – Heavy metal contamination can wreak havoc with many body systems, but no evidence of heavy metal contamination has emerged.
High Omega-3 Levels – Omega 3 is the good omega oil but omega-6 (at the right level) provides important functions as well. In general, the ratio of the severely ill patients’ omega-3 to omega-6 levels is out of balance. Davis chalked up the too high omega-3 levels to supplementation and an excellent diet :).
Cell Lysis – too many cells dying and dumping their DNA into the blood can cause problems – but not in ME/CFS.
Mitochondria Levels – energy production in ME/CFS patients could be impaired by low levels of mitochondria but the numbers of mitochondria are fine.
Inflammation – evidence of inflammation is present, but Davis warned that we don’t know what is triggering that inflammation and what positive effects it might be having. He noted that the immune activation could be present without a trigger.
Energy Production – Dramatic differences are continuing to show up in metabolic testing (metabolomics). With one third of metabolites greater than two standard deviations below normal, metabolomics is providing the best window into ME/CFS yet. The severely ill patients are showing significantly more metabolomic abnormalities than the moderately ill ME/CFS patients. That suggests that Davis’s idea that the severely ill provide a clearer picture of this disease could be true.
Genes – The genomic studies have identified a gene new to ME/CFS research which has been found, if I remember correctly, in every severely ill patient. Expressed mainly in the brain, the gene has been connected to autism – an interesting connection given Bob Naviaux’s findings of similar metabolomic results in the two diseases. Davis suspects that ME/CFS is primarily a metabolic disease and is not centered in the brain. That would be good news given the difficulty of studying the brain and accessing it via treatments.
In general, Davis believes the genetic predisposition to ME/CFS is different; instead of featuring a couple of rare polymorphisms, it appears to be manifesting as increased levels of a series of common polymorphisms. Showing that, he said, requires a different kind of approach from what most geneticists do.
Biomarker
Finding a biomarker, Davis said, is essential for proving to the world that ME/CFS is not all in one’s head. He holds out the most promise for the nanoneedle and its billion data points. Thus far, the stats are impressive. The nanoneedle has found dramatic declines in the energy production of all 17 ME/CFS patients but none of the healthy controls when faced with a stressor. The relatively small sample size becomes less significant in the face of a statistical finding like that. (The possibility that that result could be caused by chance is 5×10(-7) (or, if I can get my zero’s correct p<.0000007).) You hardly ever see probability factors that strong in biology.
The nanoneedle has clearly uncovered something dramatically different happening in ME/CFS patients. It’ll be exciting to see how the nanoneedle tests out in other diseases and to learn more about exactly what it is uncovering. As it is now, its potential seems immense. After all the bad luck with ME/,CFS the nano-needle is a case of serendipity striking. It basically fell into our laps – Davis’s lab began working on it before he got heavily involved in ME/CFS, and here it is playing a major role in Davis’s search for the cause of ME/CFS.
The OMF’s blood flow study is another case of serendipity striking. it came about when SJSU researchers heard about Davis’s work and approached him. Davis said the results were too preliminary to talk about that, but thus far, ME/CFS patients’ red blood cells were showing reduced deformability and slowed movement. Davis wants a smaller capillary tube to mimic the blood flow through the smaller capillaries, so his lab is doing what it does and creating one.
During the question period, Davis acknowledged that the sedentariness the severely ill ME/CFS experience is likely having massive physiological effects. In truth there’s no way to tell how much effect it’s having. You can find sedentary healthy controls to match up with sedentary but still somewhat active ME/CFS patients, but it’s impossible to find healthy controls who’ve laid in bed for a year. The closest match are astronauts who laid in bed for a month to mimic the effects of space flight, but Davis’s attempt to access NASA’s blood samples failed. (The samples had been lost).
Since the conference, the Open Medicine Foundation has opened a new ME/CFS Center at Harvard, led by long time Davis collaborator, Ron Tompkins. Tompkins, who has participated in numerous studies on sepsis and burns, will be extensively analyzing muscle biopsies of ME/CFS patients. Almost all the studies of ME/CFS have analyzed the blood, but Davis felt that direct analysis of muscle cells could be critically important. A blog on that is upcoming.
Conclusion
If we could just get them to take it on the road…
The talks were received with real interest. In fact, I had got the feeling that they were amongst the two most interesting talks in the conference. Both speakers were treated to a bunch of questions. Dr. Bateman waved off my surprise at the reception they got stating the researchers are always interested when they hear about ME/CFS, it’s the doctors she had trouble with. The conference organizer stopped by to remark about how fascinating the talks were. She seemed genuine.
Thinking about it I could see why. It’s probably not often that researchers are treated to a fascinating field they probably know nothing about – one goal of the conference – and in such an enticing way. Nobody is better than Dr. Bateman at explicating the clinical side of this illness in a clear and vivid way and Ron Davis was at his best – cajoling, joking with, and even gently taunting his audience. These guys are pros. My one thought as I left the talk was how we could get this duo to take their talk on the road…
I wish they would focus on the following issues: insulinoma, (HFI) Hereditary Fructose Intolerance, (PERM) Glycine Antibodies, (SPS) Gad-65 Antibodies, Silent Migraines with migraine medicines & diet & or without Chocolate skin Allergy testing, Narcolepsy Migraines medicines & Glucose tests of Nasal fluids spontaneous spinal brain sinus fluid leaks…Last, Sero Negative Q Fever treat with both chronic CDC antibiotics see what happens after one month & use muscle biopsies to grow Q Fever cultures & PCR testing…
That’s quite a list. To me it shows how vast the possibilities are. Hopefully we will be able over the next couple of years to narrow them down. Davis’s molecular approach is removing some possibilities and opening up others.
I was a patient of Dr.Paul Cheney for many years and I always argued with him that toxic exposures could cause the many, confusing symptoms of CFS. He mentioned that there was a toxic factor in Tahoe but never said what it was. At last,toluene! My work involves researching toxic exposures that cause birth defects. We have worked with Gulf War veterans because we have found increases in certain birth defects in their children. There were 31 reproductive toxicants in the Gulf War environment. One of these was Dursban which I believe triggered my own illness in 1984. This pesticide was widely used in the Gulf and although it is now banned from indoor use, it is still used on food crops. We live in a environment that becomes more toxic every day. Why aren’t we spending more time studying those possible triggers?
Hi I’d be interested in reading more about Dursban and its use in the Gulf war. Was it a mosquito or bug spray?
My only issue with toxin exposure triggering GWI was that many marines who were never deployed on the ground and were waiting on the ships at sea hundreds of kilometres away still got sick.
Which has me wondering about the powerful antigen loaded vaccines designed to protect against biological weapons. That to me seems to be the most common denominator in GWI
Unless Dursban was used on board the ships too? Perhaps the combination of a pesticide and those powerful vaccines was too much for their immune systems to handle
Dursban is an organophosphate pesticide with a chlorinated structure. A member of our scientific advisory board identified a pattern of birth defects associated with Dursban exposure in the mother during pregnancy. This helped to get Dursban removed from indoor use.Re.the Gulf,there were many other toxins in the Gulf War environment including the multiple vaccines you mentioned; permethrin treated uniforms; the anti-nerve gas agent pyridostigmine; CARC; smoke from oil fires; depleted uranium; possible low levels of chemical warfare agents; etc. In our data, some of the sick veterans who were not deployed worked with contaminated gear that was sent back. These vets had received vaccines, but they had no access to their vaccine records and they didn’t all receive the same thing. Plague, botulin, anthrax?
Hi there for me too, I was exposed to a termite insectide which played havoc with my immune system and later I developed ME/CFS.
Would I be able to get an appointment at the me/CFS Center at Harvard? I have had me/CFS since my early 30’s. I was finally diagnosed by Anthony Komaroff around 1995; I had lost my teaching career and was severely ill with me/ CFS. I am now 72 and hardly go out and my symptoms have gotten worse. I hope there is research being done on the aging of those of us still alive and suffer with this horrible disease!
Thank you
I think at this point its going to be a purely research center but there will at some point be an active treatment component. I will ask Ron Tompkins about that, though.
Cort – I am near Boston and would be interested in participating in research as well. Please keep me in the loop! Let me know if I should contact Dr. Tompkins directly. Thanks!
I, too, live in the Boston area and am very interested in volunteering for any research studies or, eventually, treatment trials if that happens. Pretty standard story: Sick since 1994, I was diagnosed by Drs. Hugh Calkins and Peter Rowe at Johns Hopkins. I lost career, marriage, home, friends, etc. At 73, I refuse to give up hope that I can find a way to improve and be a more active part of my grandchildren’s lives. Thank you for all your dedication and work in our behalf.
Good suggestion about the aging CFIDS/ME population. I also fall into that category (age 67 ME for 27 years). This illness is not static and symptoms change, come and go over time. Some symptoms you think are done reappear years later, and even after years of being ill new symptoms arise. What’s happening long term in the bodies of those of us who have been ill for so long, and will new treatments also work on those who have been ill for years. Good questions to pursue.
Hello Arlene Smith. I too started with this in 1978 & now I am also 72 yrs. old. Yes, I am older so it does feel worse. I was divorced 3 yrs. before this all started plus raising 2 young boys on my own. It’s been as you know horrific. So many side effects. The pain I can manage but the fatigue it’s just comes more then not & I am like a zombie. I too am more house bound & memory getting worse. (People see me like a normal person). I walk me dog from 15 min to sometimes 40 min. I hope & pray this year someone will hit the mark of what it is…..
Glad to see CFS info being talked about. Diagnosed in mid ‘90’s. It’s a silent disease and limits everything I can’t do anymore. Plus I have fibro and excruciating pain.
There is an herbal blend that I’ve been using now for about 6 weeks called Kyungheechunggan-Tang-01 or KCT-01. It is a combination of individually inexpensive herbs for the control of inflammation pain ……and its results have been amazing for me. I realize that some/much of your pain may be related to a different pathway but if it is at all related to the TSPO activation in Microglia (as the ME/CFS researchers are finding), this should prove helpful to you. If you’d like any more info that I can provide, I’d be happy to do so. You can contact me at mark.elitemedical@gmail.com (this is an email I created for a different reason but I use it for my ME/CFS correspondence as well).
Another great blog, on great work Cort.
Can these talks be video’d and put online? How useful it would be if GPS could be encouraged to see this information and start treating people with belief and support.
Yes’ Gp’s and clinical specialist it could plus should be part of their least training:
Ron Davis’ his inventions are born from the necessary.
Thank you.
A casualty of ME/ CFS.
I saw my doctor last week and attempted to tell her about the fact that there is now medical information online about ME/CFS, even the CDC gave way a bit and has included a link to the IOM’s report on ME/CFS.. making it easily acceptable..
I shared that a lot of information on ME/CFS has been learned in the past year and YouTube now offers up videos on many new talks, conferences and presentations on ME/CFS from the scientific community…Some online sites are offering CME credits to doctors that visit and read the information presented.
She walked out without even acknowledging my information.
When I inserted a link to the IOM’s report on ME/CFS in a message I sent my doctor via the Peace Health Patient Connection I got a message back from her MA, stating that I cannot send limks to my doctor on their messaging feature.
I haven’t had any luck getting my physicians or her team to be willing to take the initiative to look at the truly scientific info that’s available.
My best guess is that they are waiting for informatiom to fall into lapse from a source they Trust. I can’t see you then considering me as a patient to be trustworthy
Dear Maschelle,
Why are you still wearing yourself out to get to a doctor who doesn’t even listen to you? I know it can be hard to find a good doctor, but it can be done, and you are worth the effort. Move on! You can do much better. More to the point, that kind of abuse creates stress that will only make you sicker. It’s counterproductive. You are the one who should be getting up and walking out, and oh, by the way, you don’t owe payment to a doctor who refuses to communicate with you or treat your illness. File a complaint with your insurance and with the state medical board if you have the energy. Hang in there, I know how hard it is. It took me years to get to the right person. On the way I found some real losers but also decent doctors who would at least listen and try to understand and find ways to help. Then I found an internist who specializes in AIDS, Lyme, and CFS (because they have so much in common). And that is where I have stayed. God bless and best wishes.
Great ? article! Thank you
Great work sneaking into the conference, Cort! Way to get the story! I think it’s so interesting what Dr. Bateman said at the end, about researchers always being interested in ME/CFS, it’s the doctors who are not.
I suppose it is because the researchers see something they can pursue to make headway while the clinicians, besides not being educated about ME/CFS in medical school, are at a loss as to what to do with patients. Researchers feel empowered and intrigued but clinicians feel helpless as to what to do. I too am an aging ME/CFS patient, having gotten sick 32 years ago in 1986 after a visit to Tahoe the year before. I think we need to put our focus on finding a way to prevent ME/CFS in the first place, finding a way to heal new patients who have the best chance of recovering in the first 3-5 years to prevent lifelong illness and pediatric/young ME/CFS patients. At 71, I too would love to have a few good years before I die but I’ve accepted that that is unlikely. Now we need to fight for the young people. I at least had my family, my education, career established at 39 years old when I got sick. The children and young adults may face a permanent illness unable to establish anything resembling a life of their own. Of course, I hope any research will benefit us all. Great article, Cort!
Hi Esther, my daughter got sick on her 13th birthday….almost 10 years ago. She has no memory of what it is to feel normal.
I’m a 35 yr old Esther who has had this for 4 years now, mostly bedridden the whole time. On the verge of moving beyond those 3-5 years they say determine if you will or won’t get better, I’m absolutely terrified, and can’t bear the idea of research giving up on any of us who have had it for a longer time.. I feel like my life has been cut wayyy too short, but I also see people much older who got it later who feel the same way. To me the research is showing that nothing is incurable, it just hasn’t has the funding and research it needs yet. If they can help one group of us they can help all of us. Don’t give up hope for all of us at various stages with it!
I’ve had ME/CFS since I was 14. I had no family, no higher education and am now 69. I really don’t want to be at the end of the queue when there is a treatment, but would fight to be at the head of it.
Dr. Bateman was my doc for many years when I lived in Utah. I really miss her valuable perspective and treatment approach’s. Since I have arrived to San Diego County I have not been able to find a physician of her caliber, or any, in general Maybe I need to have some Tele-Medicine!
Bobbi, are you able to travel? You might look into seeing Dr Montoya or the Center for Complex Diseases (Drs Chedda and Kaufman) in the Mountain View, CA area. I am happy to hear you speak of Dr Bateman as after 2 yrs on a wait list I recently was offered an appointment in early September. Which I am planning on being at then.
Dr. Montoya at Stanford has a 2+ year wait list.
San Diego is over 400 miles away from Palo Alto and Mtn. View, and it is about a 13 hour drive, due to having to pass thru L.A. & Bay Area traffic. Utah isn’t much longer to get to.
Theresa Dowell and RN with ME/CFS who can prescribe medications has opened a practice in Flagstaff Az. I have a blog on her story coming up.
H Chritiane! Can you share any info gained in your appointment please? Thank you!
One factor not addressed was toxic mold. What is the latest understanding about its possible role in CFS? Is it possible that one’s CFS like symptoms are actually the result of exposure to toxic mold? what are the best tests to determine one’s exposure to toxic mold and how would one remediate such exposure?
Good question. I think that Lipkin is looking for fungi and other kinds of pathogens in his NIH funded study.
Yeah i was exposed to toxic mold but so was my roommate and she is 100% fine so that’s still not the root cause unless those of us sick have been re-exposes multiple times.
http://www.me-ireland.com/cheney2.htm
I never will forget, in 1991 I was sitting in a hotel room with Dr. Suhadolnik when he was first presenting these data on RNase-L. He was showing these electrophoretic gels. [Electrophoresis is a method of separating out different chemicals in a mixture; they appear in different places on a gel slide.] You incubate human lymphocyte cytoplasms with a target messenger RNA. [Lymphocytes are immune system cells, and cytoplasm is the substance of the cell, excluding the nucleus and the cell wall. The purpose of the experiment is to see what RNase-L does to the target RNA.] The RNase-L digests the target RNA into little pieces, and the pieces migrate all the way down the gel, and you can basically see little pieces of the RNA target displayed on the gel. He showed the gels of CFIDS patients, and of course he’s a wonderful man and a wonderful scientist, and he’s all excited about these blank gels he’s showing to the group huddled in the hotel room. He says, “Look! Look, do you see this? Do you see this?” And I looked at these gels, and I said, “But Robert, there’s nothing on the gel.” And he said, “I know, I know; don’t you understand?” I said, “No.” He said “Well, it’s because the RNase-L digested everything, digested it all completely, into such little tiny pieces that they had migrated completely off the gel into the gutter.” He went on to say that the RNase-L of these patients will digest in 60 seconds a target ribosome that the RNase-L of a normal human being cannot digest in 60 minutes of incubation. [Ribosomes are spherical bodies within cells that are the sites of protein synthesis.]
When I finally understood that this tremendous rate of destruction of messenger RNA was going on, it suddenly dawned on me; I went from not understanding why these people were so sick to understanding why they were so very sick. And I remember the hairs standing up on the back of my neck as I realized, “I now understand this. I understand why they can be that sick, yet not really look like they should be that sick, because they have a disturbed physiologic system that’s simply over-producing RNase-L and destroying messenger RNA” [and their cells are so badly damaged that they can’t function].
It also explains why hunting for evidence of RNA viruses in the blood of ME patients is a waste of time. Our cells could be teeming with viruses, but once it hits the blood it’s gone in seconds.
Years ago there was an effort to rename the illness REDD, so they couldn’t miss this clue.
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This written statement was sent out by Ken Wilber in October 2002 to his close friends. Since I get many requests by visitors to this site about this topic, I have posted it here, with permission of Ken Wilber. FV.
RNase Enzyme
Deficiency Disease
Wilber’s statement about his health
hi folks,
several people have asked about my health, so let me give a brief rundown on the situation.
the condition i have is called RNase Enzyme Deficiency Disease (i love the acronym: REDD). it is thought to be either fully or partially responsible for a host of illnesses, including multiple sclerosis, myalgic encephalomyelitis, ALS, inflammatory rheumatoid arthritis, Gulf War Syndrome, fibromyalgia, to name a few.
for a long time its contours were unknown, but there is now a definitive test (95% positive) and it is considered a discrete, well-defined clinical entity, although accurate information about it is rare, especially among physicians (to the extraordinary detriment of their patients).
the basic problem itself is straightforward: RNase is an enzyme produced by the human body when it is attacked by viruses or bacteria. as the name implies, RNase denatures messenger RNA wherever it find its. as it comes in contact with the invading virus or bacteria, it destroys its RNA and thus kills the invader. this is a very quick-acting defense mechanism, unlike the slower production of T cells, B cells, etc., which can take days or even weeks, and thus is one of the body’s first lines of defense.
in REDD, the mechanism that produces RNase is damaged by any number of causes, the most notable being environmental toxins. in 1985, in incline village, north lake tahoe, there was what has now become a very famous outbreak of REDD, where over 200 people came down with it (i was one of the lucky 200. treya and i were in tahoe recovering from her latest round of intensive chemotherapy). a widely circulated hypothesis is that this outbreak was triggered by a local toluene spill, but nobody really knows. the disease itself, however, is not human-to-human transmissible.
once the damage is done, the body begins producing a shortened but highly active form of RNase (37 kD instead of 80 kD). this 37 kD RNase has no turn-off mechanism, because the body only recognizes the 80 kD forms. therefore, the body keeps producing this 37kD RNase, which then proceeds to attack the RNA in literally every cell in the body.
the test for this 37 kD RNase is positive in 95% of the patients identified with REDD, and 0.00% of the population at large, which is why it is considered a definitive test and a definite clinical entity.
one of the first things damaged by this defective RNase is the glutathione system, which is one of the body’s major anti-oxidant systems. this leaves the body open to serious damage by its own free radical cascades. the areas most damaged are those that produce the most energy and free radicals, namely, the mitochrondria, or the small organelles in cells that produce all of the body’s energy.
as the condition progresses, more and more mitochrondria are damaged and destroyed. in severe cases, the person is bedridden for the rest of their lives. many of the tahoe victims are still bedridden. that means literally, with around the clock professional care.
another system quickly damaged is the body’s Th1 immune system, which is responsible for intracellular protection (i.e., protection against pathogens that attack inside the cell, like viruses and primitive bacteria such as mycoplasma). an opportunistic bug is defined as one that is already present pretty much everywhere (and is already crawling all over you), but only attacks when a portion of the immune system fails. in the case of REDD, the opportunistic viruses are hhv6, epstein barr, and CMV; and on the bacterial side, mycoplasma. over 70% of REDD patients have active hhv6, and over 60% have active mycoplasma infections. for the population at large, it is less than 3% for both of those.
those are the symptoms common to all forms of REDD. additional symptoms vary depending upon which other systems are hit hardest by the body’s own free radical cascades. if brain tissue, the result is myalgic encephalomyelitis, functionally indistinguishable from MS (and MS patients also have >60% active hhv6 and mycoplasma). crippling forms of chronic fatigue, rheumatoid arthritis, Gulf War syndrome, and ALS have been linked to this cluster. although the condition is often still called cfids (chronic fatigue immune dysfunction syndrome), it applies only to severely debilitating cases. yuppie depression it ain’t.
the first phase of the illness lasts about 5 yrs, and comes to an end, ironically, when the body’s capacity to synthesize protein is so badly damaged that it can no longer make any RNase, either. the person then enters a second phase, which lasts about ten years, where things are relatively quiet in terms of the illness itself, it’s just that their physical activity is severely compromised and they live in what has been called a “functional bubble,” often having only a few hours a day of walking-around time. fortunately, i had cultivated a lifestyle that never required a body (:-), so i had a pretty good middle ten years (roughly, all of the 1990s).
the third phase begins when the cumulative damage to various tissue systems starts to take a toll. basically, it just opens the body up to new attacks by the 37 kD RNase. every time you get an infection, cold, flu, or fever, your body produces interferon, which tells cells to start producing RNase—which in this case is, of course, defective. so more mitochrondrial damage, etc.
the basic symptom is “hypoxia,” or lack of oxygen in the cells (due to damaged mitochrondria), so you feel like you are suffocating most of the time, and you’re often bedridden around the clock (literally). also fortunately for me, this means mega meditation. it also means depression, sadness, and pain, not so much for the pain in this body, but the pain of what this body can’t do.
weirdly, of course, my spirit-mind just keeps writing books, and during this last really severe period (the last half year), i managed about 800 really good pages. often written in bed, but no matter.
the central issue for me has never been the mitochrondrial damage per se, which i have always been able to handle fairly well, although it was nonetheless a total pain. (interestingly, REDD damages the aerobic system, and not so much the anaerobic system—which is why, although i didn’t know it at the time, i stopped jogging and starting weight lifting….) rather, the central problem is when i get one (or two or three) of the opportunistic infections on top of the REDD. think of the worst case of flu you’ve ever had, subtract 80% of your energy, and that’s sorta what it’s like—but fortunately it only lasts for 6 or 8 months…..
much of this information (including the existence of the 37 kD RNase, extensive mitochrondrial damage, the 70+% infection rates with hhv6 and mycoplasma) has only been discovered in the last 5 years or so, which is why i previously didn’t talk about it per se—i didn’t know “it” was an it. i simply handled whatever it was and went on about my dharma.
some of you remember the really bad staph infection i had about 5 years ago. i did indeed have a staph infection, and at the time it appeared that was the culprit. but that never really made total sense, no matter what the doctors said, because staph doesn’t cause those types of symptoms. looking back, it is now virtually certain that i had opportunistic mycoplasma (which can be killed by 6 to 12 months of dual antibiotics—the same antibiotics they coincidentally but fortunately put me on for the staph infection). so the reason i got better after about 8 months of antibiotics was not because it killed the staph, but the mycoplasma.
at any rate, starting last spring i began running a chronic fever, which really put me down in a rather unpleasant and prolonged fashion, with mitochondria croaking by the buckets full and me on oxygen (a very cool trip). i am now two months into a 6 month or longer course of dual antibiotics.
there are now tests for all 6 of the major opportunistic bugs that come along for this ride. because my problems have always been when one of those is added to the REDD, in the near future i will undergo tests for all these, so i can knock the little shitheads off one by one. compassionately, of course.
as for what specifically triggers the damaged RNase, nobody knows, although environmental toxins are a leading factor. i learned from a researcher last week that harvard thinks they found a retrovirus. if so, that’s the most likely culprit. it’s still not human-to-human transmissible, so i personally hope it is a retrovirus, since that would mean that there is at least the possibility that an hiv-like protease inhibitor cocktail could attack the actual cause of the illness. but we shall see…
And yes, I do remember that solvent spill Wilber is talking about.
Hi Erik, would you happen to know the mechanism by witch this smaller RNase destroys/damages glutathione or would it be more a correlation that more of this smaller RNase goes hand in hand with less glutathione? Thx, dejurgen
“one of the first things damaged by this defective RNase is the glutathione system”
Actually Vincent Lombardi found that the test was faulty. The way the test was done was causing the issue; i.e. the RNase L problem was not in the body. I don’t think anyone has researched RNase L in ME/CFS in years..
You’ll have to be more specific Cort, which test done by who? Several groups have looked at this in several ways. One group correlated both increased RNAse activity with decreased RNAse inhibitor mRNA expression, which is unlikely to be a coincidence or due to a faulty test.
Thanks Cort ever so much. Yes, Dr Bateman and Dr Davis make a formidable team.
My question is: when you conclude about what Dr Bateman said, that early diagnosis and early treatment could alter the prognosis, are you suggesting she is saying that this is how it will be once they find the cause and the treatment?
Obviously, I can’t help but think what would this mean about those who have been sick for so long?
And the question someone posed about being sedentary was also of interest. Were any of the ramifications of this status described?
You are doing phenomenal work Cort.
My sense is that Dr. Bateman believes that if a person with ME/CFS can get to a good doctor early that can alter their prognosis. My guess is that that’s her experience. If you think of Jen Brea’s story – she pushed too hard and never recovered – it makes sense. Maybe the person doesn’t become well (or maybe some do ???) but maybe they don’t get nearly as bad as they would.
Sad to say the majority of us are too sick to get to the few knowledgeable doctors and the waiting lists are LONG. We’re most often too sick to travel the distance, plus none take Medicare. I’ve been sick for 29 years beginning at the age of 24. We need this taught in medical schools starting NOW, needless to say100+ years ago would have been good. We need something to take to our physicians to educate them and have an easy way to test for all these things that the few experts test. Another 2 weeks in bed and I feel like I’m dying. It doesn’t get easier or less scary and you always wonder just how much your body can take.
Bateman is spot on in her description of what is some sort of common sense. Meeting a doctor with knowledge early on, taking proper actions, will definitely have impact on prognosis. It’s like Cort says, it won’t fix you, but could have major impact avoiding getting to bad. By the way, this is not a future description, this is now! The major problem of course, is that many (long term) ME-patients have experienced the total opposite meeting no knowledge and no advice early on, getting into a very harmful push-crash cycle when trying to push through. Brea is one example out of millions, this is unfortunately classic, this is the “normal”.
Proper actions early will be important for every disease I guess, but so da.. important when it comes to ME. Partly because of no treatment at this point in time, not at least because we know that a push-crash cycle over time at some point will shut down your system with irreversible effect and in many ways demolish prognosis.
So what Bateman says will apply mostly to new patients. And it is so important to have focus on this why we (still) await research. One of the really nasty things is the passive approach of “we just have to await research”. There is so many things to work with that could contribute in a positive way, at least minimizing damage – it is a paradox (while awaiting research) not investing more in meeting a doctor with knowledge and good advice early on. If we don’t have all answers yet, we do have knowledge of what not to do early on.
Is there like an “advice for early on” sufferers?
I may have had some version of it for a very long time but just crashed in 2015 and started healing but crashed again. I definitely need to pace myself better but sitting/laying around all the time is so hard when all i want to do is dance and have a life…i know, we all feel that way.
it’s scary to think that we only know this stuff because you had the guts to crash a conference, many thanks. I have FM so it is extremely tough to assess how relevant some of these findings might be to me. not to be my usual downer here but I always feel that I am approaching the end of my life stuck with a complex disorder no one understands and no one really cares about except other sufferers and a tiny handful of underfunded researchers. but we soldier on until we can’t.
You can thank Ron for my crashing the conference. It was the kind of smaller, much more informal conference. It was a bit of jolt when I found out I was sitting next to the organizer! But she was great….
I would be surprised if MUCH of what we learn about ME/CFS does not apply to FM as well. In Dr. Bateman’s experience these two diseases are on a continuum. If you have significant pain and fatigue and have been diagnosed with FM you would surely be on her continuum.
If you are worried about missing info like this you can subscribe to OMF newsletter.
Cort has indeed been kind (and brave 😉 ) enough to bring this info to us early by sneaking in, but OMF always makes sure patients get to find out their research progress. I am certain you don’t need to be scared we would have never found this out.
I thought I was unique, but I have a twin in the world!
Dr. Bateman talks about a patient who was running high school cross country in 1979, became ill. Had to give up exercise, because it made her feel sick afterwards.
Struggled through college, tried teaching, but had problems being upright. Misdiagnosed with a psych disorder.
That’s the story of my life. Just change the year to 1978.
Cort, thank you so much for sharing this! This is so much appreciated from the ME/CFS Community and I just want to personally thank you.
Dr. Bateman and Dr. Davis are truly world class individuals that we’re very lucky to have continuing to advocate for this devastating disease.
I had one question regarding Dr. Bateman’s remarks with sleep and attributing to the concept of central sensitivity. If this is indeed attributing to the sleep problems with ME/CFS patients, mind-calming techniques would be the remedies correct? I.E. – yoga, meditation, etc?
I ask because when I went to the Mayo Clinic in November 2017 (where I was diagnosed with ME/CFS), they shared their belief that this condition stems from Central Sensitization and they provided me a list of essentially mind-calming techniques to try and treat (I’m aware now how much Mayo still has for room in terms of ME knowledge). Unfortunately there was no impact on my symptoms or sleep after meticulously trying – so I would be curious to what Dr. Bateman would try and treat for sleep then if she’s aligned with that theory.
I found meditation helps somewhat but it really doesn’t help me fall asleep. Meditation helps reduce stress but doesn’t directly help me to sleep. I found it easier to stay awake another hour in a low light room and then go back to bed. Repeat as needed.
I have found listening to Binaural beats for sleep have allowed me to get 7-8 hours of sleep. They are on YouTube and for various lengths of time. I use at least the 8 hr ones. And there are hundreds to choose from. I’m bed/house bound 90% of the time. I’m on a sleep medication but was only getting about 5 hrs of sleep. So using the combo now and am going to ween off the medication to see what happens.
Thanks Cort for being sneaky and providing us with this info?
🙂
I went on HRT about 3 months ago, and find my sleep experience transformed. I can still have difficulty in falling asleep (though to a much lesser degree) but my sleep is a much better quality and I wake up feeling much more refreshed. Trying to wake/get up in the morning was hellish after insomnia and poor quality sleep, but it’s much easier now.
Ladybird, can I ask what HRT is?
I’m on HRT (Hormone Replacement Therapy) for menopause symptoms that were off the scale.
I do sleep better now the sweats and burning hot flushes that left me unable to breathe have stopped. But I don’t reckon my sleep is any better than it was before menopause. And I can’t say it’s helped other symptoms. In my case, HRT just dealt with the symptoms for which it was intended.
It seems to me that, although there are many commonalities, we all have different responses to this illness. Therefore it must affect something that interacts with all sorts of systems in the body. Because of this, my favourite theory is it’s to do with the systems that are supposed to be self-regulating – things we can’t have any conscious control over. Eg the hypothalamus and other things that control homeostasis in the body. My general temperature control is totally still up the spout, despite HRT. I have underactive thyroid, asthma, need to take antihistamines all year round and have hypersensitivity to alcohol, caffeine and adrenaline (in local anaesthetics). I briefly stop breathing in the night sometimes but apparently don’t have sleep apnoea (huh?). My digestive system varies from day to day, as does muscle strength/freezing and balance – though that’s not do do with my ears apparently.
So it seems that different systems are affected in different people and therefore different symptoms result – and different remedies are needed. That’s why I prefer the theory about homeostasis not working. That’s just my A Level Biology and online research speaking, I’m certainly no expert – except perhaps for myself and my own symptoms and treatment.
In the absence of medical treatment, we all have to become our own experts with this condition!
So I’m finding this site invaluable. Many, many thanks Cort!
My diet has improved since reading your articles and following the links. I’ve given up added sugar and processed carbs but can’t give up carbs completely as it makes my skin flake off! Bizarre or what?! However, I’m really enjoying eating seeds, nuts, goat’s cheese, fruit and veg as well as favourite things like meat, eggs and porridge from my previous diet.
The amazing thing is I’m managing to loose weight at long last – even though I can’t exercise. I’ve also found drinking salted, filtered water (1 Litre a day) helpful for dizziness and brain clarity. And I actually like it – I just add a little stevia for sweetness. It was on the article about blood volume.
It seems I’m one of the lucky ones who found a medic quite early (after a few false starts!) who understood the importance of pacing. That really is the key for me. However, I’ve moved house several times since then (relapse warning!) and in this latest place I haven’t even brought up the subject of ME/CFS with my current GP. I’m a coward! But I’m lucky to have understanding family and friends – most of them anyway! 🙂
Forgive my ignorance but could someone explain what central sensitivity is?
Central sensitization is over-activation of the circuits in the brain that process pain and other stimuli which makes it hard to rest and sleep. There is also increased sympathetic nervous system activity which does the same.
Central sensitization in a concept that comes from pain research, used in attempt to explain increased sensitivity to pain.
There have been attempts, outside of scientific research, to apply the concept to other contested and poorly understood conditions such as CFS, IBS, fibromyalgia, etc. Used this way, it’s bordering on a biopsychosocial concept with no real evidence, and I’m actually horrified to see a CFS clinician use it.
I presume that you aren’t aligned with Dr. Bateman then? I know what you mean, but I’m also curious just based on how renowned Dr. Bateman is.
I’m not sure what you mean by aligned. I disagree with any clinician that attempts to use central sensitization to explain anything other than abnormal pain nociception. There’s just no science to back up such claims.
I don’t understand your objection. There are millions of unproven hypothesis (they are hypothesis because they are yet to be unproven, after all) and central sensitization is just one of them. It is a hypothesis even in pain medicine I think, and it is neurological, not “biopsychosocial”.
I understand the history of abuse. But rejecting anything that even remotely conjures psychology will only do a disservice for the research and the patients.
Yes, central sensitization, and central sensitivity syndrome, are just hypotheses and have no place in clinical practice. It will need years of research and translational work before this, which is a large reason why I’m horrified to see a well known CFS clinician use it. There’s already enough pseudoscience in clinical practice with CFS, we don’t need more.
Sorry, but central sensitization is treated as a biopsychosocial concept.
http://www.empr.com/aapmanagement-2016/the-biopsychosocial-model-to-chronic-pain-treatment/article/524998/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1820749/
It’s even attractive enough of a concept in this context that Peter White has attempted to draw a line straight between central sensitization and psychosomatic disorders, which they consider CFS to be.
https://www.ncbi.nlm.nih.gov/pubmed/25598410#
I vehemently reject any psychological approach to ME as it is what truly harms patients.
Please cover all the bases Weyland. I’m not sure about behavioral means of treating central sensitization. I do know that behavioral means can be quite helpful in helping people with chronic pain. I include by the way, meditation and mindfulness practices in behavioral means.
But central sensitization is also treated with drugs such as Lyrica which has been shown to calm the microglia down and reduce the activation of pain pathways and tools such as transcranial magnetic stimulation which do the same.
In that article you post White characterizes central sensitization as having a physiological origin:
“Functional somatic syndromes are common and disabling conditions that all include chronic pain, and which may be related to central nervous system sensitisation. Here, we address the concept of central sensitisation as a physiological basis for the functional somatic syndromes.”
It should be noted that people with autonomic nervous system diseases can benefit from “behavioral treatments” that slow the breathing and calm the mind and body down. In fact, the ANS – which is clearly involved in ME/CFS and FM is a system that can be directly modified by “behavioral” activities.
The point is that behavioral activities whether they are associated with pain, cardiovascular illnesses, even autoimmune illnesses – See the Nakazawa series of blogs on this website – can be helpful.
“It should be noted that people with autonomic nervous system diseases can benefit from “behavioral treatments” that slow the breathing and calm the mind and body down.”
I can follow both weyland’s and Cort’s point:
* Cort’s point; things like pacing is a form of behavioral treatment: change your behavior to take into account your very low energy levels and very long recuperation times; it does work well!
* weylands point; 9 out of 10 times or worse the behavioral treatments are just voodoo science forcing to do just the opposite as what is helpful, causing massive physical damage to hordes of patients and justify widespread patient abuse by health care professionals and insurers.
Thanks for the link, weyland. I read both and I’ll just comment on the first that seems more controversial.
The article states that “The concept of central sensitization posits that once an injury occurs, pathways become sensitized and hyperexcitable.” Even in this biopsychowhatever model, they clearly states that the central sensitization is a neulogical concept. And that they are using it as part of their model does not make it biopsychosocial concept.
I think it is unfortunate that we are so sensitized to the psychobabble that some charlatans parade, that we reject anything that the psychiatrists make use of as psychological.
Hi, my diagnosis from Mayo Clinic Rochester was Central Sensitization resulting in symptoms of CFS and Fibromyalgia. Central Sensitization, while originally from pain research, is now understood at Mayo – who are a conservative organization – to be an over-sensitized nervous system with many possible precursors. They freely admit that it is unknown if the symptoms are rooted in pathological cause or epigenetic response to a substance or trauma, and only offer ways to reduce symptoms. If Mayo feels comfortable using it this way, so should Dr Bateman…and as someone who’s life turned around thanks to this approach, I’m horrified that you would attempt to undercut it like this. Here’s what I’m backing this with: “In 2010 Nijs et al.[19] provided guidelines to aid the recognition of central sensitization on musculoskeletal patients.
In their paper, they suggest that a patient’s medical diagnosis can offer insight into the likelihood of the presence of central sensitization (fig 1) and this in conjunction with observable features (fig 2) can inform the therapist as to the presence of central sensitization.” The observable features are the same symptoms presented by CFS patients. https://www.physio-pedia.com/Central_Sensitisation_/_Sensitization
(Cort, this comment seems to have gotten lost somehow. If it wasn’t received previously, please have this one posted).
Thanks for the link, weyland. I read both and I’ll just comment on the first that seems more controversial.
The article states that “The concept of central sensitization posits that once an injury occurs, pathways become sensitized and hyperexcitable.” Even in this biopsychowhatever model, they clearly states that the central sensitization is a neulogical phenomenon. And that they are using it as part of their model does not make it biopsychosocial concept.
I think it is unfortunate that we are so sensitized to the psychobabble that some charlatans parade, that we had to reject anything that the psychiatrists make use of as psychological.
So Gad you could provide us with the info from this conference. Any updates on the Cortene trial?
cort, so glad that you could attend this conference.this kind of information is encouraging!…on another note- there are people who became ill with me/cfs at tahoe earlier than 1985. myself in 1982, and a friend of mine in 1984. so i have to assume that there are more.
I visited Tahoe in November 1981 and ended up with CFS as well. I remember being bitten all over by some no see em mite.
How can we duplicate this on doctors forums, talks???
Appreciate this, Cort! I am severely affected, housebound, mostly bedbound, isolated due to more severe sensory overload… but can still walk to the kitchen. Dr. Davis’ finding on little to no viral activity in the severe patient study agrees with my experience, as I have gotten a cold or flu maybe two or three times in the past 16 years. I began to get symptoms a couple of times, only to have them leave within mere hours, while my husband was sick for 2 weeks. My immune system blows them out! Unfortunately, the latest new thing my daughter (same level of functioning as me) started is Pridgen’s combo with patient X (see Cort’s blog), and I was planning on starting an antiviral (first time) hoping for some help, for a while at least. After 4 months, my daughter is no better. Dr. Davis’ findings on viral activity in severely ill ME/CFS patients seem to indicate this is a dead end treatment idea for us. What a bummer!
Here’s a question: Are enteroviruses that Dr. Chia looks for and treats, which don’t show up in the blood, considered by Dr. Davis? Or not? If it’s due to a strong overactive immune system, would they also be hard to find? Is it to be assumed that severely ill PWCs then would also not have evidence of enteroviruses, and thus not respond to Chia’s treatments, and Equilibriant? Any thoughts?
I’m just a laymen. I don’t know about enteroviruses but I believe Dr. Chia believes forms or fragments of enteroviruses are left in the muscles. I don’t know if they would show up in the blood or not.
It’s not a belief, enterovirus RNA in ME muscle tissue is a replicated finding at this point.
OMF has recently finally acknowledged that this enterovirus RNA may not survive long enough in the blood to be detected, presumably due to RNAse degradation. According to their statement they haven’t even yet figured out how to approach this problem.
https://www.omf.ngo/2018/04/11/the-hunt-for-elusive-pathogens/
Firstly, severe ME patients do have evidence of enterovirus and Dr. Chia himself has documented this in a severe patient of his that committed suicide. He found the virus itself in his brain tissue. I am unsure of his overall success treating severe patients. In the example above, the patient unfortunately did not respond well to pretty intensive antiviral treatment. There are no highly effective antivirals yet for enterovirus, so immune modulation has to be used which is just not as effective, especially in an ME patient.
Dr. Davis unfortunately so far has decided not to perform any enterovirus serology testing in his research, which is inexplicable. This testing is a cornerstone of Dr. Chia’s clinical protocol and, with limitations, can indirectly show the presence of an enterovirus in the body.
OMF started by looking for DNA viruses because it’s the low hanging fruit. Cell free viral DNA in the blood is not as fragile. Viral RNA in the blood is highly subject to enzymatic degradation by RNAse, the activity of which is increased in several diseases, including ME.
OMF has recently stated that they still aren’t even ready to begin looking for RNA viruses such as enterovirus and they’re still trying to come up with a means to do so. Their journey to look for viruses in ME hasn’t even yet begun.
https://www.omf.ngo/2018/04/11/the-hunt-for-elusive-pathogens/
I don’t buy a singular viral cause at all. I think all sorts of viruses can trigger the illness, but not one in particular.
Dr. Davis is doing all he can with the funding he has. He definitely plans to look for RNA viruses.
I have a far greater weakness to a variety of virus then bacteria. I have a simple observation:
During the night virus become much more active with me then during the day. I have for example a viral scar as my doctor calls it. The speed at with it can grow at night from hard to notice to filled to burst with virus loaded liquid is amazing: 1 to 2 hours. A simple cold invades me also in a few hours at night and withdraws largely during the day.
Colds behave also like a half retrovirus in me: I can have no cold for weeks but be outdoors and get a cold draft on my neck or chest and boom: instant cold that night. Even if I did not meet a single person that day and don’t know a single person that has the cold.
I think it might be interesting to look into this.
So much great information. Interesting that Dr. Davis believes CFS is a metabolomic issue. I wonder if samples obtained from the “all of us” research program can be used to test the levels of metabolites in healthy people and in people with CFS.
On omega 3s out of balance with omega 6s, I am fairly sure from my early self-experimentation and the work of an early CFS doctor, Dr. Martinovic, that there is over-utilisation of omega 6s. This fits with other drivers of cyclooxygenase activity suspected in CFS and ME. I would be interested in identifying eicosanoid involvement in connection with this.
Really great read Cort – thanks so much for your effort in getting in to this conference and writing an excellent post covering it all for us. Very interesting. Love your writing!
I’m trying to wrap my head around this idea of over-active immune system blasting out viruses etc – I don’t get sick much myself and so this makes some sense to me, but when I do get sick, it can be bad and without fail it crashes me terribly for 4 months afterwards. Still trying to understand what’s going on here..
Has anyone studied how stem cells can help ME/CFS?
Helen, I’m with you! We need this guy to try out this procedure on one of us. I’ll even volunteer, having not much to lose after a lifetime with this illness. They are curing every autoimmune disease known to man with this procedure. And some insurance plans actually cover it.
https://www.stemcellresearchfacts.org/dr-richard-burt/
Hi Cort
Has Prof. Davis advanced the Nanoneedle to 17 patients ?
Last time he mentioned 10 patients
I’m pretty sure they’ve tested at least 20 patients so far.
Wow Janet thanks that is really amazing !!
Nice reporting, Cort. It’s great you are killing two birds at once by combining traveling and work.
There was a paper a couple years ago that measured the cytokine levels in athletes every hour after an intense exercise and showed how the exercise triggered immune system commotion for several days The resulting pattern surprisingly looked like what CFS patients go through after an exercise.
I think the non-invasive inflammation meter that Davis is working on, if it ever materializes, a big if, could go a long way in unraveling the mystery of CFS and managing the symptom. The standard cytokine panel takes too long, too expensive and too invasive for a real time use. A meter that can read out the values in real-time will be infinitely more practical and could serve as a fatigue meter. It’ll have to be highly sensitive though, since it is not really the inflammation magnitude, but likely the hyper-sensitivity to inflammation that causes CFS.
As for the severely ill patients being “clean”, that is probably because they are home-bound. I didn’t catch any cold or flu for several years when I got sick with CFS. (I used to say “I never got sick ever since I got sick”). Now that I’m a bit more socially active, I’m starting to get them again.
Really interesting article Cort. I’m particularly interested in the comment about the possible genetic link with autism as I have sons with autism and another with severe ME, I also have fibromyalgia and possible milder ME, with other autoimmune issues and autism in the wider family. My husband and his wider family appear to have no such problems. I would be very interested in the gene and if it could be tested for. Do you know what it is?
I don’t know about the genetic link but I do know that Naviaux has said that the metabolomic results in ME/CFS and autism are quite similar and that he believes the two are linked – one occurs earlier in life and one later. Your case certainly suggests a genetic connection may be driving those metabolomic similarities.
Cort, thanks again for all your work with this.
In regards to Transcranial Magnetic Stimulation (TMS) helping with a subset of patients that may support the Central Sensitization theory, is there any written/published evidence? Or mainly just anecdotally at conferences or symposiums and such?
I ask because the Mayo Clinic advised possibly on using TMS as a treatment method – albeit it was from a very preliminary external study. So I was just curious where you have seen it from.
Many thanks again
Did the big data study test Mitochondrial functioning? If so, do we know the results…
I am a very severe bedbound patient in Australia.. I have had a muscle biopsy done and I believe the tissue should be still at the hospital… Cort or Janet would Dr Tomkins be interested in using this tissue for their studies? I could try to get it sent…
I,too, have autistic children. I am a 16 year CFS veteran. I thought that the difference between us had something to do with hormonal changes, with the boys having testosterone from the get go along with neurological dysfunction, and when my estrogen began to recede in my mid-40’s, my testosterone levels increased on a relative basis and my “adult onset autism” kicked in.
Cort, I am 78 yrs old, retired FNP, onset 6yrs ago of FM immediately after unavoidable 15 min. exposure to bromine and Chlorine. CFS followed within a few weeks., then with dysautonomia & SEID. Now w/ MCAS usually food/allergy related. Treated by MD in Mill VAlley after I understood that there was no physician in town where I lived, who had any real experience. I started on very low cho diet, Guaifenisine& acetominophen BID . cut pain by 60% This is the Dr. St. Albans UCLA protocol from the 60’s. I also take multi antioxidants and stinging nettles for MCAs, I sleep well now, but have to PACE myself exersizing. Still very limited. Thank you for staying with ME research. I live in Tacoma WA, Are you aware of any MD here or in Seattle for ME ?
Hi Linda,
Congrats on finding some things that help. I’m afraid I don’t know of MD’s there – there probably are some – I just don’t know of them.
Stay tuned, though. Health Rising should be to help with finding doctors pretty soon.