The Newcomer
Phair came to this disease like many others have – he knew someone (a neighbor) who had it. When a piece on ME/CFS by Tracie White showed up in the Stanford Alumni magazine in 2016, he contacted Laurel Crosby in Ron Davis’s Stanford lab and has been volunteering ever since. He noted that, “Without that story, I wouldn’t be here.”
Phair got involved in Ron Davis’s work after reading about it in the Stanford Alumni magnazine
Without that story, we wouldn’t be talking about a new hypothesis for chronic fatigue syndrome (ME/CFS) – one which could – we’re a long way off from demonstrating this – but one which could, if it’s correct, offer a cheap, simple and quick solution to ME/CFS.
That’s the power of sharing. The more sharing – the more we spread the word about ME/CFS – the better chance we have of finding the person who produces the breakthrough that turns this disease around. Who knows? It could be Robert Phair…
Weird Data
Robert Phair had chanced on something that nagged at him. It was a metabolic result in the Severe ME/CFS Patient study that just didn’t make sense to him. Many of us would probably move on to what we did understand, but the disconnect really bugged Phair.
As Ron Davis later explained, it’s often the oddball results that intrigue good scientists. They’re more interested in what they don’t know than in what they do. When something doesn’t fit their conceptions, it bugs the heck out of them. They feel compelled to figure it out.
The saga of the ozone hole demonstrates how ignoring anomalous data can have severe consequences. Atmospheric researchers had been getting and deleting weird data from the upper atmosphere in their models for years. Because it didn’t fit their conceptions, they simply assumed it was an outlier and eliminated it. Doing so for much longer, they later realized, could have had enormous consequences – the data actually indicated that a hole in the ozone layer was forming.
When Phair dug into his strange data, it ended up opening a new world for him — and perhaps for us, too.
When Phair turned his attention to some anomalous data a “metabolic trap” was revealed
In a way, it was no surprise that Phair dug in the way he did: figuring out answers to complex biological questions is what he does for a living. Phair is an engineer and biologist who’s made a career out of understanding the functioning of complex systems. Phair’s company – Integrative Bioinformatics – uses a process called mechanistic kinetic modeling, which allows researchers to test complex hypotheses against experimental biomedical data. The mathematical descriptions of those systems that kinetic modeling creates allows researchers to assess the dynamics of those systems; i.e. to describe how they work and how they can be changed.
A “Metabolic Trap” Emerges
As Phair dug deeper into the possible causes of the weird data, a “metabolic trap” – a kind of biological sinkhole – opened up before his eyes. Once the process – which involved amino acid oxidation – started, he saw no way for an ME/CFS patient to get out of it without outside help (e.g. a treatment). Looking further, he and Davis realized it could conceivably explain some fundamental symptoms in ME/CFS.
Since then, he’s been creating model simulations to test his hypothesis. Thus far, he’s created kinetic models of the central metabolic systems in the body (mitochondrial electron transport chain, TCA cycle, fatty acid beta oxidation, amino acid oxidation, glycolysis and pentose phosphate pathway, purine synthesis and degradation, and NAD synthesis).
It would be impossible to escape Phair’s metabolic trap without help
Using Davis’s genomics data from the Open Medicine Foundation’s Severely Ill Big Data Project, Phair has examined the exons (the part of the DNA which actually codes for proteins) of 100-plus genes involved in energy production. First, a variant commonly found in the general population — but which was more commonly found in ME/CFS — popped up. Digging deeper two more gene variants were found.
I asked Phair if he had finished up the genetic testing – the answer was far from it!
No. Most CFS investigators focus on rare SNVs. To me it’s just a matter of logic that predisposing genetic factors for ME/CFS must be common, not rare, in the population. Otherwise you can’t explain the many well-known CFS epidemics like Incline Village and Lyndonville. The downside of this logic is that common mutations are common! So, we still have many thousands to examine. Fortunately, we have colleagues at Stanford and at Harvard who are great at big data analytics.
There are two sides to modern systems biology – the mechanistic hypothesis testers like me, and the statistical hypothesis generators – like all the AI ads you see on your devices. We think these two groups of researchers should be working together on tough problems like ME/CFS.
Further analysis suggested that these gene variants may significantly, and in a negative manner, impact the functioning of key enzymes that process important metabolites involved in energy production, brain and immune functioning. When Phair added the impaired enzyme functioning to his metabolic modeling to determine if it could account for the strange metabolomic finding, he found that it could.
Testing the Hypothesis
That hurdle passed, it’s time to test the hypothesis experimentally — something, Davis noted, that Stanford has the tools to do. (Stanford was recently rated the third best medical research school in the country.) Davis and the OMF has made testing Phair’s hypothesis a major focus.
The team will use “tracer” metabolites to determine if the cells with these mutations are, in fact, functioning less effectively. Phair said they should know if the metabolic trap is present in the white blood cells of ME/CFS patients by the end of summer.
The potentially very big news regarding Phair’s metabolic trap is that, as noted above, if it works out – Ron cautioned that’s a big “if” at this point – it could conceivably lead to a cheap, fast and effective treatment. It might also be able to help explain how some autoimmune diseases occur.
Because the treatment strategy would involve tweaking one of the major systems in the body, though, it has the potential to do either good or harm. Worried that in the wrong hands, it could backfire – making ME/CFS patients worse – Davis and the Open Medicine Foundation are keeping the details of the possible metabolic trap under wraps until they know more about it.
Looking ahead, I asked Phair what’s next if the “metabolic trap” hypothesis passes the next hurdle?
If the metabolic trap can be demonstrated experimentally in cells from CFS patients and not in healthy controls, we’ll begin the search for ways to return such cells to normal. With a little luck, as Ron says, this might turn out to be the easy part.
The tougher question is what’s next if we cannot demonstrate the metabolic trap in these easily obtained blood cell types. People tend to think one cell is as good as another, and for genomics that’s true, but there are well over 300 different cell types in the human body, and it’s likely that only some of them are affected in ME/CFS. But which ones, and how can we get those cells to study?
Maybe we’ll have to move to stem cells. Our current thinking, though, is that we should be able to induce the metabolic trap in cells carrying the mutations we’ve identified. So that’s the first backup plan.
Oh, and it’s always possible the metabolic trap will turn out to be “a beautiful theory destroyed by an ugly fact.” I wake up many mornings thinking of another reason I might be wrong – then I try to find a way to test that possibility. It’s how science works.
Phair has put out a call for whole genomic data from ME/CFS patients.
Whole Genome Data
We are seeking CFS/ME patients who have had their genomes sequenced and who would be willing to share their data for research purposes.* Your data would help us test theories about gene variants that may have predisposed you to developing CFS/ME when you encountered the infection or other stress that was the cause of your case of CFS/ME. We cannot provide feedback or use the data in studies. Nevertheless, confirmation or refutation of what we find in professionally acquired and processed WGS or exome sequencing data could help us a lot in our search for something that helps every ME/CFS patient.
You can reach me at rphair@integrativebioinformatics.com. I am working on CFS as a volunteer because I have a friend with the disease and another friend whose son is severely ill with CFS. There is no charge for my work on CFS.
Your data would be most comprehensive and powerful in the form of .VCF (Variant Call Format) file but we will work to find a way to analyze your data in any format you are able to provide.
Please also tell us your age and gender and write a paragraph or a page with a description of how you came down with ME/CFS. A list of current symptoms is optional, but desirable.
*23andME, Ancestry.com do not do whole genome sequencing but could be helpful. Find out about WGS here. Companies that do it include Illumina, 10xGenomics, Veritas, and Qiagen. As of 2016 a whole genome sequence from Illumina or Veritas costs about $1,000 but Illumina hopes to bring the price down to $100 in the next 3-10 years.
Robert Phair on using 23andME/Ancestry.com
23andMe covers only 3 of the five variants that are important to the current metabolic trap hypothesis. So 23andMe data sometimes works and sometimes has insufficient information. The 23and Me file that I need has a filename like this: genome_firstName_lastName_Full_date_time_in_digits.txt
so if it was mine it would be something like
genome_Robert_Phair_Full_20180315085441.txt
.zip instead of .txt is also fineIf you can open the file in a text editor it should begin with a header that looks like this:
# This data file generated by 23andMe at: Wed Jun 14 12:04:30 2017
#
# This file contains raw genotype data, including data that is not used in 23andMe reports.
# This data has undergone a general quality review however only a subset of markers have been
# individually validated for accuracy. As such, this data is suitable only for research,
# educational, and informational use and not for medical or other use.
#
# Below is a text version of your data. Fields are TAB-separated
# Each line corresponds to a single SNP. For each SNP, we provide its identifier
# (an rsid or an internal id), its location on the reference human genome, and the
# genotype call oriented with respect to the plus strand on the human reference sequence.
# We are using reference human assembly build 37 (also known as Annotation Release 104).
# Note that it is possible that data downloaded at different times may be different due to ongoing
# improvements in our ability to call genotypes. More information about these changes can be found at:
# https://www.23andme.com/you/download/revisions/
#
# More information on reference human assembly build 37 (aka Annotation Release 104):
# http://www.ncbi.nlm.nih.gov/mapview/map_search.cgi?taxid=9606
#
# rsid chromosome position genotypeThis will be followed by many thousands of lines each corresponding to a single genetic variant.
Ex-Weightlifters / Bodybuilders
Phair is interested in knowing the supplement intake of ex-weightlifters or bodybuilders as they came down with the disease. He’s also interested if anyone doing these activities was taking in any extreme amounts of one particular food or drink.
Regarding this question, Phair said he was asking more out of curiosity than necessity. For me, I’ve always been interested in the number of people who were workout nuts – as I was – who fell prey to ME/CFS. Phair said:
I have a hunch surrounding people who train hard and fall victim to ME/CFS, but I’m not in a position to test that hunch in patients. I’m in the gym 6 hours a week myself, so there’s a kind of camaraderie behind my question. The stories of athletes in films like Unrest contain just as many new clues as do the more frequent stories of the first crash.
To me understanding crashes is critical. One of the most compelling features of the metabolic trap is that it provides a straightforward explanation for the initial crash. I’ll read every response that patients might share on these issues, because you never know when unexplained details you’ve been storing for a long time will suddenly merge into a simple theory.
We cannot use data acquired this way in our publications, because we can’t vouch for the diagnosis or the sequencing pipeline. And two, we cannot provide feedback to individual patients who send us their whole genome VCF files. Nevertheless, confirmation or refutation of what we find in professionally acquired and processed WGS or exome sequencing data could help us a lot in our search for something that helps every ME/CFS patient.
Conclusion
Davis and the Open Medicine Foundation must be happy to see the Severely Ill Big Data Project already paying dividends: the “metabolic trap” hypothesis was birthed out of it.
Phair’s growing presence at Davis’s lab is notable for several reasons. Phair’s definitely got some skin in the game – he’s got a friend with ME/CFS – but it’s clear two years into his work on ME/CFS that intellectual excitement is a big driver. Having folks like Phair and the Cortene team find fertile ground in ME/CFS is good news indeed for a field that needs as many bright minds as possible.
On that note, sometime this year, Davis and the OMF will start making data from the Severe ME/CFS Big Data project available to outside researchers. We’ll see what other ideas it may spawn.
Do relapse/remitting ME/CFS patients fit this hypothesis? Is it possible to fall in and out of the “metabolic trap”?
Great question. Unfortunately I have no idea…What an interesting subset you are in! For me it’s pretty darn boring…
Interesting. as someone who newly is suffering from this illness I like to mention that something stuck out to me when he said bodybuilders Informer weightlifters. Before I got sick I was under a difficult amount of stress and I also was a big weightlifter in the gym it was my favorite hobby I was always in the gym pushing myself to the Limit and I have an idea that that has somehow contributed to my illness
John,
Thanks for asking. There are two scenarios in which the metabolic trap could produce a relapsing/remitting form of the disease. But it’s still just a theory until we do some experimental tests.
Dr. Phair. I carry a diagnosis of Andersen Tawil syndrome. It is an intermittent periodic paralysis. Mitochondrial dysfunction is frequent among patients with ATS. I am constantly researching for information dealing with the disorder to share with others in my facebook group. Many in my group carry comorbid mitochondrial issues and would likely qualify for a diagnosis of ME CFS. I also have my genetic data. Within a few days of looking through my data and running different livewello templates I discovered I have a pathological mutation for ampd1. I then decided I should check to see if I also have issues with atp1a2 electron transport. Sadly my data didn’t translate and was seen as abiguous. However, with a little more looking I discovered this information. An atypical presentation of periodic paralysis that is responsive to coq10. https://www.researchgate.net/publication/315507524_Hypokalaemic_periodic_paralysis_due_to_a_novel_ATP1A2_mutation_a_new_periodic_paralysis_gene. Every step I take I have so many more questions. I do have genetic data through Genes for Good that I am willing to share if you are interested. There may be some others in my group of facebook members who possibly would share as well.
Interesting as some people with ME sometimes have a kind of paralysis.
Responding to Cort and Karen – paralysis is also common among people who have developed mold sensitivity and/or were demonstrably exposed to toxic molds. I experienced that; it has stopped since I started a technique called mold avoidance. For what it’s worth, I have been diagnosed with fibromyalgia by several doctors and ME/CFS by others.
Ha….I was thinking of Julie Rehmeyer…
I love your philosophy that you never know where the answers might be found.
My illness started in 1985
With mono/EBV and also a ruptured ectopic pregnancy. I was very ill for 8 years and never regained my baseline health. I was always very athletic and active in various sites and outdoor activities. I have T-Cell LGL leukemia AND sIBM. I’ve had genetic testing: mitochondria DNA, testing for a UT research project for people with multiple food and chemical sensitives performed at Emory University, and 2 generic tested for MD. I also have muscle and bone marrow biopsy results. Would any of this help you with your west for answers? I’m a patient of Dr. Bateman here in SLC.
Thanks for all you are doing Dr. Phair I have a few questions & points I want to bring to your attention one is I am seeing some now being diagnosed with either (SPS) Stiff Person
Syndrome or (PERM) Glycine Antibodies are you able to look into this in your work there? Also there are people now testing Positive to a new blood Genetic test put out by Dr.
Joshua Milner Team from the NIH-NIAID also he put out some Videos for awareness now on YouTube under tryptase I think there are now 4 or 5 Videos the test they found they have 2,
3 or 4 copies of the tryptase Gene inherited at Birth from each Parent I heard they are now trying to Block tryptase & also seeing if 2 of the new Arthritis medicines could be
helpful in the lab in mice the test is in a Houston Texas lab results take about 3 to 4 weeks cost is $169.00 they require an MD referral as it is a Genetic test carried out the site
is here key in tryptase on the Home page http://www.genebygene.com & also I have seen a full recovery a Military Male Nurse was treated by Army Doctors they even Published saying he had
Sero Negative Q Fever so I wonder if we have this undetected he was treated 18 months CDC both antibiotics & fully
recovered from illness, I also heard of a Woman with an infection in her ear with CFS a waterborne parasite they say is huge in Asia I believe it was the Philippines she got
infected I have heard Viet Nam vets would bring this back with them & transmitted it to other people in North America…You mentioned about products we took prior to
becoming Sick I was Boxu=ing in top condition I was using pure Brewers Yeast so maybe this did something to my system back then I have CFS Fibro EDS3 as well recently diagnosed
this is my email here mraidangwalsh@gmail.com…thank you & all the best in your work God bless you 🙂
Insulinoma is also being diagnosed & missed in many so are Brain, Sinus, Spinal fluid leaks as well Ian Carrol Stanford Pain Clinic also Duke University Radiologists find these as well in CFS Fibro EDS patients & last ‘crossovers’in EDS some have multiple types from EDS3 with VEDS or EDS3 & Tenascin X etc
Glucagon Stimulation testing for Hypopituitarism found in numerous in UK Endocrinology the Team now continuing their work in Dubai on large amounts of patients so something wrong with the Pituitary also years ago Dr. Mark Demeitrick
Published one of the best ME/CFS papers on ME/CFS on the Hypothalamus I believe…Cortef also used in Montreal Endocrinology years back small doses 5 mg in Published CFS
work Dr. Beverly Pearson Murphy was involved in this trial & she said it is not Depression they also used Cortef in patients with depression nonresponders to antidepressants & a Patent was filed as well…Small dose 5mg Cortef max 10 mg a day
Kia ora Robert. In regards to your interest in athletes my 10 year old son (from New Zealand) was doing up to 4 hours a day of rugby league, running, wrestling and jiu jitsu when he came down with CFS. He wanted to become a professional sportsman. He had Epstein Barr & CMV virus simultaneously 6 months prior to this. He was bed bound for months. 15 months later he can sometimes attend school for a few hours but if he does any physical exercise he crashes hard. Obviously he was not taking supplements! he also eats 10 fruits & veges a day as per gut health diet and eats plenty of meat and fish and dairy protein. Thank you so much for your work it gives us hope that he may regain his life.
I also have remitting/reoccurring ME/CFS. The first big occurance happened when I was 16 and worked a summer job – on my feet all day. The second was in college walking everywhere and staying up late studying. I’m now 55 and can trace each crash – with recovery taking longer each time – to a major life occurance involving increased physical and mental stress. Each crash has left my periods of remittance more debilitating. Following a big crash about 5 years ago, I was severely ill for two years – bed bound most days. While I have recovered enough to go back to work, that is all I can do. I can’t walk more than 50-100 yards most days and half of my work is completed in a recliner. I would like to do whatever I am able to assist in research. I will check out the full gene testing and send results when I can. Thank you for helping us!
I too can trace each big crash to a life occurrence that put me under physical and/or mental stress. It occurs when I just keep pushing and pushing myself.
I wonder if that is what happens in the cases of athletes who develop ME, and if it is not only illness that causes ME to develop but anything that puts you under strain. So, illness puts your body under strain, as does exercising a lot, as do life events.
I felt into the trap many yeas ago (15) and then relapsed after antibiotics.
John, I wondered this too when I first read about the metabolic trap hypothesis. I’ve also wondered if the hypothesis might be an explanation for why some treatments like LDN tend to work temporarily for ME/CFS patients, and then “stop working.” I know this is a common issue. It’s happened to me more times than I can count.
I’ve had my 23&Me done, but I don’t think that’s a whole genome thing. What kind of genomic testing is helpful?
I think 23andME is whole genome but I will check with Robert.
Unfortunately, it is not. They inly do parts of genome that are most known, to keep the costs affordable for customers
Hi Cort, I’m feeling desperate?
I had 23 and Me done. How can I get my results over to you.
Hi Nancy,
I wish I could help but I’m not up on genetic testing. I am, however, getting my results done by SelfDecode and I will report on it. I will do a blog then on how to interpret our genetic test results. If I don’t do that second part please remind me 🙂
Aaron, Thanks for asking. 23andMe does not do whole genome sequencing. Instead they measure genotypes at a large number of well-documented single nucleotide variants (SNVs). For the metabolic trap hypothesis, only some of the key variants are covered by 23andMe, so for some patients I can tell if you fit the hypothesis and for others, there won’t be enough information in just 23andMe.
Robert – thank you so much for your work on this horrific disease. To not bombard you with unhelpful information can you provide more details under what scenarios you would like our 23andme raw data?
Margie and Aaron, 23andMe covers only 3 of the five variants that are important to the current metabolic trap hypothesis. So 23andMe data sometimes works and sometimes has insufficient information. The 23and Me file that I need has a filename like this: genome_firstName_lastName_Full_date_time_in_digits.txt
so if it was mine it would be something like
genome_Robert_Phair_Full_20180315085441.txt
.zip instead of .txt is also fine
If you can open the file in a text editor it should begin with a header that looks like this:
# This data file generated by 23andMe at: Wed Jun 14 12:04:30 2017
#
# This file contains raw genotype data, including data that is not used in 23andMe reports.
# This data has undergone a general quality review however only a subset of markers have been
# individually validated for accuracy. As such, this data is suitable only for research,
# educational, and informational use and not for medical or other use.
#
# Below is a text version of your data. Fields are TAB-separated
# Each line corresponds to a single SNP. For each SNP, we provide its identifier
# (an rsid or an internal id), its location on the reference human genome, and the
# genotype call oriented with respect to the plus strand on the human reference sequence.
# We are using reference human assembly build 37 (also known as Annotation Release 104).
# Note that it is possible that data downloaded at different times may be different due to ongoing
# improvements in our ability to call genotypes. More information about these changes can be found at:
# https://www.23andme.com/you/download/revisions/
#
# More information on reference human assembly build 37 (aka Annotation Release 104):
# http://www.ncbi.nlm.nih.gov/mapview/map_search.cgi?taxid=9606
#
# rsid chromosome position genotype
This will be followed by many thousands of lines each corresponding to a single genetic variant.
Thanks for asking.
Many of you have sent me 23andMe data, which I really appreciate. Recently, I received my first version 5 (v5) 23andMe data set from a CFS patient and to my surprise, 23andMe v5 appears to be no longer measuring ANY of the 5 single nucleotide variants (SNVs) (aka SNPs) that are important to the metabolic trap hypothesis.
I did a brief search and found this post on Reddit
https://www.reddit.com/r/23andme/comments/3dd3lp/snp_coverage_analysiscomparisons_23andme_v3v4/
that compares 23andMe v3 and v4. This analysis asserts that each version both adds and subtracts SNVs. If someone reading this has the programming skills to verify this analysis and extend it to v5, that would be awesome.
So at least for my metabolic trap project, please don’t spend your money on 23andMe v5. It won’t help.
Also, if you’re thinking paying for sequencing data, I’d recommend whole exome sequencing, not the more expensive whole genome sequencing (WGS). Just sayin’.
Robert Phair, I am a patient with ME and I have the original 23andme genome sequencing version (I had the test done in 2013 before the FDA crackdown). I’m happy to send mine to you if you’re interested.
Robert – I’m also a former Ironman triathlete, with a PB of 12:00; marathon PB of 3:37. Within weeks of my second Ironman race in late 2009, I developed ME/CFS symptoms.
Sorry, catching up on the full thread, Robert. 🙂 I also had a period of “remission” (didn’t feel 100% but was much better) in 2013, where I was able to complete a 5:20 half Ironman, and 12:26 Ironman. During that period, I felt like I was not quite able to keep up with some of the people I used to beat, and I still noticed shortness of breath episodically with no asthma.
The whole genome DNA sequencing cost is more than $2K.
I think its admirable how many people want to contribute to Robert’s work :). I came across a 2016 article on Veritas which indicated they were doing it for $999. – https://www.genomeweb.com/sequencing-technology/999-whole-genome-sequencing-service-veritas-embarks-goal-democratize-dna#.WsTs7IjwbIU
Prices are rapidly falling. I got mine from Dante Labs at considerably less than that. Their prices fluctuate but generally around £500 (which I know is still expensive if you don’t have a personal reason for testing).
https://www.dantelabs.com/collections/our-tests
If you have episodes of paralysis email them before you pay normal prices though. They’re interested in finding currently unknown Periodic Paralysis mutations. Only if this is a clear problem for you though, we don’t want to muddy that data with a load of ME data!
(There’s considerable overlap between ME and Periodic Paralysis experiences so this is an alternative diagnosis to be aware of, though PP is rare)
Thanks a lot for the information.
I wanted to order 23andme in the next weeks, but if it doesn‘t include the SNPs that are important for the theory I won‘t order it. Does anybody know if there is another (maybe cheaper than the whole genome sequ.) alternative that would include the imporant SNPs?
Must be possible to be sent to Europe though :/
This work sounds fantastic. I thought i’d leave a comment as a former athlete & bodybuilder who now has moderate ME/CFS and is unable to work. Hopefully my story may give a few clues.
My first crash was a few days/weeks after I came down with a really bad stomach flu while abroad. Coincidently, i’d been for a run the night before I came down with it.
A week later after returning to the UK, I felt like i’d just about recovered from the stomach bug but could tell that a bit of fatigue was still lingering. I decided to go to the gym to try and shake it off but while dumbell pressing around 40kg on each arm, I felt an odd palpatation sensation and immediately became detached from my surroundings…my legs turned to jelly, vision and hearing went strange and I felt like I was dying. I stumbled to the changing room and called for a paramedic. It took about 45 minutes of laying down for me to feel normal ish again. I managed to return to work but for the next 2 years my energy declined and I kept having mini hypoglygemic episodes if I didn’t eat every 2-3 hours or walked too far. I still managed to go to the gym as long as I ate significant amounts of food pre-workout. Slowly joint pain set in and I found that I had to take energy bars with me even on short ish walks of 1-3 miles.
Eventually I had another mega crash at the gym while on chest press, but this time I never recovered and am down to about 30% of my pre illness energy level. I’ve always found that using my arms crashes me way quicker.
Supplements wise I was taking barely anything in the way of whey or creatine etc, maybe this is the problem? I was just eating very healthily, plenty of chicken, fish & rice, dark chocolate etc.
That’s very interesting Adam because I also experienced the hypo attacks and always had to take energy bars with me even if walking for only 30 minutes because I could crash so severely everything would go black and I would experience massive adrenaline attacks. Even now 18 years later I never go for a walk without a bar in my bag but rarely need it these days.
My illness started with 2 weeks of what I thought was flu but think now it might have been EBV. Things were never the same after that. It was 1979 and although I did get energy back I suffered with frequent vertigo and migraines. I picked up so many infections and viruses and by 2000 was in full blown ME. The hypo attacks started from 1996 after yet another gut bug. Campylobacter poisoning in 1998 finished me off I think.
Previous to this I was swimming 32 lengths 3 times a week as well as walking my 2 dogs twice daily plus I did part time teaching so I think you could say I was an active person before ME hit.
Adam this is very similar to me! I wasn’t a bodybuilder but I was very active. I was training a martial art hard, did yoga 2x/week, swing dancing, sometimes a jog, sometimes some light strength training.
The day of my first big crash that led to full-blown ME/CFS, I had spent a few hours that morning doing my martial art training. I was well hydrated but don’t think I ate quite enough.
I believe that I started having a severe hypoglycemic attack. Hypoglycemia seemed to arise concurrently with ME/CFS. Incredible weakness, glazed expression, inability to think/speak, heart pounding, dry mouth, feeling lightheaded and like I might pass out, numb/tingling in my mouth…all the signs. I eventually drank three glasses of orange juice and my friend called an ambulance. After the OJ I didn’t get worse, but I didn’t bounce back. In normal, straight hypoglycemia, when you get your glucose up you’re fine. But I just never recovered.
This was almost three years ago. Still sick from it. My vision immediately went wonky, I have visual disturbances like “visual snow” now, and PEM that is triggered both by over-exertion (so, I can’t do anything active anymore, ever) and also triggered by low blood sugar. Low blood sugar had *never* been a problem for me before! I have to eat every few hours, and if I get low, and eat quickly, it doens’t get that bad. I still feel crappy (because my ME/CFS baseline is of course not fun) but if I don’t get to food soon enough, it triggers a crash. Even after eating and getting my blood sugar back up, I don’t just bounce back. I have to lay there, not moving or speaking, for a while. It just wrecks me.
Wow! This story is so similar to mine although I wasn’t doing any exercise at the time. I came down with a really bad stomach bug on Christmas day of 1982 and my life has never been the same since. Prior to the stomach bug, I was a sugar addict and junk food junkie. After the stomach bug, I developed a severe case of reactive hypoglycemia and lost so much weight I looked anorexic despite the fact that I was eating the same number of calories. I could no longer tolerate sugar at all and I still can’t to this day. I struggled along for several years before completely collapsing and becoming bedridden with ME/CFS in 1988. It’s been a real roller coaster ride for me ever since.
That’s interesting about the hypoglycemia because I developed that too with ME/CFS. I had a glucose tolerance test done and it dropped to 33. What was so very strange though, is that even after my blood glucose returned to normal, I still felt bad for more than two days after.
Environmental conditions make all the difference for me. At my worst, I was housebound and mostly bedridden. However, much to my surprise, I have found that in a pristine desert environment, I do not experience hypoglycemia and can exercise near normal.
I too had a life-long (+4 decades) addiction to sugar and junk food for lunch before developing CFS. Although sugar and a bad diet may not be the cause of CFS, I’ll always believe the over-consumption caused the conditions that allowed CFS to develop in my body. My husband rarely consumed sugar or junk food and did not develop CFS.
I wonder what’s in the energy bars that’s not in a normal diet?
I just had a thought, I bet we body builders all also had a lot of surgars in our diets, I always went hypoglycaemic without it as a kid and teenager. So I was always eating. Drank a lot of coke, ate a lot of meat dairy and eggs too. Also had protein shakes but they often tasted too sweet.
I wonder if that created some sort of intolerance to something in that appalling diet?
I see the Gulf War Illness patients (a similar, but still different disease) are being tested on some sort of simple sugar.
Btw I improved dramatically on a vegetarian almost vegan diet but had to remove leptons (I think that’s the name) from that diet too. Meaning beans most grains aren’t allowed. So it’s stricter than a vegan diet but removing them helps. Just make sure you get all your amino acids. Have plenty of green smoothies and keep the fibre in them. Blend a good 2-3 mins. If you add fruit put it in last and pulse the blender a few times so it doesn’t get too processed. Interesting studies show fruit releases sugars slowly if still reasonably intact. Which keeps the blood sugar levels healthy zone without the reboundimg lows.
Most people now know not to ‘juice’ fruit as you’ll end up with sugar spikes. (That’s were fruit got its negative press)
Anyway I still have ME but am a lot, lot better 🙂
I have seen patients with this illness finally diagnosed with an insulinoma, it is something missed in many & found by the 72 hour in Hospital water fast measuring Glucose, Peptide C & Insulin
levels most do not reach 72 hours to be diagnosed it is the Gold Standard test I see it also in EDS Hypermobility as well…Also, Hereditary Fructose Intolerance (HFI)Genetic testing should be
ruled out so should spinal fluid leaks & even Silent Migraines (SM)I read one recovered & another had (SM) with a chocolate skin Allergy the skin test performed at an Allergist Office…I saw
the article on Patient’ online it was unsder Silent Migraines some can have headaches some do not, avoidance also of Sprays is also paet of recovery some stay away from Coffee, all Sodas,Cheese etc.
This is very interesting. How do I convince a Doctor to Do this genetic testing?
This “crash” is EXACTLY in line with my experience. Same trigger. Same terrifying symptoms around the chest. Same result – a continuous massive reduction in the seeming ability to produce and maintain energy.
I have had Family Tree´s Family Finder, Y-DNA37 and mt-DNA Full Sequence test done, but I don´t know if that is of any help for you. I live in Sweden and have Fibromyalgia and ME/CFS. 2009 I got a influensavaccination and after a severe influensaepisode in the beginning of 2011 I never get well. I was diagnosed in april 2015 in Gothenburg, Sweden.
All inspiring news. Can anyone explain why Ron Davis’ team will not share information with the Stanford ME/CFS clinic? It doesn’t seem to make sense and Davis’ team sounds like they’re willing to share as much as possible toward finding a cure.
It’s not true that they won’t share! They’ve done a lot of sequencing and gene expression work for Montoya’s group and are always willing to share. The Severely Ill Oatient Study data is now online and available to researchers as well. Ron is always willing to share.
I just clicked on his link, I got a big red screen that said it was a possible ‘phishing’ site…….? I’m willing to share my 23&me info although it was just an ancestry test.
I guess that was the link to Whole Genome Testing? I’ve update that to this – (you can click on the links by going to the post – they don’t show up in the comment)
*23andME, Ancestry.com do not do whole genome sequencing. Find out about WGS here. Companies that do it include Illumina, 10xGenomics, Veritas, Qiagen. As of 2016 a whole genome sequence from Illumina or Veritas costs about $1,000 but Illumina hopes to bring the price down to $100 in the future.
I’m a relapse/remitting ME/CFS patient who had gradual onset instead of sudden. So am interested in the answer to the question John posed as to whether this new idea would apply to this subset.
I also have gradual onset ME (now for c. 14 years, but it only got diagnosed as ME 4 years ago) and would love to know if the metabolic questions would fit our subset?
Nita and Julieanne,
It’s likely the metabolic trap idea can account for relapsing-remitting ME/CFS. I can imagine a scenario where it would give gradual onset, but I have no data for this scenario.
When you say gradual onset, how do you identify the starting point? Do you mean you had symptoms a long time ago, but they kept getting worse? What symptoms were the first symptoms?
Dr. Phair: Thank you for your response and your interest in ME/CFS. It is deeply appreciated. To answer your question, there are three situations that I think contributed to my ME/CFS. 1. Difficult pregnancy, never fully recovered to pre-pregnancy level of wellness. 2. Horrible case of the flu, never fully recovered back to healthy. 3. Being sprayed with white powder by a crop duster near an Oklahoma wheat field. All three happened within a 30 month period of time. Within a year of these events, I could not longer play tennis, could not continue on a softball team and had to stop playing in an indoor volleyball league, simply too exhausting. After another year had passed with continuing and more debilitating additional symptoms of ME/CFS, I knew for sure I was quite physically ill. Then after being ill for nearly 5 years I had my first partial remission. I have had several over the 42 year I’ve had this illness. Each subsequent partial remission lasting a shorter period of time and when ended I was in worse condition that when the remission started.I am now basically limited to my bed/recliner and am housebound.
First symptons: 1. fatigue 2. muscle pain 3. minor, but noticeable shortness of breath 4. unrefreshing sleep 5. what we now call PEM 6. minor, but noticeable cognitive impairment (understanding complex math and or scientific data, when it had not been a problem before and word-finding)
Nita, Thanks for your message. Your description of partial remission is important to me. Can you tell me how many hours or days it took from the time remission started until you reached the best you felt during that remission? How long did these remissions last? Similarly, when remission failed, how many hours or days did it take to fall into that worse-condition-than-when-the-remission-started?
In order for the metabolic trap to be correct, it has to be able to account for these remission dynamics. Any details of the timing that you can recall would be helpful. Thanks again.
I hope you don’t mind me butting in but I thought it may be helpful to tell you that I too have partial remissions.
What has happened with me is that a job/life will get really stressful or requires a lot of energy, and I’ll keep trying to push through it and then I have a big crash. It usually then takes months, or even over a year to get back to nearly the level I was at before the crash (although with each remission I don’t get quite back to where I was, and I haven’t had ‘normal functioning for over a decade).
The remissions can last for a few years, the most I have managed is about 4, but I will then crash again if I hit a stressful patch of life and try and push myself too much (I also push myself physically at these times, as it becomes apparent that I no longer have the energy to walk to work, say, but I keep pushing to do it anyway).
When I begin to struggle but keep pushing through I can manage this for a few months then I fully crash.
I’m not sure if this helps at all. Thank you for the work you are doing.
Ive been ill 16 years and would like to get my genome tested and sent to be included . What is the best way to go about doing this so the necessary data will be provided.
Hi Andrea. I don’t the best way as I’m completely new to WGS. (I just found out this morning that 23andME was not WGS.) I don’t know if Robert has anything more to add but I just put some links to WGS testers in the blog. From what I can tell it costs about $1,000 but prices may drop dramatically over the next 3-10 years. It’s a quite competitive field
Hey gang, for all interested – Veritas Genetics has been offering coupon code “DNASPECIAL” for $100 off WGS. However, I believe the .vcf file might cost extra, although Veritas includes interpretation and some genetic counseling. I’m happy to share my results with you, Robert, when they’re available.
Nice! Thanks SA
Robert,
I was very fit and taking supplements before I got CFS. But I don’t have genetic data to share. Would you still be interested in my story? Or is it unhelpful without genetic data?
I have the same question. Is shortversionstory interesting even without genetictest?
I live om Norway but will be hounered to contribute. Have been ill for 5 years. First year severly ill,latest able to have some activity outside the house.
I am the same. I was a very healthy 12 year old who had danced, done horse riding and loved sports. I went on my first skiing trip with my school and hurt my back really bad but it healed quickly. On return from skiing I came down with the flu and soon after my first ME symptoms appeared – leg pain! If you want more info don’t hesitate to ask. Lorna
I haven’t bothered with a gene scan yet either, since there didn’t seem any use for it. I am intrigued by the part about this involving TRP metabolism. TRP worsens my symptoms (blocked by taking BCAAs with it), so that seems very definitely involved. Other observations have pointed to elevated QUIN and picolinic acids. Other observations point to the electron transport chain being involved. It seems that reducing levels of superoxide and peroxynitrite increases my symptoms severity. If your model indicates that reduced peroxynitrite is involved, and you need a blood or CSF sample from someone showing this effect, I’d be willing to volunteer.
This project should definitely contact the Genes for Good, a research study conducted at the University of Michigan. The major goalis to engage tens of thousands of individuals in genetic research. The primary tool to accomplish this is the Genes for Good Facebook App. Participants engage in the study through the App, answer health-related questions, and view summaries of selected survey questions. They have a FaceBook page that solicits participation https://www.facebook.com/Genes-for-Good-1396987533961180 Website link: https://www.google.com/search?q=Genes+for+Good&ie=utf-8&oe=utf-8&client=firefox-b-1-ab
Catherine,
Thanks for pointing out Genes for Good. I did not know about this project. I will look into it.
Regarding the question about why Ron Davis is team wants to keep the specifics close to the vest , I’m attempting to get a comment in here . But am having a very difficult time with language right now, and have erased this many times, as speech to text is having an extremely hard time understanding what I’m saying. Typing or swiping the comment in on my tablet is quite simply not an option for me as my brain and muscle memory both malfunction when it comes to the placement of letters or how to spell them using a keyboard or a pencil for that matter . so if this is horribly grammatically incorrect please understand the reason as I am tiring extremely rapidly right now from so many attempts to get this written.
Okay, here goes…
In the article it was stated that if the hypothesis proves to be true the fix is going to be very simple and I assume it is easily accessible and affordable. For me that brings to mind things like supplements and herbal remedies Pact oh my gosh into a pill and things like that. I don’t really think they’re talking prescriptions because they say we would easily able to get a hold of it.
Another fact that was stated was that if the hypothesis is incorrect the thing that would have been a cure 4 an accurate hypothesis would actually be very harmful to our specific illness.
Since people have a tendency 2 jump on rumored dietary and or supplemental fixes for everything that the human mind can imagine needs fixing it is highly likely that either a company would attempt to capitalize on this at our expense before it’s even been approved as an actual cure.
And the patient community is suffering horribly with very little to no validation and a huge need to return to our lives that have Ben just held it Bay from us dangling like a carrot before the nose of a horse. This community is very likely to try and see if this thing works before it’s safe to do so. And even though we’ve been told it will make us very sick if they are wrong and to wait, most of us are too desperate to not at least try it. That is why I think Ron Davis wants to keep this close to the vest until they know whether or not the hypothesis is true. I think that’s a very wise idea because sadly people have the need of warnings being printed on grocery bags that a plastic bag is not a toy. And that speaks to the apathy we tend to have towards whether or not something can be harmful to us.
I find that some people actually do not know that herbs can be harmful when used incorrectly. And some things cannot be taken if you are on certain medications whether they are natural or chemical. I’ve heard people say if it’s sold over the counter has to be safe. Honestly I have a family member who believes that. Paragraph
We certainly don’t want to take what we perceive to be a possible cure and end up making ourselves horrifically worse. I think I use the word horrific Lee twice in this comment and I hate text to speech right now.
I think I got that spit out correctly enough. I’m reading along hoping it makes sense even if it’s the wrong word is phonetically close to what I’m saying in most cases.
A different topic I would like to address briefly this time. He mentioned that they were curious if exercise fanatics that have any CFS me CFS have used a specifics supplement or dietary things that they hyper focused on. I know that there have been two things that I hyper focused on right before I got ill and only just quit consuming a large amount of those better for me items in my diet. and I hyper focused on those for 16 years thinking that they would be good for me. I’m really curious to find out what those items are that he was referring to. It’s fascinating and quite possibly a very realistic idea. and how often do you find out something that is supposed to be good for us on the food pyramid suddenly gets kicked off the good foods pyramid and branded wickedly bad for us? and then we find out we’ve been eating these things every single day thinking they were good for us and we were actually making ourselves messed up and more likely to get a deadly illness.
Okay I’m done. I feel like my brain is pretzel shaped right now and it feels really weird in my head. Wow
Thanks for struggling through the voice to text. That is exactly why Ron Davis is holding back on providing more information. He explained to me that the metabolic trap involves some very basic systems and tweaking them the wrong way could cause some large problems. If they proceed further with the trap Ron said they would test possible treatments under controlled situation; i.e. under a doctor’s supervision.
Thanks Cort. Would you be able to explain a bit more what a metabolic trap is. Just a hypothetical example would be good.
The other issue is that folks are severely ill, and they need help asap.
As for the relapsing types, my daughter actually did improve and then relapsed, and this was the pattern for some time, now however, it’s just sort of flatlined.
Alex3619 had a nice example
http://forums.phoenixrising.me/index.php?threads/a-metabolic-trap-for-me-cfs.58606/#post-968485
How can you get to be part of this experiment. My Dr….Kaufman works with OMI. I wld love to be a guinea pig and am involved in several other studies right now. I wld like to try to take something/anything that would change the way I feel…..incredibly sick every day of my life.
I am in the Severely Ill Study, the Big Data Study and the CDC Study being conducted through Dr. Kogelnik. I have learned nothing new abt my condition from any of these studies yet. I hope someday to learn something that will make me feel even one iota better.
Thanks, Lisa in CA.
So glad you’re in all those studies Lisa – you are contributing to the science big time.
I think the Metabolic Trap study is probably going to take cells and test them. If the hypothesis holds up I’ll imagine that they’ll move to trying to get patients out of the metabolic trap. At that point I would think you’re sitting pretty really with all this data they have on you.
This is very interesting. I too wonder what supplements body builders who got this disease used beforehand. Because i got I’ll after 10 weeks of intense weightlifting, and supplementation of high doses of Tricreatine Malate (creatine mixed or bound with malic acid) and whey protein. Both creatine and malic acid interfere with ATP production and citric acid cycle.. i’ve been thinking a lot about that after i got ill. I’m a non responder to normal creatine monohydrate but in the past trikreatine malate increased strenght and energy. This time not so much, but the fatigue set in 4 days after i quit. From there it was a week of steep downhill slope into ME/CFS.
This, togather with about 1 year of high tempo, lots of colds/influenza, stress etc.. but something triggered me over the edge.
What I would like to know is if using antibiotics after infection in lungs,stomach or operation triggers this metabolic change. I have heard many stories of people using antibiotics and then getting me/cfs. I read somewhere that certain antibiotics can impact mitochondria negatively.
Zara, I’m one of those people. I had a very bad tooth infection, took Azithromycin, started having gut pains and a short time after that caught a very bad cold or flu and never recovered.
I’ve been wondering about this myself. I got ME/CFS after having mono. Unfortunately I went to the doctor three times (Stanford clinic of all places) and the doctor prescribed me three back to back courses of antibiotics, until I finally trusted my own judgement and said this isn’t right, went to the ER where they did a monospot test. Did taking all those antibiotics during my mono push me into this state?
I too have heard many stories surrounding antibiotics. Most are complicated by having many things happening at the same time. But the general idea that antibiotics might impact mitochondria makes some sense on purely logical grounds because mitochondria were almost surely bacteria before they were adopted into the current apparently-symbiotic relationship with more complex cell types.
It’s still possible that mitochondria are dysfunctional in ME/CFS, and when I first started thinking about ME/CFS I was definitely thinking mitochondria. But lots of people have looked and no one has reported a major mitochondrial defect. I always encourage people to read the Vermeulen 2014 J Transl Med paper which shows resting and peak exercise cardiac output are normal in Fukuda-defined ME/CFS. This is on the first exercise day, not the second when PEM makes it impossible to reproduce the previous day’s work, but it tells us that the heart, which is a completely oxidative organ completely dependent on mitochondria, is working fine.
I can’t rule out mitochondrial involvement, but I’m pretty convinced that it’s not ALL mitochondria that are affected, and it’s difficult to explain how an antibiotic could affect just the mitochondria in some organs.
One thing that’s pretty clear is that there are many external stressors that serve to push a predisposed person “over the edge” and into a state from which it is difficult to escape. Some of us think that state is what’s common to all cases of ME/CFS. In this regard, I think Dr. Robert Naviaux is right. Our first priority has to be: Why can’t patients recover? This is why the nature of the metabolic trap seems so important to me.
Robert and Cort, I am a patient of Dr. Bateman and participated in a study that Dr. Alan and Kathleen Light at the University of Utah are doing. I gave blood samples that they are using to study gene variants. I thought they had said they were studying my whole genome? I wonder if this is WGS testing and if you could correlate with them? I have severe CFS and POTS. I would be happy to be a part of any research that could find answers about this disabling disease! Thanks to both of you for your work and dedication!!
Continuing on antibiotics..
Since there were in the past outbreaks in hospitals with patients getting me/cfs..can it be that these patients were getting antibiotics for their infection..hence the outbreak of me/cfs….
Maybe these patients had received antibiotics in early life…and when receiving a dosis later in life resulting in damaged mitochondria. Read an article about effects of antibiotics in early life on metabolism.
It would be interesting if medical long term records of patients could be gathered and analyzed..as to what communalities are there.. we as patients tend to forget details we think are not important..but could be crucial.
I used to run 40 Miles a week even after having my first child. Two years after having my second child, when I tried to get back into running, I came down with CFS. Now I crash after things like cleaning my home for Easter. I am on day 3 of feeling the effects.
The HIV / AIDS condition seemed to have been taken on, studied, and “solved” at a much faster rate than ME/CFS is taking. Why?
Much simpler! Very early on epidemiological studies indicated a pathogen was involved. From there it was a matter of identifying it and coming up with a treatment for it. Even way back then they were able to find it fairly quickly. Today they would find it almost immediately.
ME/cFS is not transmissable; a pathogen could be involved but its not an infectious one.
Rob – Massive funding (still ongoing) for HIV/AIDS research. Negligible funding for ME/CFS research. There’s your answer.
Saw an interesting documentary that explained this very well. The gay community was a strong bonded community that was used to adversity, that turned all their energy into changing the usual practice of running studies from one drug/one study to the cocktail approach study. Things were able to move much faster after that.
I developed CFS when I took cisapride and Methylpolysiloxane (Brand name – Normagut) under the supervision of a Gastroenterologist for two and a half years. Initially I started getting a lot of flatulence and then mucous. six months down the line I had full blown fatigue. I could not even get out of bed on my own. I am taking antidepressants and supplements. I am now house bound but not bed bound. I want to know whether the intestinal aspect of CFS is being considered in this study.
When I was at Dr. Klimas’s office last week I entered my Ancestry DNA into a PureGenomics program and it showed some very interesting results. I already knew I was heterozygous for the MTHFR gene but I also have 3 others mutations in the methylation cycle. One of them is a CBS mutation which apparently causes an upregulation in the methionine cycle of the metabolism. I’ve been on a high protein diet because I read that we have problems with carbohydrate metabolism. I felt even worse on high protein and now realize that high protein is bad with a CBS mutation. Supplementing with folate and b12 also can make things worse when the methionine cycle is out of wack because the folate and methionine cycle are interconnected.
Dana, It’s probably too late for you to see this, but I am homozygous MTHFR c677t, and have other methylation variances. I can’t afford to see Dr. Klimas and haven’t had much success with the functional medicine people I’ve consulted with. Would you be open to communicating with me off this site? I’m on Facebook. Tanja Bugas, Littleton, Colorado
Hmm, I am homozygous on CBS C677T as well, I eat a lot of protein. I am not sure not eating it makes me better, just hungier.
If there were a “cheap, simple, and quick solution” to ME/CFS, safe to say we would have found it already, given everything (including the kitchen sink) that we and our alternative doctors have tried over the years. Forgive my cynicism, but this sounds more like just another grab for research funds that ends up going nowhere. Well, everybody has to eat, and I hope I’m wrong.
Rick,
Well, I worked on this for 2 years as a volunteer before receiving research funding to test the metabolic trap theory. People died of bacterial infections for thousands of years before the first cheap, simple, and quick antibiotic became available. What’s more the best medical solutions always follow from knowing the cause. Often it’s finding the cause that’s the hard part. But anyone who knows the history of ME/CFS will immediately forgive your cynicism. I hope you’re wrong too.
Dear Mr. Phair, thanks so very much for the years of effort you have put into trying to understand this nasty disease.
I have added you to the ME/CFS ‘wall of hope’ I keep to remind myself that REALLY smart, caring, and dedicated people are working to heal us. Some days looking at that wall is the thing that keeps me hanging on…
Your endeavors to seek answers on our behalf are enormously appreciated!
Rick, ha-ha, count me as a skeptic. First thing I do whenever I hear people say they recovered doing this and that is to roll my eyes.
That said, I do think Robert is onto something with kinetic modeling. If the modeling can’t reveal the actual structure of the underlying process, it can at least give us some clues. I’ve been doing it myself by building statistical model between different types of exertions that I do and my symptoms, as well as testing practically millions of micro-hypotheses. I’m coming to a quite different conclusion from Robert’s though. But then, I don’t have sophisticated equipment and data — I only have a fitbit and myself as the cohort — so my models are rather imprecise, to say the least.
TK,
Here in Silicon Valley, almost everyone is doing what you’re doing. Statistical modeling is the heart of machine learning and AI. Certainly lots of people think machine learning is the future. But I’ve always maintained (as do the statisticians when pressed) statistics was terrible at cause and effect. It’s the old dictum that “correlation is not causation.” So my models are all based on chemical kinetics and nonlinear ordinary differential equations. What’s cool about these kinetic models is that causality is explicit. This means we can test them against experimental data like those from genomics and metabolic tracers.
I could write a long complicated CFS story like most of you ,and my heart goes out to every one of you.
But I have to say I have found something magic!!!!
Yes I can hardly believe it myself.
I came across a site called, Inclined bed therapy,IBT.Put simply it is raising the head of your bed!I have been on my raised bed four weeks and am almost back to normal.I have good energy,my insomnia has gone,I don’t need to pee during the night,brain fog gone,happy feeling of well-being,memory better,can usually go all day without sleep.
I am telling every one I meet as you will see on the site this therapy helps countless problems and it’s free.
I have stopped b12injections and other pills and potions.I eat a healthy caveman diet,with low carb and low sugar as have struggled with Candida for many years.
Please please,try this,! it works!
Congratulations Jill – when it works it really works 🙂
For those interested in this check out this blog – https://www.healthrising.org/forums/resources/heads-up-an-easy-way-to-improve-sleep-for-fibromyalgia-and-chronic-fatigue-syndrome-me-cfs.415/
How much does the bed head need to be raised please. My 22 year old daughter has been sick for 9 years. This is something we have not tried.
Something to potentially think about – Erik Johnson has brought up the possibility of mycotoxins affecting people who worked/went to school in water damaged buildings during the Tahoe outbreak. Then Dr. Shoemaker states that up to 25% of the population are unable to clear out these toxins due to their genetic makeup. I’m wondering if these factors might be a piece of this puzzle?
Robert,
THANK YOU for pointing out how many former weightlifters and bodybuilders fall ill with CFS. That is exactly what happened to me. My CFS started very suddenly, but was not associated with any illness or stressful event in my life. I was, however, engaging in extremely intense heavy weight training workouts to exhaustion, working out on average 18 hours per week with weights, and loving it. Until I woke up one day and suddenly couldn’t anymore.
While I was weight training like that, I had been eating virtually the same foods every single day. They were:
-TONS of grilled chicken
-Tons of eggs
-Tons of skim milk
As far as supplements, I was taking four supplements every day:
-Whey protein
-Casein protein
-Creatine
-A preworkout called “N.O.-Xplode” (N.O. standing for Nitric Oxide)
Does CFS resulting from weight training fall in line with your metabolic trap theory?
Hi Brian,
Would you possibly have had (in the year before getting ME) often sore or painful muscles from all that heavy weight training? I’m working on some new idea and could use this input. If it would be, would the under legs (are those calve muscles, translation?) and in particular on the back have felt (over)strained (like they could feel after stretching a bit too much)?
Thx in advance,
dejurgen
Hi dejurgen,
No, I can’t say that I experienced that. i felt absolutely fantastic until the day my CFS started.
Brian,
Your story helps me. Thanks for taking the time to write it out.
Just looking back on this, I forgot to mention that I took the casein protein every night, to prevent my body from going into a catabolic state. And I ate 5 or 6 meals throughout the day spaced out less than 3 hours apart, also to keep my body from going into a catabolic state. My goal was to be in an anabolic state at all times, and I was very strict about it. Not sure if that is relevant to your research, but I thought I would mention it just in case.
For the question of bodybuilding triggering ME/CFS, I think the muscle damage triggers the immune system in a similar way as viral infections do. It’s the immune system activation that triggers ME/CFS, and the precise trigger isn’t really important. Thus it certainly should fit into the metabolic trap theory.
A moderate amount of exercise will boost the immune system, whereas intense exercise performed by elite athletes who have the capability to perform at high levels will suppress aspects of the immune system. Elite athletes who overdo it will make themselves more susceptible to colds. Elite athletes are probably familiar with coming down with colds when overtraining. The reason I mention ELITE athletes is because it would be difficult for the average person to exert themselves to this degree. See https://www.ncbi.nlm.nih.gov/pubmed/17826186. Exercise and the immune system. “Exercise has a variable effect on the immune system. The underlying reasons for this variability are multifactorial and include infectious, neuroedocrine, and metabolic factors, with nutritional status of the athlete and the training load playing a role. Environmental factors such as living quarters, travel requirements, and the type of sport (team versus individual) also contribute to infectious risk. Regarding the direct effect of exercise on the immune system, moderate exercise seems to exert a protective effect, whereas repeated bouts of strenuous exercise can result in immune dysfunction. Understanding the relationship between exercise and infectious disease has important potential implications for public health and for clinicians caring for athletes and athletic teams.” Full text: https://sci-hub.tw/10.1016/j.csm.2007.04.011
Regarding muscle damage, or Delayed-Onset Muscle Soreness (DOMS): There is a localized immune response to the damaged muscle: See http://www.humankinetics.com/excerpts/excerpts/recent-research-provides-insight-into-muscle-soreness
“Mononucleated cells in muscle are activated by the injury, providing the chemical signal to circulating inflammatory cells. Neutrophils (a type of white blood cell) invade the injury site and release cytokines (immunoregulatory substances), which then attract and activate additional inflammatory cells. Neutrophils possibly also release oxygen free radicals that can damage cell membranes. The invasion of these inflammatory cells is also associated with the incidence of pain, thought to be caused by a release of substances from the inflammatory cells stimulating the pain-sensitive nerve endings. Macrophages (another type of cell of the immune system) then invade the damaged muscle fibers, removing debris through a process known as phagocytosis. Last, a second phase of macrophage invasion occurs, which is associated with muscle regeneration.”
Viral infections produce a different kind of immune response: https://www.immunology.org/public-information/bitesized-immunology/pathogens-and-disease/immune-responses-viruses
A special cell of the immune system called a T cell circulates looking for infections. One type of T cell is called a cytotoxic T cell because it kills cells that are infected with viruses with toxic mediators. Natural killer cells also kill virally-infected cells. Virally-infected cells produce and release small proteins called interferons, which play a role in immune protection against viruses. Viruses can also be removed from the body by antibodies before they get the chance to infect a cell.
HOly shit!! i was taking no-xplode for years as well before falling sick, but in my case it was differennt i felt sick because of many antibiotics, worngly prescribed, doctors ruined my life, probably no-xplode helped too years before… my story is very long. i had CFS for two days only (two whole days in bed) after a sore throat, antibiotics and a work out session, the next day i fell in bed for two days,… after that y recovered for almost a whole year until y fell sick again after many antibiotics… i guess this has alot to do with microbiome.
Robert, thank you SO MUCH for looking into your hypothesis!
Gail, I know that 23andMe testing does not cover the part of chromosome 6 where the HLA-DR genes are.
Hi there and thank you for your wonderful work on CFS,
I like to share my story as a CFS patient who used to be an avid weight lifter. I was 26 years old at the time (12 years ago) and I was in graduate school and very active. I had a very busy social life and I was doing very heavy strength training at the gym, running, doing yoga and swimming. Now looking back it looks like I was really driving myself too hard, but when you are 26 you dont ever think about these things. Anyhow, one night I went out with my friends and we had dinner and the next day I woke up with tremendous amounts of bloating. I literally looked pregnant. I was not feeling tired and had no other symptoms aside from this insane amount of bloating. I continued with my heavy exercise routine and went on with life in spite of the bloating and IBS-C symptoms that had suddenly developed overnight. Two weeks later after the onset of the bloating I went to a hot yoga class (bikram yoga). It was VERY hot and on this day i found myself feeling very strange but I decided to power through the class and finish it. By the end of the class i felt like I was dying. I still remember this strange sensation of impending doom and the feeling that something was very wrong. Even people in the yoga class were looking at me and wondering if i was ok. I left the class and that night i felt like i was having a nervous breakdown. I hoped the next day i would wake up and things would be back to normal. Well, things were not. I woke up and immediately felt like I couldn’t walk. I laid down right beside my bed on the floor and did not move. I stayed in my apartment for two weeks and survived on the kindness of friends. I gradually got enough energy to go out but since then I have been a shell of my former self. The cognitive dysfunction is the worst part. I have no social life and live a fairly meaningless existence. What keeps me going is the hope that some day someone finds a cure. And the work that people like you are doing is basically my reason to be alive.
Amazing story Haach! It’s the really fit people who get so ill who really blow my mind. How does anyone think this can be psychological when such extreme debilitation occurs almost overnight to very healthy people.
Have you read Jamison Hill’s stuff? Another former weightlifter and gym rat.
Keep on hanging on. You never know might be around the corner.
I’ve had my DNA sequenced by both 23andMe and Ancestry (I am adopted and I’m looking for bio parents). I have a feeling that 23andMe does a better job but does Ancestry use the same 3 out 5 markers? I have downloaded all my raw data and would the same markers? I would be happy to provide both if it would help in any way.
Unfortunately neither have the kind of data Robert is looking for.
When I do some short electric bicycling (with very low resistance) then I have to breathe less then at rest. In fact then I have to breathe surprisingly little even compared to an average person. To me that seems like I have an efficient aerobic mechanism as long as the time and effort are low enough. Beyond short and (very) low intensity breathing needs go up very sharp.
Would such behavior fit the metabolic trap? If so, then it would seem to have an on/off time that is very short (on time far less then an hour, off time hours to days when really overdoing it). Might be somehow helpful information. I must add I learned diaphragm breathing since some time and that made my breathing more efficient.
Reading this post -in which NAD is mentioned- first thing in the morning made my day!!
After spending months identifying triggers of oxidative stress (in my case food and chemical sensitivities) followed by avoidance of those triggers combined with support of antioxidant enzymes (Zn, Mn, Se, Liposomal Glutathione) and high levels of B6, my body is finally able to tolerate my efforts to boost levels of NAD and FAD (NR, B2+VitD) and I’m feeling better for it! It leads to intermittent muscle aches which thankfully I can control through Magnesium oil and Creatine. I recently started taking amino-acids but am avoiding tryptophan, tyrosine and anything that enhances the methylation cycle for now until I am stronger. I’ve got a long way to go but at least I am getting somewhere.
Cortene sounds promising for moderate to severe cases of ME/CFS as Cortene seems to enable bypassing of the downregulation of adrenal and thyroid functions. Not sure if properly understand Cortene yet and if the above is accurate but it sounds promising. On the other hand, for mild to moderate ME/CFS cases, could it be as simple as finding and avoiding triggers of oxidative stress (genetics, genomics, elimination diets, endotoxins), supporting the body in neutralising oxidative stress and following a (personalised) supplementation protocol to recover? I so hope so!!!
If you’re interested in raising NAD+ levels, look at the supplement from LIAS Research. It is pure NAD+ not NR or NMN or other niacin metabolites.
I read an article in which it is claimed that NAD+ is first metabolised to NR before it can enter the cell and apparently then metabolised to someting else again before it can enter the nucleus or mitochondria after which it is metabolised back to NAD+. I may have misunderstood though…But I think I am now getting off topic with regards to the content of this thread so I’ll leave it that. The website of LIAS research has a lot of info indeed. Thank you for that!
Which of the WGS tests done by Illumina should be ordered? There are several to choose from. I became ill in 2004 after a significant GI infection. I was a healthy, active person with a fast paced life as a senior level executive when I became ill. Got better but not well (“stable”), under a doc using Dr Jacob Teitelbaum’s protocol, but then fully relapsed several years later after exerting past limits. Have never been able to get back to “stable” & continue to be mostly housebound & bed/chair confined at times 6 yrs later.
I can’t afford gene testing, but can contribute with a short history:
1. Extreme stress at work that lasted weeks.
2. Unable to sleep at all for five nights due to this stress.
3. Jet Black stools passed that smelt revolting.
4. Terrible throat soreness / fever symptoms. G.P. gave huge doses of I.V. antibiotics for 7 days straight.
5. Following this: The “worse case of mono (Glandular Fever ) the doctors had ever seen” hospitalized me for one week.
6. Never got better. (That was 23 years ago). The 1st 5 years were the worst (bedridden).
7. Health improved slightly with aiding digestive process. D.H.E.A. helped. Easily digestible protein helped (whey).
8. For many years symptoms plateaued and were managed.
9. Last 3 years E.B.V. has reactivated twice with serious health setbacks.
Hope that helps.
Tryptophan,ether directly or thru whey protein.
I took Tryptophan for sleep prior to onset.
Now I can not get close to anything that even smells of Serotonin. Serotonin Syndrome light, not so lite???
Ron P said he had problems with tryptophan. That might be through the IDO-kynurenine pathway, rather than the TPO-5-htp-serotonin pathway. TRP made me seriously suicidal, as well as increasing my ME symptoms. 5-htp didn’t bother me at all, so I think my serotonin pathway is working okay, but my kynurenine pathway isn’t.
If 5-htp gives you problems, then that’s different from me. If it doesn’t give you problems, but TRP does, it’s likely your kynurenine pathway involved. Just something to consider…
There are many smart insightful people on this thread. Sometimes I read what you write and just smile because some of you are just a few technical details and a ton of genomics data behind where I am with the metabolic trap hypothesis. Of course, that doesn’t mean the hypothesis is correct, but it does make me happy that, thanks to OMF, we can test it.
Adding to the ideas around serotonin overload… many ME/CFS patients have sensitivities to SSRIs and SNRIs. I am one of them – both Wellbutrin and Cymbalta made me terribly sick.
I haven’t had my genome sequenced yet so cannot offer that data unfortunately. As a very long term patient, however, I am interested in why hormonal upheaval might have impacted my presentation of the disease.
I first became ill in 1970. I didn’t have a ‘pin point’ moment but as 1970 dawned I was what I would consider healthy (albeit with some MCS and sensitivity issues from either i) birth or ii) a smallpox vaccine when I was was 17 months old maybe?) but when 1970 closed I was unwell and I would never be well again.
My disease cycled in relapse / remission form until I had children in the late 1980s (although since 1970 my ‘best’ non pregnancy remission would be classified at about 75% of normal… which is great looking from a perspective of about 25 to 30% now).
I had 2 pregnancies in very close succession (not intended 😉 ) and had severe hyperemesis gravidarum for the first 20 weeks of each. For the final 20 weeks of each I went into an almost ‘overnight’ remission to about 80% of normal. I remember describing it to a friend as ‘being set free from a cage’. I didn’t have a diagnosis at this point, I wasn’t diagnosed until 1990.
After I had my children the trajectory of my disease changed from this ‘cycling’ pattern to a continuous downhill presentation. I became mainly housebound in 1994 and have become increasingly more disabled every year since then.
There are other points in my history which might be significant such as sudden very severe allergies starting after (?) swine flu in 2011 tipping over into bodywide neuropathic pain later that year.
If any of this detail is helpful to you Dr Phair, and you wish to interrogate it more I’m very happy to speak with you via email. I’m in the UK but would be happy to send any samples that might be useful if doable. Equally if none of this resonates with your hypotheses feel free to ignore it!
Thank you for your work, it sounds very interesting.
I have ME with sudden onset since 2001. I am unable to work and just about manage to look after myself with various degrees of fluctuating capability.
I have had DNA testing by My Heritage which I presume uses similar processes to 23andMe? If so I presume the data is not good enough for you to use and unfortunately I cannot afford WGS testing, which is a shame because this disease runs in my family with my mother and aunt suffering from it. My aunt is a half sister on my grandmother side if that’s any help.
Good luck with your research, will look forward to hearing more about it in the future.
I was spending a lot of time in a chair in front of a computer just prior to becoming ill and had developed what my doctor called “overuse injury” in my arm and wrist.
Had a great physical therapy program for a few weeks.
The very first thing they did was establish a baseline by having me perform a series of challenges, including cycling as hard and fast as I could for a certain period of time. That day I started feeling like I was coming down with something, but it went away.
At the end of the physical therapy I was given exercises to take home. I misunderstood and did a whole weeks’ worth of exercise in one day. Later that week I came down with a flu that has never left.
Thanks for this great article, Cort and thank you Robert for your work.
LOL! I’m sorry CJ. I shouldn’t laugh, but this is the most unfortunate way of coming down with CFS I’ve ever heard. Doing a week’s worth of exercise in one day by a mistake! But, yeah, a small mistake could change our lives forever, I know. It’s like stepping into a crosswalk and then run over by a bus.. I constantly think about my mistake too and wonder how different my life would have been if I didn’t.
The same thing has happened to me. At first I noticed I was not recovering from lifting and losing strength. I decreased how much work I was doing and how often. One day I just blacked out and I can not hardly do anything now. I pushed snow off the driveway for 10 minutes and my body shuts down for 3 days.
High protein intake depletes vitamin A, which is not a common nutrient in the standard American diet and thus isn’t likely to be repleted without effort. Vitamin A was commonly known as the “anti-infective vitamin” before it was swept aside by the use of antibiotics. Vitamin A has a lot of impact on immunity. It’s also necessary to secrete mucus (including the gut mucosa where “good” bacteria communicate with the immune system) and to maintain the integrity of the gut. Vit A is also necessary for hematopoiesis so deficiency causes a type of anemia. Zinc and B6 are the other biggies for proper amino acid metabolism. Vit A stimulates ceruloplasmin for proper iron and copper metabolism. In the overall scheme of CFS/ME, I still think there’s room for multifactorial nutrient deficiencies, for example, low B6 or low vit A causing normocytic anemias. I’m also interested in whether gut inflammation caused by dysbiosis depletes B6 and tryptophan or causes anemia of chronic inflammation. So it’s not just the primary nutrient deficiency that causes problems, it’s the web of deficiencies. For example, low bioavailable iron means vit A and D cannot be hydroxylated, which impacts calcium metabolism, DNA transcription, hormones, et cetera. Aromatic amino acids cannot be hydroxylated to form neurotransmitters, impacting mood, energy, sleep, et cetera. Collagen proteins cannot be hydroxylated. Energy production is reduced due to limited copper or iron. Et cetera, et cetera. I would think that,not does the underlying cause need to be corrected, but all of the nutrient deficiencies would have to be discovered and corrected before one could restore their health. (This is my jumble of thoughts that I haven’t figured out how to turn into a possibly productive conversation.)
“High protein intake depletes vitamin A”
I never heard of this nor thought about it. I just assumed vitamin A deficiency was something of the past.
It may however relate to a few things:
* Many consider high protein intake diets as inflammatory.
* I believe that when we go anaerobic that we start lacking glucose at the place of consumption. Anaerobic energy production consumes glucose at a very rapid pace as it only delivers very few ATP per molecule of glucose. As our blood volumes and likely blood flow are low, replenishing it at the site of consumption could be insufficient. This could locally drive glucose levels very low. This would, combined with our high adrenaline (fight-or flee hormone) very rapidly convert our protein stocks to glucose for anaerobic energy production. This would temporary and locally produce overwhelming amounts of purine that need to be processed as fast as possible. That would produce excessive amounts of local uric acid witch does not solve well in blood. That would result in uric acid crystal formation in capillaries obstructing blood flow making local supply of blood, oxygen and glucose even more problematic speeding up the destructive process.
* If the above would happen, it would likely cause a massive inflammation / immune reaction combined with massive hydrogen peroxide / ROS production. Uric acid is an anti-oxidant so producing massive amounts of oxidants (peroxide / ROS) would be helpful in removing / preventing the blood-vessel blocking uric acid crystals. That would be a bit in line with Naviaux’s view on “oxidative shielding”.
* Cleaning up the mess after local hypoxia / ischemia is a very inflammatory process.
* It would go hand in hand with low / depleted protein stocks in our blood, such as is seen in some metabolic studies.
* https://www.ncbi.nlm.nih.gov/pubmed/20181784 says: “Vitamin A deficiency increases protein catabolism and induces urea cycle enzymes in rats.” thus vitamin A deficiency may increase this very inflammatory process.
* This hypothetical process would be devastating to blood vessels. Repairing them would be crucial. Retinoic acid, derived from vitamin A, is a hormone like growth factor for epithelial cells. These are everywhere and are important in blood vessel health. Repairing the blood vessels if they were broken likely could use this growth factor.
* And: secondary vitamin A deficiency can be caused by… …”chronic exposure to oxidants” (oxidants like self produced peroxide) according to https://en.wikipedia.org/wiki/Vitamin_A causing some sort of vicious circle.
It would also be another thing that helps explaining the observation why the two main working (and seemingly opposite) keto and vegan diets both work. One contains much fat and vitamin A is fat-soluble hence found in many fatty foods. The other contains plenty of beta-carotene (leading to vitamin A) and reasonable amounts of fat. The decades long pushed high-carb low-fat diets to lower cholesterol however often don’t.
One of the things common in many body-builders and heavy weight lifters is this (very) high intake of protein. Let us assume it increases inflammation risk.
Body building goes hand in hand with rapid muscle building. Muscle building goes hand in hand with deconstruction-reconstruction. That process involves muscle inflammation too.
Body building and heavy weight lifting puts a lot of strain on the muscles, certainly if not done perfect. The load in kilograms is high to very high. Releasing the weights causes mechanical shock waves with far higher forces then average. Balancing causes only part of some muscles to be used. For example the calves could be stressed almost exclusive at the outer edge when correcting balance. If only for example 20% of the muscle cross section bears the entire heavy weight than that is a very strong local force, as if the weight was 5 times as high. And it is unbalanced loading of the muscle: very high tension at the edge and few tension or even compression at the other edge of the muscle (often seen in mechanical loading of “beam like” structures). This could help pull muscles “apart”. That could cause plenty of micro damage in the muscles, needing repair and inflammation. When releasing the weight while having poor balance, immense local tension could occur from combined unbalance muscle loading and strong shock waves.
So body builders and heavy weight lifters may activate / “prepare” plenty of processes that involve inflammation. That’s why I asked Brian the question about muscle pain.
In healthy people pro-inflammation and anti-inflammation components are in balance repairing tissue damage at a healthy rate. Now add a flue. That requires immediate (very) strong immune reaction. A very strong immune reaction should increase pro-inflammatory chemicals a lot too IMO. With all those underlying pro-inflammatory factors and body-wide supposed micro damage to the muscles lying their waiting it might cause a massive body wide inflammatory reaction on top of the needed immune reaction.
That could be a bad position: massive body wide inflammation is not without its risks. Just imagine the purple and swollen gout toe and see it happen all over the body: deadly inflammation?
So the body may be caught in another trap: increasing immune functioning in order to defeat the flu or reduce body wide inflammation. Both at once may not be possible. One may well end up with both a heavy inflammatory process and a weak reaction to the flu virus leaving it extra chances to wreak havoc. If it happened it could induce a sudden virus onset of healthy to ME.
I had a gradual onset, but like many ME patients even a flu vaccination can set me back in a major way. I believe ME causes massive local damage, requiring massive inflammation. In order to keep it “safe” the body must limit it to not have extreme destructive massive body wide inflammation. But now add a flu vaccination that needs strong up-regulation of the immune system. That would fuel the body wide inflammation too much again requiring setting things in the middle once more: long time too much body wide inflammation and too weak immune response to the vaccination.
Maybe it also could link to ME being much more virus triggered then bacteria triggered: if a bacterial infection gets out of control then antibiotics can save the day. If correct, the “setting in” of ME would not be immediate: most people only get antibiotics in a delayed fashion when it is obvious something is going wrong.
It could also help explain the many cases of people getting ME after taking some antibiotics: maybe they did not succeed enough to get both inflammation and infection in safe zones in a timely fashion?
Endurance sporters such as marathon runners also often “collect” plenty of muscle inflammation after their heavy sport. Again, as long as they are healthy the inflammation is overcome. Add stress, injury and infection and it may be insurmountable. Endurance sporters often have a very carb-heavy diet as well, leaving few healthy fats and vitamin A.
It is but a hypothesis but it could work out.
A new treatment for lupus will be launched this year. Normally this drug cures lupus after several injections. This illness has similitude with ME/CFS…
http://www.immupharma.co.uk/
Great to see progress in an autoimmune disease. Check out this link – http://simmaronresearch.com/2018/04/hope-mecfs-autoimmune-subset-german-researcher-steps-forward/ – for more on an autoimmune subset in ME/CFS.
Let’s dial this comment back a bit. Not even the company is claiming it’s a cure. Results from the phase II trials showed a 53% improvement in symptoms among patients taking the drug once a month, a 45% improvement in patients taking it twice a month, and a 36% improvement in those on placebo. At best, we have an incremental advance for some lupus patients that appears to be well tolerated. Which would actually be huge for SLE, given how many drugs have failed.
I want to reply to several things mentioned above.
1- The hypoglycemia issue. I have always had hypoglycemia and sugar cravings. I need to eat something every couple of hours.
Has anyone looked into this aspect? Is it a part or a contributing factor to CFS?
2-A few people mentioned taking antibiotics before CFS symptoms set in. I doubt if this was a contributing factor for me. However, I did develop a cold sore (HVS1) for the first time after taking zythromycin. I took it 2 more times and each time a more intense cold sore developed. My friend, who is a nurse, had the same experience. We have wondered if that particular antibiotic some how caused the cold sore virus to develop.
Does anyone have any comments of either of these items? Has there been research on hypoglycemia and/or antibiotics and CFS?
I wonder whether hypoglycemia is caused by induction of endogenous syntesis of d-ribose which maybe is triggered by low levels of adenosine. Adenosine is precursor for ATP and D-ribose apparently is needed to make adenosine (for energy) but d-ribose has also been shown to induce hypoglycemia. This leads to a catch22 because hypoglycemia may inhibit endogenous synthesis of D-ribose potentialy leading to depletion of ATP which will in turn will interfere with sugar metabolism etc. So maybe once a critical low level of adenosine has been reached, then the body can no longer synthesise d-ribose and therefore no longer raise levels of adenosine leading to chronic fatigue and impaired sugarmetabolism???
I too have always had hypoglycemia and sugar cravings and need to eat every few hours. I hadn’t come across this as being common in ME before I read this thread.
I was a brain athlete… meaning an accountant who worked an amazing number of hours during income tax season. Everybody around me would say ” I don’t know how you do it” . For many years, I had crashes that I would not recognize as such. And then the ultimate crash. I got better by stopping it all and eating what my body would ask: butter (vitamin A ? ) and salt. Potato chips became my medication, every day at 5 o’clock.
As I always say, a CFS hypothesis should at least explain the post-exertional sickness, our cardinal symptom. The problem working with only serverely ill patients though is that PEM is not pronounced with them. They are constantly sick, the boundary between PEM and non-PEM is a blur. Or, more likely, they are in constant state of PEM. Moderately ill patients, on the other hand, can function almost normally when they are well rested. The real disability for them is PEM that puts them in bed for days or weeks when they go over their limit imposed by CFS.
It’s not clear to me what this metabolic trap exactly is even after reading about amino acid oxidation. But one of the weakness of any metabolic hypothesis is that they don’t explain PEM cleanly. Can exertion drive their cells into dysfunctional metabolic state and then recover after days or weeks? Possible, but they’ll have to find a simple way to explain the relationship between exertion and metabolic genes going out of whack, before testing any prediction.
As for the body builders that Phar is looking for, I’m not one of them, but I did end up in CFS after repeated over-training. Wrestling/judo are the most energy thirsty anaerobic sports and I used roll with the boys 2 hours a night. I used to get sick weeks at a time whenever I practiced 4 times a week. 3 times were my limit, obviously. One day I never recovered from the over-training syndrome and hence my problem got reclassified as CFS.
PEM seems to be somewhat separate from the other ME symptoms. I’ve found an effective PEM blocker (cumin, regular, not black). For me, it blocks exertion-triggered PEM completely, but doesn’t reduce the baseline ME symptoms. My guess is that ME and PEM involve the same metabolic pathway leading to symptoms, but have different triggers. For me, cumin blocks one of the triggers.
I also get an increase in symptom severity from mental stimulation, such as driving or socializing. This is similar to PEM, and to the baseline ME symptoms, but the delay time is different from exertion-triggered PEM, so I consider it a different pathway for triggering symptoms. So, perhaps we have a chronic trigger (ME) for symptoms, and physical exertion and mental exertion each triggers increased severity.
I’ll also point out that physical exertion does not seem to affect the severity of my baseline ME symptoms. PEM makes me feel worse, but with that blocked, I can do very strenuous activities without negative effects (aside from normal fatigue). So, I disagree with Peter’s claim that ME is affected by exertion. PEM is a symptom of ME, and is affected by exertion.
Interesting – regular cumin – thanks for the idea. I will try it.
Nico, how do you take cumin and what a dose is helpful for you? Works cumin also, when you are in an the awful state of PEM, or is it necessary to take the cumin before the effort?
I wonder if PEM is caused by depletion of IMP (a precursor of ATP) in the body through exercise……….maybe because ribose synthesis via the Pentose Phosphate Pathway cannot keep up…….(low G6PD activity??)
Ribose apparently can induce IMP synthesis……does this mean that D-ribose supplements could positively influence exercise tolerance?
However, IMP synthesis uses ATP……..so supplementation with d-ribose should be started at very low levels and titrated upwards because if one gets the dosage wrong one could induce a crash and make things worse…..
I really wonder…….
TK makes important notes on PEM. You can name variations of symptoms that have value and maybe give som clues, but to sum up ME in 2-3 sentences.
1. Exceptionally low tolerance for any form of exertion
2. Overdoing(which says nothing) will cause an absolute and abnorm payback
3. The payback will be extreme both in symptoms and in time
You use 1 unit, you pay a 100. That is the hallmark of ME. We need to repeat this over and over again.
It may be costly and hard, but any study should ideally focus on and try to do good measures of PEM. It may not reveal the final cause, but if one could mend this, that would be of immense value for patients.
Like TK I came down with fully developed ME after substantial overtraining in a possible combination with “quiet” mono. The first is maybe something you could label as “not very smart, the “quiet” mono not easy to know. The combinations is scary.
At last, a significant point is that a ME-patient when well rested, these patients may function almost “normally”’for a very short amount of time, ref “Moderately ill patients, on the other hand, can function almost normally when they are well rested. The real disability for them is PEM that puts them in bed for days or weeks when they go over their limit imposed by CFS.”
Thanks for all the research efforts. I hope they are financially rewarded at some time, and that the CFS/ME community is also rewarded with some relief!
My daughter became ill 9 years ago at 13 years of age. In that time we have had at least three tests done of urinary organic acids which outline amino acid profiles. Also numerous other metabolites tested. Would this be helpful?
Would the Family Tree Mitochondrial test be of any benefit to the researchers? If so, please explain what to do to submit the data. It looks like the Ancestry test is not of value.
As a semi-professional genealogist & avid amateur, I have established contact with a wide range of known family members as well as DNA matches. My father [who was an MD] & I believe that my mother had CFS & that I inherited the problem from her. Looking back, I can see “footprints in the sand” indicative of CFS starting in childhood. In addition, I have at least one first cousin who also has it. I don’t know if family clusters are of interest.
This is very promising. I’ll try about anything at this point! I’ve battled this since 1993 and blood tests have shown latent EBV in my blood, possibly from a misdiagnosed case of mono in college. It’s really taking a toll on me. I would love to be involved in the research of ME/CFS but there aren’t any opportunities here in Kansas City.
This is in response to Karen Carr Biehl’s post on April 6, 2018 about being diagnosed with Anderson Tawil Syndrome, a disease that causes her to experience intermittent, temporary paralysis. Have you ever been tested for autoantibodies to acetylcholine receptors? A lack of acetylcholine can produce temporary paralysis and is seen in people suffering from Myasthenia Gravis (MG), an autoimmune disease you may already be familiar with, in which the body attacks and damages, impairs, or destroys the acetylcholine receptors at the muscular junctions. There are two types of acetylcholine receptors, nicotinic and muscarinic. Usually, it’s the nicotinic acetylcholine receptors that are affected in MG. However, there have been several research studies over the years that have identified autoantibodies in the muscarinc acetylcholine receptors of people with ME CFS. This subset of ME CFS patients usually suffers from some form of autonomic nervous system disorder. In my case, my worst ME CFS symptoms manifest as autonomic dysfunction with an impaired parasympathetic (“rest and recover”) nervous system and possibly and over reactive sympathetic (“fight or flight”) nervous system. Having researched the role of the vagus nerve, in regulating the parasympathetic nervous system, I decided to try a vagus nerve supplement called Parasym Plus recommended by a Physiologist who recently worked on me. It contains a proprietary blend of a form of acetylcholine and l-carnitine, the latter of which I was already taking, along with numerous other vitamins and supplements, since becoming ill with ME CFS in July of 2016. My vitamin and supplement regimen includes COQ10, Glutathione, D-Ribose, the Methyl forms of Folate and B12 (since I suspect I carry either one or both defective MTHFR genes), the active form of B6, Zinc, Magnesium, Turmeric, Alpha Lipoic Acid (this has helped tremendously in terms of pain control from Fibromyalgia), and high dose Vitamin C. I developed ME CFS following a viral infection later confirmed to be a reactivated case of EBV. Since then, I have tested positive for other viruses linked to ME CFS. In any case, shortly after beginning the new supplement, I experienced an improvement in my symptoms for the first time in nearly two years. It’s certainly not a cure but it has given me some hope since nothing had improved my symptoms even marginally and for those that did, the improvement was temporary. Presently, I’m being tested for the autoantibodies to the acetylcholine receptors so it will be interesting to see my results. I’m convinced, as I’m sure so many other people are, that there are many subsets of ME CFS patients and the disease develops and the symptoms manifest differently based on our own unique “footprint” which includes our genetic defects and susceptibilities, our internal “wiring,” viral, bacterial, and parasitic infections, exposure to environmental toxins, and physical and emotional trauma.
Thank you for all of your work. I would caution you, however, in assuming gym rats working out for a couple hours a day, should be a category. You need to assess a mother/housewife/cook from scratch/home gardener/lawn service, animal caretaker, occasionally helping out on the farm and with livestock and crops, just to name a few. Living in a hot humid area of the US. I have been to a gym, and I have done all of the above, putting in a lot more hours and sweating more than I care to admit.
My health problems started when I was 7 in 1950 with a tonsillitis infection. In those days doctors did not want to operate in the summer months unless absolutely necessary because the hospitals were filled with children suffering from polio. So my tonsillectomy was held off hoping to get past that season. Unfortunately, I soon came down with all the symptoms of Polio and I was rushed to the hospital for a spinal tap and other tests. It showed a non-polio bacterial infection that had settled in my kidneys resulting in Nephritis. I was on Penicillin shots every 2 hours for two weeks and then Penicillin pills for the next 6 months. I was put on complete bed rest for six months and put on a no salt, no protein diet of baby food fruits and vegetables. I did recover, but I was never “normal” again. Tired, aches and pains, extreme allergies to just about everything, supersensitive to everything, constant rounds of antibiotics for bronchitis and sinusitis. Unable to tolerate inoculations because of allergic reactions. I was finally diagnosed with MPS in the 1980’s and FMS in 2000. I am sure I would qualify for CFS as well. Taking allergy shots for over 45 years has made life tolerable. I do have resident simplex 1 viruses that show up in bloodwork when they are active. I have found that taking l-lysine on an empty stomach can keep them in check if I increase the amount when they re-activate. My energy levels are greatly improved by taking inositol at high levels several times a day. It acts as a transporter for thyroid hormones. I also take lots of vitamin supplements because my many food allergies and intolerances (which I cannot avoid if I want to live) result in a hyperactive digestive tract so I do not get the full value of what I eat. The end result is I can live a fairly normal life and hardly ever get sick anymore, but still have hypersensitivities, aches and pains from the MPS trigger points and arthritis. I take Tylenol, heat, massage and electrical therapy for that. I have to be careful not to overdo my activities or I will pay for it for days afterward. I have had my DNA done by Ancestry so I guess it does not help this project, but I can’t afford the cost of the full test.
Is there a deadline of when you would need information from ME patients, including Genome Sequencing?
Also, I’m in the Palo Alto area and would be willing to be available for any other studies or samples you may need.
Thank you! Please email Julie Wilhelmy in Ron Davis’s lab and let her know you are available for donating blood. wilhelmy@stanford.edu She will get back to you with the details. Thanks again. It’s so helpful. We need healthy controls too, so if you know people, especially around age 25-50, please have them contact her. Thanks again.
Janet
“My energy levels are greatly improved by taking inositol at high levels several times a day”
That is very interesting, thank you for sharing. Inositol is made from G6P in the body so maybe by taking inositol, G6P is freed up for use in the Pentose Phosphate Pathway instead, potentially leading to de novo synthesis of ATP for energy (via ribose). If it turns out that I cannot (yet?) tolerate low amounts of D-ribose as a supplement, I will try inositol.
Moira, I learned about inositol when I was participating in the Fibrom-L discussion group awhile back. Several participants had mentioned they were trying a protocol used by a doctor who was treating CFS and FMS patients with some success. I think he was from the Carolinas–don’t remember his name. Anyway the idea was to take 650-1000 mg with food for a few days and see if there was any help to energy levels. If not, to increase the dosage gradually every few days. If you got to a certain level and there was no benefit to discontinue. I think the upper level was 10,000mg. If you found at some point that there WAS a benefit in energy, you continued to increase the dosage until there was no additional benefit and back off to the last level that gave you the benefit. It worked for me. The amount I stopped at was 2600mg in the morning (for me 8-10 am)and 1950mg in the afternoon(3-6 pm). That afternoon dose takes me functional right up to midnight. I have to be sure to take it by 6 pm, because if I take it later, I will be up most of the night!
Another interesting note–there was a study published with the last two years concerning diabetes and pre-diabetes that had a surprising outcome. A large number of people who were considered pre-diabetic were followed over a long period of time. They wanted to see which ones progressed to full blown diabetes and which did not. Then they looked at lifestyles, medications and supplements between the two groups to see what differences there might be. They expected medications diets and lifestyles to contribute to the outcome. They were surprised to find that every one of the participants who were taking supplemental inositol did NOT develop diabetes no matter what their lifestyle or diet or medications or other supplements. All other factors were mixed in results. Most of those not taking inositol went on to develop diabetes
My husband was a good example of that. He had tried inositol and found it helpful for energy as well. He loved cookies and carbs. He was overweight and had become rather sedentary. Both his parents had become diabetics. Looking at his health records, you would assume he was diabetic. He lived well into his 70’s (longer than his parents) and died from congestive heart failure and MRSA, but he never became a diabetic. After reading that study, now I think I know why.
Cort,
To your knowledge has anyone done a survey on antibiotics taken before developing CFS? Could we do one via this site? Or is it a mute point considering how most people have been on antibiotics.
my daughter was an olympic level swimmer until senior hs year. finally at pediatric healthcare was told she has been a strep carrier always in there for strep and always given antibiotics and shots they said she had to have, starting hs once given 3 shots at one sitting against my better judgement but her mom is big on pushing the kids past theyr limits and needles suposed for prevention. then got mono then the slide .. and eventually told after the multiple shots and then the momo, they could no longer manage her and sent us to childrens hospital and its been every one of the best hospitals in the boston area for multiplying symptoms like stomach function ibs?, no energy even after sleep cf?, sick off all food including every med given, tinitus etc etc etc…. now seeing integrative specialists. mystery illness(s) my 24 yr old daughter fighting this having every test eastern medical has since jr high school…finally had to drop out last semester at best college with a mono crash $120000 in debt…just our portion… trying to be supportive parent in financial crisis
So, so sorry to hear this….:(
So much pain and difficulty. Why we must keep fighting…
For sure we could do a survey. As you note thought I imagine that that everyone has had courses of antibiotics at some point but some have had more than others. I probably did just a couple of times when I was a kid.
Might be a good idea to also put in the options:
“Took antibiotics multiple times but the same type of infection came back multiple times. Then after another infection and taking another round of antibiotics I got ill”.
and
“Took antibiotics but it was never clear that the original infection was wiped out”.
ME often starts after viral, parasite or mold infection but rarely after bacterial infection. If Lyme disease were a variant of ME then this is the only major exception IMO. But Borelia is renown to be very difficult to threat with antibiotics. So if we include that one too we come too:
ME often starts after any type of infection as long as antibiotics, antivirals, anti… don’t kill off the infection soon and good enough.
Nowadays for example they often give people with mono immediate antivirals with good result to recovery. I imagine that could also mean: less chance for ME or MS later on. If wright it could also mean: having less effective antibiotics due to overuse and bacterial resistance may lead to a growing ME epidemic in the future.
So: is the biggest cause of ME after antibiotics the antibiotics itself or the failure of them to eradicate the infection? Even if bacterial infection markers are gone, slumbering viral infection often take opportunistic advantage of a strong bacterial infection. Sorting this one out may use the help of a big data study IMO.
About antibiotics
Maybe problem could also be that after antibiotics the dead bacteria is not being cleaned or cleared out by the body ( due to a genetic fault in the part responsible of cleaning out toxins etc).Thus it becomes toxic. And this stuff can easy move in the blood from one place to the other..the immunesystem reacts on it..setting of an upregulated offensive..this leads to inflammation..and toxins build up even more damaging mitochondria..
Just a thought…
I was sick as a baby..due to contaminated water..i became a baloon..swallowed body..in hospital they gave me shots..of antibiotics maybe, dont have a record of this..i survived. When i was 7 i got toncilites without treatment..then i felt very ill and fatigued..after i experienced episodes of fatigue..when i reached 32 i got a bad flu amd received that year 4 timed antibiotics due to infections..and ever since worsening ME.
I too lifted quite heavily and did HIIT training. I fell ill my senior year of highschool and played football and lacrosse. When I came down with Mono, I was currently lifting 6 days a week and doing High Intensity Interval Training for 4 of those. This included boxing, swimming, running on incline, etc.. I used an altitude mask for conditioning, ate chicken breast, grapefruit, and other healthy options for almost all meals, and was taking a supplement called Hydroxycut. I was in the best shape of my life before I came down with mono and found myself never getting better. Hope this helps
Hope somebody keeps us informed of pricing at Illumina or other WGS firms. If Illumina testing is considered diagnostic for disease, I’d probably do it right away. Otherwise, I’d like to wait until the price drops to the low hundreds.
Sorry if I am a little late to this.
I have a weightlifting story from the beginning of my illness and I will also share my experience with exercise during my illness.
One morning in 1996 I woke up paralyzed. When I regained my ability to move I went to a walk-in clinic and was diagnosed with the flu. The strange thing was I felt completely better the following day, so I went to work. Around this time, I developed afternoon headaches. Every day around 1 o’clock I had a headache. I felt strange and had waves of soreness, tiredness, poor concentration, head pressure, headaches, itchy skin, blurry vision and extreme light sensitivity. I was weight lifting at the time I became ill. Nothing too extreme though. 3 times a week for 45 minutes with cardio every other day. I started getting a migraine within minutes of completing my weight workouts. I had no option but to stop working out. My diet at that time would have included a lot of rice, canned tuna, rice cakes, peanut butter and cottage cheese. I drank a protein shake that had skim milk, whey powder and a banana in it.
Approx. 7 years into my illness I was diagnosed with FM. Around year 10 of my illness I started running. It went mostly well for the first year and a half. Lots of running injuries and sometimes I could be found crying on the side of the road because it was so painful, but I did it. I could only ever run 3 days a week and my 10k time over 3 years never improved. My body did not recover fast enough to add a 4th run day. Around year 13 of my illness I was diagnosed with CFS. Even though I was running, I was told that my treadmill test showed that I was a little out of shape and that I should exercise more. So, I continued to run. One day I was 10 minutes into a run and I hit the wall. Zero energy. Had to sit down, have a gel and some water. Did not help. It was a very slow, painful walk back to my starting point. Every run after this was the same. 10 minutes into the run I would burn though my glycogen stores and have nothing left. So, I quit running. Around year 15 I found a specialist and was diagnosed with ME. A few months before my ME diagnosis I had decided to give cycling a try. I did alright riding 10k, 20k and even 30k. One day I went for a ride that was supposed to be 50k but turned out to be 70k. It was a tough ride because it was more than twice my previous distance. It was difficult, but I was not surprised because it was a big ride. After the ride I was tired but otherwise fine. The following day I was tired but fine. Two days after my ride I was not fine. I got a migraine. My migraine lasted for 7 days. I had never in my life experienced a 7-day migraine before this. I had many 7-day migraines after the initial one. 7-day migraine if I walked 3 blocks to the post office. 7-day migraine if I dared shower and make dinner in the same day. I quit cycling. 6 years after my 70k bike ride I am still housebound and at times bedridden.
Unfortunately, I can not afford to have my whole genome tested. I am hoping to have the 23andme testing done in the near future.
I believe I contracted CVS around 1980 in Incline Village. I have had several flair ups since then that have cost me jobs etc. In 2006 I had a tramatic physical and emotional experience that caused my CFS to flair up and by 2011 I had to quit my job or be fired do to this illness. It’s 2018 and it is getting worse. I can only pray that someday there will be a cure or at least a way to keep anyone else from getting this. The depression alone from people thinking you are crazy is bad in itself.
My CFS story started in 2006 I was 16 years old and I was a workout freak, use to lift or play sports 6 days a week multiple times a day while taking protein powder drinks twice a day. I got some stomach infection and got sick for 1 week but recovered fine. I was under a lot of stress then about 6 weeks after my initial stomach illness got some infection again and thats when my CFS started I got diagnosed by Dr montoya at Stanford.
My CFS is moderate compared to most I can still try to work out just cant go for long at all until my muscles hurt so bad and they cant go any longer but I never crash from regular activities or stress. The only time I’ve crashed was 5 years ago after a ACTH stress test which is an ACTH injection testing my adrenals which caused my fatigue and muscle pain to increase 5x the next day that never returned to my original CFS state. I also use to be able to sleep 12 hrs a day but would still be tired now I’m even more tired but find it hard to fall asleep and only can sleep 8 hrs a day.
I have seen to order my genome on the website illumina, veritas, etc… but I don’t find the page or link to buy the test… could you give me this ? I live in france and would like to participate for the study.
Does anyone have an idea of what we might see as a treatment for this hypothesis?
“23andMe covers only 3 of the five variants that are important to the current metabolic trap hypothesis.”
does anyone know what those variants are? I’d like to look them up… (the “rs” numbers)
Reading all the very interesting but quite sad stories involving so much because of so much suffering got me to wonder if people who one might consider to be on the “lazy” side ever got the illness too or is it only the ones like myself who were used to pushing on or through any physical difficulties we might have been experiencing. Ultimately did this way of leading our lives actually contribute to us getting ME?
I would love to know the answer to this and wonder whether it would add anything as to what is going on with us and why we cannot get back to normal.
Dear Robert, Cort, Ron and all who are trying to find the cause of our illness, thank you! thank you! thank you!!! I have tears of hope in my eyes that you will succeed so that we can finally start addressing the cause of our illness leading to new approaches to correct it and get us back to health.
As with many of you, my severe FM was triggered by very high stress…mine from work. I’ve had to be homebound the last 2,5 years with this hell on earth. Looking back, maybe it was always lurking in the background? Rob, I’ll email you a quick summary of history if it’s of any help. I too am willing to be a guinea pig if it means finding a cure.
I do believe there must be some genetic predisposition at work as I have 2 cousins who also have been diagnosed, one is now in a wheelchair following a stroke and is only in her early 50s.
In my research and trying to connect the dots, I’ve come across the relationship between stress-> gut bacteria-> brain fog and successfully treating FM and c.difficile with fecal microbiata transfers. Has this already been considered?
Please let me know if you need the info! Keep us posted please!!!
I hope you can get your family into a study Agnes! Please sign up with the SMCI’s Biobank and Patient Registry 🙂
Robert and Cort,
Would you be interested in talking to several women that were diagnosed with CFS/FM after taking a drug called Lupron?
Also, would sharing my amino acid / organic acid testing be useful to your research?
You took lupron also? I attribute all my symptoms to lupron. It happened so quickly after lupron that there has to be a connection.
After passing the bar exam, I started an internship at one of the busiest prosecutor’s office in the country. I also had to take on another job. I was also obsessed with working out and had more energy than the average person. The only meat I ate was fish. I had undiagnosed Celiac disease. Suddenly, the steps I used to take two at a time, I had to use a handrail. I felt as if weights were put on my ankles and arms,and I felt short of breath. My white blood cells were low. I think the trigger was mono. I was a patient of Dr Lerner, and I did achieve a semi-recovery for a while where I was able to work out again. I did have relapses which took about 3 days to recover. Once off treatment I eventually crashed when I was doing the work of 3 APA’s. I now go to Stanford’s CFS Clinic. I did 23andme, and had some DNA work done by a mitochondrial Dr. at the Cleveland Clinic. Have also been to Mayo, not sure of all the tests they ran.
Dr. Phair mentioned above in comments his preference for exome rather than whole genome, but I didn’t see any comment as to how/where to get this. Am one of the lucky ones who can afford to do this. Please advise. I am near Stanford and a patient of Drs. Montoya/Bonilla; got sick at 61 and am now 65, so too old for most other studies. Lifelong athlete until 4 years ago and hope to run again some day.
I would like to order 23andme kit there are two kids at there webpage I’m confused as what should I order can someone please tell me? Also the other labs Robert put sounds good speacially 10xgenomics if Im willing to test with 10xgenomics what test should I required ???? Please tell me
I was sick with a virus every month for at least a year before contracting CFS/ME I also had weird cold sensations accompanying these viruses. I have had ME for almost a year and have not had any viruses – instead, apart from having low energy I feel cold all the time, have random pains, and my sleep cycles are all messed up. So a metabolic change makes sense. Mine started when I was going through a lot of stress. I wonder if you can have CFS/ME without cognitive dysfunction?
i will just tell you all that i am 58….i got sick when i was living in a motel room for 6 months while going to school. I got violently sick one night …diahrea..vommitting . It never left me. Two weeks after getting sick i developed an ulcer…sore aching muscles and joints, aching jaws also. It continued to grow inside of me until one chemical overexposure tipped me over the edge. I ended up in hospital due to a slipped disc that would not heal. While in hospital i decided to stop eating for 5 days. When i began to eat again, my body took off and began to work the way it was supposed to. I got home from hospital and was re exposed to the hardwood floor finish that contained tolyuene and benzene …tipped me over the edge and down i went again..this time for good. Ive had cfs ever since. Terrible waste of a life! I was such a talented artist, taxidermist etc.
just to add to the above comment…i also was on tetracycline as a child for many months for acne that never did take the acne away. Doc said..”oh..just keep taking them”. That was back in the 70s when abx were becoming a popular candy for folks
I have had CFS for so long it has literally become my life. I have no doctor who takes it seriously. Summer has its special challenges because of heat intolerance on top of labile BP, low blood volume, and what I suspect are arrythmias. Just recovered from another bout with pneumonia. I need to wait for a health crisis for someone to believe me. Some things are new, some things are worse, and some things are better. All in all, I still think I have become far less functional, and I do not dare even do volunteer work anymore.
I am always interested in new findings, and it would make sense if CFS had subtypes like mental illness or cancer. Just because the precipitating factors, cause, course, and prognosis of what we may assume a a single condition is different for different people, it does not mean the illness is just an hystercal fabrication.
I was recently reading something about VCZV and CFS because I got chicken pox as an adult, and became sick not long after, in my second year of grad school. I was able to finish and graduate with honors, pass the licensure exam.while I had the flu, but ironically I cannot work. My plan was to do research in PTSD. Some dreams die hard.
Does anyone have relapses that actually only last a day or two when there is a weird ambient light outside that most other people cannot see? It is sort of hazy but it is not hazy ? I have talked with a few other people who have an auto-immune disorder (I.e. MS) who can see the wired light. I have charted humidity and atmospheric pressure and it does not correlate with my relapse days and the weird light . Possibly ozone or CO?
My story. I was diagnosed with CFS in 1994. For 5 yrs I was pretty ill but managed to work as a home health physical therapist. During this period I tried just about everything – hydrogen periods IV drips, naturopathy, many different meds and supplements, vit C drips ect ect. In 1999 I did 4 things – got rid of my husband, gluten free diet for 6 mos, very mild moderate exercise in the form of running with gradual increase in distance but never more than 6 miles and Adderrall My daughter had just been diagnosed with ADD and my MD said “hey maybe you are suffering from adult ADD”. He put me on Adderrall and since I function as a full time physical therapist and currently swim 1 mile 3 to 4 x/ week. I can no longer run due to muscle pain . I will say I am not totally normal. I hesitate to make any social plans because I know I might not be up to it physically. Intermittently I get the horrible fatigue, achiness, light headedness, my eyes don’t work and different than most CHF sufferers horrible nausea and this weird pain deep between my ears that is not an earache nor a headache just this weird pain. These last 2 symptoms are bad on those days with the weird light . And usually my relapses are just a day to 3 days . They come suddenly, usually associated with the wierd ambient light outside and leave suddenly. Please note before it is even light outside I feel the symptoms so it is not caused by the light but by something causing the light.
My history. I had recurring severe tonsillitis starting at 10 years old. I was a national level competitive swimmer starting at 10 years old. This was in the day swimmers were commonly overtrained ( 1966 to 1975). When I was 16 years old, training in water 4 to 6 hours a day, I was severely ill for 3 days. I had a fever of 103 degrees F plus. The doctor came to my home twice and did blood tests. I tested negative for mono and everything I was basically undiagnosed ( at that time overtraining was not recognized). I returned to training probably in less than a week but was never the same as a competitive swimmer, however, I was not sick with CFS.
At least I don’t think I was.
I quit swimming about a year later . I achieved 2 university degrees. Married along the way. Exercised a lot Ran 6 to 20 miles 4 to 6x / week. Taught > 25 advanced high impact aerobic classes a week. I did continue to get sore throats, swollen glands and bronchitis a lot and had pneumonia twice. ( by the way finally had a tonsillectomy at 17 years old) but did not suffer from the S&S of CFS.
I had my first and only child at 38 years old and 1 1/2 years later had a sore throat, swollen glands and flu ( don’t remember if I had antibiotics at that time but probably did and regardless was treated with antibiotics multiple multiple times in the past for my throats) Immediately after that I had S&S of CFS lasting 5 years as the above story tells. After 1999 I have had relapses some lasting longer than the day or two described above related to the wierd ambient light but those longer lasting relapses were always related to some psychological or physical,stress.
I wanted to share my story for 2 reasons. First, To let people know about the Adderrall which may not be an acceptable answer to many ( probably depending on how desperate one is and how bad one is suffering ) Second, to see if others see the wierd light on particularly bad symptom days because this might give us a clue to cause and or treatment.
P.S. Since the multiple failed treatments I did go through between 1994 and 1999 I really do not follow the current research much and I never ever go to the doctor. I just do what I can to get by – but it really is no life
I heard of a drug causing this light but can’t remmember what it was….darn. I believe the light does go away over time in that case.
Looking forward to Stanford Symposium this Saturday.
I was a martial arts fanatic. After hospitalization with MRSA infection and obscene numbers of IV antibiotics and even post surgery oral antibiotics, I had a steady decline.
I did add testosterone replacement therapy after this event as it seemed my production plummeted.
Bed ridden for a few year, I did erase my gut with antibiotics again and even Epsom salt to evacuate gut. Then produced fecal transplant capsules at home using centrifuge, and triple encapsulate for late GI delivery.
Would say that I recovered 50% of my life. Still looking for answers to recover more fully, and beleive that the metabolic trap is likely the key.
Seems to me that there is likely something in our blood plasma (like an antibody) that is interfering with cell receptors.
I hope that Dr. phair will give some details enough for those of us who cannot afford doctor supervision and are willing to test on ourselves safely.
** I have found anecdotal success with methylated b6,b9,b12, but something still missing. **
Thank you for the volunteer work Dr. phair. You deserve a nobel already in my book.
If you have questions, my email is first initial last name at gmail.
Hello Dr. Phair, I read an article that said you think high tryptophan might cause this disease. I took tryptophan supplements in 1989 for several months and had a decline in my health that I’ve never really recovered from. I will be very interested in the results of your research. Thank you
I have had ME/CFS for many years and am disabled at this point because of it. My crash started when I took Lupron for endometriosis pain. The pain quickly started. The severe fatigue quickly followed. I was 37 at the time and went from being very active to severe fatigue almost overnight. Prior to my health issues with endometriosis, my husband had had a severe injury on his job and I was taking care of three kids, two of which had health issues, one is autistic and one has mild cerebral palsy. I did the 23 and me years ago so have the old version testing. I believe you are looking for ID02 and of the three I have two of the three. I will send you the details when I can figure out how to do that. I appreciate all you are doing. I would love to get my life back. I have found that eating a high antioxidant cocoa flavonoid shake has helped improve my quality of life but symptoms persist overall.
My son was very healthy and active until the age of 15, although he always had problems to fall asleep. Then he began going to the gym to lift weights, and became obsessed to the point of training almost every day. I don’t remember exactly what he was eating most, but he was certainly eating eggs and drinking plenty of milk. After about 7 months of intense work in the gym he crashed. Almost suddenly he did not have the strength to lift half of what he lifted before, and felt constantly tired. Over time his sleeping deteriorated further, and started experiencing brain fog. His form of CFS/ME could be considered mild to moderate. He has had it for more than 3 years now. Recently we found out that he is intolerant to various foods, particularly grains, eggs, and milk. He is on a diet now. He has not diarrhea anymore (which he had often before), but all other symptoms are still there.
Learned some new stuff with very detailed information.
firstly:
Is there a site dedicated to self-reporting by ‘overnight’
recoverers, for those rare individuals who recover ‘overnight’.
Would seeing their metabolomics inform the trap, or further
muddy the waters?
secondly:
Is it feasible, at some point in time, where patients could pay to have a lab tech run their samples without their being part of the particular research study itself.
The money could help fund the tech’s salary. And the results would provide a depth of samples of potential immediate and/or future value.
And patients could thus be involved in a new way, instead of feeling left out of studies.
Search and compare surgical treatment prices, medical treatment prices,
diagnostic tests price etc among various hospitals near your location with just a single click.
Thank you for the article about the metabolic trap