Life Continues to Happen. Health Rising’s hiatus continues…
Sometimes life gets in the way…
Two botched neuters resulted in 5 trips to the emergency room, a massive surgery to save one dog’s life (thankfully successful), 3 days in intensive care, a new infection, another surgery to fix blown sutures, two early morning returns, a trailer breakdown, major dental work, and two trips to Phoenix.
Two weeks later, things are looking better. The dogs got a good report from the vet yesterday and hopefully over the next ten days or so, the cones will come off and they will be back in business.
Health Rising’s Quickie Summer Donation Drive is On!Not surprisingly, my Oura ring has marked many high stress days, but I have been taking care to rest, and my sleep has been OK, and I am fine. Onto the blog!
The Open Medicine Foundation’s BioQuest Project
Geoff’s Narration
The GIST
BioQuest – the goal: find 5-20 molecular biomarkers for ME/CFS.
“A quantifiable biomarker is urgently required to assist in and accelerate a correct ME/CFS diagnosis. Although ME/CFS often causes severe disability, the lack of a clearly understood aetiology and corresponding diagnostic biomarker fuel a significant level of scepticism, trivialisation, marginalisation and misunderstanding of ME/CFS in wider society, including among medical personnel.” From “The search for a blood-based biomarker for Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS): from biochemistry to electrophysiology” Feb. 2025
My eyes widened when I looked at the Open Medicine Foundation’s Large-Scale Biomarker Project (BioQuest) study. It’s the kind of bold study that this big (in so many ways) disease and small field needs.
The big data biomarker approach. The goal: distill ME/CFS into its molecular subsets.
The BioQuest study is aimed at uncovering a holy grail in ME/CFS – biologically proven subsets in ME/CFS. This isn’t “we’re looking for biological subsets” approach; it’s a “we’re going to find, document and validate biological subsets in ME/CFS” project. The study is bigger – not just a little bigger but more like a magnitude bigger – than anything that’s been attempted before. In a field larded with 20, 30, 50, maybe 100-person studies, it’s a 1,000-person study.
It’s not just the size – it’s the scope. The OMF is throwing multiple omics assessments (metabolomics, lipodomics, proteomics, cytokines and clinical findings) at their samples in an attempt to uncover biomarkers.
It’s not easy for a poorly funded field like ME/CFS to come up with potentially game-changing studies, but by cleverly leveraging assets from other studies, the Open Medicine Foundation has found a way to do it.
THE GIST
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Strong biomarkers, if they are found, could turn ME/CFS from a complicated, mysterious disorder into a series of clearer ones.
Life continues to happen. Botched neuters, emergency surgeries, stays at the doggie ICU, early morning returns, etc., have kept Health Rising from publishing blogs. Hopefully, over the next week the dog issues will be resolved.
- Is the Open Medicine Foundation’s BioQuest study the big biomarker study we’ve all been waiting for? At 1,000 samples strong, I think it is. The BioQuest multiphase project will used multiple omics’ analyses (metabolomics, proteomics, cytokines, etc.) in an attempt to, once and for all, find, document and validate molecular biomarkers that identify the subsets that everyone believes are present.
- I talked with Danielle Meadows PhD about the study (see YouTube interview in the blog). The massive study has been under development and gathering funding for several years, but with the samples headed to the labs as we were speaking, it was now underway.
- The study size dwarfs anything that has been done before. It includes 400 ME/CFS, 400 age and sex matched healthy controls, and 200 samples from multiple sclerosis, burnout syndrome, depression and long-COVID patients.
- The study benefits by using patients that come from a large geographic area, the inclusion of fatigue, and sedentary producing diseases (multiple sclerosis, burnout syndrome, long COVID) that will allow OMF researchers to filter out biological signals caused by simply being sedentary or fatigued.
- It hopes to produce between 5-20 molecular biomarkers (or signatures) that are able to identify distinct subsets in ME/CFS.
- It is phase one of a three phase project. In this first phase of the project, testing the samples will occupy the rest of this year. The artificial intelligence/bioinformatic analyses that assess the data will form the most time and resource intensive part of the study and will likely last all of 2027.
- If biomarkers are found (I would be shocked if they weren’t), the next phases of the project – verification and validation – will commence. These phases will involve testing on new sets of patients, including those with other diseases.
- This project has the potential to be transformative. History has shown that when a field transitions from small, fragmented studies to large-scale, biomarker studies that achieve validation, the impact on the disease can be huge.
- Blood test(s) for ME/CFS would erase stigma, validate the disease, result in quick diagnoses, make it easier to get disability insurance benefits, illuminate core factors in ME/CFS, enable researchers to target specific subsets, increase research funding, and get drug companies interested in this disease.
- Time will tell. Biomarkers can be weak or strong. They can point to secondary or core factors. The Alzheimer’s field spent a decade in a fruitless pursuit of what turned out to be a secondary factor – amyloid beta. On the other hand, mechanistic biomarkers that define core issues can quickly lead to treatments. Lupus, for instance, had no specific treatments until biomarker studies uncovered an “interferon signature” group and the first lupus drug was developed.
- Suddenly, we seem to be awash in ambitious studies that are attempting to get at the exact molecular drivers of this illness. The OMF’s BioQuest study, Amatica’s huge gene expression study, Precision Life’s mechanistic approach, and Liz Worthey and Camille Birch’s recent whole genome study suggest that the field is becoming more and more confident that it can, as Ian Lipkin asserted earlier this year, begin to unravel this complex disease.
- When I asked Danielle what excited her about the ME/CFS field right now, it was no surprise to hear that it was a focus on precision medicine’s ability to identify subtypes and provide treatments for them.
- We’re clearly light years ahead of where we were even five years ago. Seven years ago, I talked to Sadie Whittaker, Solve M.E’s Chief Scientific Officer, who came from the cancer field. She said that, above all, the ME/CFS field needed big data sets – the kind of data sets that turned breast cancer from one disease to ten diseases – and resulted in precision medicine treatments.
- Seven years later, the OMF is embarking on the biggest data set yet, and precision medicine is becoming a kind of buzzword in ME/CFS. While we don’t have it yet, it’s no longer a pie-in-the-sky idea but something numerous research groups feel is within reach.
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A Talk with Danielle Meadows PhD
I talked with the OMF’s Vice President of Research Programs and Operations Danielle Meadows about the study. Danielle has a PhD in Biomedical Engineering and has been in the middle of an impressive array of large efforts.
She was the Senior Scientific Officer for the huge CareEvolution Platform (which the unhide Solve M.E. effort is using), she developed and executed the project plan for the mobile health platform for the NIH’s RECOVER study, was a Project Director for a Scripps Research’s Long COVID Randomized Controlled Trial, and a Project Manager of the NIH’s All of Us Research Program.
The time is ripe for a study like this. Findings from small studies that continue to cohere around general themes suggest that biological subsets are simply waiting to be found. There’s been a lot of buzz around several possible biomarkers, including a Raman spectroscopy biomarker – a DNA conformation biomarker, a biomarker in the spinal fluid, or one using flow cytometry, but these require complex and/or expensive procedures.
The OMF, on the other hand, is looking for “a biochemical signature for ME/CFS that can be conveniently evaluated through a blood test.”; i.e. something that can easily be tested for via a standard lab.
Danielle said that creating the study design, raising funds for it, etc., has been underway at the OMF for several years. The study was announced in December 2024 and with the samples being transported to the labs has begun.
This study could not have been have happened without past efforts at the OMF Collaborative Center at Uppsala, and the Chronic Fatigue Initiative (thanks, Hitchens Foundation!) and to biobank samples, as recruiting new patients is expensive. These rigorously characterized samples from doctor-diagnosed patients include 400 people with ME/CFS, 400 healthy controls, and, as a bonus, 200 people with either multiple sclerosis, exertional malaise (burn out syndrome), clinical depression, and long COVID.
Broadscale Effort
“The important thing is if it’s a robust enough signature for ME/CFS, we’re gonna be able to see it with, you know, a panel of things. If it was one molecule, two molecules, we’d probably already have found it.” Danielle Meadows
The OMF’s broad approach – which incorporates metabolites, proteins, cytokines, etc., – strengthens the likelihood of finding verifiable biomarkers.
The OMF’s broadscale approach to measure over 10,000 proteins, metabolites, cytokines, etc., gives it a better chance to find strong biomarkers than say a single proteomic or metabolomic study.
Bringing fatiguing, sedentary producing diseases (multiple sclerosis, burn out syndrome, long COVID) into the mix also gives the study a leg up that will allow OMF researchers to filter out biological signals caused by simply being sedentary or fatigued. The study also benefits from two ME/CFS cohorts that derive from a large geographic area,
If this study follows OMF practices in other studies (that is, if it uses Somascan technology and processes the samples in highly controlled, high-throughput environment), the problem of “batch effects” that have confounded other studies will be reduced.
Five to 20 Molecular Signatures Expected
“We think we’re set up in a pretty good position, where if there’s something there to find, we’re gonna find it.” Danielle Meadows
No one expects to find a universal biomarker. The OMF expects to find from 5–20 molecular signatures. The number will depend upon how strong the signals are. Generally, researchers want to see 30-50 people with similar findings to identify a subset. That suggests that 400 ME/CFS samples could result in from 8-15 subsets – if really strong signals are found. For me, I would be very happy if the study was able to identify 3 or 4 significant subsets.
“We would not be able to conduct this study without AI. The analysis that I think we’re hoping to do is going to be hugely, hugely reliant on artificial intelligence and machine learning and all these sorts of things.” Danielle Meadows
A study of this size and complexity, not surprisingly, will take time. Danielle said the sample collation and testing will occupy the rest of this year and then AI/bio-informatics work will be the most time and resource intensive part of the study. It will likely last all of 2027. The OMF is already engaging with bioinformatics specialists to help guide the vast amount of analysis that will be needed.
Validation
Rome is not built in a day, and validating a biomarker will also take time. Biomarkers, after all, can impact everything from diagnosis, to research, to drug trials, and validating them does not happen overnight.
First, in the discovery phase, a wide net is cast to identify candidate biomarkers. Then, in the verification and validation phases, the candidates are tested in new samples and assessed against candidates from number of other diseases. The crucial step comes when outside researchers and labs validate the original findings. Once that is done – if it is done – ME/CFS is potentially off to the races.
Impact
History has shown that when a field transitions from small, fragmented studies to large-scale, biomarker studies that achieve validation, the impact on the disease can be transformative.
Large biomarker studies have provided the key that unlocked treatments for other diseases.
The validation of the HER2/neu oncogene in breast cancer in the 1980s led to the first targeted treatment for breast cancer. Large-scale studies indicating that B-cells play a crucial role in multiple sclerosis directly led to the development of a drug, Ocrevus (ocrelizumab), that specifically targeted them. Similarly, lupus moved from a kind of wastebasket autoimmune disease to a targeted one when omics’ studies identified an “interferon Signature” which resulted in the first new lupus drug in 50 years (Benlysta) being successfully tested and approved.
On the other hand, too much faith in the beta amyloid biomarker in Alzheimer’s, which identified a secondary instead of a core factor in Alzheimer’s, resulted in a decade of failed clinical trials. It’s possible, but probably not likely, that ME/CFS contains too many subsets (20-50) even for a 1,000 sample study to uncover.
A strong biomarker would be able to reliably distinguish ME/CFS from similar diseases (fibromyalgia, long COVID). The impact that strong, validated diagnostic biomarkers – if they are found – would have on the ME/CFS field could be immense. A mechanistic biomarker (i.e., a biomarker that directly identifies a core driver of the illness) could even quickly lead to targeted drug trials and effective treatments for a subset of patients.
“If we can identify subtypes, I think it goes a long way toward also just convincing larger pharmaceutical companies to take interest.” Danielle Meadows
- Doctor’s Office – People with ME/CFS would get diagnosed much more quickly, and the stigma patients face in doctors’ offices would fade. Subsets that point to specific treatment options could result in quicker, more effective treatments.
- Insurance and Disability – No more exercise tests needed to get disability? A validated finding could result in patients more quickly getting disability and insurance benefits.
- More Effective Research Studies – Research studies today are inhibited by having to assess symptomatically similar but biologically heterogeneous cohorts of patients. Being able to target biologically defined cohorts of ME/CFS would erase the “wastebasket” theme that has so inhibited researcher interest. Increased researcher interest and funding should allow researchers to drill down on specific kinds of ME/CFS. The OMF raised money from its supporters for this study but, call me naïve, if this study is successful, I would be shocked (shocked!) if the NIH didn’t provide ample funding for follow-up studies and ultimately, clinical trials. Funding the validation studies would, hopefully, not be a problem.
- Drug Companies Get Involved – Drug company interest (or lack of it) has been a huge hurdle. Pharmaceutical companies would feel more confident in testing their drugs. Identifying subsets would allow them to target drug trials to specific groups of patients. Ultimately prognostic biomarkers that allow them to assess how well a treatment is doing would be developed. Finding a prognostic biomarker was the breakthrough that allowed drug companies to uncover multiple drugs to stop HIV/AIDS in its tracks. It all starts with finding diagnostic biomarkers.
A Field Slowly Begins to Turn…
Strong biomarkers, if they are found, could turn ME/CFS from a complicated, mysterious disorder into a group of clearer ones.
Even if strong, validated biomarkers are not immediately found, it’s hard to imagine this study not being very helpful. Molecular signatures that researchers can drill down on will surely pop out. At the very least, researchers will have a better understanding of ME/CFS, and better cohorts to study. Plus, further analysis of any molecular signatures found could result in validated biomarkers – it will just take more time.
I would be shocked, though, if the study didn’t ultimately result in validated biomarkers. Everything tells us that the deeper researchers dig into the molecular roots of ME/CFS, the more they find.
Suddenly, we seem to be awash in ambitious studies that are attempting to get at the exact molecular drivers of this illness. The OMF’s BioQuest study, Amatica’s huge gene expression study, Precision Life’s mechanistic approach, and Liz Worthey and Camille Birch’s recent whole genome study suggest that the field is becoming more and more confident that it can, as Ian Lipkin asserted, begin to unravel this complex disease.
When I asked Danielle what excited her about the ME/CFS field right now, it was no surprise to hear that it was a focus on precision medicine’s ability to identify subtypes and provide treatments for them.
We’re clearly light years ahead of where we were even five years ago. Seven years ago, I talked to Sadie Whittaker, Solve M.E’s Chief Scientific Officer, who came from the cancer field. She said that, above all, the ME/CFS field needed big data sets – the kind of data sets that turned breast cancer from one disease to ten diseases – and resulted in precision medicine treatments. Seven years later precision medicine is becoming a kind of buzz word in ME/CFS. While we don’t have it yet, it’s no longer a pie-in-the-sky idea but something numerous research groups feel is within reach.
What about long COVID? LIINC’s long-COVID biomarker effort called “VIPER” is underway. VIPER doesn’t have, to my knowledge, a 1,000-person study, but it is an uber-organized, large-scale effort to test possible biomarkers. Right now, the VIPER is focused on finding pathogen biomarkers, but it will, at some point, expand them. It’ll be fascinating to compare BioQuest’s and VIPER’s results.
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Geez Cort! I was wondering where you were. I’m so sorry! Neutering is not rocket science. (Vet tech here) I know of only 1 botched job in 10 years with multiple hundreds of animals of all kinds. 1 could be a fluke but 2 at the same time is very suspicious. I hope you are negotiating paying for the pain, suffering, and emotional distress of you all! In case they object you might just mention the State Board of Vet Medicine that issues licenses. They would be providing the service for free if it were my dogs. Or they could look forward to explaining how they screwed up so badly to the board that can put restrictions on their license to practice. I really hope you find another vet!!
Thanks for the overall better news. Progress is being made, if slowly! Take good care.
Thanks Tracey. My partner knows a long time breeder who said she’s never seen such a thing. Despite the fact that the vet in question has regularly been getting reports regarding these two dogs they have never contacted us to ask how they are doing – so we are not happy campers and will see if we can do anything to recover the costs of several surgeries not to mention the stress of watching one young and very healthy dog nearly die.
This was well written, Cort. Thank you.
There are only 3 issues I am worried about concerning BioQuest – since it’s obviously well thought out and well organized (in my opinion).
1. In smaller studies, we have seen the effect that stimulating PEM has on increasing accuracy, sensitivity, and specificity. ie. MicroRNAs. So the question is will trying to find proteins, metabolities, cytokines and lipids in this study be effected by not stimulating PEM in the samples?
2. Will the sex data be disaggregated so we can if the markers are different for women and men?
3. For the Alzheimer’s blood test, the FDA asked for a study where the blood test was validated against using objective markers – MRI and Spinal Tap. In the case of ME/CFS, our only recognized objective marker is the 2-Day CPET. There is of course Dr. Moreau’s Cuff and Hexoskin for stimulating PEM and objectively measuring what occurs for 5 days as well. But it isn’t recognized, and as far as know, is only being used in Montreal.
So the question becomes, shouldn’t we be preparing for eventual validation of a BioSignature or a Biomarker by creating a Biobank for Biosamples taken from (2-Day CPET studies and 2-Day CPET ME/CFS diagnosis and additionally preparing a PEM biobank for biosamples taken from stimulating PEM by 2-Day CPET and Moreau’s Cuff?
Thank you for writing about OMF BioQuest.
Great question! I would think that our chances of finding a biomarker would be MUCH enhanced by using an exercise stressor. I think this “a Biobank for Biosamples taken from (2-Day CPET studies and 2-Day CPET ME/CFS diagnosis and additionally preparing a PEM biobank for biosamples taken from stimulating PEM by 2-Day CPET and Moreau’s Cuff?” is a wonderful idea.
Unfortunately, that would require that people exercise before taking their diagnostic test and that would complicate the OMF’s attempt to find a biomarker “that can be conveniently evaluated through a blood test.”
Let’s hope they find what they’re looking for in these samples – and that researchers continue to use exercise/cognitive stressors to unlock ME/CFS.
Thank you, Cort.
I just wanted to be clear, I think we need the 2-Day CPET/ Moreau’s Cuff to validate any ME/CFS biomarkers (for the FDA).
I want a diagnostic blood test so that PEM doesn’t have to be stimulated.
I don’t believe we should have to do what harms us to prove we are sick.
Which is why I think it would a better use of our time, energy, and money if we collected BioSamples from ME/CFS patients during diagnosis through 2-Day CPET (voluntarily) and used in ME/CFS studies with provoked stressors.
Like before doing the 2-Day CPET at Workwell, or at Cornell et cetera. Participant would sign a form saying they consent to bloods be taken Day 1,2, and 3, 4, and 5. That bloods can be biobanked at X Location. Participant is willing to fill out questionnaires and authorizes limited medical records to confirm symptoms and diagnosis. Something to that effect. It’s inline with what would be needed for FDA approval, and would probably also meet specifications to take biosamples from patients in PEM (idea from Christoph Ströck ).
Ultimately, I think we need to get at least 3 steps ahead of the FDA for a BioSignature. It’s not going to be easy. The rules never apply to us, so we need to apply the rules before they shut us out from them.
So the samples are used to help find and validate the biomarker.
Rather than just being used once.
At one point, the FDA is going to be asked for the BioSignature to go up against an objective biomarker to prove accuracy, sensitivity, and specificity – and I want to us to be 3 steps ahead.
I want that guy at the FDA who wants to cancel our biomarker for Swiss Re so badly, to stand up and say, “but it hasn’t been compared against an objective marker. ”
And for our representative to stand up and say clearly with the words ringing out, “It’s been done. done. done.”
“I just wanted to be clear, I think we need the 2-Day CPET/ Moreau’s Cuff to validate any ME/CFS biomarkers (for the FDA).”
Got it.
“Like before doing the 2-Day CPET at Workwell, or at Cornell et cetera. Participant would sign a form saying they consent to bloods be taken Day 1,2, and 3, 4, and 5. That bloods can be biobanked at X Location.”
Great idea! I used to wonder if these biobanked samples were ever being used but this study demonstrates in spades how valuable they are. I sincerely doubt the OMF could have done this study if they had to collect 1000 new samples – it’s too expensive.
I would hope that every NIH funded study that assessed samples got them into an ME/CFS biobank. If we’re going to do these mammoth studies we need lots of accessible samples.
Cort –
First – THANKS so much for everything you do for those of us with this oh-so-entertaining disease. I always head to your website for a clear explanation of new studies and other news.
Second – I’m so dadgum mad about what happened to your dogs that I did a little research into the complication rates of neutering male dogs, and they are minuscule! That original vet was just some kind of boxing-glove-wearing, butter-fingered monster.
Anyway, hope this info helps in some way…
https://www.caninejournal.com/dog-dying-during-spay-neuter-surgery/
Neuter Complication Rates
A study of five Canadian veterinary private practitioners found a total complication rate (both during and after surgery) of 19% for neutering male dogs.
The RCVS Knowledge database’s reported outcomes from 17,056 dog neutering surgeries between 2005 and 2023 included:
• 76.69% had no abnormalities or complications
• 12.42% had abnormalities, but no treatment was required
• 10.27% had complications that required treatment
• 0.58% had complications requiring surgical intervention*******
• 0.04% fatality
•
Why Trust Canine Journal?
Sally has over 20 years of experience in human health sciences communications, including 10 years as an expert on pet health conditions and treatment. She’s part of a dedicated team of canine professionals and long-time dog owners at Canine Journal. We spend countless hours researching the best care, training methods, and pet products, not only for our own pups but for all of our readers.
skeptvet.com/2018/11/new-report-on-complication-rates-for-neutering-surgery-in-dogs-and-cats/
(This guy lives in Britain, so these are British statistics. Also, I was a little put off by the name of their website – skeptvet – so I did some looking, and I think they’re a vet or other veterinary care worker who writes a blog about being skeptical about some of the more out-there treatments people get conned into for their animals, NOT about veterinary medicine).
Total complication rates for routine castration or spaying have been reported from 2.6%-33% of cases.The majority of these complications are minor and require no treatment. Complication rates vary considerably from practice to practice and are generally reported to be higher in studies of surgeries performed by students in training. Reported death rates are less than 0.1%.1-5 (1-5 was superscripted)
The RCVS has recently released the results of data collection on complications of neutering. Though not the result of a controlled, prospective research process, this audit report is based on over 30,000 individual surgeries, so it at least represents a potentially powerful source of data. The specific variables that affect outcome of neutering surgery in individual animals can’t be identified, and there is the problem of patients who can’t be followed and whose outcome is unknown. However, this type of data complements the research evidence already available and gives us a general sense of the complication rates in the UK for these common procedures.
Routine Neuter Complication Rates
The outcomes measured were cases with no complications, those with minor complications not needing treatment, problems needing medical treatment, problems needing surgical treatment, and fatalities. About 8% of the cases in the database were not available for followup, and these were not included in the calculation of complication rates.
Complications for Male Dogs:
Outcome. Frequency Percent Cum Percent
Abnormal but
no treatment necessary 977 11.4% 11.4%
Abnormal requiring
medical treatment 796 9.3% 20.6%
Abnormal requiring
surgical intervention 61 0.7% 21.3%
Fatality of animal 6 0.1% 21.4%
No abnormality
present 6763 78.6% 100.0%
Total 8603 100.0% 100.0%
(These were the references he used for his first paragraph).
References
1 Pollari FL, Bonnett BN, Bamsey SC, Meek AH, Allen DG.Postoperative complications of elective surgeries in dogs and cats determined by examining electronic and paper medical records. Journal of the American Veterinary Medical Association 1996;208(11):1882-6.
2 Howe LM. Short-term results and complications of prepubertal gonadectomy in cats and dogs. Journal of the American Veterinary Medical Association 1997;211(1):57-62.
3 Pollari FL, Bonnettt B.N. Evaluation of postoperative complications following elective surgeries of dogs and cats at private practices using computer records. Canadian Veterinary Journal 1996;37:672-8.
4 Burrow R, Batchelor D, Cripps P. Complications observed during and after ovariohysterectomy of 142 bitches at a veterinary teaching hospital. Veterinary Record 2005;157(26):829-33.
5 Root Kustritz MV. Effects of surgical sterilization on canine and feline health and on society. Reprod Domest Anim. 2012 Aug;47 Suppl 4:214-22.
Wow – thanks so much for that, Louise. That will be very helpful!
We have missed you Cort. So many blessings to you and your four legged friends xxx
Thanks, Michelle. I missed doing the blogs. They’re a source of excitement for me 🙂
Is this at all similar to what Amatica Health is doing?
It’s similar in its size – Amatica is aiming for 1000 samples because it believes it needs that many samples to uncover subsets. BioQuest is more comprehensive in that it includes metabolomics, proteomics, lipidomics and other measures. It is not, however, doing gene expression I don’t believe. How nice it would be if both studies coming from different angles and different patients uncovered similar subsets. (Talk about validation!)
Just imagine if the USA ceased being such a warmonger and invested 1% of its war budget into health research.
Disgrace
If I remember correctly studies have shown that a $1 invested in medical research more than pays for itself. There’s certainly enough research interest to sustain a 5fold increase in funding. Thankfully, Congress is still behind the NIH and the dramatic cuts proposed were not enacted. I would love to see a big increase, though.
HERE!! HERE!!
So grateful to hear that you and pups are on the other side of this very stressful and difficult time you have been going through! Thank you for letting us know what challenges you have been facing. Good to hear your sleep is better.
And always thank you for keeping us all informed of ongoing research.
Thanks, Jeanie. I think we’re on the downward stretch. May it be so 🙂
Hi Cort,
I have been following you from the day I got a diagnosis (some 14-15 years) and I can’t believe we are both still here…
Over the years I have been sick, I lost a few cats. After each death (they passed at 15 to 20 y/o), I crashed.
You are a precious ally that could not be replaced so please take good care of yourself.
There actually may already be a very good candidate for such a test. A few years ago researchers published a test that was able to very clearly separate all of 35 healthy controls from 35 ME/CFS patients and 35 close relatives from ME/CFS patients. The research was published in the highly respected Natures Magazine. The researchers concluded their results were statistically not significant, but the graph shows strong diagnostic potential when interpreted differently.
In the three following comments I present the short summary and the intermediate length summary both made by an LLM followed by my original comment for more detailed information.
@Cort: if you find this information valuable, please forward to the correct contact at the OMF. If you have questions, please reply to this specific comment.
Short LLM made summary:
“The Lupo et al. (2021) paper in *Scientific Reports* (https://www.nature.com/articles/s41598-021-86425-6) may already contain the starting point for a diagnostic marker.
**Figure 3B is striking:** salivary microbiota analysis produces three completely non-overlapping clusters—healthy controls, ME/CFS patients, and close relatives—with perfect separation. All 35 samples in each group cluster distinctly. The authors dismissed this as statistically insignificant, but the visual separation suggests strong discriminant potential.
**A simple validation would test this:**
Define decision boundaries around the three clusters (mathematically or visually)
Collect new samples from each group, analyzed identically
Plot results on the same figure
If >90% of new samples classify correctly, the marker has strong potential
**What this would show:** Not a complete ME/CFS diagnosis, but objective biological evidence that a patient is *not* a healthy control. This addresses a critical gap—ME/CFS patients currently lack any simple, objective test to counter dismissal as psychosomatic.
**What remains:** Testing specificity against other fatiguing illnesses (fibromyalgia, Lyme disease, etc.) and determining cost-effectiveness.
The data is published, peer-reviewed, and waiting for validation. This seems worth exploring.
Intermediate length LLM made summary:
The Lupo et al. (2021) paper in *Scientific Reports* (https://www.nature.com/articles/s41598-021-86425-6) may contain a starting point for a diagnostic marker.
**The striking finding:** Figure 3B shows salivary microbiota analysis producing three completely non-overlapping clusters—healthy controls, ME/CFS patients, and close relatives—with perfect separation across all 35 samples per group. The authors note this explains only 2.1% of total variance and dismiss it as statistically insignificant. However, this visual separation suggests strong discriminant potential that may have been overlooked.
**Why this matters:** ME/CFS patients currently lack any simple, objective biological test to demonstrate they are not healthy controls. This creates barriers to medical recognition and disability support. A biomarker showing “patient is not healthy” would be valuable even before determining specific diagnosis.
**Validation approach:**
Define mathematical boundaries around the three clusters
Collect new samples (suggested: 20-30 per group) analyzed identically
Test classification accuracy on held-out samples
If accuracy is high (>90%), proceed to specificity testing
**Remaining questions:**
Does the marker generalize beyond this cohort?
How specific is it (does it distinguish ME/CFS from fibromyalgia, Lyme disease, depression)?
What is the cost, and can it be optimized?
The data is published and peer-reviewed. This seems worth exploring as a starting point.
My usual self:
Actually there may be already a test that can validate that at the very least ME/CFS patients are *not healthy*. And the research for it has been published in the highly praised Natures Magazine. They just seem to have failed to see the diagnostic potential.
(I have no idea if it could be made cost effective)
Look at https://www.nature.com/articles/s41598-021-86425-6 with title “Potential role of microbiome in Chronic Fatigue Syndrome/Myalgic Encephalomyelits (CFS/ME)”, figure 3.B in specific.
The study set up and size:
* A total of 105 subjects: 35 patients and 70 control subjects were enrolled. The healthy control population constituted of two distinct groups: 35 patients’ relatives without CFS/ME and 35 healthy subjects not belonging to the patients’ families (Table 1). Twenty-six CFS/ME patients were females and 9 were males
* extensive study of intestinal and oral microbiome
=> The study of salivary microbiome (easier to take samples!) is IMO by far the most promising. In figure 3B it shows perfect separation between healthy controls, ME/CFS patients *and* close relatives of ME/CFS patients. All three groups with 35 individuals are *very clearly* distinguishable (for the chosen people in this study).
=> Unfortunately the authors dismissed this graph as statistically insignificant. My engineering education and experience thinks differently:
Step 1:
Draw three ellipses around the separate groups. There is even a bit of room to make them bigger. (Ideally determine the optimal ellipses by math, but just anyone could use three color markers since the separation is so clear). Just make sure none of the ellipses overlap.
Step 2:
Take samples from new groups of patients, healthy controls and close relatives of patients. Take samples exactly as these researchers did.
Step 3:
Do exactly the same math to get figure 3 A first and then 3 B.
Step 4:
Plot the math result on the exact same figure as seen in 3 B. If doctors manage to get for example 20 samples of each group into the right ‘basket / bin / ellipse’ for *new* people that did not belong to the original study groups, then we have a winner!
Important notes:
* Ending up in the ‘ME/CFS’ group actually means ‘definitely not in the healthy control group’. The study did for example not include MS patients, FM patients, cancer patients… Further tests to determine specificity are needed *but* at the very least in its current form it would indicate that patients are *not belonging to the healthy group* and that is observed by a BIOmarker (salivary microbiome).
* Cost of such a test is unknown, but could be reduced with further optimization since its statistical potential appears to be very high
* Cost or precision could be optimized by combining sample results from the patient under test and the patients’ close relatives (the same accuracy by using the cheapest markers of both patient and close relatives instead of using markers of patient only)
* The test (IF the original study had a sufficiently representative patient selection) would be a one shop ‘patient is not healthy’ test for all subgroups (that were present in the initial study). Not just a collection per subgroup.
* Since the test appears to be that convincing, it could be used for directing future research (find out how it comes it is so well possible to separate patients, patients’ relatives and healthy controls by only studying salivary microbiome, follow up healthy families that already have a similar microbiome to ME/CFS patients’ relatives as an early indicator for possible risk…)
May it be possible (and even plausible?) that the salivary microbiome changes reflect some sort of endogenous microbial reactivation? Then the question would be is this is a truely uniques signature as other chron. inflammatory disorders may also go along with endogenous reactivations?
I’d say my first guess is that it signals some (possibly specific) form of chronic immune activation at the mucosal barrier altering the microbiome composition.
Some species of the microbiome will suffer more then others under situations of chronic increased levels of oxidative stress and other chemicals the immune system releases.
Microbial communities already regulate themselves by producing sort of toxins against each other, like acetic acid, alcohols, up to natural antibiotics to compete among each other. By producing more of what they tolerate well and other species tolerate less, they carve them some competitive advantage at the cost of other species. That’s how peniciline was discovered. It’s a toxic used by microbes against competing microbes. Here the immune system sort of acts as a similar balancing player.
Another factor is that muccin is vulnerable to oxidative stress too, changing the properties of the muccus layer if ROS is increased. That happens in muco disease. That alteration in muccus would add on top of the recent research saying that 80% of ME/CFS patients had alterations in oral muccus genes. Just like in this research, they found a greater impact of oral muccus then gut muccus properties.
Where that chronic (but moderate) increase in immune activation comes from is another question. The thing is however that a period of stronger or longer lasting infection (like having the flu or acute EBV infection affecting epithelial cells and spreading via saliva) could put extra stress on the oral muccosal layer and that in turn could trigger a stronger response of the oral immune system to food, oral antigens, oral pathogens and parts of the own oral microbiome. That could (help to) keep the increased activation of the oral immune system going, even after removal of the original trigger. It hence could help create or reinforce a vicious circle.
The oral microbiome may be less in mass then the gut microbiome, but it is more exposed to all sorts of pathogens and environmental influences as non of it is yet neutralized by stomach acid. And it is in close relation to the nasal system, which has a rather direct link without blood-brain-barrier to core parts of the brain.
Your thoughts are very interesting! Personally I notice clear oral mucosal changes (bumps, streaks, ulcers) correlating clearly with PEM. The oral microbiome and inflammatory response should clearly be studied. Thanks for the literature link!
When I am in better conditions and avoiding pollen like hell, I get clear transparent nasal watery fluid. When not (most of my life) it’s sticky yellow that gets worse with nasal infection or allergen exposure. The brown-red colour comes when I have the many ‘micro-bleedings’ due to the immune system being too aggressive to my epithelial layer (up to frequent nasal bleeding).
You’ll find this paper interesting:
https://www.atsjournals.org/doi/10.1165/rcmb.2020-0168OC
saying “NETs Thicken Mucus and Decrease Mesh Pore Size (Microrheology)”
So immune activation in the form of neutrophils forming NETs do alter muccus properties and how muccus interacts with potential pathogens.
That also has a direct impact on nasal microbiome: those microbes live on something. Part of them are specialised in ‘eating’ or degrading muccus as an important food source. When the ‘food source’ of part of the microbiome changes from ‘perfect’ muccin embedded in plenty of water (roughly 1:100 ratio if I recall well) into a sticky dehydrated semi solid yellow oxidized dot of glue, it’s only logical that that may require another specialisation to live on that as ‘food source’. And the muccin eating microbes are only a small part of the global microbiome in the gut at least, so it makes sense that only a small fraction of them is remarkably altered. That may explain the big difference (three very distinct groups) matched with only an ‘statistical insignificant change’ (2.1%) in figure 3.B in the original paper (top comment).
The alteration due to ‘compromised muccus layer’ may be big, but the specific marker to look for may be on microbes having a very close interaction (such as using it as food) with muccin itself. That can combine a very big difference in oral microbes between humans with a drastic alteration in people with ‘muccin altered in specific ways’.
So hence that is why I see it as a possible marker for chronic oral mucosal (and / or epithelial) inflammation. That would be more specifc then just chronic inflammation, that could have less focus on the oral zone. Even modest inflammation might do in people with muccin gene mutations.
With the findings “NETs Thicken Mucus and Decrease Mesh Pore Size (Microrheology)” it also opens another window on what may be going on. When not having full immune attack, a bit of increased oral immune reaction would embed some NETs and decrease pore size a bit. NETs or neutrophil extracellular traps ‘are like barb wire’ damaging anything alive or organic getting near it. So they decrease pathogen viability (and microbiome too…). And they decrease pore size and hydration, reducing speed and chances for pathogens to invade. So in other words NETs turn the muccus layer into a defensive wall, and it’s a gradual thing from 0 to 100% and then broken when the mucus is so dry it’s discontinuous and detaching from the epithelial layer it needs to protect. In being *a gradual feedback mechanism* (untill it’s broken), it provides inherent negative feedback and ‘allows’ for a whole range of ‘stable-ish’ setting points. That is not unsimillar as many of us getting stuck to a fixed ceiling in between PEMs (and that ceiling varying a lot between patients). When the muccus is broken up (no muccus neither dry or wet) protecting only parts of the epithelial layer, the system is clearly broken in this view and cannot fullfill it’s function anymore with reasonable quality.
Stumbled on this idea when I came to the conclusion that chronic inflammation had to have a clear impact on the muccus properties including chemical ones itself, not just the epithelial and related cells and barriers and the thickness of the muccus layer.
Thinking of it, I do at times have ‘sticky thick saliva’ too. It’s still white but no longer clear then. Not just yellow nasal muccus.
Also thinking of it, the idea of compromised muccus layers offering the potential to form a vicious circle on one hand and it forming a natural negative feedback system on the other hand is a bit broken. The opt out is being past the point that muccus is continuous or fails to cover all surfaces but I do not observe that as a necessity with me.
A better opt out is: the NETs embedded into the muccus themselves can and will interact with the ROS released from live cells, forming even stronger products like hypochlorous acid (HOCl). That could well turn the total effect into a complex equilibrium between negative and possitive feedback.
When there is a global stress to the body, ROS production of both the immune cells and the epithelial cells (very close to embedded NETs in muccus) would increase body wide. That may shift the properties from more liquid ‘perfect’ muccus to more yellow sticky mucus filled with NETs. In common English: a temporary spike in ROS production would create sticky boogers (filled with highly reactive NETs). And those clear out in one to multiple days if the source of immune activation is gone. => Part of PEM? (Note, no, removing them all shouldn’t help, restoring equilibrium is a complex thing).
Similar for the gut. And it’s there better observed that a PEM flare goes hand in hand with an increase in gut immune activation and extra upsetting the microbiome for some time then in the oral and nasal microbiome.
Every dentist will tell you that gum inflammation is common in those with a weak immune system. And that something is wrong with the immune system in ME we already know.
For me lactic acid bacteria lozenges are a great support with these problems.
The border between my teeth and gums does get painfull when I overdo it, feeling inflamed. Since last year I use it as one of my early warning signals that I use to try and stay out of PEM.
I have never heared about lactic acid lozenges. Thanks for pointing to them.
My pleasure. My dentist helped me with this. In the beginning of my illness I worked myself through the Open Medicine Foundation’s PEM Avoidance Tool-Kit. It recommends to make everything you can to control other (or super-)infections.
Since you know a lot and write here a lot. Have you seriously considered the research into HHV6b reactication as ME’s pathomechanism?
https://www.brunel.ac.uk/research/projects/reactivation-of-herpesviruses-in-chronic-fatigue-syndrome
I belong to the herpes antiviral reponders. Therefore for my group I believe the case is solved.
I fear that it might take many more years until the fact that herpes plays a central role in the major group of patients who fulfill the CCC will be widely acknowedged. Almost everyone seems to believe that the ME puzzle is highly complex. And herpes as an explanation gets not considered because folks can’t imagine anymore that ME might have a simple pathomechanism.
Something similar happened in the 19th century when the British wanted to figure out the problem behind scurvy because they lost so many sailors.
After a couple of decades a doctor actually figured out that svurvy could be cured with oranges. Still, he didn’t publish his findings because he and everyone else in the field was invested into a very complicated theory of the links between nutrition and health. Thus, he went on to write another paper on how he had found more proves in his scurvy research for said complex theory.
It took several more decades until these sailors got their oranges.
“I belong to the herpes antiviral reponders. Therefore for my group I believe the case is solved.”
I have some help of antivirals too, but limited. I have looked more into another herpes variant, EBV, since I have had a strong infection as an adult.
In general, I do not believe ME/CFS is all about herpes virus. For HHV6b reactication the strongest indication is figure 6A in https://pmc.ncbi.nlm.nih.gov/articles/PMC8378328/ where there are two subgroups: the ones on the left where more HHV6b reactication means more symptoms and the one on the right where more HHV6b reactication means less symptoms.
When looking at the scales of the figures, the negative correlation between pain and neurocognitive issues versus viral load is bigger for the right group then for the left group. In simple words: patients’ symptoms worsen more with lower HHV6b load then they improve with lower HHV6b load in the left subgroup.
That there are two opposed reacting subgroups isn’t that odd. Herpes virusses have co-evolved with us for countless generations and seem to have addapted to become a mix between pathogenic and potential beneficial effects.
Pathogenic for ME/CFS: HHV6b reduces capillary regrowth, which is already an issue in ME/CFS. https://www.pnas.org/doi/10.1073/pnas.0905535106
Potentially beneficial: Herpes virusses have ‘learned’ to modulate immune strength to suit their needs, which may help in reducing excessive immune activation. https://www.pnas.org/doi/10.1073/pnas.0905535106
That said, for the subgroup worse at higher HHV6b loads, I do see how good antivirals may be quite helpfull. Yet in many / a majority of cases, I doubt that that alone will restore health back to former health. Am I guessing right that you improved on them but are far from fully healed?
Aciclovir supresses my flares fully so that I could go back to work. Not full time because the drug makes me dizzy and I feel drugged. But for a substantial amount of time.
However, I have decided not to continually go on the drug (and I don’t have a doctor at the moment who prescribes the drug to me) because I have chatted with others who also benefitted from aciclovir but told me that they had to increase dosage after some months until one of them didn’t have activity anymore. I think that could be because of the development of resistancies. I want to avoid that at all costs.
I only use it in emergency situations now, for example when traveling. In my daily life I am pretty stable at the moment because I have learned to rest and pace well. If I have a flare, I have it under control again by resting after 1-2 days,
As long as i can’t see that an immune therapy is coming up for us that restores my symstens capacity to suppress my ME flares fully I want to preserve the highest activity possible for emergency situations.
“Its all in your head”…couldn’t be more true.
I went swimming for the first time in years. the shoulder and head and spine movement changed EVERYTHING.the next day I got blood blisters inside my mouth the size of nickels
……3 days ago I did a liver flush.
What came out in the toilet blew me away…litterally hundreds of stones ranging from the size of 1mm all the way up to the diameter of a canadian 25 cent piece.
My bloating that ive had since 1993 has decrease by half!!
Maybe this paper holds another key. Near all metabolomics and other research allways tries to compare measured values in ME/CFS to HC (healthy controls). Normally this makes perfect sense.
But this paper says that all 35 relatives of the 35 ME/CFS patients had clearly such a distinct oral microbiome compared to healthy HC that it opens up opportunities:
If it is not the patient with ME/CFS that would alter the relatives oral microbiome after he gets ME/CFS, then it reveals that only a certain subgroup of the population seems to be vulnerable to ME/CFS. What’s more, it reveals what likely is ‘the natural healthy target state for this subgroup and with it for ME/CFS people’.
That is rather significant! It would say that trying to ‘bring back’ ME/CFS patients values to those of healthy controls is sort of a lost case, as that would not be their (the ME/CFS patients) ‘natural healthy state’, but that of people who won’t get ME/CFS in the first place. And since all 35 relatives of ME/CFS patients had a clearly altered oral microbiome, it near states that the relatives of ME/CFS patients themselves can’t reach a natural homeostasys state similar to HC. Then what are the chances that the weakened ME/CFS patients themselves could? Slim to none?
=> Maybe we are chasing the wrong target! Maybe we need to include THREE groups in every single ME/CFS research study: ME/CFS, HC and relatives of ME/CFS and try and find out what makes up the difference between the healthy relatives of ME/CFS patients and their relatives. It may reveal what makes up the lock keeping a person *vulnerable to ME/CFS* locked up (ME/CFS measurements) compared to a person *vulnerable to ME/CFS* but NOT locked up (healthy relative).
I hope it is clear what I mean to say. We may be chasing the wrong goal. Finding what locks us up in ME/CFS may be near impossible when we compare the patients who are locked with people who (almost) can’t be locked into this state.
I may have missed that but if this study fails to include the most basic of all clinical characteristics of ME/CFS – namely PEM – it will be an epic fail as it will analyze apples and oranges together. Yes, they will find “subgroups” – but they are meaningless.
Let me again say this clearly: any study which searches for “biomarkers” of ME/CFS must flag their samples by the two distinct pathobiological entities that make up ME/CFS: PEM and non-PEM. These two clinical manifestations represent completely different pathobiological dimensions – treating them together as if they were one will create murky waters and nothing but (again) confusion. We have had this for too long now (see the cytokine studies done through decades without adding any meaningful insight).
Hello HRP, you mean PEM-state and non-PEM state in a patient, right? It gets really interesting with rolling PEM ;). I’d say, don’t hesitate and enter directly into discussion with the authors. I couldn’t find an email adress for Danielle Meadows, but have written to Cort to see if he might forward her an email asking to please include separate types of sensory hypersensitivities into their symptom questionnaires (if any). (They were missing in the symptoms list of the big OMF study on what helps patients as far as I remember, and are under-researched in my opinion, particularly compared to their high burden of suffering in ME/CFS – I rank them sharing the top spot with exertion intolerance in my case.)
I now realise it’s probably moot if pre-existing samples are being used, but wouldn’t it be nice if one could try and correlate big data with one symptom in the hopes of learning more about that symptom.
Oh, and IMO there might be a third state. too: Overactivated (push state, adrenaline, etc…). Not unlikely to be present when a patient is on adrenaline/highly activated during a special appointment for a study.
That state when you feel untypically energetic, know you’re overdoing it but can sometimes hardly stop the action.
Have asked myself what the test results are worth in that case.
Dear Cort,
So very sorry to hear about your awful experiences with your dogs and glad to hear that they are hopefully recovering. We had something similar though luckily on a lesser scale with one of our Bernese some years ago, and nearly lost him after a routine castration. It has left a deep insecurity about the operation so that we now use an implant route seems to work well. there is nothing like a sick or injured dog for knocking the stuffing the stuffing out of one. Hope your own stress levels can now go down and cuddles with your animals can help you recover too. As always thank you for all your hard work to help us all. it is really appreciated.
Sending many pats and extra treats to the dogs (sounds like you deserve some treats too!)
This study ressembles another one sponsored by OMF and performed by Moreau & al. In Feb 2023, they published an article in Nature where “they identified 11 micro RNA associated with PEM and ME/CFS symptom severity”.
https://www.nature.com/articles/s41598-023-28955-9
Do you have any information that this new study is also looking at the same miRNAs?
Dr Moreau also has an upcoming study that might be worth covering: https://www.omf.ngo/raspberry-me/
Thanks for your great work Cort ! <3
So glad the dogs are doing better and so sorry you had to endure all that. What stood out to me is the line, “we’re light years ahead of where we were five years ago.”
In the swirl of information that enters my swirling mind, it is impossible to come to any big picture conclusions about the state of things. Over the years I’ve found this site to be the most trusted source for ME/CFS info. So this one statement carries a lot of weight for me (and I think is doing the same for people with ME/CFS who are regular visitors to this site?) and I can’t help but to think how valuable this optimistic conclusion would be for all the folks out there who are not familiar with this site.
Why is healthrising still promoting the fascist Twitter/X website? The far right is a huge treat to disabled folks.
we don’t promote fascist Twitter/X – but we do use it. It is still easily best way to get the message out and is critical for us. So for me with my political inclinations I hold my nose and use it and hope that something better comes up to replace it.
I don’t think talking to russian bots is an effective way to get the message out, compared to talking to humans on bluesky or using more modern social media.
I have moments of hope. But to be honest, I really don’t think we are light years ahead of where we were five years ago.
Study after study seems to suggest certain things are abnormal in ME/CFS – for example the immune system, or metabolism – but there never seems to be a genuine advancement in the field. Things feel like they are going around in circles to me.
Unfortunately, this illness must be really really complex. A real illness of complex systemic abnormalities.
Perhaps AI will help us unpack all this complexity.
I completely agree. I do see studies, but there’s no real progress. This is partly because there’s too little funding and interest from doctors to replicate studies. We’re indeed going around in circles.
What I do see is that many “abnormalities” are being found that relate to various systems. The autonomic nervous system, the vascular system and blood circulation, immune system, and energy system seem to be the most dysfunctional or have been adapted for survival.
I think the fight-flight stress system is malfunctioning or has become damaged as a cause of this disease. However, it could also be that this system is actually compensating for… insufficient blood flow/oxygen to the brain and organs. Or an energy problem. This is the cycle in which this disease operates.
Smelling the cover up since the beggining
My best hunch is mercury from both dental amalgam fillings and childhood vaccines.
Mercury being passed through the placenta if your mother had mercury dental amalgams
When i received my third clott shots (covid vax) my armpit swelled the size of a grapefruit.
When i was given molibdimum in my IV when I first became ill, I ended up with grapefruit sized lumps all over the entire chest area.
I strongly react to metals of all kinds. Hypersensitivity to the 100th degree!!
At my worst,using an electric drill would cause me to become very very sick due to the emfs.
There has to be a way to calm all of this
Yep. Despite my cynicism, perhaps drugs that act on multiple systems, like GLP-1 agonists, do actually offer some potential. If ME/CFS really is a multi system illness.
I see Carmen S. In Germany is starting a trial. Would be interested to know her rationale, as on the surface it doesn’t seem to obviously link to her theories.
Check out the latest blog 🙂
Thanks for this Cort.
I have long COVID/ME/CFS. A year and a half so far, some typical symptoms, but not the worst…
I am planning to write a book on long COVID in medical-political-historical perspective.
I’m trying to get a definition of “biomarker.” It’s confusing, because there appears to be a huge number of “objective biological abnormalities” already found–see Komaroff’s recent: https://www.sciencedirect.com/science/article/pii/S2666379125003325. What’s the difference?
Thanks in advance if you can help!
Peter
One issue is that there are lots of different kinds of biomarkers. I think what we’re looking for is a “diagnostic biomarker”. I don’t know if that helps or not but good luck with the book 🙂
Thank you so much for your continued efforts to keep all of us in the loop. It’s much appreciated. When I have some money I plan to send some of it your way!
Thanks, Helen!
Hello! I’ve had long covid since 2020. I’ve also had my entire genome sequenced. Is there anything I can contribute? Is there anything I can take from what you guys have done to help me or at least research my genome to look for certain things? I’m desperate lol ty !
Check out this blog and email Liz Worthey and/or Camille Birch. 🙂
https://www.healthrising.org/blog/2026/02/15/whole-genome-chronic-fatigue-causes/