The key item is to realize every antibiotic make different changes, often very different changes. Studies on the U.S. National Library of Medicine document many antibiotics and their changes. We use that information and the Artificial Intelligence Engine (which is not Machine Learning or Chat_GPT like) to compute the substances that will best compensate, as well as substances that may amplify the changes caused by the antibiotic.

Process Is Simple

Go to https://microbiomeprescription.com/Library/ModLookup and enter the name of the antibiotic. The database contains most of the brand names used around the world. Enter the name, for example: amoxicillin. Surround it with % % on each end. Click [Search]

This will take you to a page similar to below

The resulting page is shown below

Clicking on Bacteria Detail will list the bacteria that decreases and those that will increase! Yes, antibiotics will encourage the growth of some bacteria.

Below this are the items that impacts these bacteria, Most items impacts multiple bacteria. Balancing the impact is done by the Artificial Intelligence.

In this taking Vitamin B1 supplements (or foods rich in B1) should be avoid for sometime after finishing the course of antibiotics. Similarly with Hesperidin (polyphenol). You may not know what has it — so just click the food icon 🍱 to see the foods:

Similarly with any To Add items that you are not familiar with, for example: resistant starch,

That is it — Lookup, click suggestions, for anything unfamiliar look for the food icon and just click. Often there is no need to buy supplements when you can get sufficient from food. For example, you get 4.3 grams of resistant starch by eating a 100 grams (3 oz).

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.

I have written about this in the past:

• A mouth full – for better or worst [2014]
• Oral Probiotics [2015]
• Your mouth can trigger flares [2017]
• Science based mouth wash for ME/CFS [2019]
• Probiotics for mouth, sinus and eyes [2019]

When I first started Microbiome Prescription the main and most popular provider was uBiome (dearly departed) which explicitly offered oral microbiome analysis. I had about a dozen uploads. Eventually I stopped support because there was not going to be sufficient uploads, even if I was waited for a decade.

Stomach Acid does not nuke probiotics!

This is a common internet legend which disagrees with both studies and common sense!!!

Common Sense Anyone?

This is the key question: “If you have a bacteria in your gut, how did it get there?”

Assuming that you do not believe that bacteria has perfected teleportation, then there is just one route: Through the mouth, the stomach, etc. It is the great trek!

Studies Supporting No or Little Impact

There are two German probiotic that are suspended in water, added to water and drunk. These studies indicate that they do survive! In fact, they persist!

• Persists: Symbioflor-2 E.Coli
• Symbioflor-1 [2012] Enterococcus faecalis

Looking at Vet Practices, adding probiotic to food or water is well establish. Some sites actually advocates opening capsules. Custom Probiotics advocates all of their probiotics be taken in a glass of water.

Where does this myth come from?

I strongly suspect marketing — if you compare the cost per BCFU from Custom Probiotics to your usual health food store probiotic capsules you will see the costs can be 10x higher in the capsules That is NOT the cost of putting them into capsules. In marketing, claims about the importance of capsules is differentiate product to get you to buy brand X and not Y.

People are also willing to pay for convenience. Buying flour to bake a load of bread is much cheaper than buying a ready made load of bread. At our local coop, a custom loaf of bread was selling for $11.95 — people are lazy.

Vendor Distractor?

I also suspect that stomach acid eliminating probiotic has been used as an excuse by many vendors. The likely cause of probiotics not staying around is where they were sourced: Human or Animal. “In general, their optimal growth temperature ranges between 36–38°C and 41–43°C for human and animal origin strains,” [2011] A probiotic bacteria is unlikely to thrive at a temperature 7°C (or 12°F) from it’s preferred temperature. It will likely reproduce less and be less robust (allowing other bacteria to beat it up).

This comes back to my old soapbox: Buy Only Probiotics where the STRAIN (and not just the species!) is listed – and that specific strain has been researched (Ideally for the condition that concerns you. Use this link to look up most, for example periodontal disease), and that the origin is human. I would suggest constantly emailing the manufacturers!!! It is likely the only way that the situation will improve.

Oral Microbiome Is associated with many conditions

• ” In conclusion, this study suggests significant associations of the Oral Microbiome diversity with certain mental health dimensions such as depressive symptoms and anxiety.” [2023] [2022][2020]
• Oral Microbiota, Its Equilibrium and Implications in the Pathophysiology of Human Diseases: A Systematic Review. [2022]
• Share 
• Profiling the oral microbiomes in patients with Alzheimer‘s disease.[2023]
• Unlocking Modifiable Risk Factors for Alzheimer‘s Disease: Does the Oral Microbiome Hold Some of the Keys? [2023]
• Oral and intestinal dysbiosis in Parkinson‘s disease. [2023]
• Oral and gut dysbiosis leads to functional alterations in Parkinson‘s disease. [2022]
• Changes in Oral Microbial Diversity in a Piglet Model of Traumatic Brain Injury. [2022]
• Fungal Infections Of The Oral Mucosa. [2023]
• Implications of oral streptococcal bacteriophages in autism spectrum disorder.[2022]
• Oral Microbiota Changes Contribute to Autism Spectrum Disorder in Mice.[2022]

My impression is that any condition with a neurological component (i.e. brain fog, impulse control, etc) is likely to have ORAL microbiome dysfunction.

Going Forward

There are many products available, for example, see this list. They will likely contain one or more of the following. For a bigger list, see researched probiotics here: mouth, sinus and oral.

• Bacillus Coagulans
• BLIS K12,
• BLIS M18,
• lactobacillus acidophilus,
• lactobacillus reuteri,
• lactobacillus paracasei,
• lactobacillus salivarius,
• salivarius thermophilus
• Symbioflor-1 [2012] Enterococcus faecalis

The “salivarius” indicate where it was first identified (mouth saliva). So it is normally in the mouth.

The key is for the probiotic to stay in the mouth for sufficient time to dislodge some other residents. To me, this appears to suggest:

• Brush and rinse after every meal
• You could do things like break apart an Oregano Oil capsule or drop Monolaurin flakes into the mouth and hold them there for as long as you can tolerate them…
• Take one or more lozenge afterwards… I would suggest taking one at a time, then perhaps change to a different one when dissolved. There are a few probiotics that are available as pressed pills. If the taste is not too bad, I personally use Miyarisan(jp) [clostridium butyricum] and shin biofermin (jp) [Bifidobacterium bifidum, Enterococcus faecalis, Lactobacillus acidophilus] in this manner. Some others to consider:
  • BioGaia Prodentis Mint Lozenges [Lactobacillus Reuteri]
  • Flora, Super 5 Probiotic Lozenges [Lactobacillus Acidophilus: 60% Bifidobacterium Bifidum: 15% Lactobacillus Bulgaricus: 15% Streptococcus Thermophilus: 5% Lactobacillus Salivarius: 5%]
  • NOW Supplements, OralBiotic™, [Streptococcus salivarius BLIS K12]

The ideal would be to take an oral microbiome test that reports percentile ranking of each bacteria (against other oral samples). I do not know of any one providing that. uBiome likely had that data, but they are no more.

For more Analysis Posts on Long COVID and ME/CFS click here.

Back Story

I’m male, 5’ 10”, currently 145 lbs, 60 years old. I first became ill suddenly in 1987, with what at the time seemed to be food poisoning or a stomach bug. The nausea, stomach upset and loss of appetite lasted months after, I became bedridden. Dozens of tests, doctors, revealed nothing.

Gradually over time, the symptoms subsided and I began to eat and gain weight again. After about a year and a half, I became functional, but never recovered to my previous state. This has been the course of life since. The symptoms would reoccur, last several months, then subside. With no definitive cause for beginning, nor treatment for ending.

The ongoing fatigue over the years was relentless. I somehow managed to complete a 30 year carrier, and took retirement at first opportunity. Doctors speculated that my work was a stress factor responsible for my condition, and retirement would solve it. It didn’t.

For the past several years, I’m mostly housebound, able to go outside and do minor tasks on occasion. Currently, my worst of symptoms are LPR/ reflux related. Not in the traditional sense, mine is a gas/ aero, that I believe is being caused by severe dysbiosis/ imbalance.

I cite this study as an example,

Accompanied with voice loss, throat and chest pain, severe at times.

A recent endoscopy showed “mild gastritis”. Doctors offer me benzodiazepines and antidepressants, stating my symptoms do not correlate with their findings.

Previous endoscopes/ colonoscopies were unremarkable. Gastric empty test normal.

I have tested negative for SIBO several times. IBS Smart test, h pylori, celiac, mast cell (MCAS), all negative.

Numerous diets, eliminations, supplements, herbs, prescribed medications have brought no help or relief. Most have made symptoms worse.

I did manage to have a biopsy taken and sent to Dr John Chia, to test for entero virus. It came back highly positive, however, I am somewhat skeptical that it could be a red herring. My vague attempts with pre/ probiotics resulted with increased gas and/ or diarrhea.

One clue, on two occasions (1995, 2014) after having colonoscopy, I mysteriously had remissions afterwards, that lasted several months. The speculation, is that the prep somehow created a reset of bacteria/ flora. I recently tried to replicate, by doing a prep cleanse. However, despite drinking a full gallon plus, I ran out of solution before being completely cleared out. I felt a brief improvement, but have suffered with horrid lower gas/ flatulence since.

Not the result I was after.

Initial Comments on Back Story

For myself, stress was the trigger of each of my ME/CFS episode so the speculation by his MDs was reasonable. The 1987 event, and the resulting cascade of the microbiome is the root concern. The microbiome evolves, just like society evolves. In 1987, most homes had a VCR and a few lucky people had digital pagers. Today, very few have VCRs (in use) and almost every one has a smart cellular phone. In 2023, arguing whether the right choice should be BetaMax or VHS has become irrelevant. Similarly, focusing on the cause in 1987 is really irrelevant. It may have been a virus, Lyme disease or a dozen other culprits – it is very unlikely to be relevant to addressing today’s microbiome.

Analysis

Looking at the distribution by frequency, we see an over-population of bacteria with low levels.

The Bacteria over 90% and Bacteria under 10% are a simple statistic to understand. If you have 188 different genus and true randomness then you would expect around 19 in each group. We has 12 over 90%, close, but a whopping 61 under 10% — that 32% of all bacteria, not 10%!!! In other words, we have a massive number of different bacteria at low levels. It is not a problem of a few bacteria being too high.

Percentile	Genus	Species
0 – 9	61	76
10 – 19	20	16
20 – 29	14	16
30 – 39	9	8
40 – 49	15	20
50 – 59	14	14
60 – 69	16	20
70 – 79	10	22
80 – 89	17	22
90 – 100	12	21

Looking at Dr. Jason Hawrelak Recommendations for levels, he was at the 99.7%ile and the very few misses for being ideal.. they were border line.. (i.e. 15.1 versus 15; 0 versus 0.0001). In short, almost an ideal microbiome by that criteria.

Going Forward

Doing the usual 3 suggestions sets, we

•  Standard Lab Ranges (+/- 2 Std Dev) – 9 bacteria
•  Box Plot Whisker – 43 bacteria
•  Kaltoft-Moltrup Normal Ranges – 85 bacteria

The list of top suggestions look very close to what I was taking for my own remission (pre-microbiome analysis days).

• rosmarinus officinalis (rosemary)
• thyme (thymol, thyme oil)
• peppermint (spice, oil)
• lactobacillus paracasei (probiotics)
• lemongrass oil
• Human milk oligosaccharides (prebiotic, Holigos, Stachyose)
• neem
• syzygium aromaticum (clove)
• Sumac(Rhus coriaria)
• cinnamon (oil. spice)
• Ajwain (trachyspermum ammi)
• Curcumin
• lactobacillus casei (probiotics)
• thiamine hydrochloride (vitamin B1)
• aloe vera
• ashwagandha (withania somnifera)
• garlic (allium sativum)
• olea europaea (olive leaf)

Looking at the to-avoid

• vsl#3 (probiotics)
• walnuts
• lactulose
• amaranth
• barley, oat
• arabinoxylan oligosaccharides (prebiotic)
• fish oil
• saccharomyces cerevisiae (probiotics)
• low protein diet : typically seen when B-vitamins are wanted.

The full details are below

Going over to the Food Site we see:

• Chicken and Turkey Liver being at the top of the list

mg per 100 grams	Significant amount	Nutrient
25800	Significant	Protein
13.925	Significant	Niacin
12.9	Significant	Iron, Fe
4.293	Significant	Retinol
2.313	Significant	Riboflavin
0.84	Significant	Pyridoxine (Vitamin B6
0.56	Significant	Folic acid
0.02113	Significant	Vitamin B-12

Pass 2 — Looking at Prescription items

One non-prescription showed up near the top, an item that I have used with good effect: monolaurin. The top antibiotics list include:

• piperacillin-tazobactam (antibiotic)s [Penicillin]
• benzylpenicillin sodium (antibiotic) [Penicillin G]
• hyoscyamine (l),(prescription) – “It can treat muscle cramps in the bowels or bladder. it can treat symptoms of irritable bowel syndrome (IBS), colitis, and other digestive problems.” [Src]
• minocycline (antibiotic)s [Tetracycline] – used by many ME/CFS physician, and also by me. It has many good characteristics (neuroprotective, cross body-brain barrier, etc)
• tobramycin (antibiotic)s – usually only used for eye infections
• ampicillin (antibiotic)s [Penicillin]

The above have various risks, and should be review carefully. My own preferences would be minocycline first, then hyoscyamine [because IBS is a factor for this patient]. I should note that using a different algorithm without consensus (Special Reports for your MDs) reports contrary results.

Feedback on Antibiotics

Another freak incident that resulted in a five month remission. In 2011, I had one tonsil that became huge. The other remained completely normal. Doctors were suspect of cancer, and both were removed. Thankfully, it was not cancer. So they didn’t look any further to determine the cause.

But at 49 year old, this was no picnic. Rough surgery and recovery, but it followed with probably the most significant remission of all. It was an amazing turn around, all symptoms backed off, energy returned to nearly normal. After 5 months though, symptoms began to return, and within the year I was back to my previous state

I was on amoxicillin for several weeks after the surgery. When the symptoms began to return, we became suspect that it was the amoxicillin that had done something. My doctor put me back on it, but there was no improvement. Whatever had taken place, was a random-chance occurrence. Maybe the amoxicillin was responsible, by creating a shift in bacteria balance.

I found that Cecil Jadin’s protocol is what I tend to advocate. One of the key reason is that it was it was tuned from many years of clinical experience at the Pasteur Institute for Tropical Medicine for what they termed as an “Occult Rickettsia” infection. The basis of it is rotating different families of antibiotics. The mathematics are simple — first round may eliminate 90% of the issues with 10% being resistant. A different antibiotic usually require a different type of resistance, so 90% of the remaining 10% is eliminated.. leaving just 1%. Doing a third round, takes us down to 0.1%

I speculate that the few survivors from your first round of amoxicillin slowly rebuild . Because these bacteria were the survivors, those with resistance genes. The repopulated gut was largely resistant, hence no effect from this antibiotic later. Think of it as a boxing match. You landed a good punch — but instead of landing more punches, the opponent was able to recover and block the same punch later.

Later, discussion of this story with a well-meaning gastrologist, he had me do a week of xifaxan. He felt certain, based on my story, it would get me back to the previous gains. It made me horrid sick, lasting for weeks after stopping it. There was no improvement.

My preference is not to pick antibiotics by symptoms (or what worked for the prior patient), but from the bacteria results that are desired. Results are not guaranteed — rather, IMHO this approach has higher probability of being successful.

Looking at Probiotics

First, using KEGG data: as is typical for most ME/CFS people (and consistent with the ME/CFS conference reports from 1998): Escherichia coli (Symbioflor-2 or Mutaflor). The next common one is Bacillus subtilis (natto), Clostridium butyricum, Lacticaseibacillus casei, Enterococcus faecalis.

From the consensus list we see a good overlap and have in order:

• lactobacillus paracasei (probiotics)
• lactobacillus casei (probiotics)
• lactobacillus casei shirota (probiotics) – Yakult
• bacillus subtilis natto (probiotics)
• symbioflor 2 e.coli probiotics

bacillus subtilis natto is the source for a supplement called nattokinase, which dissolves fibrin deposits and also an anti-inflammatory [2021]. It is also available not as a probiotic, but in a Japanese Dessert Food called Natto. Natto is an acquired taste.

My probiotic suggestions would be the following (at sufficient dosage, see this page):

• 2 weeks of Bacillus subtilis (perhaps 10 BCFU daily)
• 2 weeks of lactobacillus casei (perhaps 48 BCFU daily)
• 2 weeks of one of the E.Coli probiotics (Mutaflor: 4 capsules per day, starting at 1 and slowly increasing)

Then repeat. Note that some probiotics are strong avoid, for example: saccharomyces cerevisiae / saccharomyces boulardii.

Taking Herbs

There are a large number of herbs cited above. In keeping with my philosophy of avoiding resistance, take some of herbs for 2 weeks and then change to others herbs for the next two weeks. The question is how to take it? I know that some will claim that tinctures are more effective; IMHO, tinctures are very effective for reducing back accounts!

My personal practice is to take herbs in one of two ways:

• Buying them in bulk, organic and making our own 000 capsules. Most store purchased herb capsules do not appear to be organic, often with additional ingredients “to make them better” – which is often marketing hype.
  • We take them immediately prior to meals so that the stomach acid produced to handle the meal, also dissolves the active ingredients from the herbs.
• Taking them as a hot tea. Some herbs are horrible tasting… those tend to end up as capsules.

Many, but not all, herbs have documented dosages with links to studies (which can be informative for how to take). For example: Neem: 120 mg/day, Olive Leaf: 700 mg/day, Curcumin: 3 gm/day. My general rule of thumb is one 000 capsule with each meal.

Questions

Q: Curious to know, do you think there may be an advantage of using this method with probiotics, to deliver past the stomach, farther down the gut?

A: I know this common belief, but have not seen any clinical studies demonstrating it. What I have seen is probiotics delivered as a liquid in water, are documented to persist for weeks after a single dose. That is, the specific strain delivered was not detected before but was detected in subsequent weeks. This indicates that this belief is very questionable. Personally, I tend to use single documented strains of probiotics from Custom Probiotics and follow their directions. I do keep food at least a hour away from taking probiotics so stomach acid production will be quiet.

On a related issue, remember that the gut is downstream from the mouth and nasal passages. The source of bad bacteria may be there and may account for repopulation over time. One probiotic that has been shown effective for the nasal passages etc is Symbioflor-1. There are a few hard tablet probiotics out there (for example, Miyarisan — Clostridium butyricum). I have often just put them in my mouth and let them dissolve there.

NOTE: I will be doing a follow up post on The oral microbiome, coming soon!

This post started out seeking to confirm or debunk the claim located here.

The method was very simple because we have a continuous stream of samples from before COVID, before the COVID vaccination and after the majority of people uploading samples would have been vaccinated. If this massive change is happening then the pre-COVID bifidobacterium count (by lab) would be much higher than the post-COVID vaccination bifidobacterium counts.

My results: there was no statistical significance between the averages

• Pre 2020-01-01: Average Count 20380 on 118 samples, Std Dev 98300
• Post 2022-06-01: Average Count 26111 on 406 samples, Std Dev 72700

That is a 28% increase when a decrease was expected from the above talk.

I am open data, so you can pull the data and check the calculations:

Volatility of Numbers

I was also curious to see if there was any apparent month by month pattern, so I pulled the statistics for biidobacterium, shown below. It is illuminating to a statistician like me, perhaps confusing or concerning to people with poor understanding of statistics (who would expect the numbers from month to month to be similar).

		Thryve			BiomeSight
Year	Month	Average	Std Dev	Obs	Average	Std Dev	Obs
2020	7	32438	131646	24	27929	35826	14
2020	8	25456	43405	21	7683	8948	9
2020	9	13410	19329	17	18501	22566	14
2020	10	84056	148144	18	4370	7390	20
2020	11	18598	34049	9	4926	8197	13
2020	12	10078	17108	16	1841	2718	29
2021	1	68152	172405	20	12436	20675	32
2021	2	101600	163980	30	17289	55509	45
2021	3	57957	103248	17	14482	33774	33
2021	4	21979	42967	30	7700	24436	46
2021	5	24693	51744	56	14257	33608	38
2021	6	28166	84491	39	21465	85762	51
2021	7	47023	105209	39	22620	67229	51
2021	8	60283	82398	43	18427	79784	37
2021	9	62438	92929	28	12002	19635	41
2021	10	13121	29924	24	5922	8565	38
2021	11	11515	27095	57	9996	24966	58
2021	12	28582	80191	17	11498	29919	63
2022	1	15114	28760	38	7076	15149	50
2022	2	24816	59069	32	11707	27202	52
2022	3	10486	23995	33	20243	51539	47
2022	4	10207	21580	57	7916	18288	69
2022	5	33471	82497	80	10304	23719	81
2022	6	23861	60126	53	8053	21994	235
2022	7	26797	109435	40	10709	20439	62
2022	8	67707	132108	60	8085	17190	85
2022	9	13926	17622	28	12635	21332	92
2022	10	9090	14049	45	9627	21171	89
2022	11	10296	19034	39	7293	12150	61
2022	12	3186	6194	21	10887	21390	42
2023	1	10224	18215	41	13302	21612	89
2023	2	10604	22883	52	9103	19781	72
2023	3	65953	78173	30	13566	34256	57

My conclusion is that you need to have two things to get good results:

• All of the samples should be processed by the same lab at the same time. Different batches of reagents may cause different results.
• You need good sample sizes, at least 100+
• You need to be very very careful not to cherry pick data (example below)

An example from Thryve/Ombre data above, with a sample size of 30, the average was 101600. Later a sample size of 21 reported just 3186. Conclusion: going back to school caused family bifidobacterium to tank!

On sample size of 100 issue:

This is an update of my 2016 post: Low Iron – A Gut Bacteria Connection. One key addition is that Vitamin A supplementation may have significant positive impact.

The microbiota shifts the iron sensing of intestinal cells [2016]. “The amount of iron in the diet directly influences the composition of the microbiota. Inversely, the effects of the microbiota on iron homeostasis have been little studied….Commensal organisms (Bacteroides thetaiotaomicron VPI-5482 and Faecalibacterium prausnitzii A2-165) and a probiotic strain (Streptococcus thermophilus LMD-9) led to up to 12-fold induction of ferritin in colon.”

Probiotics to Take

• Probiotic strain Lactobacillus plantarum 299v increases iron absorption from an iron-supplemented fruit drink: a double-isotope cross-over single-blind study in women of reproductive age[ 2015 ].[2017] [2019] [2020] [2021]
• Effects of Lactobacillus casei on Iron Metabolism and Intestinal Microflora in Rats Exposed to Alcohol and Iron.[2022]
• “No significant differences were found between the two yogurts (one with live  cultures and the other without) in terms of their effects on serum iron, AST and ALT levels.” [2013] – so only certain  bacteria are involved. Most lactobacillus do not have an effect [2007]
• Oral administration of Bifidobacterium longum CECT 7347 ameliorates gliadin-induced alterations in liver iron mobilisation [2013].
• “we show that a panel of probiotics are not able to respond to increased iron availability, and identify an isolate of Streptococcus thermophilus NCIMB 41856 that can increase growth rate in response to increased iron availability.” [2011]
• Vitamin A modulates the expression of genes involved in iron bioavailability [2012] [2019]
• Heat-Killed Lactococcus lactis subsp. cremoris H61 Altered the Iron Status of Young Women: A Randomized, Double-Blinded, Placebo-Controlled, Parallel-Group Comparative Study [2022]

Likely No or Negative Effect

• “Bifidobacterium bifidum.. decreased amounts of calcium and iron released from bread.” [2012]
• Probiotics Lactobacillus reuteri DSM 17938 and Lactobacillus casei CRL 431 modestly increase growth, but not iron and zinc status, among Indonesian children aged 1-6 years [2013].
• “we show that a panel of probiotics are not able to respond to increased iron availability, and identify an isolate of Streptococcus thermophilus NCIMB 41856 that can increase growth rate in response to increased iron availability.” [2011]
• Probiotic bacteria reduce salmonella typhimurium intestinal colonization by competing for iron [2013]. “Thus, iron availability impacts S. Typhimurium growth, and E. coli Nissle reduces S. Typhimurium intestinal colonization by competing for this limiting nutrient.” – So E.Coli probiotics and iron deficiency may not play well together.
  • ” Intestinal bacteria compete for the essential nutrient iron, leading to replacement of pathogenic Salmonella by the probiotic Escherichia coli Nissle, which is better equipped with iron acquisition systems, and resolution of infectious colitis.” [2013]

This is a person as in this prior set of posts, A Microbiome Trek Continues thru the land of ME/CFS.

There are two key differences that needs to be understood

• Difference in numbers reported (of bacteria and percentiles)
• Will the suggestions change?

Comparison of Results: Thorne to Biomesight

The samples were only a few weeks apart, so similar data. The ratio of bacteria reporting is 6x more for Thorne than Biomesight, so the expectation would be similar shifts for most of the others.

Key Difference: Bacteria Percentiles come from Thorne, the other percentiles are computed against a composite of other samples (until we get sufficient samples). The Conditions, Enzymes and Compound estimates are likely unreliable (we compare against all tests and not other samples from the same procession) and we will ignore in this analysis.

Many of the criteria are identical between tests: Outside Range for JasonH, Medivere, Metagenomics , MyBioma, Nirvana/CosmosId and XenoGene. So for people using those criteria — there is no difference between the tests.

The Bacteria over 90% and Bacteria under 10% are a simple statistic to understand. 10% should be under 10% and 10% above the 90%ile to have a balance microbiome.

With Thorne we have 3226 bacteria and true randomness then you would expect around 322 in each group. We find 239 over 90%, close, but a whopping 1577 under 10% — that 48% of all bacteria, not 10%!!! In other words, we have a massive number of different bacteria at low levels. It is not a problem of a few bacteria being too high (which is a common belief about gut dysfunction), but many only have token amounts.

For Biomesight, we have 503, and thus would expect 50 and 50. For over 90%ile, we have just 25, and for under 10%, 108 bacteria. The high %ile is just 50% of expected and 200% of expected for low with Biomesight; Thorne is just 75% of expected for high, but a massive 489% of expected for low.

Criteria	Thorne Sample	Biomesight
Bacteria Reported By Lab	3226	503
Bacteria Over 99%ile	193	10
Bacteria Over 95%ile	212	18
Bacteria Over 90%ile	239	25
Bacteria Under 10%ile	1577	108
Bacteria Under 5%ile	1411	44
Bacteria Under 1%ile	1106	3
Different Labs – Items Skipped
Pathogens	162	34
Outside Range from JasonH	6	6
Outside Range from Medivere	16	16
Outside Range from Metagenomics	7	7
Outside Range from MyBioma	5	5
Outside Range from Nirvana/CosmosId	17	17
Outside Range from XenoGene	35	35
Outside Lab Range (+/- 1.96SD)	189	8
Outside Box-Plot-Whiskers	685	27
Outside Kaltoft-Moldrup	1753	91
Condition Est. Over 99%ile	6	6
Condition Est. Over 95%ile	15	7
Condition Est. Over 90%ile	24	10
Enzymes Over 99%ile	93	10
Enzymes Over 95%ile	673	118
Enzymes Over 90%ile	1131	647
Enzymes Under 10%ile	312	150
Enzymes Under 5%ile	262	75
Enzymes Under 1%ile	183	12
Compounds Over 99%ile	230	100
Compounds Over 95%ile	498	463
Compounds Over 90%ile	684	606
Compounds Under 10%ile	1350	599
Compounds Under 5%ile	1336	580
Compounds Under 1%ile	1324	569

Comparison of Results: Thorne to Ombre

The Bacteria over 90% and Bacteria under 10% are a simple statistic to understand. If you have 3226 bacteria and true randomness then you would expect around 322 in each group.

• For Ombre we would expect 59 over 90%ile and under 10%ile. close. We have 22 or 37% of expected for low %ile and 117 or 200% of expected for low percentile.

Many of the criteria are identical between tests: Outside Range for JasonH, Medivere, Metagenomics , MyBioma, Nirvana/CosmosId and XenoGene. So for people using those criteria — there is no difference between the tests.

Criteria	Thorne Sample	Ombre
Bacteria Reported By Lab	3226	588
Bacteria Over 99%ile	193	2
Bacteria Over 95%ile	212	10
Bacteria Over 90%ile	239	22
Bacteria Under 10%ile	1577	117
Bacteria Under 5%ile	1411	67
Bacteria Under 1%ile	1106	6
Different Labs – Items Skipped
Pathogens	162	34
Outside Range from JasonH	7	7
Outside Range from Medivere	14	14
Outside Range from Metagenomics	5	5
Outside Range from MyBioma	8	8
Outside Range from Nirvana/CosmosId	18	18
Outside Range from XenoGene	46	46
Outside Lab Range (+/- 1.96SD)	189	5
Outside Box-Plot-Whiskers	685	34
Outside Kaltoft-Moldrup	1753	129
Condition Est. Over 99%ile	6	0
Condition Est. Over 95%ile	15	0
Condition Est. Over 90%ile	24	0
Enzymes Over 99%ile	93	0
Enzymes Over 95%ile	673	9
Enzymes Over 90%ile	1131	101
Enzymes Under 10%ile	312	165
Enzymes Under 5%ile	262	65
Enzymes Under 1%ile	183	2
Compounds Over 99%ile	230	38
Compounds Over 95%ile	498	236
Compounds Over 90%ile	684	332
Compounds Under 10%ile	1350	248
Compounds Under 5%ile	1336	159
Compounds Under 1%ile	1324	33

My personal opinion is that Thorne is better because the more bacteria reported, the greater the statistical significance of over and under representation. On the positive side, all three samples agree on the shifts of bacteria patterns

Analysis

The distribution continues to match a common pattern with ME/CFS microbiomes, an over abundance of low percentile bacteria. This is also seen with the prior Biomesight sample. This shift is made much stronger with Thorne because more genus and species are reported. It also emphasis the shifts seen above.

Percentile	Genus	Species
0 – 9	417	628
10 – 19	85	82
20 – 29	60	85
30 – 39	42	69
40 – 49	34	32
50 – 59	59	339
60 – 69	26	60
70 – 79	16	28
80 – 89	15	31
90 – 99	21	142

Percentile	Genus	Species
0 – 9	24	33
10 – 19	32	37
20 – 29	15	23
30 – 39	9	11
40 – 49	9	16
50 – 59	8	14
60 – 69	8	9
70 – 79	10	17
80 – 89	7	15
90 – 99	6	10

Treatment Dilemma

The usual algorithm is to increase bacteria with low percentiles and decrease those with high percentiles. When you have a huge numbers of low percentile then the question arises: Do you really want to increase these, or do you want to eliminate them entirely to get them off the radar? It is a valid question, but to do that, we have to make increase/eliminate suggestions on 417 genus. That is not practical (given the sparseness of data and limited knowledge of so many genus). My working hypothesis is that keeping to the usual algorithm is the best way to go. Let the bacteria make the determination of winners and losers.

Going Forward

I am going to build two consensus reports. One for Thorne and one for the latest Biomesight, then use the “Uber Consensus” report on the Multiple Samples tab. The purpose is to see whether there are really significant differences in suggestions between the two sample reports.

We are going to do 4 basic suggestions for each:

•  Standard Lab Ranges (+/- 2 Std Dev) Thorne: 53 bacteria,BiomeSight: 8 bacteria
•  Box Plot Whisker Thorne: 86 bacteria,BiomeSight: 21 bacteria
•  Kaltoft-Moltrup Normal Ranges Thorne: 215 bacteria,BiomeSight: 70 bacteria
•  Percentile in top or bottom 10% Thorne: 1508 bacteria,BiomeSight: 130 bacteria

The results had 581 suggestions. I did a Pivot tables of Take Counts against Avoid Counts to visualize the similarities between each set of suggestions going into the uber suggestions. I read the pivot table below as indicating that the suggestions were equivalent with 73 items being to Take with no Avoid, and a further 72 items with just 1 avoid. We have lots of choices in agreement

Counts	Takes
Avoid	0	1	2	3	4	5	6	7	8
0		4	5	16	23	1	1	1	22
1	3	2	3	7	11	6		72
2	3	3	11	10	19	5	29
3	20	6	9	11	5	47
4	15	18	9	4	29	1		1
5	12	10	1	44		1
6	3	2	25			1
7		37
8	13

What are some of the top suggestions?

• bacillus subtilis (probiotics)
• whole-grain barley
• high fiber diet
• Cacao
• noni
• dates
• aspartame (sweetner) — which is always a tricky one to suggest
• Taxifolin
• Sriracha sauce
• wasabi
• Cilantro

As with the prior reports, Escherichia coli probiotics is at the top of the KEGG computed probiotics, typical for ME/CFS. From the consensus, we have:

• bacillus subtilis (probiotics)
• bifidobacterium infantis,(probiotics)
• bifidobacterium pseudocatenulatum,(probiotics)
• clostridium butyricum (probiotics),Miya,Miyarisan
• lactobacillus reuteri (probiotics) – which produces a powerful natural antibiotic, Reuterin
• bifidobacterium pseudocatenulatum li09,bifidobacterium catenulatum li10 (probiotics)

The absence of most Lactobacillus is not surprising because they are hostile to Escherichia Coli. My pivot conference report from 1998 had this bacteria being low in ME/CFS patients. With Thorne, we can get actual numbers (16s numbers for Escherichia Coli are questionable). This person Thorne Results is at the 27%ile for Escherichia and 29%ile for Escherichia Coli, which is consistent with that conference report and the KEGG computation for probiotics.

Out of interest, I looked for the %ile on the Thorne results of the consensus suggested probiotics:

• bacillus subtilis (probiotics) – 66%il1
• bifidobacterium infantis,(probiotics) – 0%ile
• bifidobacterium pseudocatenulatum,(probiotics) – 16 %ile
• clostridium butyricum (probiotics),Miya,Miyarisan – 92%ile
• lactobacillus reuteri (probiotics) – 32%ile

Having the actual percentiles for the strains used in probiotics allows us to tune the suggestions. In this case, we should skip any probiotics with bacillus subtilis or clostridium butyricum. There is no point in taking them. On the other side, you have confirmation that the suggested probiotics are likely to have an impact. I give the Thorne results a big 👍 because you can actually determine the probiotics that you likely not benefit from. The 16s results only report a few probiotic species (with questionable accuracy).

The Extras from the Thorne Results

This person did not see the next data on Thorne’s Web Site — but it was in the data CSV file to upload. The virus count with a few having percentiles. The ones without percentiles are rare ones without data.

And Fungi too!

For both of these sets of data, values over 90% should be researched. Fungi are of special concern because they can both be treated often and may also indicate a mold issue around the person.

User Feedback

Thanks Ken! .. and yikes . Mold is my nemesis. I’ve been trying to figure if I’ve had mold / moldy house for years. I did an ermi for the entire house and got a 2 which is really low. Recently I did an air test all around the house and it was pretty low minus a car which I knew was an issue and I’ve been trying to avoid. I’m trying to decipher if it’s a past issue and I can’t detox or current 

Attached is my air test.

Question: yellow highlights on Thorne. Those were 90%+ , there were some non highlighted 90% + results. Should I only research the ones you highlighted?

I should have a new mold urine test result coming too which I’ll send your way once I get it!

Answers: As a general and very rough rule, count the number of items reported (Virus: 35, Fungi:50). Take this number and multiple by a percentile – say 99%ile, and round up. For Virus and Fungi it is 1. This is the number of false positives that would be expected with 99% or higher.

You appear to have an issue. Your mold test fortunately identifies the genus and where it is located. The HVAC and washing machine hints that it is brought into the house, likely on clothes. The attic appears free of the ones that you are high in. I noticed that Malassezia is not reported in the mold test.

Bottom Line

IMHO, getting a Thorne sample is a definite should do at least once. Why? some of your issues may be fungi or virus related. The difference for suggestions of using Thorne, BiomeSight or Ombre is slight. The differences are reasonable given the sparseness of the data that we have for suggestions.

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 uber focus for the last few years has been on the microbiome. The reasons are simple: relatively rich amount of data to work from, detail tests can be done without a Physician’s Order, and treatment can often be done without a prescription.

In no way am I saying that the microbiome is the complete picture. It is simply the easiest to doddle in.

The analogy of a dice is good to get the entire picture. Actually two dice … because often you feel like crap as a result of a roll of the die in the craps game of life.

Some Sides of The Die

The following are the sides that come quickly into mind, they are likely more

1. SNP/DNA issues. Many conditions have associations with specific DNA mutations.
2. Infections (Past or Present)
3. Environment
4. Minerals
5. Vitamins
6. Organic Acid and Other Metabolites
7. Microbiome
8. Epigenetics

Chances are that a condition will develop when two (or more) die are rolled with bad values

Worked Example

I am using Chronic Fatigue Syndrome (CFS) / Myalgic Encephalomyelitis (ME) because I am most familar with the existing literature. The same can be done for many other conditions – for example Autism.

SNP/DNA for ME/CFS

A few examples of findings

• Genetic association study in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) identifies several potential risk loci [2022]
• Autoimmunity-Related Risk Variants in PTPN22 and CTLA4 Are Associated With ME/CFS With Infectious Onset [2020]
• Glucocorticoid receptor DNA methylation and childhood trauma in chronic fatigue syndrome patients [2018]
• Coagulation Issues can be DNA based (i.e. Sticky Blood or Micro-Clots). For example, I have the Prothrombin G20210A mutation which was a direct contributor to my own ME/CFS
• IgG subclass deficiencies in chronic fatigue syndrome. [1988]

Infections (Current or Past)

Side Note: Many cancers are associated with specific virial infections.

• The persistent viral infections in the development and severity of myalgic encephalomyelitis/chronic fatigue syndrome [2023]
• Viral studies of chronic fatigue syndrome.[1994]
• Studies on enterovirus in patients with chronic fatigue syndrome. [1994]
• Incidence, risk and prognosis of acute and chronic fatigue syndromes and psychiatric disorders after glandular fever. [1998]
• Post-Lyme borreliosis syndrome: a meta-analysis of reported symptoms. [2005]
• Share 
• [Systemic Mycoplasma blood infection in fibromyalgia and chronic fatigue syndrome]. [2004]

Environment

• Stress: May be work, childhood etc. It was a trigger for my own ME/CFS
  • Stress-Induced Transcriptomic Changes in Females with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Reveal Disrupted Immune Signatures [2023]
  • Intimate Partner Violence and the Risk of Developing Fibromyalgia and Chronic Fatigue Syndrome [2021]
  • Glucocorticoid receptor DNA methylation and childhood trauma in chronic fatigue syndrome patients [2018]
  • Effects of early childhood trauma on hypothalamic-pituitary-adrenal (HPA) axis function in patients with Chronic Fatigue Syndrome [2014]
• Fungi and Mold (at home or work)
  • Fungal spores: hazardous to health? [1999]
  • Is there any relation between moldy building exposure and chronic fatigue syndrome? [2006]
• Chemical Exposures
  • [Chronic fatigue syndrome and multiple chemical hypersensitivity after insecticide exposure]. [2005]
  • Chronic fatigue and organophosphate pesticides in sheep farming: a retrospective study amongst people reporting to a UK pharmacovigilance scheme [2003]
  • A preliminary investigation of chlorinated hydrocarbons and chronic fatigue syndrome. [1995]
  • Exposure to Gulf War Illness-related agents leads to the development of chronic pain and fatigue. [2021]

Minerals

This can be a function of environment, diet, water quality.

• Vitamin and mineral status in chronic fatigue syndrome and fibromyalgia syndrome: A systematic review and meta-analysis [2017] 
• Does Coenzyme Q10 Plus Selenium Supplementation Ameliorate Clinical Outcomes by Modulating Oxidative Stress and Inflammation in Individuals with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome? [2022]
• Multivitamin mineral supplementation in patients with chronic fatigue syndrome. [2014]
• Improved chronic fatigue symptoms after removal of mercury in patient with increased mercury concentration in hair toxic mineral assay: a case. [2012]
• Magnesium and chronic fatigue syndrome. [1991]

Vitamins

• Analysis of dietary intake and selected nutrient concentrations in patients with chronic fatigue syndrome.[1998]
• Efficacy of Vitamin D Supplementation in the Improvement of Clinical Status in Patients Diagnosed with Fibromyalgia Syndrome: A Systematic Review. [2022]
• Neurochemical abnormalities in chronic fatigue syndrome: a pilot magnetic resonance spectroscopy study at 7 Tesla [2022]
• Evidence of widespread metabolite abnormalities in Myalgic encephalomyelitis/chronic fatigue syndrome: assessment with whole-brain magnetic resonance spectroscopy.

Organic Acid and Other Metabolites

Within this, stomach acid and blood pH is included.

• Evidence of widespread metabolite abnormalities in Myalgic encephalomyelitis/chronic fatigue syndrome: assessment with whole-brain magnetic resonance spectroscopy. [2020]
• Hematologic and urinary excretion anomalies in patients with chronic fatigue syndrome. [2007]
• Urinary and plasma organic acids and amino acids in chronic fatigue syndrome. [2005]
• Lowered oxygen saturation and increased body temperature in acute COVID-19 largely predict chronic fatigue syndrome and affective symptoms due to Long COVID: A precision nomothetic approach. [2023]

Microbiome

A quick copy and paste. For many other conditions, see this page.

📓 Potential role of microbiome in Chronic Fatigue Syndrome/Myalgic Encephalomyelits (CFS/ME). Scientific reports (Sci Rep ) Vol: 11 Issue 1 Pages: 7043 Pub: 2021 Mar 29 Epub: 2021 Mar 29 Authors Lupo GFD , Rocchetti G , Lucini L , Lorusso L , Manara E , Bertelli M , Puglisi E , Capelli E , Summary Html Article Publication

📓 Gut Microbiota Interventions With <i>Clostridium butyricum</i> and Norfloxacin Modulate Immune Response in Experimental Autoimmune Encephalomyelitis Mice. Frontiers in immunology (Front Immunol ) Vol: 10 Issue Pages: 1662 Pub: 2019 Epub: 2019 Jul 23 Authors Chen H , Ma X , Liu Y , Ma L , Chen Z , Lin X , Si L , Ma X , Chen X , Summary Html Article Publication

📓 Correction to: Open-label pilot for treatment targeting gut dysbiosis in myalgic encephalomyelitis/chronic fatigue syndrome: neuropsychological symptoms and sex comparisons. Journal of translational medicine (J Transl Med ) Vol: 16 Issue 1 Pages: 39 Pub: 2018 Feb 23 Epub: 2018 Feb 23 Authors Wallis A , Ball M , Butt H , Lewis DP , McKechnie S , Paull P , Jaa-Kwee A , Bruck D , Summary Html Article Publication

📓 Potential role of dengue virus, chikungunya virus and Zika virus in neurological diseases. Memorias do Instituto Oswaldo Cruz (Mem Inst Oswaldo Cruz ) Vol: 113 Issue 11 Pages: e170538 Pub: 2018 Oct 29 Epub: 2018 Oct 29 Authors Vieira MADCES , Costa CHN , Linhares ADC , Borba AS , Henriques DF , Silva EVPD , Tavares FN , Batista FMA , Guimarães HCL , Martins LC , Monteiro TAF , Cruz ACR , Azevedo RDSDS , Vasconcelos PFDC , Summary Html Article Publication

📓 Human Gut-Derived Commensal Bacteria Suppress CNS Inflammatory and Demyelinating Disease. Cell reports (Cell Rep ) Vol: 20 Issue 6 Pages: 1269-1277 Pub: 2017 Aug 8 Epub: Authors Mangalam A , Shahi SK , Luckey D , Karau M , Marietta E , Luo N , Choung RS , Ju J , Sompallae R , Gibson-Corley K , Patel R , Rodriguez M , David C , Taneja V , Murray J , Summary Html Article Publication

📓 Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome (Microbiome ) Vol: 5 Issue 1 Pages: 44 Pub: 2017 Apr 26 Epub: 2017 Apr 26 Authors Nagy-Szakal D , Williams BL , Mishra N , Che X , Lee B , Bateman L , Klimas NG , Komaroff AL , Levine S , Montoya JG , Peterson DL , Ramanan D , Jain K , Eddy ML , Hornig M , Lipkin WI , Summary Html Article Publication

📓 A Pair of Identical Twins Discordant for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Differ in Physiological Parameters and Gut Microbiome Composition. The American journal of case reports (Am J Case Rep ) Vol: 17 Issue Pages: 720-729 Pub: 2016 Oct 10 Epub: 2016 Oct 10 Authors Giloteaux L , Hanson MR , Keller BA , Summary Html Article

📓 Support for the Microgenderome: Associations in a Human Clinical Population. Scientific reports (Sci Rep ) Vol: 6 Issue Pages: 19171 Pub: 2016 Jan 13 Epub: 2016 Jan 13 Authors Wallis A , Butt H , Ball M , Lewis DP , Bruck D , Summary Html Article Publication

📓 Chronic fatigue syndrome patients have alterations in their oral microbiome composition and function. PloS one (PLoS One ) Vol: 13 Issue 9 Pages: e0203503 Pub: 2018 Epub: 2018 Sep 11 Authors Wang T , Yu L , Xu C , Pan K , Mo M , Duan M , Zhang Y , Xiong H , Summary Publication Publication

📓 Gut-associated lymphoid tissue, gut microbes and susceptibility to experimental autoimmune encephalomyelitis. Beneficial microbes (Benef Microbes ) Vol: 7 Issue 3 Pages: 363-73 Pub: 2016 Jun Epub: 2016 Feb 3 Authors Stanisavljevic S , Lukic J , Momcilovic M , Miljkovic M , Jevtic B , Kojic M , Golic N , Mostarica Stojkovic M , Miljkovic D , Summary Publication Publication

📓 Increased d-lactic Acid intestinal bacteria in patients with chronic fatigue syndrome. In vivo (Athens, Greece) (In Vivo ) Vol: 23 Issue 4 Pages: 621-8 Pub: 2009 Jul-Aug Epub: Authors Sheedy JR , Wettenhall RE , Scanlon D , Gooley PR , Lewis DP , McGregor N , Stapleton DI , Butt HL , DE Meirleir KL , Summary

Epigenetics

This is where an event, like stress, causes the behavior of DNA to change. Your DNA is the same, just a “switch” is turned on or off.

• Dynamic Epigenetic Changes during a Relapse and Recovery Cycle in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome [2022]
• Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients.[2021]
• Changes in DNA methylation profiles of myalgic encephalomyelitis/chronic fatigue syndrome patients reflect systemic dysfunctions. [2020]
• Lower ambulatory blood pressure in chronic fatigue syndrome. [2009]

Going Forward with Treatment

My attitude is evidence based action with testable models. If you walk into a physician’s office, it is unlikely that they will be aware with the many sides of the dice. Usually, they want simple “follow the recipe book” cases where what to do is clear.

For myself, I had the luxury of unbelievable, unlimited, medical coverage for a few years. I found some of the DNA issues, and to quote a physician “You are extremely lucky with that mutation, it is very treatable” — I became a piracetam addict when needed. Most people do not have that luxury.

Looking at 8 items above, I ask the same question:

• Is it objective measurable?
  • Can you get the test (willing MD, cost)
• Is it treatable?
  • Do we have actual clinical studies showing treatment is effective?
    • Is the treatment just symptom relief or remission?
  • What are the risk of side-effects?

If getting information from a test is not clearly actionable, then it does not help with treatment and not worth the expense. Testing for testing sake is a luxury for the rich.

My Criteria in evaluating new proposed models. “

Many people will advocate that just one of these 8 sides of the die needs to be done for a cure. IMHO, if the model does not address most of these factors, it is likely to work for only a few.

For me, the Microbiome model appears the best to use.

• Microbiome tests are cheap and do not require a MD to be involved — Objective
• We have hundreds of studies showing substances alters the microbiome
• Risk of side-effects with non-prescription items is low

And it is connected to the other factors above well.

• Many of the organic acid and metabolites are produced by the microbiome. Thus correcting the microbiome is likely to resolve this I compute many of these using Kyoto Encyclopedia of Genes and Genomes data.
• Vitamins and Mineral absorption is deeply influences by the microbiome too!

If you have DNA information, for example on your methylation, this impacts your microbiome and the reverse. Being tested for DNA SNPs that does not have effective treatment is a waste of money. The individual’s microbiome is greatly influenced by their DNA. They co-exist and co-operate. In some cases, the microbiome bacteria can produce anticoagulants and fibrinolytics which can counter some coagulation issues.

WARNING ON PEOPLE PROPOSING MODELS

Over the last 30 years, I have constantly seen people proposing this model or that model. Usually the model is focusing on a single aspect of one the die sides above. For ME/CFS, it was the search for an occult virus that was the root cause of this condition. This often comes out of a need to reduce to the simple in whatever specialty that the researcher or physician is trained in. The wages of over-specialization in modern medicine. Be wary of any model that does not offer a concrete explanation for all of the laboratory results in the literature. Often models will cherry-pick studies and ignore the majority of other studies, or do vague hand waving.

The cause is almost never just one of the above factors, but typically many.

Recently I have been getting several emails from people with status updates. I thought that I should share a few of them. I have not gotten any negative feedback (Are all of my readers Canadians who are too polite to complain?)

Also good news. I’ve managed to correct much of my microbiome. I’ve reversed the NIH gnavus ans prausnitzii signature that is very common in ME. My prausnitzii is now 21%! It was something like 0.2 two years ago.

And my lactobacillus and bifido are in the very bottom range of healthy for the first time in two years. Also three lactobacillus strains from vivomixx appeared on my 16s for the first time. Proving that even artificial probiotics can populate the gut albeit temporarily. 

I intend to continue and get another test in three months. While my physical symptoms have improved a lot my light sensitivity and brainfog are still not great to be honest and I have no idea why. Leaky gut can I think be ruled out becuass gnavus is so low and I barely react to eggs anymore (I’ve had issues with eggs since I was a kid). But I have some work to do still.

I really love the website and get a ton of use out of it.  I hope you stick with it and keep updating it and making it better.

Mold is what got me initially too.  Retrospectively.  When we moved to our new house is when my decline actually started.  And then when we redid our master bath, there was a bunch of mold, and I got real sick real fast.

In essence, I had all the triggers.  Every single one of these:

1. Viral or bacterial exposure (listed in order of severity) – COVID and RSV
2. Trauma – to intestines
3. Food poisoning – Bacterial and fungal
4. Prolonged Stress – Luxonis.com startup, I’m the founder
5. Environmental Toxins – Mold in our MASTER BEDROOM

Oh forgot to mention I took lactobacillus Rhamnosus based my my research before I noticed your big red note to not take it and other lactobacillus because they block the impact of heparin.  I think that’s what really got me!

Haven’t pooped for 3 days since that mistake!  Before that pooped every day for 14. 

As an update, I’m nearly 5 weeks in and am beginning to feel better.  My energy levels are perhaps the best they’ve been in the last 5 years.  I’ve still got a very long way to go but the results thus far are promising!

I’m taking 5-7 foods/ supplements, 2-3X a day.  And every 2 weeks I’m rotating all of it to prevent antibiotic resistance.  In another month I plan to retest myself and make the necessary adjustments to my protocol.  

The other reason I’m writing is that a friend with similar fatigue issues and a histamine intolerance has just gotten tested and is joining my journey to recovery. 

First, there is a body of literature indicating that the microbiome plays an important part in many conditions. The last one in this list of citations agrees with my hypothesis for the last 7 years: “Multi-kingdom gut microbiota analyses define CONDITION-X severity and in some case the syndrome.“

Citation
Reversion of Gut Microbiota during the Recovery Phase in Patients with Asymptomatic or Mild COVID-19: Longitudinal Study. Microorganisms (Microorganisms ) Vol: 9 Issue 6 Pages: Pub: 2021 Jun 7 Epub: 2021 Jun 7 Authors Kim HN , Joo EJ , Lee CW , Ahn KS , Kim HL , Park DI , Park SK , Summary Html Article Publication
The gut microbiome of COVID-19 recovered patients returns to uninfected status in a minority-dominated United States cohort. Gut microbes (Gut Microbes ) Vol: 13 Issue 1 Pages: 1-15 Pub: 2021 Jan-Dec Epub: Authors Newsome RC , Gauthier J , Hernandez MC , Abraham GE , Robinson TO , Williams HB , Sloan M , Owings A , Laird H , Christian T , Pride Y , Wilson KJ , Hasan M , Parker A , Senitko M , Glover SC , Gharaibeh RZ , Jobin C , Summary Html Article Publication
Gut Microbiota May Not Be Fully Restored in Recovered COVID-19 Patients After 3-Month Recovery. Frontiers in nutrition (Front Nutr ) Vol: 8 Issue Pages: 638825 Pub: 2021 Epub: 2021 May 13 Authors Tian Y , Sun KY , Meng TQ , Ye Z , Guo SM , Li ZM , Xiong CL , Yin Y , Li HG , Zhou LQ , Summary Html Article Publication
Gut Microbiota Interplay With COVID-19 Reveals Links to Host Lipid Metabolism Among Middle Eastern Populations. Frontiers in microbiology (Front Microbiol ) Vol: 12 Issue Pages: 761067 Pub: 2021 Epub: 2021 Nov 5 Authors Al Bataineh MT , Henschel A , Mousa M , Daou M , Waasia F , Kannout H , Khalili M , Kayasseh MA , Alkhajeh A , Uddin M , Alkaabi N , Tay GK , Feng SF , Yousef AF , Alsafar HS , Summary Publication
Gut microbiota dynamics in a prospective cohort of patients with post-acute COVID-19 syndrome. Gut (Gut ) Vol: Issue Pages: Pub: 2022 Jan 26 Epub: 2022 Jan 26 Authors Liu Q , Mak JWY , Su Q , Yeoh YK , Lui GC , Ng SSS , Zhang F , Li AYL , Lu W , Hui DS , Chan PK , Chan FKL , Ng SC , Summary Publication
Alterations in microbiota of patients with COVID-19: potential mechanisms and therapeutic interventions. Signal transduction and targeted therapy (Signal Transduct Target Ther ) Vol: 7 Issue 1 Pages: 143 Pub: 2022 Apr 29 Epub: 2022 Apr 29 Authors Wang B , Zhang L , Wang Y , Dai T , Qin Z , Zhou F , Zhang L , Summary Publication
Alterations in Gut Microbiota of Patients With COVID-19 During Time of Hospitalization. Gastroenterology (Gastroenterology ) Vol: 159 Issue 3 Pages: 944-955.e8 Pub: 2020 Sep Epub: 2020 May 20 Authors Zuo T , Zhang F , Lui GCY , Yeoh YK , Li AYL , Zhan H , Wan Y , Chung ACK , Cheung CP , Chen N , Lai CKC , Chen Z , Tso EYK , Fung KSC , Chan V , Ling L , Joynt G , Hui DSC , Chan FKL , Chan PKS , Ng SC , Summary Publication
Alterations in Fecal Fungal Microbiome of Patients With COVID-19 During Time of Hospitalization until Discharge. Gastroenterology (Gastroenterology ) Vol: 159 Issue 4 Pages: 1302-1310.e5 Pub: 2020 Oct Epub: 2020 Jun 26 Authors Zuo T , Zhan H , Zhang F , Liu Q , Tso EYK , Lui GCY , Chen N , Li A , Lu W , Chan FKL , Chan PKS , Ng SC , Summary Publication
Challenges in the Management of SARS-CoV2 Infection: The Role of Oral Bacteriotherapy as Complementary Therapeutic Strategy to Avoid the Progression of COVID-19. Frontiers in medicine (Front Med (Lausanne) ) Vol: 7 Issue Pages: 389 Pub: 2020 Epub: 2020 Jul 7 Authors d`Ettorre G , Ceccarelli G , Marazzato M , Campagna G , Pinacchio C , Alessandri F , Ruberto F , Rossi G , Celani L , Scagnolari C , Mastropietro C , Trinchieri V , Recchia GE , Mauro V , Antonelli G , Pugliese F , Mastroianni CM , Summary Publication
It Ain`t Over `Til It`s Over: SARS CoV-2 and Post-infectious Gastrointestinal Dysmotility. Digestive diseases and sciences (Dig Dis Sci ) Vol: Issue Pages: Pub: 2022 Mar 30 Epub: 2022 Mar 30 Authors Coles MJ , Masood M , Crowley MM , Hudgi A , Okereke C , Klein J , Summary Publication
Integrated analysis of gut microbiome and host immune responses in COVID-19. Frontiers of medicine (Front Med ) Vol: 16 Issue 2 Pages: 263-275 Pub: 2022 Apr Epub: 2022 Mar 8 Authors Xu X , Zhang W , Guo M , Xiao C , Fu Z , Yu S , Jiang L , Wang S , Ling Y , Liu F , Tan Y , Chen S , Summary Publication
Respiratory dysfunction three months after severe COVID-19 is associated with gut microbiota alterations. Journal of internal medicine (J Intern Med ) Vol: 291 Issue 6 Pages: 801-812 Pub: 2022 Jun Epub: 2022 Mar 17 Authors Vestad B , Ueland T , Lerum TV , Dahl TB , Holm K , Barratt-Due A , Kåsine T , Dyrhol-Riise AM , Stiksrud B , Tonby K , Hoel H , Olsen IC , Henriksen KN , Tveita A , Manotheepan R , Haugli M , Eiken R , Berg Å , Halvorsen B , Lekva T , Ranheim T , Michelsen AE , Kildal AB , Johannessen A , Thoresen L , Skudal H , Kittang BR , Olsen RB , Ystrøm CM , Skei NV , Hannula R , Aballi S , Kvåle R , Skjønsberg OH , Aukrust P , Hov JR , Trøseid M , NOR-Solidarity study group. , Summary Publication
Dissecting the role of the human microbiome in COVID-19 via metagenome-assembled genomes. Nature communications (Nat Commun ) Vol: 13 Issue 1 Pages: 5235 Pub: 2022 Sep 6 Epub: 2022 Sep 6 Authors Ke S , Weiss ST , Liu YY , Summary Publication
Multi-kingdom gut microbiota analyses define COVID-19 severity and post-acute COVID-19 syndrome. Nature communications (Nat Commun ) Vol: 13 Issue 1 Pages: 6806 Pub: 2022 Nov 10 Epub: 2022 Nov 10 Authors Liu Q , Su Q , Zhang F , Tun HM , Mak JWY , Lui GC , Ng SSS , Ching JYL , Li A , Lu W , Liu C , Cheung CP , Hui DSC , Chan PKS , Chan FKL , Ng SC , Summary Publication

Looking at what is statistically significant in samples uploaded to the citizen science site, we see that only BiomeSight has sufficient data. It identifies 36 taxa/bacteria at present. With more samples coming in, this may increase. Before looking at the bacteria, I like to look at the enzymes — why? different bacteria produce the same enzymes so it is an elegant way of clustering bacteria by what they produce.

KEGG Enzyme data

In this case, I am blown away on the number of statistically significant shifts! If you want more information about these enzymes, see BRENDA or/and Kyoto Encyclopedia of Genes and Genomes.

There are 197 with P < 0.001. Give there is 8000+ enzymes, that suggests around 8 may be false positives.

Enzyme Name	ECKEY	With Long COVID	Without Long COVID	T-Score	DF	Probability
(S)-3-hydroxy-3-methylglutaryl-CoA acetoacetate-lyase (acetyl-CoA-forming)	4.1.3.4	130357	52076	13.57	666	P < 0.001
4-amino-5-aminomethyl-2-methylpyrimidine aminohydrolase	3.5.99.2	151693	69126	13.48	666	P < 0.001
dihydrourocanate:acceptor oxidoreductase	1.3.99.33	135133	55921	13.44	666	P < 0.001
nucleoside-triphosphate diphosphohydrolase	3.6.1.9	145528	63523	13.38	666	P < 0.001
poly(deoxyribonucleotide)-3′-hydroxyl:5′-phospho-poly(deoxyribonucleotide) ligase (ATP or NAD+)	6.5.1.6	129475	51779	13.34	666	P < 0.001
poly(deoxyribonucleotide)-3′-hydroxyl:5′-phospho-poly(deoxyribonucleotide) ligase (ATP, ADP or GTP)	6.5.1.7	129475	51779	13.34	666	P < 0.001
acetyl-CoA:kanamycin-B N6′-acetyltransferase	2.3.1.82	128673	51662	13.32	666	P < 0.001
acetyl-CoA:2-deoxystreptamine-antibiotic N3-acetyltransferase	2.3.1.81	130200	53104	13.28	666	P < 0.001
(1->4)-alpha-D-galacturonan reducing-end-disaccharide-lyase	4.2.2.9	128038	50989	13.28	666	P < 0.001
alpha-maltose-6′-phosphate 6-phosphoglucohydrolase	3.2.1.122	130496	53951	13.28	666	P < 0.001
D-serine ammonia-lyase (pyruvate-forming)	4.3.1.18	128576	51987	13.23	666	P < 0.001
ATP phosphohydrolase (ABC-type, iron(III) enterobactin-importing)	7.2.2.17	130373	54180	13.15	666	P < 0.001
protein-Npi-phospho-L-histidine:D-mannose Npi-phosphotransferase	2.7.1.191	140701	62807	13.14	666	P < 0.001
protein-Npi-phospho-L-histidine:D-mannitol Npi-phosphotransferase	2.7.1.197	129284	53723	13.06	666	P < 0.001
ADP-alpha-D-glucose:alpha-D-glucose-1-phosphate 4-alpha-D-glucosyltransferase (configuration-retaining)	2.4.1.342	134654	58028	13.04	665	P < 0.001
aryl-ester hydrolase	3.1.1.2	151171	72377	13.02	666	P < 0.001
ATP phosphohydrolase (ABC-type, Fe3+-transporting)	7.2.2.7	142152	66111	12.86	666	P < 0.001
palmitoyl-CoA hydrolase	3.1.2.2	149499	71728	12.83	666	P < 0.001
ATP:[protein]-L-tyrosine O-phosphotransferase (non-specific)	2.7.10.2	131925	57360	12.75	666	P < 0.001
D-psicose 3-epimerase	5.1.3.30	143416	68284	12.74	666	P < 0.001
D-tagatose 3-epimerase	5.1.3.31	143416	68284	12.74	666	P < 0.001
penicillin amidohydrolase	3.5.1.11	139138	66165	12.62	666	P < 0.001
D-aspartate:[beta-GlcNAc-(1->4)-Mur2Ac(oyl-L-Ala-gamma-D-Glu-L-Lys-D-Ala-D-Ala)]n ligase (ADP-forming)	6.3.1.12	145356	70261	12.57	666	P < 0.001
2′-(5-triphosphoribosyl)-3′-dephospho-CoA:apo-[citrate (pro-3S)-lyase] 2′-(5-phosphoribosyl)-3′-dephospho-CoA-transferase	2.7.7.61	149196	74697	12.46	666	P < 0.001
ATP:3′-dephospho-CoA 5-triphospho-alpha-D-ribosyltransferase	2.4.2.52	149957	75781	12.39	666	P < 0.001
2,4,6/3,5-pentahydroxycyclohexanone 2-isomerase	5.3.99.11	146254	73538	12.37	666	P < 0.001
acetyl-CoA:citrate CoA-transferase	2.8.3.10	150367	76318	12.36	666	P < 0.001
L-aspartate:tRNAAsx ligase (AMP-forming)	6.1.1.23	132939	61720	12.22	666	P < 0.001
4-phospho-D-erythronate:NAD+ 3-oxidoreductase	1.1.1.409	134073	62914	12.19	666	P < 0.001
4-phospho-D-threonate:NAD+ 3-oxidoreductase	1.1.1.408	134073	62914	12.19	666	P < 0.001
poly(deoxyribonucleotide)-3′-hydroxyl:5′-phospho-poly(deoxyribonucleotide) ligase (ATP)	6.5.1.1	143883	68128	12.15	666	P < 0.001
ATP:D-erythronate 4-phosphotransferase	2.7.1.220	133631	62696	12.13	666	P < 0.001
ATP:D-threonate 4-phosphotransferase	2.7.1.219	133631	62696	12.13	666	P < 0.001
ATP:D-glycero-alpha-D-manno-heptose 7-phosphate 1-phosphotransferase	2.7.1.168	156157	78491	11.99	666	P < 0.001
2-lysophosphatidylcholine acylhydrolase	3.1.1.5	160874	86814	11.71	666	P < 0.001
UDP-alpha-D-glucose:1,2-diacyl-sn-glycerol 3-alpha-D-glucosyltransferase	2.4.1.337	159960	87248	11.57	666	P < 0.001
N-succinyl-LL-2,6-diaminoheptanedioate amidohydrolase	3.5.1.18	151482	82849	11.49	666	P < 0.001
acetate:holo-[citrate-(pro-3S)-lyase] ligase (AMP-forming)	6.2.1.22	163245	90493	11.44	666	P < 0.001
D-tagatose 1,6-bisphosphate D-glyceraldehyde-3-phosphate-lyase (glycerone-phosphate-forming)	4.1.2.40	140814	72879	11.44	666	P < 0.001
L-iditol:NAD+ 2-oxidoreductase	1.1.1.14	181524	109886	11.34	666	P < 0.001
alkylated-DNA glycohydrolase (releasing methyladenine and methylguanine)	3.2.2.21	172169	89028	11.33	666	P < 0.001
oligosaccharide 6-alpha-glucohydrolase	3.2.1.10	161628	93712	11.12	666	P < 0.001
(3S)-citryl-CoA oxaloacetate-lyase (acetyl-CoA-forming)	4.1.3.34	185375	105009	10.73	666	P < 0.001
S-adenosyl-L-methionine:tRNA (adenine22-N1)-methyltransferase	2.1.1.217	157938	92817	10.69	666	P < 0.001
S-adenosyl-L-methionine:16S rRNA (cytidine1409-2′-O)-methyltransferase	2.1.1.227	183689	114027	10.56	666	P < 0.001
S-adenosyl-L-methionine:23S rRNA (cytidine1920-2′-O)-methyltransferase	2.1.1.226	183689	114027	10.56	666	P < 0.001
sn-glycerol 3-phosphate:quinone oxidoreductase	1.1.5.3	177064	110486	10.54	666	P < 0.001
L-glutamate:tRNAGlx ligase (AMP-forming)	6.1.1.24	165448	97402	10.38	666	P < 0.001
D-glycero-D-manno-heptose 7-phosphate aldose-ketose-isomerase	5.3.1.28	213475	135248	10.25	666	P < 0.001
beta-D-glucose 1,6-phosphomutase	5.4.2.6	253383	169933	8.98	666	P < 0.001
type II site-specific deoxyribonuclease	3.1.21.4	245864	165266	8.77	666	P < 0.001
uroporphyrinogen-III carboxy-lyase (coproporphyrinogen-III-forming)	4.1.1.37	266562	184417	8.59	666	P < 0.001
ATP phosphohydrolase (ABC-type, Ni2+-importing)	7.2.2.11	141054	86367	8.56	666	P < 0.001
acetyl-CoA:oxalate CoA-transferase	2.8.3.19	133160	80149	8.41	666	P < 0.001
5-phospho-alpha-D-ribose 1,2-cyclic phosphate 1,2-diphosphophosphohydrolase	3.1.4.57	134813	82183	8.33	666	P < 0.001
Carboxypeptidase Taq	3.4.17.19	136153	84074	8.31	666	P < 0.001
(2E)-2-enoyl-CoA:NADP+ 4-oxidoreductase	1.3.1.34	134146	81935	8.31	666	P < 0.001
2′-deoxyribonucleoside 5′-monophosphate phosphohydrolase	3.1.3.89	136444	84251	8.19	666	P < 0.001
cellobiose 2-epimerase	5.1.3.11	224933	147685	8.17	666	P < 0.001
type III site-specific deoxyribonuclease	3.1.21.5	200155	141657	8.10	666	P < 0.001
D-galactonate hydro-lyase (2-dehydro-3-deoxy-D-galactonate-forming)	4.2.1.6	138933	88181	8.02	666	P < 0.001
protein-Npi-phospho-L-histidine:maltose Npi-phosphotransferase	2.7.1.208	138609	88325	7.98	666	P < 0.001
L-aspartate:NAD(P)+ oxidoreductase (deaminating)	1.4.1.21	245150	169471	7.90	666	P < 0.001
protein-Npi-phospho-L-histidine:sucrose Npi-phosphotransferase	2.7.1.211	144741	96084	7.85	666	P < 0.001
protein-Npi-phospho-L-histidine:N-acetyl-D-glucosamine Npi-phosphotransferase	2.7.1.193	152088	103970	7.64	666	P < 0.001
N-acetyl-alpha-D-glucosaminyl-diphospho-ditrans,octacis-undecaprenol 4-epimerase	5.1.3.26	259434	182387	7.64	666	P < 0.001
UDP-sugar sugarphosphohydrolase	3.6.1.45	156303	108944	7.63	666	P < 0.001
rubredoxin:superoxide oxidoreductase	1.15.1.2	147572	101699	7.40	666	P < 0.001
UDP-2-acetamido-2,6-dideoxy-L-talose:NADP+ oxidoreductase	1.1.1.367	244790	176296	7.33	666	P < 0.001
(4-O-methyl)-D-glucuronate—lignin ester hydrolase	3.1.1.117	265763	190685	7.31	666	P < 0.001
alkylated-DNA glycohydrolase (releasing methyladenine and methylguanine)	3.2.2.20	306951	231407	7.30	666	P < 0.001
S-adenosyl-L-methionine:16S rRNA (cytosine967-C5)-methyltransferase	2.1.1.176	192348	143978	7.28	666	P < 0.001
ATP:molybdopterin-synthase adenylyltransferase	2.7.7.80	297993	218788	7.25	666	P < 0.001
UDP-N-acetyl-alpha-D-glucosamine hydro-lyase (inverting; UDP-2-acetamido-2,6-dideoxy-beta-L-arabino-hex-4-ulose-forming)	4.2.1.115	287717	211984	7.24	666	P < 0.001
UDP-2-acetamido-2,6-dideoxy-beta-L-talose 2-epimerase	5.1.3.28	245857	178308	7.23	666	P < 0.001
ATP phosphohydrolase (ABC-type, molybdate-importing)	7.3.2.5	157815	111902	7.18	666	P < 0.001
sucrose:(1->4)-alpha-D-glucan 4-alpha-D-glucosyltransferase	2.4.1.4	148095	102284	7.16	666	P < 0.001
UDP-N-acetyl-2-amino-2-deoxy-alpha-D-glucuronate:NAD+ 3-oxidoreductase	1.1.1.335	172209	124841	7.08	666	P < 0.001
an acyl-[acyl-carrier protein]:phosphate acyltransferase	2.3.1.274	185445	139090	7.05	666	P < 0.001
FMNH2:NAD(P)+ oxidoreductase	1.5.1.39	156478	107179	7.02	666	P < 0.001
cellobiose:phosphate alpha-D-glucosyltransferase	2.4.1.20	165795	117785	6.98	666	P < 0.001
4-beta-D-xylan xylohydrolase	3.2.1.37	308412	233667	6.87	666	P < 0.001
crossover junction endodeoxyribonuclease	3.1.21.10	341116	260719	6.82	666	P < 0.001
nucleoside-2′,3′-cyclic-phosphate 3′-nucleotidohydrolase	3.1.4.16	321464	242830	6.82	666	P < 0.001
UDP-glucuronate 4-epimerase	5.1.3.6	280650	207501	6.80	666	P < 0.001
S-adenosyl-L-methionine:precorrin-2 C20-methyltransferase	2.1.1.130	293271	227548	6.79	666	P < 0.001
S-adenosyl-L-methionine:cobalt-factor-II C20-methyltransferase	2.1.1.151	293124	227408	6.78	666	P < 0.001
dipeptidase E	3.4.13.21	204290	149503	6.73	666	P < 0.001
GTP:alpha-D-mannose-1-phosphate guanylyltransferase	2.7.7.13	331462	252998	6.69	666	P < 0.001
ATP:1,2-diacyl-sn-glycerol 3-phosphotransferase	2.7.1.107	333291	259697	6.61	666	P < 0.001
L-selenocysteine selenide-lyase (L-alanine-forming)	4.4.1.16	337172	260622	6.56	666	P < 0.001
1,4-beta-D-mannooligosaccharide:phosphate alpha-D-mannosyltransferase	2.4.1.319	300427	227352	6.54	666	P < 0.001
4-O-beta-D-mannopyranosyl-N-acetyl-D-glucosamine:phosphate alpha-D-mannosyltransferase	2.4.1.320	300427	227352	6.54	666	P < 0.001
sortase B	3.4.22.71	161358	119363	6.52	666	P < 0.001
cobalt-precorrin 5A acylhydrolase	3.7.1.12	160731	118900	6.48	666	P < 0.001
6-carboxy-5,6,7,8-tetrahydropterin ammonia-lyase	4.3.99.3	329010	253328	6.47	666	P < 0.001
precorrin-8 11,12-methylmutase	5.4.99.60	161359	119806	6.46	666	P < 0.001
precorrin-8X 11,12-methylmutase	5.4.99.61	161359	119806	6.46	666	P < 0.001
UDP-alpha-D-glucose:NAD+ 6-oxidoreductase	1.1.1.22	341877	267968	6.45	666	P < 0.001
4-O-beta-D-mannopyranosyl-D-glucopyranose:phosphate alpha-D-mannosyltransferase	2.4.1.281	294563	221546	6.44	666	P < 0.001
O-acetyl-ADP-D-ribose carboxylesterase	3.1.1.106	232755	178380	6.39	666	P < 0.001
2′-deoxyribonucleoside-5′-diphosphate:thioredoxin-disulfide 2′-oxidoreductase	1.17.4.1	355018	281224	6.39	666	P < 0.001
3′-ribonucleotide phosphohydrolase	3.1.3.6	303202	229568	6.38	666	P < 0.001
acetyl-CoA:alkane-alpha,omega-diamine N-acetyltransferase	2.3.1.57	341806	269466	6.32	666	P < 0.001
5,10-methylenetetrahydrofolate:glycine hydroxymethyltransferase	2.1.2.1	356606	283241	6.30	666	P < 0.001
carbonic acid hydro-lyase (carbon-dioxide-forming)	4.2.1.1	321295	248957	6.29	666	P < 0.001
L-isoleucine:tRNAIle ligase (AMP-forming)	6.1.1.5	364094	292209	6.24	666	P < 0.001
DNA-6-O-methylguanine/DNA-4-O-methylthymine:[protein]-L-cysteine S-methyltransferase	2.1.1.63	365615	293975	6.16	666	P < 0.001
NADH:hydroperoxide oxidoreductase	1.11.1.26	323275	252045	6.11	666	P < 0.001
L-glutamate:tRNAGlu ligase (AMP-forming)	6.1.1.17	321496	262066	6.08	666	P < 0.001
bleomycin hydrolase	3.4.22.40	314461	243175	6.08	666	P < 0.001
L-cysteine-S-conjugate thiol-lyase (deaminating; 2-aminoprop-2-enoate-forming)	4.4.1.13	363963	293237	6.08	666	P < 0.001
UDP-alpha-D-glucose:alpha-D-galactose-1-phosphate uridylyltransferase	2.7.7.12	170072	129650	6.05	666	P < 0.001
peptidoglycan amidohydrolase	3.5.1.28	363233	293964	5.99	666	P < 0.001
adenine-DNA deoxyribohydrolase (adenine-releasing)	3.2.2.31	355124	285300	5.95	666	P < 0.001
D-phosphoglycerate 2,3-phosphomutase (2,3-diphosphoglycerate-dependent)	5.4.2.11	319582	250208	5.95	666	P < 0.001
tRNA N6-(3-methylbut-2-en-1-yl)-adenine37:sulfur-(sulfur carrier),S-adenosyl-L-methionine C2-(methylsulfanyl)transferase	2.8.4.3	370115	301224	5.93	666	P < 0.001
10-formyltetrahydrofolate:5′-phosphoribosylglycinamide N-formyltransferase	2.1.2.2	363374	295358	5.89	666	P < 0.001
peptidase Do	3.4.21.107	276660	224637	5.87	666	P < 0.001
poly(deoxyribonucleotide)-3′-hydroxyl:5′-phospho-poly(deoxyribonucleotide) ligase (NAD+)	6.5.1.2	372463	304412	5.85	666	P < 0.001
methionyl aminopeptidase	3.4.11.18	372462	304426	5.85	666	P < 0.001
prenyl-diphosphate:adenine37 in tRNA prenyltransferase	2.5.1.75	371863	303924	5.84	666	P < 0.001
ATP:pyridoxal 5′-phosphotransferase	2.7.1.35	329032	261786	5.80	666	P < 0.001
L-rhamnose aldose-ketose-isomerase	5.3.1.14	307393	241401	5.80	666	P < 0.001
peptide-methionine:thioredoxin-disulfide S-oxidoreductase [methionine (R)-S-oxide-forming]	1.8.4.12	257798	203935	5.76	666	P < 0.001
deoxyribonuclease IV	3.1.21.2	353617	287404	5.73	666	P < 0.001
alpha-L-rhamnoside rhamnohydrolase	3.2.1.40	318053	252744	5.68	666	P < 0.001
ATP phosphohydrolase (ABC-type, Zn2+-importing)	7.2.2.20	331254	264520	5.66	666	P < 0.001
L-rhamnulose-1-phosphate (S)-lactaldehyde-lyase (glycerone-phosphate-forming)	4.1.2.19	307632	243590	5.63	666	P < 0.001
6-deoxy-6-sulfo-D-fructose:D-glyceraldehyde-3-phosphate glyceronetransferase	2.2.1.14	173	33	5.60	41	P < 0.001
ATP:L-rhamnulose 1-phosphotransferase	2.7.1.5	319257	255641	5.50	666	P < 0.001
ATP:glycerol 3-phosphotransferase	2.7.1.30	271460	223970	5.50	666	P < 0.001
(R)-S-lactoylglutathione methylglyoxal-lyase (isomerizing; glutathione-forming)	4.4.1.5	341379	280079	5.36	666	P < 0.001
exodeoxyribonuclease V	3.1.11.5	224710	181406	5.36	666	P < 0.001
NAD(H) phosphohydrolase	3.6.1.22	335898	275329	5.26	666	P < 0.001
L-alanyl-D-glutamate epimerase	5.1.1.20	211984	168065	5.24	666	P < 0.001
CTP:2-C-methyl-D-erythritol 4-phosphate cytidylyltransferase	2.7.7.60	342240	289619	5.12	666	P < 0.001
beta-D-fructofuranoside fructohydrolase	3.2.1.26	204815	169106	4.91	666	P < 0.001
beta-lactam hydrolase	3.5.2.6	328892	276729	4.76	666	P < 0.001
GTP 7,8-8,9-dihydrolase (diphosphate-forming)	3.5.4.25	363191	310173	4.54	666	P < 0.001
D-ribulose 5-phosphate formate-lyase (L-3,4-dihydroxybutan-2-one 4-phosphate-forming)	4.1.99.12	363190	310173	4.54	666	P < 0.001
5-amino-6-(D-ribitylamino)uracil butanedionetransferase	2.5.1.78	363021	310046	4.54	666	P < 0.001
5-amino-6-(5-phospho-D-ribitylamino)uracil:NADP+ 1′-oxidoreductase	1.1.1.193	356070	302730	4.53	666	P < 0.001
2,5-diamino-6-hydroxy-4-(5-phospho-D-ribosylamino)pyrimidine 2-aminohydrolase	3.5.4.26	356070	302730	4.53	666	P < 0.001
D-mannose-6-phosphate aldose-ketose-isomerase	5.3.1.8	349959	298038	4.51	666	P < 0.001
5′-ribonucleotide phosphohydrolase	3.1.3.5	363417	312818	4.40	666	P < 0.001
peptidoglycan-N-acetylglucosamine amidohydrolase	3.5.1.104	334065	289136	4.35	666	P < 0.001
fragilysin	3.4.24.74	7726	2137	4.30	487	P < 0.001
UTP:alpha-D-glucose-1-phosphate uridylyltransferase	2.7.7.9	180042	146829	4.27	666	P < 0.001
adenosylcobinamide-GDP:alpha-ribazole ribazoletransferase	2.7.8.26	336101	289980	4.27	666	P < 0.001
Fe(II):oxygen oxidoreductase ([FeO(OH)]core-producing)	1.16.3.2	343886	295642	4.23	666	P < 0.001
D-stereospecific aminopeptidase	3.4.11.19	146732	114608	4.23	666	P < 0.001
D-glycerate:NAD+ oxidoreductase	1.1.1.29	304790	258395	4.21	666	P < 0.001
ATP:dTMP phosphotransferase	2.7.4.9	182727	149804	4.20	666	P < 0.001
ATP:UDP-N-acetyl-alpha-D-glucosamine 3′-phosphotransferase	2.7.1.176	7304	3121	4.15	664	P < 0.001
L-histidinol:NAD+ oxidoreductase	1.1.1.23	360776	312129	4.13	666	P < 0.001
queuosine34 in tRNA:acceptor oxidoreductase	1.17.99.6	365803	318709	4.13	666	P < 0.001
L-lysine:tRNALys ligase (AMP-forming)	6.1.1.6	372837	325856	4.10	666	P < 0.001
(R)-lactate hydro-lyase (adding N-acetyl-D-glucosamine 6-phosphate; N-acetylmuramate 6-phosphate-forming)	4.2.1.126	315409	268045	4.06	666	P < 0.001
CoA-[4′-phosphopantetheine]:apo-[acyl-carrier protein] 4′-pantetheinephosphotransferase	2.7.8.7	170465	139721	4.06	666	P < 0.001
D-altronate hydro-lyase (2-dehydro-3-deoxy-D-gluconate-forming)	4.2.1.7	307568	262854	4.05	666	P < 0.001
(6R)-6beta-hydroxy-1,4,5,6-tetrahydronicotinamide-adenine dinucleotide 6-epimerase	5.1.99.6	373721	327886	3.98	666	P < 0.001
UTP:L-glutamine amido-ligase (ADP-forming)	6.3.4.2	369633	324526	3.96	666	P < 0.001
beta-D-4-deoxy-Delta4-GlcAp-(1->3)-beta-D-GalNAc6S hydrolase	3.2.1.180	300245	258391	3.94	666	P < 0.001
D-erythro-1-(imidazol-4-yl)glycerol-3-phosphate hydro-lyase [3-(imidazol-4-yl)-2-oxopropyl-phosphate-forming]	4.2.1.19	361792	316233	3.94	666	P < 0.001
1-(5-phospho-beta-D-ribosyl)-ATP:diphosphate phospho-alpha-D-ribosyl-transferase	2.4.2.17	361822	316271	3.94	666	P < 0.001
2-phospho-4-(cytidine 5′-diphospho)-2-C-methyl-D-erythritol CMP-lyase (cyclizing; 2-C-methyl-D-erythritol 2,4-cyclodiphosphate-forming)	4.6.1.12	375199	329906	3.93	666	P < 0.001
1-(5-phospho-beta-D-ribosyl)-5-[(5-phospho-beta-D-ribosylamino)methylideneamino]imidazole-4-carboxamide aldose-ketose-isomerase	5.3.1.16	361727	316261	3.93	666	P < 0.001
[poly-N-acetyl-D-glucosaminyl-(1->4)-(N-acetyl-D-muramoylpentapeptide)]-diphosphoundecaprenol:[N-acetyl-D-glucosaminyl-(1->4)-N-acetyl-D-muramoylpentapeptide]-diphosphoundecaprenol disaccharidetransferase	2.4.1.129	367331	322381	3.93	666	P < 0.001
5-[(5-phospho-1-deoxy-D-ribulos-1-ylamino)methylideneamino]-1-(5-phospho-beta-D-ribosyl)imidazole-4-carboxamide D-erythro-1-(imidazol-4-yl)glycerol 3-phosphate-lyase (L-glutamine-hydrolysing; 5-amino-1-(5-phospho-beta-D-ribosyl)imidazole-4-carboxamide-forming)	4.3.2.10	363190	317925	3.91	666	P < 0.001
dTDP-alpha-D-glucose 4,6-hydro-lyase (dTDP-4-dehydro-6-deoxy-alpha-D-glucose-forming)	4.2.1.46	363385	318389	3.90	666	P < 0.001
ATP:(d)CMP phosphotransferase	2.7.4.25	370117	325801	3.88	666	P < 0.001
L-histidinol-phosphate:2-oxoglutarate aminotransferase	2.6.1.9	372117	327934	3.85	666	P < 0.001
5,10-methylenetetrahydrofolate,FADH2:dUMP C-methyltransferase	2.1.1.148	143685	115112	3.81	666	P < 0.001
orotidine-5′-phosphate carboxy-lyase (UMP-forming)	4.1.1.23	376841	333051	3.81	666	P < 0.001
N2-formyl-N1-(5-phospho-D-ribosyl)glycinamide:L-glutamine amido-ligase (ADP-forming)	6.3.5.3	376690	332992	3.80	666	P < 0.001
alpha-D-galactoside galactohydrolase	3.2.1.22	351869	309262	3.80	666	P < 0.001
oligonucleotidase	3.1.13.3	361085	318401	3.79	666	P < 0.001
ATP:pseudouridine 5′-phosphotransferase	2.7.1.83	143192	114831	3.78	666	P < 0.001
citrate(isocitrate) hydro-lyase (cis-aconitate-forming)	4.2.1.3	370344	327004	3.78	666	P < 0.001
adenosine-3′(2′),5′-bisphosphate 3′(2′)-phosphohydrolase	3.1.3.7	363418	321345	3.74	666	P < 0.001
adenylyl-molybdopterin:molybdate molybdate transferase (AMP-forming)	2.10.1.1	155862	128309	3.71	666	P < 0.001
sn-glycerol-3-phosphate:NAD(P)+ 2-oxidoreductase	1.1.1.94	370438	328604	3.70	666	P < 0.001
isocitrate:NADP+ oxidoreductase (decarboxylating)	1.1.1.42	361230	319382	3.70	666	P < 0.001
short-chain acyl-CoA:electron-transfer flavoprotein 2,3-oxidoreductase	1.3.8.1	140972	113231	3.70	666	P < 0.001
acetyl-CoA:oxaloacetate C-acetyltransferase [thioester-hydrolysing, (pro-S)-carboxymethyl-forming]	2.3.3.1	362515	321195	3.65	666	P < 0.001
UDP-2,4-diacetamido-2,4,6-trideoxy-beta-L-altropyranose hydrolase	3.6.1.57	5601	2056	3.64	644	P < 0.001
D-mannonate hydro-lyase (2-dehydro-3-deoxy-D-gluconate-forming)	4.2.1.8	329439	288135	3.63	666	P < 0.001
ribonuclease M5	3.1.26.8	146813	119961	3.60	666	P < 0.001
(S)-4-hydroxymandelate:oxygen 1-oxidoreductase	1.1.3.46	148308	122183	3.58	666	P < 0.001
S-adenosyl-L-methionine:tRNA (carboxymethyluridine34-5-O)-methyltransferase	2.1.1.229	86	34	3.50	87	P < 0.001
5,10-methylenetetrahydrofolate:tRNA (uracil54-C5)-methyltransferase	2.1.1.74	146047	120006	3.48	666	P < 0.001
aldehyde:ferredoxin oxidoreductase	1.2.7.5	140099	114474	3.47	666	P < 0.001
cobalt-precorrin-6B:NAD+ oxidoreductase	1.3.1.106	150101	125120	3.41	666	P < 0.001
precorrin-6B:NADP+ oxidoreductase	1.3.1.54	150101	125120	3.41	666	P < 0.001
(3S)-3-hydroxyacyl-CoA hydro-lyase	4.2.1.17	146259	121343	3.40	666	P < 0.001
coproporphyrinogen-III:S-adenosyl-L-methionine oxidoreductase (decarboxylating)	1.3.98.3	183567	156750	3.31	666	P < 0.001

Looking at the weaker statistical significance (where we expect 80 to be false positive) we have just 87 items. In other words, the ones below should likely be excluded from any analysis

Enzyme Name	ECKEY	With Long COVID	Without Long COVID	T-Score	DF	Probability
protein-Npi-phospho-L-histidine:D-glucose Npi-phosphotransferase	2.7.1.199	150395	126046	3.30	666	P < 0.01
ATP:4-methyl-5-(2-hydroxyethyl)thiazole 2-phosphotransferase	2.7.1.50	189360	164062	3.30	666	P < 0.01
D-glucose-6-phosphate:NAD+ oxidoreductase	1.1.1.361	368	88	3.26	359	P < 0.01
ATP:alpha-D-Man-(1->2)-alpha-D-Man-(1->2)-[alpha-D-Man-(1->3)-alpha-D-Man-(1->3)-alpha-D-Man-(1->2)-alpha-D-Man-(1->2)]n-alpha-D-Man-(1->3)-alpha-D-Man-(1->3)-alpha-D-Man-(1->3)-alpha-D-GlcNAc-diphospho-ditrans,octacis-undecaprenol 3-phosphotransferase	2.7.1.181	386	91	3.26	346	P < 0.01
S-adenosyl-L-methionine:3-O-phospho-alpha-D-Man-(1->2)-alpha-D-Man-(1->2)-[alpha-D-Man-(1->3)-alpha-D-Man-(1->3)-alpha-D-Man-(1->2)-alpha-D-Man-(1->2)]n-alpha-D-Man-(1->3)-alpha-D-Man-(1->3)-alpha-D-Man-(1->3)-alpha-D-GlcNAc-diphospho-ditrans,octacis-undecaprenol 3-phospho-methyltransferase	2.1.1.294	386	91	3.26	346	P < 0.01
S-adenosyl-L-methionine:23S rRNA (guanine745-N1)-methyltransferase	2.1.1.187	147722	123211	3.25	666	P < 0.01
kanosamine-6-phosphate phosphohydrolase	3.1.3.92	364	88	3.25	363	P < 0.01
kanosamine 6-phosphate:2-oxoglutarate aminotransferase	2.6.1.104	368	92	3.24	365	P < 0.01
ATP:L-glutamine N5-phosphotransferase	2.7.3.13	241	33	3.23	54	P < 0.01
GDP-beta-L-fucose:beta-D-Gal-(1->3)-alpha-D-GalNAc-(1->3)-alpha-D-GalNAc-diphospho-ditrans,octacis-undecaprenol alpha-1,2-fucosyltransferase	2.4.1.308	390	89	3.22	326	P < 0.01
UDP-alpha-D-galactose:N-acetyl-alpha-D-galactosaminyl-R beta-1,3-galactosyltransferase (configuration-inverting)	2.4.1.122	390	89	3.22	326	P < 0.01
UDP-alpha-D-glucose:N-acetyl-alpha-D-glucosaminyl-diphospho-ditrans,octacis-undecaprenol beta-1,3-glucosyltransferase	2.4.1.305	390	89	3.22	326	P < 0.01
UDP-N-acetyl-alpha-D-galactosamine:N-acetyl-alpha-D-galactosaminyl-diphospho-ditrans,octacis-undecaprenol alpha-1,3-N-acetyl-D-galactosyltransferase	2.4.1.306	390	89	3.22	326	P < 0.01
fluoroacetyl-CoA hydrolase	3.1.2.29	242821	211022	3.20	666	P < 0.01
GDP-alpha-D-mannose:alpha-D-Man-(1->2)-alpha-D-Man-(1->2)-[alpha-D-Man-(1->3)-alpha-D-Man-(1->3)-alpha-D-Man-(1->2)-alpha-D-Man-(1->2)]n-alpha-D-Man-(1->3)-alpha-D-Man-(1->3)-alpha-D-Man-(1->3)-alpha-D-GlcNAc-diphospho-ditrans,octacis-undecaprenol 2,3-alpha-mannosyltransferase (configuration-retaining)	2.4.1.371	387	97	3.20	347	P < 0.01
GDP-alpha-D-mannose:alpha-D-mannosyl-(1->3)-N-acetyl-alpha-D-glucosaminyl-diphospho-ditrans,octacis-undecaprenol 3-alpha-mannosyltransferase (configuration-retaining)	2.4.1.349	387	97	3.20	347	P < 0.01
carbamoyl-phosphate:L-ornithine carbamoyltransferase	2.1.3.3	193666	169029	3.19	666	P < 0.01
ATP:L-homoserine O-phosphotransferase	2.7.1.39	169424	144404	3.19	666	P < 0.01
GDP-alpha-D-mannose:N-acetyl-alpha-D-glucosaminyl-diphospho-ditrans,octacis-undecaprenol 3-alpha-mannosyltransferase (configuration-retaining)	2.4.1.348	386	98	3.18	346	P < 0.01
16S rRNA-uridine516 uracil mutase	5.4.99.19	191228	167210	3.17	666	P < 0.01
2,3-dihydroxybenzoate:oxygen 3,4-oxidoreductase (ring-opening)	1.13.11.14	56	24	3.17	72	P < 0.01
ATP:molybdopterin adenylyltransferase	2.7.7.75	150983	127838	3.16	666	P < 0.01
GDP-beta-L-colitose:beta-D-galactopyranosyl-(1->3)-N-acetyl-D-glucosamine L-colitosyltransferase (configuration-inverting)	2.4.1.341	391	96	3.16	326	P < 0.01
pyrimidine-nucleoside:phosphate (2′-deoxy)-alpha-D-ribosyltransferase	2.4.2.2	160966	137755	3.13	666	P < 0.01
ATP phosphohydrolase (ABC-type, D-galactose-importing)	7.5.2.11	150190	126661	3.13	666	P < 0.01
protein-Npi-phospho-L-histidine:D-fructose Npi-phosphotransferase	2.7.1.202	150170	127151	3.12	666	P < 0.01
diphosphate phosphohydrolase	3.6.1.1	204902	180774	3.10	666	P < 0.01
2-oxo-acid carboxy-lyase (aldehyde-forming)	4.1.1.1	356	95	3.09	358	P < 0.01
NAD+:diphthamide-[translation elongation factor 2] N-(ADP-D-ribosyl)transferase	2.4.2.36	391	103	3.08	326	P < 0.01
GDP-4-dehydro-alpha-D-rhamnose 3-hydro-lyase	4.2.1.168	391	103	3.08	326	P < 0.01
acetyl-CoA:L-glutamate N-acetyltransferase	2.3.1.1	198282	174552	3.07	666	P < 0.01
(8S)-3′,8-cyclo-7,8-dihydroguanosine 5′-triphosphate lyase (cyclic pyranopterin phosphate-forming)	4.6.1.17	164816	142092	3.06	666	P < 0.01
GTP 3′,8-cyclase [(8S)-3′,8-cyclo-7,8-dihydroguanosine 5′-triphosphate-forming]	4.1.99.22	207283	180149	3.05	666	P < 0.01
ADP-L-glycero-D-manno-heptose 6-epimerase	5.1.3.20	33154	22635	3.03	666	P < 0.01
malonyl-CoA:malonyl-CoA malonyltransferase (decarboxylating, phloroglucinol-forming)	2.3.1.253	56	9	3.03	47	P < 0.01
N2-acetyl-L-ornithine:L-glutamate N-acetyltransferase	2.3.1.35	195917	172469	3.03	666	P < 0.01
dTDP-3-amino-3,4,6-trideoxy-alpha-D-glucose:2-oxoglutarate aminotransferase	2.6.1.106	48	25	3.01	61	P < 0.01
L-threonine ammonia-lyase (2-oxobutanoate-forming)	4.3.1.19	287308	259880	3.01	666	P < 0.01
acetyl-CoA:dTDP-4-amino-4,6-dideoxy-alpha-D-glucose N-acetyltransferase	2.3.1.209	391	109	3.01	326	P < 0.01
acetyl-CoA:GDP-4-amino-4,6-dideoxy-alpha-D-mannose N-acetyltransferase	2.3.1.227	391	109	3.01	326	P < 0.01
acetyl-CoA:polysialic-acid O-acetyltransferase	2.3.1.136	391	109	3.01	326	P < 0.01
UDP-alpha-D-galactose:N-acetyl-alpha-D-glucosaminyl-diphospho-ditrans,octacis-undecaprenol 3-beta-galactosyltransferase (configuration-inverting)	2.4.1.303	391	109	3.01	326	P < 0.01
phosphoenolpyruvate:protein-L-histidine Npi-phosphotransferase	2.7.3.9	198327	175154	2.99	666	P < 0.01
beta-D-galactopyranosyl-(1->3)-N-acetyl-D-hexosamine:phosphate galactosyltransferase	2.4.1.211	157215	134837	2.98	666	P < 0.01
acyl phosphoate:sn-glycerol 3-phosphate acyltransferase	2.3.1.275	188180	165885	2.97	666	P < 0.01
(S)-3-hydroxybutanoyl-CoA:NADP+ oxidoreductase	1.1.1.157	152442	130608	2.95	666	P < 0.01
prephenate:NAD+ oxidoreductase (decarboxylating)	1.3.1.12	209257	186558	2.95	666	P < 0.01
GDP-beta-L-fucose:beta-D-galactosyl-(1->3)-N-acetyl-beta-D-glucosaminyl-R 4I-alpha-L-fucosyltransferase (configuration-inverting)	2.4.1.65	22456	12648	2.95	648	P < 0.01
GDP-beta-L-fucose:beta-D-galactosyl-(1->4)-N-acetyl-D-glucosaminyl-R 3-alpha-L-fucosyltransferase (configuration-inverting)	2.4.1.152	22456	12648	2.95	648	P < 0.01
S-adenosyl-L-methionine:tRNA (cytidine34/5-carboxymethylaminomethyluridine34-2′-O)-methyltransferase	2.1.1.207	203298	180300	2.95	666	P < 0.01
Ste24 endopeptidase	3.4.24.84	8054	5270	2.94	642	P < 0.01
dTDP-4-amino-4,6-dideoxy-alpha-D-glucose:2-oxoglutarate aminotransferase	2.6.1.33	392	116	2.94	327	P < 0.01
formate:NADP+ oxidoreductase	1.17.1.10	9300	6092	2.93	618	P < 0.01
[biotin carboxyl-carrier protein]-N6-carboxybiotinyl-L-lysine:acetyl-CoA:carboxytransferase	2.1.3.15	344844	310616	2.92	666	P < 0.01
2-hydroxy-2H-chromene-2-carboxylate—(3E)-4-(2-hydroxyphenyl)-2-oxobut-3-enoate isomerase	5.99.1.4	48	17	2.92	88	P < 0.01
acetyl-CoA:acetyl-CoA C-acetyltransferase	2.3.1.9	152724	131247	2.92	666	P < 0.01
1H-pyrrole-2-carbonyl-[peptidyl-carrier protein]:FADH2 oxidoreductase (chlorinating)	1.14.19.56	57	8	2.92	43	P < 0.01
phosphoenolpyruvate:D-erythrose-4-phosphate C-(1-carboxyvinyl)transferase (phosphate-hydrolysing, 2-carboxy-2-oxoethyl-forming)	2.5.1.54	201875	179097	2.91	666	P < 0.01
SpoIVB peptidase	3.4.21.116	158665	137029	2.90	666	P < 0.01
ATP:adenosine 5′-phosphotransferase	2.7.1.20	8550	5745	2.90	614	P < 0.01
ATP:selenide, water phosphotransferase	2.7.9.3	160218	139060	2.89	666	P < 0.01
CTP:molybdenum cofactor cytidylyltransferase	2.7.7.76	158341	136662	2.89	666	P < 0.01
ATP phosphohydrolase (ABC-type, polar-amino-acid-importing)	7.4.2.1	199197	176858	2.86	666	P < 0.01
6-phospho-beta-D-glucosyl-(1->4)-D-glucose glucohydrolase	3.2.1.86	151359	130522	2.85	666	P < 0.01
D-mannonate:NAD+ 5-oxidoreductase	1.1.1.57	156942	135744	2.83	666	P < 0.01
acetyl-CoA:N-terminal L-alanyl-[S5 protein of 30S ribosome] N-acetyltransferase	2.3.1.267	334249	305071	2.82	666	P < 0.01
23S rRNA-uridine955/2504/2580 uracil mutase	5.4.99.24	173982	152979	2.79	666	P < 0.01
aspartyl aminopeptidase	3.4.11.21	174811	154321	2.75	666	P < 0.01
adenine aminohydrolase	3.5.4.2	165689	145730	2.73	666	P < 0.01
D-threo-aldose:NAD+ 1-oxidoreductase	1.1.1.122	318	146	2.72	529	P < 0.01
N-acyl-D-glucosamine-6-phosphate 2-epimerase	5.1.3.9	169311	149193	2.71	666	P < 0.01
(S)-2-haloacid halidohydrolase	3.8.1.2	155173	135018	2.71	666	P < 0.01
peptide-L-methionine:thioredoxin-disulfide S-oxidoreductase [L-methionine (S)-S-oxide-forming]	1.8.4.11	312546	283931	2.71	666	P < 0.01
S-adenosyl-L-methionine:precorrin-3B C17-methyltransferase	2.1.1.131	161683	141568	2.70	666	P < 0.01
S-adenosyl-L-methionine:cobalt-factor III C17-methyltransferase (ring contracting)	2.1.1.272	161548	141442	2.69	666	P < 0.01
23S rRNA-uridine2605 uracil mutase	5.4.99.22	356849	324293	2.69	666	P < 0.01
4-hydroxybenzoyl-CoA hydrolase	3.1.2.23	8515	5695	2.67	538	P < 0.01
phosphate-monoester phosphohydrolase (alkaline optimum)	3.1.3.1	350542	317857	2.67	666	P < 0.01
aceneuramate pyruvate-lyase (N-acetyl-D-mannosamine-forming)	4.1.3.3	308399	281017	2.65	666	P < 0.01
ADP-D-ribose ribophosphohydrolase	3.6.1.13	323656	296452	2.65	666	P < 0.01
Repressor LexA	3.4.21.88	194850	174370	2.64	666	P < 0.01
pectin pectylhydrolase	3.1.1.11	273240	244908	2.64	666	P < 0.01
S-methyl-5′-thioinosine:phosphate S-methyl-5-thio-alpha-D-ribosyl-transferase	2.4.2.44	8312	5582	2.62	547	P < 0.01
hydrogen:ferredoxin oxidoreductase	1.12.7.2	8245	5720	2.61	609	P < 0.01
phosphonoacetate phosphonohydrolase	3.11.1.2	9209	6261	2.60	489	P < 0.01
sortase A	3.4.22.70	170941	151298	2.59	666	P < 0.01

I will leave it to the professional microbiologists to make sense of the 190 enzymes above. I should point out that the levels with Long COVID are always higher than the control. I saw the same pattern with Salicylate sensitive – Data And Research, but not as extreme (as with much fewer significant enzymes).

Bacteria Found Significant

The strongest associations are shown below. It is interesting to note that the t-scores are lower for bacteria than for enzymes. The clustering by enzymes was beneficial. We expect less than 2 false positives in this list. Note that the degrees of freedom (Df) is reflected of frequency found. df=38 means that 40 out of 668 samples reported this bacteria.

Tax rank	Taxa Name	With Long COVID	Without Long COVID	T-Score	Df	Probability
species	Faecalibacterium prausnitzii	138151	109673	3.78	666	P < 0.001
genus	Planococcus	41	25	3.89	118	P < 0.001
genus	Anaeroplasma	19328	3766	3.49	74	P < 0.001
class	Mollicutes	5774	2610	3.65	642	P < 0.001
genus	Coriobacterium	173	32	5.41	38	P < 0.001
species	Coriobacterium glomerans	173	32	5.41	38	P < 0.001
genus	Kushneria	54	28	3.62	148	P < 0.001
phylum	Tenericutes	5774	2610	3.65	642	P < 0.001
order	Anaeroplasmatales	19328	3766	3.49	74	P < 0.001
family	Anaeroplasmataceae	19328	3766	3.49	74	P < 0.001
species	Planococcus columbae	41	24	4.85	108	P < 0.001

The less significant ones are shown below:

Tax rank	Taxa name	With Long COVID	Without Long COVID	T-Score	Df	Probability
species	Lactobacillus letivazi	28	11	3.93	12	P < 0.01
species	Clostridium fallax	84	22	3.53	32	P < 0.01
species	Corynebacterium xerosis	755	90	3.34	48	P < 0.01
species group	Pseudomonas syringae group	60	25	3.17	46	P < 0.01
species	Corynebacterium kutscheri	186	34	3.12	33	P < 0.01
genus	Comamonas	289	51	3.11	61	P < 0.01
species	Peptoniphilus indolicus	150	30	3.11	67	P < 0.01
species	Prevotella oulorum	87	52	3.06	72	P < 0.01
order	Sphingobacteriales	40382	31662	2.99	667	P < 0.01
class	Sphingobacteriia	40382	31662	2.99	667	P < 0.01
family	Azonexaceae	60	20	2.98	60	P < 0.01
genus	Dechloromonas	60	20	2.98	60	P < 0.01
family	Rhodocyclaceae	71	50	2.97	413	P < 0.01
genus	Marinospirillum	42	28	2.87	156	P < 0.01
species	Euzebya tangerina	64	46	2.79	370	P < 0.01
class	Nitriliruptoria	64	46	2.79	370	P < 0.01
order	Euzebyales	64	46	2.79	370	P < 0.01
family	Euzebyaceae	64	46	2.79	370	P < 0.01
genus	Euzebya	64	46	2.79	370	P < 0.01
species	Clostridium caliptrosporum	26	17	2.72	37	P < 0.01
genus	Pedobacter	12917	9686	2.72	656	P < 0.01
species	Sphingobacterium bambusae	480	315	2.70	579	P < 0.01
species	Prevotella corporis	1883	645	2.69	315	P < 0.01
species	Dechloromonas hortensis	34	21	2.68	56	P < 0.01
family	Sphingobacteriaceae	35765	28616	2.59	666	P < 0.01

At this point, our first set of bacteria to look at are ones with a high df (and thus most commonly seen). This is a short list when we drop parent and child with the same numbers:

Tax rank	Taxa name	With Long COVID	Without Long COVID	TScore	Df	Probability
order	Sphingobacteriales	40382	31662	2.99	667	P < 0.01
species	Faecalibacterium prausnitzii	138151	109673	3.78	666	P < 0.001
family	Sphingobacteriaceae	35765	28616	2.59	666	P < 0.01
genus	Pedobacter	12917	9686	2.72	656	P < 0.01
phylum	Tenericutes	5774	2610	3.65	642	P < 0.001

Comparing to published studies above

We have no agreement on identification of significant bacteria. The only bacteria in common was Faecalibacterium prausnitzii. This bacteria was cited in just one Pubmed studies on Long COVID. Many studies reported on it during the active COVID infection. This study reported it was lower. We found that it was higher. That study sample size was considerable smaller than us : 106 with Long COVID and 68 Control; they did not mention the significance level but used the term often seen when there was poor significance: “were characterized by”. This study cites “Faecalibacterium prausnitzii showed the largest inverse correlations with PACS at 6 months.” We are dealing with samples with different periods since onset.

The absence of bacteria in common is not unexpected given differences in methodologies. This is often seen when multiple studies on the same condition are done, non-replication of results. I refer the reader to this story

Three blind microbiologists attempt to describe the microbiome of an elephant…

See Blind men and an elephant

Comparing Suggestions

We have suggestions generated from the US National Library of Medicine studies, and we also have suggests from this analysis. These suggestions are generated by the Fuzzy Logic Artificial Intelligence on the Microbiome Prescription site. How do they compare?

Running with everything that is suggested (including prescription items) by both sets of data we found:

• Agreement on 1255 items that will help
• Disagreement on 396 items (one says help, one says hurt)

This is 76% agreement on suggestions that would help. This is surprisingly good given that Faecalibacterium prausnitzii are reported in opposite directions between these two sets. The best agreement was for:

• Drug or “Non-drug” at 90.5% – with 95 items considered
• Prescription other at 93.8% – with 933 items considered

This was not surprising because the data density for these two is good. For many other things, the data density is sparse — for example, for Prebiotics, Amino acids and Probiotics. There is almost no literature on how they impact many of the bacteria cited.

How to Use this data?

The root problem is having insufficient data in many vectors. As a fuzzy logic engineer, this does not concern me — we will simply make the best use of available data in the belief that it is better than working from no data.

The system on Microbiome Prescription uses the consensus system for treatment suggestions. You can process a microbiome using PubMed studies, process it again with the above data, and then get a list where the suggestions are in agreement. At present, the microbiome sample must be processed thru Biomesight because that is how the items of significance were detected. In time, other labs could reach sufficient data to get results.

To illustrate this process, I have done a video below using a sample from someone with Long COVID.

Related Blog Posts for those who are interested:

• Special Studies on Symptoms caused by Bacteria – v.2
• Histamine Release – Literature Review And Speculation
• Salicylate sensitive – Data And Research

Data Availability: The samples and symptoms are available at: Microbiome Prescription Citizen Science Data Share

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.

After the post on histamines, people with Salicylate sensitivity started to contact. “Me too!”. I looked at the data available and was disappointed that only 31 people have annotated their sample with this condition.

Medical Literature

This is known as  salicylate allergy, salicylate hypersensitivity or salicylate intolerance. The traditional medical view is “It’s not clear exactly what causes salicylate allergy. “[WebMD] It was associated with Lyme Disease in 1991, and in other studies to: rheumatic diseases [1961] and systemic lupus erythematosus[1979]. It is seen in up to 7% of all patients with inflammatory bowel syndrome[2004] where as it was been estimated that 2.5%[2015] of the general population has this issue. The incidence in samples uploaded to microbiome prescription with symptom annotations appears to be 1.8%. This implies a significant microbiome contribution to this condition.

In 1980, we have The uselessness of blood salicylate levels in the diagnosis of salicylate hypersensitivity. However, the level may cause issues with blood donations being received by people with this condition, see Salicylate and acetaminophen in donated blood [1986].

Diet changes appear to have minor impact as reported in Effectiveness of Personalized Low Salicylate Diet in the Management of Salicylates Hypersensitive Patients: Interventional Study[2021] and others [2021] [2016]

In dealing with Plants we have an interesting study Overexpression of Arabidopsis NIMIN1 results in salicylate intolerance [2016] with other plant based studies [2010].

Human Trials

Only one trial could be found

After dietary supplementation with 10 g daily of fish oils rich in omega-3 PUFAs for 6-8 weeks all three experienced complete or virtually complete resolution of symptoms allowing discontinuation of systemic corticosteroid therapy. Symptoms relapsed after dose reduction.”

Control of salicylate intolerance with fish oils [2008]

KEGG: Kyoto Encyclopedia of Genes and Genomes Perspective

I am by temperament, a modeler. Look at the surface layer of information, derive some suggestions of how thing work and then, critically, test the model. Failure is information also! My first model is to assume enzymes associated with salicylates are significant.

Salicylate aka o-Hydroxybenzoic acid aka Salicylic acid is compound C00805 with the following enzymes interacting with it. Conceptually, too much of some enzymes and too few of other enzymes may be the likely cause. The list include the followin:

• 1.2.1.65 salicylaldehyde dehydrogenase
• 1.14.13.1 salicylate 1-monooxygenase;      
• 1.14.13.172 salicylate 5-hydroxylase
• 2.1.1.274  salicylate 1-O-methyltransferase
• 3.1.1.55 acetylsalicylate deacetylase  
• 4.1.1.91 salicylate decarboxylase        
• 4.2.99.21 isochorismate lyase
• 6.2.1.61 salicylate—[aryl-carrier protein] ligase    
• 6.2.1.65 salicylate—CoA ligase

Data From Microbiome Prescription Samples

See Special Studies on Symptoms caused by Bacteria – v.2 for technical detail. A related post is Histamine Release – Literature Review And Speculation.

For more information on each enzyme see BRENDA or KEGG

The most significant ones from are shown below. None are a match for the candidate list above

EC	Enzyme Name	With Sal	Without Sal	TScore	DF	Probability
1.1.1.337	(2S)-2-hydroxycarboxylate:NAD+ oxidoreductase	37077	19517	3.38	666	P < 0.001
1.3.7.1	6-oxo-1,4,5,6-tetrahydronicotinate:ferredoxin oxidoreductase	334	91	4.01	222	P < 0.001
2.1.1.245	5-methyltetrahydrosarcinapterin:corrinoid/iron-sulfur protein methyltransferase	36498	18608	3.46	666	P < 0.001
2.1.1.258	5-methyltetrahydrofolate:corrinoid/iron-sulfur protein methyltransferase	36569	18689	3.46	666	P < 0.001
2.6.1.109	8-amino-3,8-dideoxy-alpha-D-manno-octulosonate:2-oxoglutarate aminotransferase	108	35	3.90	124	P < 0.001
2.7.7.39	CTP:sn-glycerol-3-phosphate cytidylyltransferase	60861	32715	3.56	666	P < 0.001
3.4.19.11	gamma-D-glutamyl-meso-diaminopimelate peptidase	39254	21501	3.42	666	P < 0.001
3.5.2.18	6-oxo-1,4,5,6-tetrahydronicotinate amidohydrolase	334	93	3.93	215	P < 0.001
4.2.1.43	2-dehydro-3-deoxy-L-arabinonate hydro-lyase (2,5-dioxopentanoate-forming)	433	103	4.57	214	P < 0.001
5.4.99.21	23S rRNA-uridine2604 uracil mutase	63603	39414	3.33	666	P < 0.001

Looking at the next level of association, we still find none of these candidate enzymes.

EC	Enzyme Name	With Sal	Without Sal	TScore	DF	Probability
1.1.1.135	GDP-6-deoxy-alpha-D-talose:NAD(P)+ 4-oxidoreductase	279	96	2.82	263	P < 0.01
1.1.1.312	4-carboxy-2-hydroxymuconate semialdehyde hemiacetal:NADP+ 2-oxidoreductase	353	105	2.68	229	P < 0.01
1.1.1.410	D-erythronate:NAD+ 2-oxidoreductase	381	117	3.32	300	P < 0.01
1.1.99.31	(S)-mandelate:acceptor 2-oxidoreductase	265	92	2.71	210	P < 0.01
1.13.11.37	hydroxyquinol:oxygen 1,2-oxidoreductase (ring-opening)	268	88	2.66	247	P < 0.01
1.17.1.4	xanthine:NAD+ oxidoreductase	34795	17231	2.81	666	P < 0.01
1.17.9.1	4-methylphenol:oxidized azurin oxidoreductase (methyl-hydroxylating)	198	83	3.00	338	P < 0.01
1.2.1.87	propanal:NAD+ oxidoreductase (CoA-propanoylating)	25104	13840	2.72	666	P < 0.01
1.2.7.4	carbon-monoxide,water:ferredoxin oxidoreductase	51730	29588	3.18	666	P < 0.01
1.2.99.7	aldehyde:acceptor oxidoreductase (FAD-independent)	34901	17791	2.71	666	P < 0.01
1.3.1.32	3-oxoadipate:NAD(P)+ oxidoreductase	268	88	2.65	260	P < 0.01
2.3.1.101	formylmethanofuran:5,6,7,8-tetrahydromethanopterin 5-formyltransferase	289	88	3.25	207	P < 0.01
2.3.1.276	acetyl-CoA:alpha-D-galactosamine-1-phosphate N-acetyltransferase	51215	29509	3.08	666	P < 0.01
2.3.2.13	protein-glutamine:amine gamma-glutamyltransferase	49247	27040	3.22	666	P < 0.01
2.4.1.245	NDP-alpha-D-glucose:D-glucose 1-alpha-D-glucosyltransferase	111	42	3.33	213	P < 0.01
2.7.1.215	ATP:erythritol 1-phosphotransferase	12084	5590	2.73	653	P < 0.01
2.7.4.31	ATP:[5-(aminomethyl)furan-3-yl]methyl-phosphate phosphotransferase	289	88	3.25	207	P < 0.01
2.7.4.33	ADP:polyphosphate phosphotransferase	36369	19252	2.68	666	P < 0.01
2.7.7.83	UTP:N-acetyl-alpha-D-galactosamine-1-phosphate uridylyltransferase	51217	29512	3.08	666	P < 0.01
2.7.9.6	ATP:rifampicin, water 21-O-phosphotransferase	1458	427	2.99	575	P < 0.01
3.1.1.104	5-phospho-D-xylono-1,4-lactone hydrolase	12119	5680	2.70	656	P < 0.01
3.1.1.81	N-acyl-L-homoserine-lactone lactonohydrolase	12121	5591	2.73	653	P < 0.01
3.4.23.43	prepilin peptidase	104657	72966	2.58	666	P < 0.01
3.5.1.110	(Z)-3-ureidoacrylate amidohydrolase	12177	5917	2.63	661	P < 0.01
3.5.4.44	ectoine aminohydrolase	268	85	2.71	234	P < 0.01
3.5.99.5	2-aminomuconate aminohydrolase	309	106	2.72	177	P < 0.01
3.6.1.15	nucleoside-triphosphate phosphohydrolase	26554	15567	3.28	665	P < 0.01
3.6.1.7	acylphosphate phosphohydrolase	60707	38253	2.67	666	P < 0.01
4.2.1.147	5,6,7,8-tetrahydromethanopterin hydro-lyase (formaldehyde-adding, tetrahydromethanopterin-forming)	309	101	2.77	192	P < 0.01
5.3.1.15	D-lyxose aldose-ketose-isomerase	58198	37194	2.64	666	P < 0.01
5.3.1.34	D-erythrulose-4-phosphate ketose-aldose isomerase	12039	5560	2.71	642	P < 0.01
7.5.2.4	ATP phosphohydrolase (ABC-type, teichoic-acid-exporting)	25268	12222	2.91	666	P < 0.01

So, model 1 is a bust — none of the suspected enzymes showed up as being statistically significant. This echoes The uselessness of blood salicylate levels in the diagnosis of salicylate hypersensitivity[1980]. However one thing stands out…. for each of the enzymes estimates above — the amount with salicylate sensitivity is in every case more than those without it. This is unusual.It hints that the issue is over production of enzymes.

Microbiome Significances

Only Biomesight has sufficient data to do an investigation with. The most significant ones all had an interesting characteristic matching that seen with the enzymes — Too MANY.

Tax_name	Tax_rank	With Sal	Without Sal	Tscore	DF	Probability
Fusobacteriia	class	21983	3330	3.52	346	P < 0.001
Chroococcaceae	family	588	165	3.42	286	P < 0.001
Fusobacteriaceae	family	25628	3687	3.63	305	P < 0.001
Hungateiclostridiaceae	family	8534	2649	3.69	201	P < 0.001
Lachnospiraceae	family	297116	203706	4.2	667	P < 0.001
Rhodanobacteraceae	family	2453	656	3.32	478	P < 0.001
Syntrophobacteraceae	family	115	36	3.57	184	P < 0.001
Acetobacterium	genus	3977	1250	3.92	657	P < 0.001
Blautia	genus	141777	87110	4.2	667	P < 0.001
Chroococcus	genus	588	165	3.42	286	P < 0.001
Clostridium	genus	30531	18614	3.45	667	P < 0.001
Furfurilactobacillus	genus	91	38	3.48	270	P < 0.001
Hungateiclostridium	genus	8178	2229	3.94	200	P < 0.001
Luteibacter	genus	3734	764	4.07	387	P < 0.001
Fusobacteriales	order	21983	3329	3.52	346	P < 0.001
Syntrophobacterales	order	135	45	5.06	331	P < 0.001
Fusobacteria	phylum	21983	3330	3.52	346	P < 0.001
Bacteroides fluxus	species	2722	318	3.41	517	P < 0.001
Blautia glucerasea	species	4228	664	3.86	550	P < 0.001
Blautia schinkii	species	1710	265	4.14	558	P < 0.001
Caloramator uzoniensis	species	300	85	4.53	328	P < 0.001
Chroococcus minutus	species	588	165	3.42	286	P < 0.001
Clostridium akagii	species	113	43	4.37	311	P < 0.001
Furfurilactobacillus siliginis	species	91	38	3.51	271	P < 0.001
Luteibacter anthropi	species	3734	764	4.07	387	P < 0.001

Looking at the next level, we have a lot less BUT THE PATTERN OF OVER ABUNDANCE continues:

Tax_name	Tax_rank	WithMean	WithoutMean	Tscore	DF	Probability
Desulfovibrionaceae	family	8811	5037	2.61	641	P < 0.01
Xanthomonadaceae	family	2131	642	3.16	556	P < 0.01
Bilophila	genus	6608	3415	3.25	587	P < 0.01
Caldicellulosiruptor	genus	581	289	2.67	617	P < 0.01
Fusobacterium	genus	2795	683	2.76	289	P < 0.01
Holdemania	genus	572	296	3.04	589	P < 0.01
Lachnospira	genus	49628	28041	3.22	667	P < 0.01
Macrococcus	genus	2425	419	3.28	222	P < 0.01
Thiorhodococcus	genus	64	28	2.67	108	P < 0.01
Desulfovibrionales	order	8840	5039	2.63	643	P < 0.01
Bacteroides finegoldii	species	7458	2163	3.15	552	P < 0.01
Blautia obeum	species	12039	5596	2.68	642	P < 0.01
Fusobacterium gonidiaformans	species	3980	833	3.12	134	P < 0.01
Shewanella upenei	species	92	46	3	157	P < 0.01

Cross Validation of The above

We know of only one thing known to help, Omega-3 / Fish Oil. We have this information in our database and find that it decreases the following (from multiple studies):

• Lachnospira
• Lachnospiraceae
• Furfurilactobacillus siliginis
• Blautia

A single study suggests that it increases Clostridium / Clostridium akagii (Child). This is a 80% validation rate implying that the Artificial Intelligence suggestions on a person’s microbiome is likely to be effective.

Putting this data to Use

The first step is simple, take 10 g daily of fish oils rich in omega-3 for the first 6-8 weeks. Get relief. Warning: the study states that if you stop, you will revert. It is insufficient to correct the bacteria shifts.

If you do not have a BiomeSight sample on hand…

Go to Citizen Science Special Studies, Enter Salicylate in the search box. The page should give you two buttons as shown below.

The results may change as more samples are uploaded and annotated with symptoms. This research is dynamic and live!. Clicking the green button will show a list of item to take or add to your diet.

The second item is likely more important items that feed the bacteria that are too high. You want to reduce or eliminate these.

There is still more information available on actual diet (foods that you may eat), by clicking on

We know the fish oil helps, let us verify that by clicking on [FIsh, shellfish and their products]. We see fish — specifically salmon! And Walrus liver is a to-avoid!

Returning to the red button, we see a list of off-label usage of drugs mixed into the results. The top ones:

• Risperidone is used to treat a certain mental/mood disorder called schizophrenia.
• Acarbose is used with a proper diet and exercise program to control high blood sugar in people with type 2 diabetes.
• meomycin is used to decrease the risk of infection after certain intestinal surgeries.

Step 2 Order a Suitable Test

You will likely need at least 3 tests, the data is based on Biomesight tests. Order some. If you live in the US, you could order an Ombre Test (this gets more technical because you will need to download some big files [FASTQ] from their site and then upload to Biomesight for them to process them).

You will likely be doing the above for 5-6 weeks before you get your data available on BiomeSight.

Log in to Microbiome Prescription

Go to [Research Features]

Then find on that page, the Experimental section, and click v.2 Of Special Symptom Associations

Select your latest sample (if more than one) and then the condition

The bacteria that definitely match the pattern will be automatically checked.

You should scan for any close matches and check those boxes. For example, above the without symptoms slightly.

Now click the [Add to Hand Picked LIst] button at the top

A new window will appear with the items that you have selected.

Just click [Get Suggestions] and then scope the type of suggestions you wish

Then click the Get Suggestions button on the top left

Your suggestions may be similar (the sample that I am using was for someone with this issue)

The food list may also change

WARNING: Many items suggested may trigger a Salicylate reaction. Consider doing the 6-8 weeks of Fish Oil before starting any items that could trigger a reaction.

This reaction could be caused by bacteria resisting change (similar to a Jarisch Herxheimer)

The usual pattern is to implement the changes for 4 week, do a new sample. Keep doing the changes until the results come in. So this is the likely time line for some

• Week 0: Order Kit, start general list
• Week 1: Take test #1 and send in
• Week 4: Get results, upload and get 1st personalized set of suggestions
• Week 8: Take test #2 and send in
• Week 10: Get results, upload and get 2nd personalized set of suggestions
• Week 14: Take test #3 and send in
• Week 16: Get results, upload and get 3rd personalized set of suggestions

Depending on results, repeat. Your desired result is to have NO Matches with the pattern (and hopefully have eliminated the issue).

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.