What is CFS Remission Site About?

I have been observing the Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) community for almost 35 years. I have been an active member of this community. I have also been in remission for it, but deeply interested in understanding it; I have had several relapses. I wanted to prevent future relapses hence great interest in reading and researching.

Microbiome Analysis as a path with good results

My main focus in 2023 is on the microbiome of ME/CFS people. I have a collections of reviews of individual microbiome samples reviews available. The data from the suggested tests are processed using the free expert system at Microbiome Prescription. So far, every person who has done this route and repeated the microbiome tests have reported subject improvement and objective improvement. It can be a long journey, we take one step at a time.

During those decades I have seen a huge number of theories, suggested treatments and clinical findings. I have seen many “this cured me” which failed to deliver remission for anyone else. I have seen treatment plans proposed / sold by well-meaning MDs that worsen the condition and persisted for years. I see this still going on today for both ME/CFS and Long Hauler COVID.

My training is in science: mathematics, statistics, general sciences. I have been an instructor in those areas at many universities, colleges and even high schools. My remissions resulted from following gold or silver standard evidence. I have read several thousand published papers on ME/CFS (with and without brain fog).

What is on this site?

Most of the posts results from reading a new paper, readers asking questions, seeing a question asked on some online groups. The posts follow this pattern:

  • The question or concern that started the post
  • A review of all literature on the US National Library of Medicine, conference papers, etc.
    • Quotes provided from papers or their titles
    • Links to the paper so people or their medical professionals can read for themselves
  • A bottom line section which are my conclusions inferred from the literature.

To quote Seargent Friday from the old Dragnet TV Series, “All we want are the facts, ma’am“.

Use the site as an Encyclopedia

There is another similar site, Encyclopedia Myalgic encephalomyelitis, [me-pedia.org], which I also use. I actually have had more page views than that site! What the difference? I seem to cover things in more depth. I just searched for “grapeseed” on that site and found nothing. I searched on this site and literally had dozens of posts cited. Resveratrol Revisited [2015], Resveratrol Recap [2017], Mast Cell Moderators — non-drugs and suspect bacteria [2023]

The fastest way to find information is to go to google search, enter site:cfsremission.com followed by what you are interested in.

I Promote No Protocol, I promote evidence based treatment.

As a statistician, I recognized that ME/CFS consists of many, many, many, different subsets. To treat successfully means getting information. I know that my own ME/CFS was usually triggered by the interaction of an inherited coagulation defect (Prothrombin G20210A a.k.a. Factor II Mutation) interacting with stress and a microbiome that goes bad with stress. What works for me may not work for another with ME/CFS.

My Unified Model of ME/CFS and Long COVID

I have a hypothesis on the causes of ME/CFS and a treatment approach (not a protocol) that is likely to reduce the severity of ME/CFS. Some may go into remission.

The Cause of ME/CFS

The cause is rather simple: anything that causes an alteration of the microbiome. This may be food poisoning , an infection (COVID, Flu, Lyme, Epstein-Barr virus), a vaccination, a prescription or over the counter drug, pesticides, bad diet. This alteration and happenstance cascade into a microbiome dysfunction that mucks up your system. Too much of some metabolites /chemicals are being produced, too little of others, the chemicals used by the body are “hacked” and the body manifests a huge variety of symptoms.

Treatment Approach

Over the 30+ years, I have been a good mathematical modeler. Trying to find a model that agrees with all of the facts, explains all of the observations and last, can make predictions that are testable. Not that many years ago I came to the realization that the microbiome dysregulation model was an extremely good fit. More important, it made predictions that could be tested.

A 1999 study in Australia found a common pattern with ME/CFS patients microbiome. If something helps ME/CFS then it is likely that this same thing would influence the bacteria found to move closer to normal. This post from 2013, Finally! Someone verified the 1999 Studies – Thank you Kenny De Meirleir! shifted me further down this path. Finding that the most effective antibiotic protocols for ME/CFS and Lyme would also correct the reported microbiome function (see Why Jadin’s Antibiotics Protocol usually work — Pasteur Institute got the solution right and the explanation wrong? ).

I keep monitoring ME/CFS studies. My current effort is dealing with improving the ability to correct the microbiome. This is done on a separate site, Microbiome Prescription, and a separate blog site.

I have a page linking to people experience with this approach. Each person is different.

Analysis Posts on Long COVID and ME/CFS

I believe that most ME/CFS people will improve significantly with microbiome testing followed by appropriate adjustments. This is often an iterative approach (test-adjust-repeat).

Overview of this Blog and the Microbiome

My ideas on this blog have evolved, as more and more information becomes available. This post is an attempt to bring readers up to date with my current thinking. I am striving to be transparent in my logic — showing the evidence I am working from, and my thought processes.


Notes to Treating Physicians     Quick Self Start on treating CFS


Analysis of Microbiome/stool with recommendations

Site: has moved to https://microbiomeprescription.com/

  • Over 30 different tests are supported. See this page

The data is available in an online collaborative python workbook for analysis. See this post.


Microbiome Definition of CFS/FM/IBS

A coarse condition that results from:

  • Low or no Lactobacillus, AND/OR
  • Low or no Bifidobacteria , AND/OR
  • Low or no E.Coli , AND/OR
  • A marked increase in number of bacteria genus (as measured by uBiome) to the top range
    • Most of these genus are hostile to/suppress Lactobacillus, Bifidobacteria, E.Coli
    • Several are two or more times higher than normally seen
    • The number of bacteria genus goes very high (using uBiome results), but most of them are low amounts.
      (“Death by a thousand microbiome cuts” and not “Death by a single bacteria blow”)
  • The appearance of rarely seen bacteria genus in uBiome Samples.

A finer definition would be a condition with a significant number of abnormalities in the ‘Autoimmune profiles see this page for the current criteria (i.e. over 25%).

The specific genus and their interactions determine the symptoms seen — likely due to the over- or under-production of metabolites (chemicals). Other autoimmune conditions may share these core shifts. The specific high and low bacteria determine the symptoms if the person was the DNA/SNP associated with the symptoms.

Replace the metabolites produced by the missing bacteria

Replacing the metabolites should result in the reduction of symptoms associated with a deficiency of these metabolites.

See this post for the study references. These items should/could be done continuously.

Other Supplements Reported to Help

Bootstrapping Bifidobacterium and Lactobacillus

The items below were found in studies to increase bifidobacterium and lactobacillus:

Unless the bifidobacterium and lactobacillus (B&L) are human sourcedthere is almost zero chance of taking up residency. Taking probiotics will not allow B&L to get established. In fact, there are grounds to believe that most commercial probiotics actually reduce your  native B&L. You want to encourage your native B&L. See this post for citations.

Bootstrapping E.Coli

The E.Coli probiotics below are human sourced and known to take up residency in the human gut.

  • Core: D-Ribose a preferred food that it uses
  • Mutaflor probiotics — E.Coli Nissle 1917
  • Symbioflor 2 — multiple strains

Dealing with the other microbiome shifts

The other microbiome shifts appear to be in different clusters of microbiome shifts. This 2017 paper by Peterson, Klimas, Komaroff, Lipkin (and a stack of other CFS researchers) makes that clear in its title: “Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome”.

The best way at present to proceed is to order an analysis from uBiome. (Disclosure: I have no financial interest in this company.) When your get your results back, log in, click on the “Compare” tab, then go to “Genus,” and click on “ratio” twice, so the results are in descending order.

This is the “hit list” of what you are trying to reduce. DataPunk provides a nice summary of what we know about these. See, for example, Alistipes:

At this point, we run into a logistical challenge.  You want to avoid items that are “Enhanced By” (which is in common across all of the high items) and take the items that are “Inhibited By” (which are not on any of the “Enhanced By” lists).  You may also wish to reduce foods that are high in items listed in “Nutrients/Substrates.”  It becomes a jig-saw puzzle! I have done this exercise for many readers’ uBiome results:

I have discovered that DataPunk is not absolutely current, and have started creating posts based on its data, and then added studies from 2016 and 2017 to the page. Past pages are below, for current list MicrobiomePrescription site.

General Suggestions (no uBiome results)

Some of these items are contraindicated with a few uBiomes that I have reviewed. This likely is why person B reports no results while person A reports improvement. Example: Magnesium is usually very helpful — but there are a few cases where it encourages overgrowth of undesired  bacteria.

Probiotics

Most probiotics do not take up residency. They are “here today, gone tomorrow”. Their primary role in my model is producing natural antibiotics against other bacteria. For example:

Probiotics should be rotated: 2 weeks on a specific one, then several weeks off. As a general rule, you want about  6-12 B CFU taken three times a day (or 2-3 times the recommended dosage) — but work up slowly because you may get be a major herx! In general, do not take Lactobacillus with Bifidobacteria or with E.Coli etc. Keep to one family per cycle. You do not want them to kill off one another!

Why 3x per day? Because almost none of them are detected after 12-24 hrs. So to keep them — and the production of natural antibiotics — going, you need to keep taking them during the day. See this post for citations.

The following probiotics commonly seem to help people with CFS/Lyme/Fibro:

Some probiotics, however, may make your symptoms worse! And, unfortunately, most commercial probiotics contains some of these. At the moment Bifidobacterium animalis, Saccharomyces boulardii and Lactobacillus acidophilus are on my best to totally avoid list.

  • “. The findings show that the six species of Bifidobacterium differed in their ability to relieve constipation. B. longum, B. infantis and B. bifidum were the most effective in relieving constipation, B. adolescentis and B. breve were partially effective and B. animalis was not effective. Furthermore, edible Bifidobacterium treated constipation by increasing the abundance of Lactobacillus and decreasing the abundance of Alistipes, Odoribacter and Clostridium. .” [2017]

On my neutral list (no clear benefit) is Lactobacillus Plantarum.

Teas

Some teas can also be antibiotics (among other roles). There are two teas that seem to produce significant results quickly:

Again, rotate and, if practical, change brands too. Their antibiotic compounds are different from different sources.

Herbs and Spices

The best choice needs examination of your microbiome (i.e. uBiome results) and doing the work cited above.  Survey results found:

  1. Neem and Oregano with 80% improving
  2. Olive Leaf and Licorice with 56% improving
  3. Thyme with 50% improving
  4. Wormwood and Tulsi with 33% improving

Other things

If you do not know your microbiome, then see https://cfsremission.com/reader-surveys-of-probiotics-herbs-etc/  for suggestions. Your results will vary because your microbiome vary.

Thick blood is an issue also — but here things gets more complicated and not suitable for this recap.

Antibiotics can have a role — but getting prescriptions for the right ones can be a major challenge.

Metabolism Shifts

From volunteered data, we can identify some distinctive shifts, see Metabolism Explorer Summary

Bottom Line

Working with the microbiome and autoimmune is like working with fragments of the dead sea scrolls. For many bacteria we can identify it — what inhibits or encourages it is not known to modern medical science.  We have extremely thin slices of knowledge –Almonds enhances Bifidobacterium, Lactobacillus (B&L)  as do sesame seeds. What about sunflower seeds? Peanuts? Cashews? We find that Walnuts help the bacteria that inhibits B&L — so we cannot safely generalize to “all seeds/nuts are helpful”.

In many cases, we find that healthy diet or supplements demonstrated to work for normal people have the opposite effect on CFS and other altered microbiome conditions. This is made even worst because most of the studies were done on males and most people with CFS are females. We end up having to swim up-stream thru good and valid suggestions — that are just wrong for us.

My model is simple to understand and allows us to filter many suggestions and candidates. With the availability of uBiome testing (without needing a prescription!) we have entered the age of explicit treatment based on your unique microbiome. We do not know the role of many bacteria involved. We do not know what will inhibit or enhanced all of these bacteria. Frustrating little knowledge!

On the flip side, many readers have reported significant improvement, reduction of prescription medication, etc. so the model and suggestions have potential and thus hope of remission! Microbiome studies are exploding on PubMed, a lot of research is being done and we can often borrow their results.

This is an education post to facilitate discussing this approach with your medical professionals. It is not medical advice for the treatment of any medical condition. Always consult with your medical professional before doing any  changes of diet, supplements or activity. Some items cites may interfere with prescription medicines.

Current Summary of Remission Approach to ME/CFS

A reader asked on Inherited Factors for ME/CFS:

Which of your posts gives the clearest explanation of how someone might begin addressing one or more possible contributors to ME/CFS? What is the most practical “how-to” guide for following the steps that led to your remission?

I understand that remission may not be possible for everyone. Still, people may want to know what I tried so they can decide whether any of those steps are appropriate for them.

I would answer this in two parts.

First, I will describe what contributed to my original recovery. Much of that approach may be difficult or impossible for many people to duplicate today because of cost, insurance limitations, and the way medical care is commonly delivered.

Second, I will describe a more practical approach that attempts to follow the same general reasoning as closely as possible.

My Original Recovery

When I was first diagnosed with ME/CFS, around 2000, I was in an unusually fortunate situation:

  • I received disability pay for one year.
  • My employer-covered medical plan paid 100% of costs, including out-of-network care, prescriptions, and dental care.
  • My physician could spend as much time with me as needed, bill for that time, and be reimbursed without major administrative barriers.

At that time, two sets of papers had been published reporting remission rates of roughly 80% to 90% using different approaches. My physician and I decided to pursue both approaches at the same time.

The plan included:

  • Extensive coagulation testing through a specialist laboratory. This included testing for inherited clotting-related factors, followed by treatment based on the results.
    • Lovenox, a low-molecular-weight heparin anticoagulant. At the time, it cost approximately $500 per month.
    • Piracetam, a compound in the racetam family, which I imported from the Czech Republic.
    • Turmeric.
  • The Dr. Cecil Jadin protocol.
    • A monthly rotation of different antibiotics.

Many of the antibiotics caused a strong die-off reaction, often described as a Herxheimer or “herx” reaction. After the reaction settled down, we added substances intended to improve penetration or effectiveness, such as bromelain.

Over several months, this approach worked for me. However, because genetic factors appeared to be involved, I did not regard it as a permanent cure. I considered it a remission.

I also came to believe that stress was an important trigger for my symptoms. As a result, I made significant lifestyle changes. In particular, I changed the kind of work I did and developed a much lower tolerance for persistently stressful work environments or managers. If a job became harmful to my health, I made it a priority to leave rather than remain in that situation.

Later Relapses

My later relapses did not always appear to have the same immediate trigger. Stress was one trigger. A flu vaccination seemed to be another in at least one instance.

There was, however, one important difference from my earlier illness: I developed gastrointestinal symptoms.

That led me back to the research literature. I found a 1999 paper describing shifts in bacterial populations associated with ME/CFS. When I reviewed the antibiotics used in my earlier treatment, I realized that they may also have corrected most of the bacterial shifts described in that paper.

Jadin’s protocol described the issue as an “occult infection,” meaning an underlying infection or infection-like process that can produce symptoms similar to those caused by the original infection. That idea helped clarify my thinking.

My interpretation was that the initial infection may have caused shifts in the gut microbiome. Even after the original infection resolved, those bacterial shifts may not have returned to a healthy baseline. In other words, some continuing symptoms may have been driven less by the original pathogen and more by the lasting changes it caused in the gut ecosystem.

That realization led me into microbiome research.

A More Practical Starting Approach

For people who want to explore this line of thinking, I would suggest a practical, lower-cost approach centered on microbiome testing and data-guided interventions.

  1. Obtain a microbiome test from Biomesight. The discount code is Micro. Use of the code provides a contribution toward the costs of maintaining the site.
  2. I prefer Biomesight primarily because we have the largest number of uploads from that testing service. A larger comparable dataset makes it easier to identify bacterial patterns that may be relevant.
  3. Transfer your Biomesight data to Microbiome Prescription.
  4. Log in to Microbiome Prescription, enter your symptoms, and review the suggestions it generates.
  5. You should also receive an Odds Ratio list of suggested interventions within about a day. I would start with those suggestions for approximately two weeks.
  6. If you see no meaningful improvement after two weeks, consider switching to the symptom-based suggestions generated by the site.

The Odds Ratio approach has received encouraging reports from several people, including some health professionals. Individual responses vary greatly, however, so it is important to introduce changes carefully, track symptoms, and involve an appropriately qualified clinician when considering prescription medicines, anticoagulants, or antibiotics.

Summary

In my experience, two areas appear to be the most promising paths to investigate:

  • Deep coagulation testing, especially where there is reason to suspect clotting-related or inherited factors.
    • 23andMe is an option: its Hereditary Thrombophilia Genetic Health Risk report covers the two common inherited clot-risk variants—Factor V Leiden in F5 and prothrombin G20210A in F2. Not complete but better than no information.
  • Microbiome testing and targeted efforts to correct unfavorable bacterial patterns.

For many people, microbiome testing may be the more accessible starting point. It is often less expensive, less confrontational, and more practical than trying to obtain extensive specialist testing or persuade clinicians to pursue less conventional treatment pathways.

One probiotic of note: Mutaflor — it is one of those bacteria found deficient in the 1999 study. My own experience is that it can cause a significant herx; on the plus side, if things are a little off, I will often use it as a preventative and take for 1-2 weeks.

This is not a promise of remission, and it should not replace individualized medical care. But it is the closest practical version of the path that led me from severe illness toward remission.

Inherited Factors for ME/CFS

A reader forwarded me a link to this new study

which included this nice diagram

This is actually OLD news

I covered this in a post from almost a decade ago, The Heart and Blood of the CFS Patient. This post cited studies from 2008. It also included this chart that bears great similarity to the above.

In new publications on ME/CFS, I too often seen results that were known and published in the past. Too often the prior studies were not cited — indicating that the researcher failed to do due diligence (or just search this site!!).

We have one factor that likely comes from DNA.

Inherited Coagulation Defects

This is another DNA variation that is over represented with ME/CFS and has been known for over a quarter century.

Addressing this was part of the plan that resulted in my remission.

Some more recent studies:

A notable 2024 plasma-proteomics study analyzed platelet-poor plasma from 15 people with ME/CFS and 10 non–SARS-CoV-2-infected controls. It found 24 proteins increased and 21 decreased in ME/CFS. Among the altered proteins were thrombospondin-1, platelet factor 4, and protein S—findings the authors interpreted as consistent with disrupted platelet/coagulation regulation and endothelial dysfunction. Complement proteins, including C9, were also lower. Its small sample size means this is hypothesis-generating rather than a confirmed biomarker panel.

Data-independent LC-MS/MS analysis of ME/CFS plasma reveals a dysregulated coagulation system, endothelial dysfunction, downregulation of complement machinery

A 2023 review in Blood Reviews concluded that multiple ME/CFS studies report platelet hyperactivation, anomalous clot formation, a more procoagulant phenotype, and endothelial dysfunction. It proposes impaired capillary-level exchange and tissue hypoperfusion as one possible connection to fatigue, cognitive symptoms, and exertional intolerance.

Cardiovascular and haematological pathology in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): A role for viruses

The “microclot” literature—especially studies using fluorescence methods, thromboelastography, and platelet imaging—has reported larger fibrinogen/amyloid-containing fibrinaloid deposits, platelet hyperactivation, and hypercoagulability in ME/CFS samples versus controls. These aggregates are hypothesized to be relatively resistant to normal fibrinolysis. However, assay standardization, replication by independent groups, and proof of clinical relevance remain important gaps

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: the biology of a neglected disease

Iron Levels — why females get ME/CFS more often?

This is more uncertain because ferritin has a complex interaction.

A 2023 Japanese study of people with Long COVID found those who went on to meet ME/CFS criteria had higher ferritin than both Long-COVID participants without ME/CFS and people without fatigue: median 193.0 µg/L versus 98.2 and 86.7 µg/L, respectively. The difference was particularly apparent in women, and ferritin correlated with fatigue severity measures.

Utility of Serum Ferritin for Predicting Myalgic Encephalomyelitis/Chronic Fatigue Syndrome in Patients with Long COVID

Other Factors

The landmark DecodeME genome-wide association study compared 15,579 people with ME/CFS against 259,909 controls of European ancestry. Its initial 2025 results identified eight genome-wide significant genomic regions. The implicated biology clustered mainly around immune response to infection and nervous-system pathways.

Possible genetic clues to ME/chronic fatigue syndrome identified in massive study

Bottom Line

I view ME/CFS as a heterogeneous condition in which impaired oxygen delivery, oxygen utilization, or microcirculatory blood flow may contribute to a state of functional tissue hypoxia—meaning tissues may not receive or effectively use enough oxygen even when routine oxygen-saturation measurements appear normal.

In this model, a person may have pre-existing vulnerabilities that leave them relatively close to a physiological threshold. These vulnerabilities could include genetic predisposition, immune dysregulation, autonomic dysfunction, endothelial or microvascular abnormalities, mitochondrial or metabolic limitations, nutrient deficiencies, chronic inflammation, or prior infectious exposures. A triggering event—commonly an acute infection, but potentially another major physiological stressor—then pushes the system beyond its capacity to recover normally.

Once that threshold is crossed, the consequences may extend far beyond the initial trigger. Reduced perfusion or impaired cellular energy production could activate stress responses involving the autonomic nervous system, immune signaling, coagulation, oxidative stress, redox balance, metabolism, sleep regulation, and neuroinflammation. These systems interact with one another. For example, impaired tissue perfusion may worsen metabolic stress; metabolic stress may intensify inflammatory and autonomic signaling; and inflammation or vascular dysfunction may further impair blood flow and oxygen availability.

This could create a set of self-reinforcing feedback loops rather than one isolated defect. It may also help explain why people with ME/CFS can have normal results on many standard resting tests while developing profound symptoms after relatively minor physical, cognitive, or orthostatic exertion. Post-exertional malaise could reflect a delayed failure of recovery systems after demand exceeds an already limited physiological reserve.

Under this framework, correcting a contributor to hypoxia—such as iron deficiency, sleep-disordered breathing, low blood volume, impaired autonomic compensation, inflammation, or vascular dysfunction—may still meaningfully reduce symptoms. But it may be insufficient by itself to produce full recovery once downstream processes have become established. Recovery may require interrupting several interacting loops and allowing time for vascular, immune, metabolic, neurologic, and autonomic regulation to normalize.

This is a conceptual model rather than an established unified explanation for all ME/CFS. ME/CFS is likely biologically diverse: tissue hypoxia may be central in some people, secondary in others, and less important in still others.

Microbiome Prescription Worked for ME/CFS But Events Went South

I got an interesting request

I wonder if you would be willing to write a blog post looking at my recent test results in comparison to last year? Confirmed diagnosis of ME/CFS. UK NHS only helps with pacing advice.

  • First BiomeSight test: 2025-04-17

Following this, 3 self-directed cycles of antibiotics, probiotics, prebiotics, and diet changes based on MicrobiomePrescription results. First 2 cycles increased my baseline and reduced symptoms dramatically, third cycle set me back slightly. Overall very positive.

Unfortunately then was hospitalised later in 2025 with a perforated and infected gallbladder, sepsis. They rotated through quite a few different harsh antibiotics trying to find one which worked. Then in December 2025 went in for surgery to remove the gallbladder, more antibiotics.

  • Second BiomeSight test: 2026-03-16

My baseline now is worse again, many symptoms returned. I am loathe to use more antibiotics while some of my bacteria are so low (Akkermansia at 0.006) even though my positive scores are dominated by antibiotic suggestions. Would like to focus on probiotics, prebiotics, herbs, supplements, diet changes for now.

Any insight would be most appreciated.

Confirming the Worst

Going over to the symptom compare tool, we see that you are now worse than a year ago. 140 of 141 symptom forecasts are significantly worse! Seeing number this much worse is unusual but consistent with his events and perception.

Going Forward

My last two post has been evaluating the alternative path — instead of attacking the bacteria causing symptoms, push the person to a statistically significant healthy microbiome. The following links may be worth a reading:

This approach matches “I am loathe to use more antibiotics” because antibiotics typically are on the avoid lists with the healthy approach and high on the to take list attacking symptoms. It is sitting on the Simple UI page.

Basic Results:

  • 52 bacteria were identified — every single one was too high.
  • I have broken suggestions into classes below. In general, I have kept them to items with an impact of at least 1.
    • Items listed are order by largest impact first.

Herbs

The top herbs are below. I was delighted {Bofutsushosan} was listed because it is well known increases Akkermansia which he is concerned about.

Food

Flavonoids

Vitamins

Common and OTC Supplements

Probiotics x PubMed

This list is done using PubMed studies.

Probiotics x R2 Model

I prefer the R2 Model because we have a lot more data to use than with PubMed. On the flip side, this does not have clinical studies supporting the choices.

The top probiotic Bacillus thuringiensis suitable for human consumption may be a challenge. Most retail products are formulated to control caterpillars, worms, or mosquito larvae in gardens and standing water, not for ingestion or probiotic use.

Non-Human Retail options

  • Home Depot sells Monterey B.T. Bacillus Thuringiensis Pint Concentrate as an online retail product.
  • Wilco Farm Stores / Farm Store lists Bonide Bt Bacillus Thuringiensis as a garden pest-control product.
  • DoMyOwn sells a dedicated Bt category and says it’s available through their store rather than big-box shelves.
  • FBN lists Bt ingredient-based products, including Bacillus thuringiensis subspecies tenebrionis.
  • DIY Pest Control lists Bt products and notes common trade names like Thuricide and Mosquito Dunks.

Summary

I look forward to see how well this alternative approach performs. It does not focus on the bacteria associated with his 141 symptoms — instead, we focus on shifting to a healthy microbiome profile (with very high statistical significance, p < 0.0001,) I would suggest retesting every 3-4 months to track progress.

Questions And Answers

Q: It’s interesting to see how some Odds Ratio based suggestions match with the Consensus Suggestions, and some vary wildly.

  • A: Suggestions are based on bacteria target and available literature. Literature is sparse and often without replication of results
    • The safest path would be to start with items that are in agreement.

Q: I had one question with regard to whole milk, dairy, and lactose. The Odds Ratio analysis suggested these were positives – this makes my life a lot easier as I was using milk to help ferment and increase the CFU of the probiotics I used last year and hoped to again, and I eat a fair amount of dairy in general (I mostly eat a vegetarian diet with occasional fish, and dairy helps with my protein intake).

However when I ran the Consensus Suggestions earlier this week I got scores of -294.9 for bovine milk products, -120 for whole cow milk, and -158.6 for lactose.

  • A: I favor the Odds Ratio. On this point as you have no issues with dairy, keep to your current usage.

Q: Does this mean I likely need to make a choice between the Consensus Suggestions route (which I followed last year) and the new Odds Ratio route?

  • A: No, you could start doing a consensus of the consensus and odds ratio. Then add in items that disagree. I would suggest using an ratio evaluation:
    • Consensus: -120 with min of -960, so -(120/960) = -12.5%
    • Odds Ratio: 4 with max of 8, so 4/8 =50%
    • Thus odds ratio would win

Postscript – and Reminder

Other posts dealing with ME/CFS or Long COVID.

I am not a licensed medical professional, and the laws where I live prohibit any activity that could be interpreted as practicing medicine or giving personal medical advice. My work is limited to academic and analytical models, and I restrict myself to the language of science and statistics rather than clinical recommendations.

I cannot tell anyone what they should or should not take. Instead, I can present information about items that, based on numerical and statistical analysis, appear to have better odds of improving microbiome-related measures. I am a trained, experienced statistician with appropriate degrees and professional affiliations, and my role is to interpret data—not to treat patients.

All information I provide is for educational and informational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Any ideas, rankings, or “suggestions” derived from my analyses must be reviewed and approved by your qualified medical professional before you decide to act on them.

The answers and explanations I provide describe my reasoning and methodology. They are not intended as medical advice for you or for anyone else, and they do not create a doctor–patient or provider–patient relationship. Always consult a knowledgeable licensed healthcare professional before starting, changing, or stopping any treatment, supplement, or health-related regimen.

Another ME/CFS Microbiome Update

This is part of this continuing saga with this person. Prior posts and the labs shown below. Repairing the microbiome is not a single test, take a pill, and you are done. It may be like a long journey by sail through the fjords of Norway: a lot of course corrections!

Person’s Summary

I would say that there is no improvement since the last test. So this is still applicable:

I have not been feeling so well lately (since the last year). I would say that my symptoms has become worse. Earlier it has always felt as I have done some progress but the last 18 months it has been the opposite. Earlier I got rid of my muscle and joint pain but it has come back and I have much bigger issues with my red nose and my body feels very stressed.

Also feel very bloated.

  • A summary of my biggest issues:
  • Get the red nose (some form of rosacea).
  • Feel fatigued (both physically and mentally).
  • Feeling stressed.
  • Brain fog.
  • Bloated.
  • Lots of gas – I fart and burps a lot.
  • Issues with allergies
  • Muscle and joint pain

For the last 4-5 years I’ve been eating large amounts of rye and oats.

  • Around 150-200 gram of rye bread every day.
  • Around 70 gram of oats every day.

Been eating low fat, low protein and high carb (specially from rye, oats, apple juice and potatoes) because this diet seem to reduce my symptoms. As soon as I start to eat high meat and high fat my symptoms get worse.

In this analysis, I am going to look at:

  • Changes since the last sample
  • Review a new approach that is being incorporated
  • Looking at suggestions and the difference between the new approach and the traditional approach

At the end, I suggest following the new approach with the motivation that the traditional approach has appeared to have stalled. The microbiome adapts to antibiotics and diet changes; rotation to alternatives often seems to be needed to keep destabilizing the microbiome dysbiosis.

Changes Between Samples

Going to Old UI/Multiple Samples we compare symptom matching values. We see that just 1 of 42 showed improvement.

Looking at the new Odds Ratio data, we see the number of bacteria identified as critical in different samples below / Odds Estimate. I am not clear on the meaning and significance…

  • Odds Estimate: The higher the number, the more likely that the person is healthy
  • Number of Bacteria: Not reliable because different bacteria contribute differently to health.
  • 2026-03-06: 59 / 1632
  • 2025-11-17: 36 / 1588
  • 2025-03-30: 20 / 1671
  • 2024-12-03: 21 / 1561
  • 2024-09-02: 36 / 1611
  • 2024-01-22: 58 / 1586
  • 2023-09-12: 38 / 678
  • 2023-02-22: 52 / 1707
  • 2022-08-11: 30 / 886
  • 2022-03-25: 24 / 1037
  • 2021-12-03: 15 / 1287
  • 2021-08-31: 49 / 757

My general reading is that from 2021-2024 there was improvement and now the person is in a new stable healthier state but with still dysbiosis. I am hoping that the switch to an alternative view of solving his health may result in further improvement. In other words, rotation of approaches.

Another View on the Same Issue

In my recent post, Turning Fixing the Microbiome Upside Down!, I introduced a different way to think about repairing the microbiome. A human–society analogy might make it clearer.

Imagine your city is struggling with homelessness, vagrancy, and petty crime. The usual response—especially in the U.S.—is to send in the police. Round up those panhandling on the streets! In microbiome terms, that’s like identifying “bad bacteria” and launching an attack.

But there’s another approach: offer housing, mental health care, and job training. You don’t punish people—you help them heal and reintegrate.

Traditionally, Microbiome Prescription has focused on detecting problematic bacteria and trying to suppress or adjust them. The challenge is that most people have many interconnected symptoms. Research often shows that substance X improves one symptom but worsens another. You end up chasing symptoms—fixing one only to see another emerge or intensify.

A more holistic alternative, which has only recently become possible, is to guide the person’s microbiome toward a naturally healthy state instead. See this post: Mathematically Derived Healthy Microbiome.

Recently I asked the head of a microbiome testing company, what statistical evidence do you have for what is a healthy or desired microbiome profile. How do you obtain the importance of each bacteria? He knew that using means and standard deviation were invalid because of the high skew with the data. His response was requesting his staff to remedy this situation, looking at odds-ratio as a starting point.


Evaluation

I am a modeler, not a medical professional. Modelers try putting together mathematics using available data and use that to generate predictions. Once the predictions are made, they are evaluated against any available facts.

Above we have some observations from the person, the model does not know this information — so we can evaluate predictions against this data.

Been eating low fat, low protein and high carb (specially from rye, oats, apple juice and potatoes) because this diet seem to reduce my symptoms. As soon as I start to eat high meat and high fat my symptoms get worse.

Comparing Suggestions

HealthSymptomsNovice
Rye-0.11-183.5-352.3
Oats0.15-179.2-742.6
Apple2.34-385.1-351.5
Potato1.32-1102.7-1418.5
High Meat2.2155.9763
Raw Meat-2.78105.521.2
High Fat Diet-.79154.4-246.1
high-saturated fat diet-.3596-291.1
low-fat diet0.86195.9378.4
Range of Values-6.82 to 5.43-2075 to 1359-2296 to 1461
Best to TakeCatechol {Catecholamines}restricted-fiber diet {low fiber diet}restricted-fiber diet {low fiber diet}

Each of the above depends heavily on the bacteria selected and the threshold used. It is interesting to see that the new “Make Healthy” is a clear winner against his observations.

What is particularly interesting with the “Make Healthy” is that values were computed for 1,632 substances. Looking at the list os suggestions, we do not have a mass of antibiotics seen on the other lists. We are not focused on reducing bad bacteria, rather on improving the good bacteria, and letting those address the bad bacteria. The top items are below.

My impression is that this is a much friendlier set of suggestions. In fact, the bottom of the list (to avoid) are pages of antibiotics and prescription drugs.

Probiotics Exploration

There are two ways of getting probiotics:

  • Using published studies on their impact. In general, each study describes one or two bacteria impacted. This results in low data
  • Using the R2 Associations: This is a modelling of their impact with hundreds of bacteria impact estimated.

The new Healthy Algorithm includes R2 recommendations

We got the following suggestions

We will explore how different algorithms evaluate these.

BacteriaHealthy With R2Healthy With StudiesSymptoms With StudiesNovice with Studies
Streptococcus thermophilus1988-1 to 4-132 to -139-132 to -139
Enterococcus faecalis1291.6-579-579
Bifidobacterium infantis1124-27676
Bifidobacterium breve3771213213
Bifidobacterium longum3651-1423-1423
Bacillus thuringiensis96n/an/an/a
Pichia kudriavzevii38n/an/an/a
Acidipropionibacterium acidipropionici22n/an/an/a
Aspergillus oryzae15.1 – 3-192 to 8-192 to 8
Lactobacillus acidophilus40-574-574

Keeping to the “When in disagreement, leave it out” a.k.a. Minimal Risk a.k.a. “Do not harm”, we have

  • Top choice is Bifidobacterium breve
  • Reasonable choice is Bifidobacterium infantis

Alternatively, Streptococcus thermophilus high value, cheap, and easy availability — it is a good candidate to try a 2-4 week experiment.

Personally, I would be tempted to try the following pattern (starting at a low dosage and increasing):

  • 3 weeks of Streptococcus thermophilus (up to 10 BCFU)
  • 2 weeks of Bifidobacterium breve (up to 20 BCFU)
  • 2 weeks of Bifidobacterium infantis (up to 20 BCFU)

Bottom Line

My personal choice would be to go with the “Healthy Algorithm” for the following reasons:

  • The traditional approach has appeared to stall, time for a change
  • It is heavily based on very statistical significance over the entire scope of bacteria involved (i.e. dense data) but it has not been validated by clinical studies.
  • I have always been unhappy about clinical studies because the data is:
    • Messy (typically in the context of one or another medical condition)
    • Small sample sizes
    • Low resolution to bacteria

I am also curious to see how well the “Healthy Algorithm” performs.

Postscript – and Reminder

I am not a licensed medical professional and there are strict laws where I live about “appearing to practice medicine”.  I am safe when it is “academic models” and I keep to the language of science, especially statistics. I am not safe when the explanations have possible overtones of advising a patient instead of presenting data to be evaluated by a medical professional before implementing.

I cannot tell people what they should take or not take. I can inform people items that have better odds of improving their microbiome as a results on numeric calculations. I am a trained experienced statistician with appropriate degrees and professional memberships. All suggestions should be reviewed by your medical professional before starting.

The answers above describe my logic and thinking and is not intended to give advice to this person or any one. Always review with your knowledgeable medical professional.

My academic training is in Operations Research with a large dosage of lateral thinking (Edward de Bono).

My academic training is in Operations Research with a large dosage of lateral thinking (Edward de Bono).

A classic story is below:

One famous story of operations research success during the war involved an analysis of Allied bombers returning from bombing missions over Europe. The military analyzed the location of shrapnel damage and bullet holes in returning bombers, to identify where to place additional armor on aircraft. Operations researchers were brought in at the last minute to do a “confirmatory” analysis, but they recommended that additional armor be placed on bombers everywhere except the places with damage or bullet holes! The operations researchers realized that analyzing damage to returning bombers involved a sampling error. It was the bombers that did not return that needed extra protection—and they needed it in the most vulnerable places (the places not damaged on the returning bombers).

In the past, most medical work has focused on bacterial shifts statistically linked to individual symptoms. Think of the “bullet holes” problem: the literature usually looks at one symptom at a time, while real patients often present with dozens.

Recently, I started using odds ratios instead. Most people know odds ratios from smoking and cancer risk, but they can be applied broadly—for example, the odds of working at Microsoft if you graduated from a particular university.

Using about 5,500 samples and roughly 350 symptoms, I built odds tables and then tested those odds ratios against a reference set of healthy individuals. To my surprise, sample after sample showed the highest odds for being asymptomatic, far more often than I expected.

On reflection, this implies we now have a well-defined, statistically grounded model of a healthy (asymptomatic) microbiome. That was the “lightbulb” moment.

Instead of hunting for individual “holes” and trying to patch them, we should look at all the shifts away from this asymptomatic model. Once those shifts and their contributions (odds ratios) are identified, we can use published research to determine what is most likely to normalize the microbiome. A long list of symptoms (bullet holes) stops being the target; the real target becomes making the microbiome asymptomatic.

Some past links:

A walk through on applying the above methodology pattern.