Overview of this Blog and the Microbiome

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

Notes to Treating Physicians

Analysis of Microbiome/stool with recommendations

Microbiome Definition of CFS/FM/IBS

A condition that results from:

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

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

Replace the metabolites produced by the missing bacteria

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

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

Other Supplements Reported to Help

Bootstrapping Bifidobacterium and Lactobacillus

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

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

Bootstrapping E.Coli

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

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

Dealing with the other microbiome shifts

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

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

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

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

  • https://cfsremission.com/2017/09/11/ubiomes-before-and-after-a-fecal-microbiota-transplant/
  • https://cfsremission.com/2017/09/03/ubiome-result/
  • https://cfsremission.com/2017/09/18/another-ubiome-review-with-bifidobacteria-overgrowth/
  • https://cfsremission.com/2017/08/27/ubiome-of-a-mcs-with-cfs-person/

I have discovered that DataPunk is not absolutely current, and have started creating posts based on its data, and then added studies from 2016 and 2017 to the page. Current pages are below (I will add more links as I research other genus)

  • Acetitomaculum: https://cfsremission.com/2017/11/14/decreasing-acetitomaculum-genus/
  • Acidaminococcus: https://cfsremission.com/2017/11/01/reducing-acidaminococcus-genus/
  • Actinobaculum: https://cfsremission.com/2017/10/21/decreasing-actinobaculum-genus/
  • Actinomyces: https://cfsremission.com/2017/11/25/reducing-actinomyces-genus/
  • Adlercreutzia: https://cfsremission.wordpress.com/2017/10/14/decreasing-adlercreutzia-genus/
  • Akkermansia: https://cfsremission.com/2017/10/14/decreasing-akkermansia-genus/
  • Alistipes: https://cfsremission.com/2017/10/09/decreasing-alistipes-genus/
  • Anaeroplasma: https://cfsremission.com/2017/11/11/decreasing-anaeroplasma-genus/
  • Anaerosinus: https://cfsremission.com/2017/11/29/reducing-anaerosinus-genus/
  • Anaerotruncus: https://cfsremission.com/2017/11/19/reducing-anaerotruncus-genus/
  • Anaerostipes:   https://cfsremission.com/2017/10/07/decreasing-anaerostipes-genus/
  • Bacteroides: https://cfsremission.com/2017/10/20/decreasing-bacteroides-genus/
  • Barnesiella: https://cfsremission.com/2017/10/15/decreasing-barnesiella-genus/
  • Bilophila:   https://cfsremission.com/2017/10/14/decreasing-bilophila-genus/
  • Blautia:   https://cfsremission.com/2017/10/29/reducing-blautia-genus/
  • Brevundimonas:   https://cfsremission.com/2017/11/04/decreasing-brevundimonas-genus/
  • Butyricimas:  https://cfsremission.com/2017/10/14/decreasing-butyricimonas-genus/
  • Butyrivibrio Crossotus:  https://cfsremission.com/2017/12/15/increasing-butyrivibrio-crossotus/
  • Caldicoprobacter: https://cfsremission.com/2017/10/15/decreasing-caldicoprobacter-genus/
  • Candidatus Stoquefichus: https://cfsremission.com/2017/11/30/reducing-candidatus-stoquefichus-genus/
  • Catenibacterium: https://cfsremission.com/2017/11/18/reducing-catenibacterium-genus/
  • Citrobacter Freundii: https://cfsremission.com/2017/12/11/reducing-citrobacter-freundii/
  • Collinsella: https://cfsremission.com/2017/10/10/decreasing-collinsella-genus/
  • Coprobacter: https://cfsremission.com/2017/11/06/decreasing-coprobacter-genus/
  • Clostridium :  https://cfsremission.com/2017/10/07/decreasing-clostridium-genus/
  • Cronobacter:  https://cfsremission.com/2017/10/21/decreasing-cronobacter-genus/
  • Desulfovibrio:  https://cfsremission.com/2017/11/05/decreasing-desulfovibrio-genus/
  • Dialister:  https://cfsremission.com/2017/11/05/reducing-dialister-genus/
  • Dorea :  https://cfsremission.com/2017/10/18/reducing-dorea-genus/
  • Eggerthella: https://cfsremission.com/2017/10/19/decreasing-eggerthella-genus/
  • Eisenbergiella: https://cfsremission.com/2017/11/25/reducing-eisenbergiella-genus/
  • Enterococcus: https://cfsremission.com/2017/10/29/reducing-enterococcus-genus/
  • Enterorhabdus: https://cfsremission.com/2017/11/05/reducing-enterorhabdus-genus/
  • Erysipelatoclostridium: https://cfsremission.com/2017/11/14/decreasing-erysipelatoclostridium-genus/
  • Faecalibacterium: https://cfsremission.com/2017/10/11/reducing-faecalibacterium-genus/
  • Flavobacterium:
  • Flavonifractor: https://cfsremission.com/2017/11/05/reducing-flavonifractor-genus/
  • Fusicatenibacter: https://cfsremission.com/2017/11/03/decreasing-fusicatenibacter-genus/
  • Gelria: https://cfsremission.com/2017/12/22/reducing-gelria-genus/
  • Gordonibacter: https://cfsremission.com/2017/10/09/decreasing-gordonibacter-genus/
  • Granulicatella: https://cfsremission.com/2017/11/25/reducing-granulicatella-genus/
  • Haemophilus: https://cfsremission.com/2017/11/19/reducing-haemophilus-genus/
  • Herbaspirillum: https://cfsremission.com/2017/10/12/reducing-herbaspirillum-genus/
  • Hespellia: https://cfsremission.com/2017/11/05/reducing-hespellia-genus/
  • Hydrogenoanaerobacterium: https://cfsremission.com/2017/12/22/reducing-hydrogenoanaerobacterium-genus/
  • Intestinibacter: https://cfsremission.com/2017/12/22/reducing-intestinibacter-genus/
  • Intestinimonas: https://cfsremission.com/2017/11/05/reducing-intestinimonas-genus/
  • Johnsonella: https://cfsremission.com/2017/11/04/decreasing-johnsonella-genus/
  • Kluyvera: https://cfsremission.com/2017/10/31/reducing-kluyvera-genus/
  • Lachnospira: https://cfsremission.com/2017/11/03/reducing-lachnospira-genus/
  • Lactonifactor: https://cfsremission.com/2017/11/29/reducing-lactonifactor-genus/
  • Leuconostoc: https://cfsremission.com/2017/10/26/reducing-leuconostoc-genus/
  • Marvinbryantia: https://cfsremission.com/2017/11/06/decreasing-marvinbryantia-genus/
  • Megasphaera: https://cfsremission.com/2017/11/18/reducing-megasphaera-genus/
  • Mitsuokella: https://cfsremission.com/2017/12/21/reducing-mitsuokella-genus/
  • Moryella: https://cfsremission.com/2017/11/11/decreasing-moryella-genus/
  • Odoribacter: https://cfsremission.com/2017/10/19/decreasing-odoribacter-genus/
  • Oscillospira: https://cfsremission.com/2017/10/15/decreasing-oscillospira-genus/
  • Oxalobacter-formigenes: https://cfsremission.com/2017/12/15/increasing-oxalobacter-formigenes/
  • Papillibacter: https://cfsremission.com/2017/11/06/decreasing-papillibacter-genus/
  • Parabacteroides: https://cfsremission.com/2017/10/17/decreasing-parabacteroides-genus/
  • Paraprevotella:https://cfsremission.com/2017/11/28/decreasing-paraprevotella-genus/
  • Parasutterella: https://cfsremission.com/2017/10/19/decreasing-parasutterella-genus/
  • Peptococcus: https://cfsremission.com/2017/11/28/decreasing-peptococcus-genus/
  • Peptoclostridium: https://cfsremission.com/2017/11/18/reducing-peptoclostridium-genus/
  • Phascolarctobacterium: https://cfsremission.com/2017/11/12/decreasing-phascolarctobacterium-genus/
  • Planomicrobium: https://cfsremission.com/2017/10/21/decreasing-planomicrobium-genus/
  • Prevotella: https://cfsremission.com/2017/10/14/decreasing-prevotella-genus/
  • Pseudoflavonifractor:https://cfsremission.com/2017/11/19/reducing-pseudoflavonifractor-genus/
  • Pseudobutyrivibrio: https://cfsremission.com/2017/10/15/decreasing-pseudobutyrivibrio-genus/
  • Robinsoniella: https://cfsremission.com/2017/10/12/decreasing-robinsoniella-genus/
  • Romboutsia: https://cfsremission.com/2017/12/09/reducing-romboutsia-genus/
  • Roseburia: https://cfsremission.com/2017/10/29/decreasing-roseburia-genus/
  • Rothia: https://cfsremission.com/2017/10/25/decreasing-rothia-genus/
  • Ruminococcus: https://cfsremission.com/2017/10/18/reducing-ruminococcus-genus/
  • Sarcina: https://cfsremission.com/2017/10/12/decreasing-sarcina-genus/
  • Senegalemassilia: https://cfsremission.com/2017/11/18/reducing-senegalemassilia-genus/
  • Shuttleworthia: https://cfsremission.com/2017/12/22/reducing-shuttleworthia-genus/
  • Slackia: https://cfsremission.com/2017/10/15/decreasing-slackia-genus/
  • Streptococcus: https://cfsremission.wordpress.com/2017/10/25/reducing-streptococcus-genus/
  • Subdoligranlum: https://cfsremission.com/2017/10/10/decreasing-subdoligranlum/
  • Succinivibrio: https://cfsremission.com/2017/11/05/decreasing-succinivibrio-genus/
  • Sutterella: https://cfsremission.com/2017/10/13/decreasing-sutterella-genus/
  • Terrisporobacter: https://cfsremission.com/2017/11/05/reducing-terrisporobacter-genus/
  • Thalassospira: https://cfsremission.com/2017/10/22/reducing-thalassospira-genus/
  • Veillonella: https://cfsremission.com/2017/11/29/reducing-veillonella-genus/
  • Victivallis: https://cfsremission.com/2017/11/11/decreasing-victivallis-genus/


Src: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4754147/

General Suggestions (no uBiome results)

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


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

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

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

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

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

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

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


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

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

Herbs and Spices

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

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

Other things

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

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

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

Metabolism Shifts

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

Bottom Line

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

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

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

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

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

Coming soon — support for all areas in uBiome

This weekend I hope to finish making changes so that throat, nose and other ubiome samples may also be investigated.

Symptoms will be linked to the email + sample date, so there is no need to re-enter symptoms. This would allow people to see the impact of changes in mouth health by changes in habits they implemented.

Recommendations will continue to be ONLY for gut — there are not enough studies to venture into other areas.  BUT, if you start chewing mastic gum (something that I have suggested before), you should see the impact on your throat and nose bacteria.

Also simplified recommendations are being worked on.

Many items appear under 3-6 different names in the literature. The citation used the term used in the study. The simplification will replace things like:

with just resveratrol (whatever the common name of a supplement is).

This will impact some recommendations because we will stop double counting or under counting some modifiers.

Simple Summary of Progress between uBiome Samples

In my earlier post, COMPARING REPEATED UBIOME RESULTS, I provided a tool but little guidance on interpreting. The key question is always whether the symptoms improved, not whether some numbers change. We do not know which numbers are significant and which numbers are just natural variation.

Model Of Onset

People see progression of symptoms since onset. Each progression is likely associated with a set of changes in the uBiome. This can be represented in the chart below (which likely have a lot more items than shown).


Model Of Recovery

Our Wishful Model

This appears to happen in two scenarios:

  • Chemotherapy for Cancer in some cases
  • Fecal Matter Transplants — but usually do not persist longer than a few weeks


Probable reality

This model comes from the model that we may have more than a dozen bacteria groups involved in the symptoms. For depression alone, we see 28!!. Being able to correct all of them in one-go is not likely. You may correct one and those not effected adapt to try entrenching themselves better (like filling the empty space of the bacteria reduced).


Interpreting results of Comparisons

I am looking at a person with two samples. I have not automated the comparisons shown below, instead I selected a sample and then went to the page and did a simple count.

Over all, we went from 31 matches to 27 matches. One increased and three decreased — I wish it was possible to do decrease across all items…

Comparison Report – Summary

The original detail was done as a quickly and dirty report comparing numbers and attempts to keep people from becoming excessively focus on numbers (which we are not certain of significance – some are likely important and some are not… we do not know for sure which ones are).

From feedback, it is clear that a simpler report, the summary, would be easier to understand and likely more beneficial

Time between samples: 10 months

Metabolism is likely the most significant

Like the profiles used above, this filters ‘noise’ and looks at the net result of a lot of different bacteria.  I have just added a new item to the report

Average Metabolism (Ideal healthy would be 1.0)

  • Early sample 1.32
  • Later Sample 1.18

In short, the metabolism is improving greatly.

New and Updated Pages

There are now two buttons available for comparison


The new report is Summary, and an example is shown below. The most significant ones are high lighted.


  • Profiles – this means the total matches for all of the conditions we have profiles on
    • We see a decrease from 59 matches to 53.
    • The individual profiles are listed in plain text
    • A decrease suggests moving away from an autoimmune state
    • This is an objective measurement
  • Symptoms:
    • Symptoms are subjective, ideally we would like to see a decrease
    • Go to the detail reports to see what symptoms changed.
  • Metabolism Average
    • This is the average of the values transcribed from uBiome.
    • A perfect (healthy) score is 1.0
    • This is an objective measurement
  • Metabolism Standard Deviation
    • This is a measure of how scattered from a healthy score you are
    • A perfect (healthy) score is 0.0
    • This is an objective measurement

Bottom Line

The new summary page give you three objective measures of your progress. For the reader above, all three objective measures improved. The subjective measure (number of symptoms) increased — we do not record severity of symptoms because that is so-so-so very subjective, just a count.

Whiplash on Recommendations

The reader found that the recommendations changed a lot between the two samples. A change is expected if progress is made. Conceptually, the number of items with a high (or low — for avoid) should decrease if progress is made.  We see this in the samples of this reader, as shown below.

Take Lists

For Example 1, we had the > 4 take

Cranberry bean flour
Bacillus subtilis natto
High Fat
Plant-rich diet
ß-lactam antibiotics
Vitamin D
Polymannuronic acid

For Example 2, the list has grown smaller, with some new items appearing

Polymannuronic acid
Ketogenic diet
Lactobacillus kefiri
Low fat diets
Lactobacillus plantarum
Bacillus subtilis natto

Avoid Lists

For Exampl1, the < -4 list

black raspberries
Acetic acid
Chrysanthemum morifolium
Isobutyric acid
Isovaleric acid
Sunflower Oil
High fruit intake
Saccharomyces boulardii
animal-based protein
High meat diet
Fraxinus angustifolia

For Example 2, the list is again smaller for < -4, with a few items in common

Navy bean
High protein diet
Carboxymethyl cellulose
Polysorbate 80
ku ding cha tea
Fraxinus angustifolia




Depression and the Microbiome Revisited

I have done a few posts on depression over the years

A friend asked me to revisit it, especially now that I have a recommendation program working.

Depression and the Microbiome – PubMed

From The role of microbiota in the pathogenesis of schizophrenia and major depressive disorder and the possibility of targeting microbiota as a treatment option [2017].

  • over-presentation of the orders of Bacteroidales and
  • under-presentation of the orders of  Lachnospiraceae,
  • Higher level of Oscillibacter and Alistipes had higher depression
  •  increased levels of Enterobacteriaceae and Alistipes
  •  reduced levels of Faecalibacterium 

Altered fecal microbiota composition in patients with major depressive disorder [2015]. adds that “Bacterial diversity was significantly higher ” and also reported additionally (for two types of depression):

  • higher Bacteroidaceae,
  • higher Butyricimonas,
  • higher Clostridium XlVb
  • higher Enterobacteriaceae,
  • higher Parabacteroides,
  • higher Phascolarctobacterium,
  • higher Porphyromonadaceae,
  • higher Rikenellaceae
  • higher Roseburia
  • higher Acidaminococcaceae,
  • higher Flavonifractor,
  • higher Proteobacteria
  • lower Actinobacteria
  • lower Fusobacteria,
  • lower Ruminococcaceae,
  • lower Veillonellaceae 
  • lower Lachnospiraceae,
  • lower Dialister,
  • lower Escherichia/Shigella,
  • lower Firmicutes,
  • lower Haemophilus,
  • lower Prevotella,
  • lower Ruminococcus

Additionally, Isovaleric acid in stool correlates with human depression.[2016] hence isovaleric acid producing bacteria appear to be another facet.

Isovaleric acid producing bacteria includes [ref]:

  • Bacillus subtilis natto
  • Prevotella
  • Porphyromonas

Automated Analysis of your Ubiome

After you logged on to http://ubiomecfsweb.azurewebsites.net/  This Depression link will show your results against the above list. As a reminder, there are other comparisons available:

The result is a report such as shown below


At the bottom is a link to recommendations for the ‘Match’ items above only. That is, the recommendations are specific to the depression symptom.



For the first one on the list, I did a google and found lots of pages saying that pomegranate helps depression!

Imagine that! With the microbiome approach, you are getting truly individualized suggestions and not proforma suggestions.


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



Interview questions from a reader

A reader sent these questions to me


An Interview with Ken Lassesen

  • Antibiotics played a key role of all three of your remissions, is that correct?
    • Correct each time the working medical hypothesis was different
      • 1st time:  Antibiotic resistant walking pneumonia (this was before CFS existed as a syndrome, the 1970’s)
      • 2nd time: CFS proper
      • 3rd time: Lyme disease (which gave a rationale for prescribing the antibiotics – since there is more resistant to prescribe antibiotics)
  • What antibiotics did you use each time?
    • The one’s in the 1970, i do not recall. I remember rotating thru several
    • 2nd time:  doxycycline, minocycline (with Olive leaf), Azithromycin
    • 3rd time: minocycline, Amoxicillian – with Olive leaf, monolaurin, neem, tulsi etc.
  • How did you choose those particular antibiotics?
    • 1st time, because of the perception that we were dealing with an antibiotic resistant bacteria — the MD tried different ones
    • 2nd time, MD was following Dr. Jadin’s protocol 
    • 3rd time, ND was following a Lyme protocol (with some negotiation from me)
    • The non-prescription items were selected based on what would shift the bacteria dysfunction reported for CFS patients in 1998
  • You’ve written at length about the Jadin protocol, though it was many years ago. [I’ll include a link to your PDF] Have your thoughts about that protocol changed any, in the years since? How many other CFS patients do you know, who’ve tried it?
    • Getting patientcounts is always difficult because when it works, the person tends to disappear and gets back to normal life fast!
    • The published rate was 70-85% went to remission. I believe it is at least 50%. A problem is that the 15+% that it did not work for are the ones in the CFS community saying it does not work! (Sample bias)
    • The protocol is still an excellent approach if you do not have solid microbiome data to work from. With that data, you can become more selective in which one(s) to use — ideally with the 15-30% of non-responders decreasing.
  • The three times you developed CFS, were your symptoms largely the same, or was there some variability of symptoms?
    • Variability in symptoms
      • 1st time, “stress cough” and cognitive collapse.
      • 2nd time, cognitive and physical collapse, MCS for a while
      • 3rd time, digestive issues appeared with the above — this caused me to review the literature in this area and I re-discovered the 1998 papers (which I had dismissed in 1999 because there was no gut issues apparent!)
  • Based on your surveys of readers, what antibiotics seem most effective, for someone with CFS?
Much Better Better no change Worst Much Word Herx Stopped Odds Ratio
minocycline 2 3 1 2 2 0 125%
rifampicin 0 0 0 2 0 0 0%
doxycycline 5 5 2 3 1 1 200%
Azithromycin 4 9 2 1 2 0 433%
Ciprofloxacin 0 3 1 0 2 2 75%
Metronidazole 0 5 4 0 1 0 500%
Amoxicillian 0 4 2 5 2 2 44%
Bacitracin 0 2 0 0 0 0
Sulfacetamine 0 1 0 3 0 1 25%
Tinidazole 1 4 1 1 0 0 500%
  •   Ranked by odds of improving:
    • Metronidazole and Tinidazole
    • Azithromycin
    • Doxycycline
    • Minocycline
  • From what you’ve seen and read, what are the biggest risks of taking antibiotics to treat these conditions?
    • Severe herx — both the patient and the MD should be aware it may happen and what to do
  • If you had to take antibiotics again, would you combine them with probiotics? If so, which probiotics come to mind, for which antibiotics?
  • Your model posits that, for most CFS cases, an illness depleted their E. coli population, and without E. coli, pathogens were able to take up residence and kill the Bifidobacterium and Lactobacillus, among others. What studies led you down this path, about the key role played by E. coli?
    • Actually my model is a stable persistent dysfunction of the microbiome. This can have many favors. Deleted E.Coli is a presentation that fits the data and is simple for brain fogged CFS patients to understand. 
    • What lead me down the stable persistent dysfunction was finding that the microbiome shift reported in 1998 and the protocol of Jadin were a match. Her protocol would counter the typical microbiome shift seen. Trying that hypothesis on for size (i.e. seeing if it’s prediction agrees with studies), found more and more agreement.   Once the model has shown to hold water, then the non-responders made sense — they were different bacteria shifts that caused equivalent changes in the body’s metabolites but those bacteria may be resistant to these antibiotics.

For the technical minded, I…

For the technical minded, I have just add a partial list of the articles that I am using.

A possible subset of CFS with a smelly symptom

This week I got an email from activist in another under served medical condition, she wrote ” Preliminary microbiome results are most similar to CFS. “. In another sense, it’s may be a variation of SIBO. There is a DNA component (as there is with CFS, FM, IBS).

A list of common symptoms include:

  • Fatigue
  • Anxiety
  • Especially temperature sensitivity,
  • Presence sensitivity, “sometimes all it takes is another person coming next to me before I get extremely hot and a prickly sensation comes over my body, this usually comes with the odor getting worse for a few moments and it’s not related to anxiety as once I get these symptoms I’ll look around and then realize someone is there”
  • General malaise
  • Randomly getting very tired
  • Recurrent sore throat
  • Bruxism
  • Difficulty processing information at times.

Some web links

Despite being known for 3000 years, still little understanding.  Trimethylamine is common in most food. it can be created by bacteria from almost any food, especially rich in protein; indoles (foods such as Brussel sprouts) inhibit enzyme “deodoryzing” trimethylamine in our liver. And, worst of all, almost nothing is known about trimethylaminuria-negative cases


  • CLINICAL CHARACTERISTICS:Primary trimethylaminuria is characterized by a fishy odor resembling that of rotten or decaying fish that results from excess excretion of trimethylamine in the urine, breath, sweat, and reproductive fluids. No physical symptoms are associated with trimethylaminuria. Affected individuals appear normal and healthy; however, the unpleasant odor often results in social and psychological problems. Symptoms are usually present from birth and may worsen during puberty. In females, symptoms are more severe just before and during menstruation, after taking oral contraceptives, and around the time of menopause. [2015]
  • “The fish malodor syndrome (also known as the fish odor syndrome and trimethylaminuria) is a metabolic disorder characterized by the presence of abnormal amounts of the dietary-derived tertiary amine, trimethylamine, in the urine, sweat, expired air, and other bodily secretions. Trimethylamine itself has the powerful aroma of rotting fish, and this confers upon the sufferer a highly objectionable body odor, which can be destructive to the personal, social, and work life of the affected individual… known since 1000BC from Mahabharata (Indian Epic)” [2001]
    • “George Preti has been working on it for 30+ years, but as his latest paper showed they can’t connect even the most severe case of TMAU to one gene” from reader
  • ” Our studies include patients who have been referred to us after being examined by numerous clinical specialists with no identification or relief from their problem. This is due in part to the intermittent nature of many of these problems as well as an apparent lack of knowledge concerning many of these metabolic problems and their relation to oral symptoms.” [1992]
  • “Individuals with the metabolic disorder trimethylaminuria may sporadically produce malodors despite good hygiene. The psychosocial impact of trimethylaminuria can be considerable. However, trimethylaminuria is difficult to diagnose without specialized tests, in part because odor production is diet-dependent, and malodors may not be present during medical examinations. Thus, the prevalence and demographics of trimethylaminuria remain unclear… Consistent with previous reports, women, particularly African American women, were significantly overrepresented among trimethylaminuria-positive patients.” [2011] – Same situation as with CFS/FM — more women than men.
    • “not necessarily – our pilot programs had more men, men are more likely to take risks, pay for experimental tests and test new treatments” reader

Clinical Studies

Current Treatment

“Treatment of manifestations: Dietary restriction of: Trimethylamine (present in milk obtained from wheat-fed cows) and its precursors including choline (present in eggs, liver, kidney, peas, beans, peanuts, soya products, and brassicas [Brussels sprouts, broccoli, cabbage, cauliflower]), lecithin and lecithin-containing fish oil supplements; Trimethylamine N-oxide (present in seafood [fish, cephalopods, and crustaceans]); Inhibitors of FMO3 enzyme activity such as indoles (found in brassicas). Use of: Acid soaps and body lotions to remove secreted trimethylamine by washing; Activated charcoal and copper chlorophyllin to sequester trimethylamine produced in the gut; Antibiotics (metronidazole, amoxicillin, and neomycin) to suppress production of trimethylamine by reducing bacteria in the gut; Riboflavin supplements to enhance residual FMO3 enzyme activity. Prevention of secondary complications: Planning and monitoring of diet to ensure that the daily intake of choline and folate meets recommendations for age and sex; no restriction of dietary choline during pregnancy and lactation. Agents/circumstances to avoid: Foods with a high content of precursors of trimethylamine or inhibitors of FMO3 enzyme activity (seafoods: fish, cephalopods, and crustaceans), eggs, offal, legumes, brassicas, and soya products; food supplements and “health” foods that contain high doses of choline and lecithin; drugs metabolized by the FMO3 enzyme; circumstances that promote sweating (exercise, stress, and emotional upsets). ” [2015]

  • “Dr. Shephard now admits dietary restrictions are even more complicated – other food compounds that should be avoided are Ergothioneine, betaine. And the network of microbes messing up with it is quite large ” – reader

New Symptoms Added for this subset

The following overlap in some cases, and do not in others

  • Comorbid: Malodor
    • Any type of odor problem of uncertain origin
  • Comorbid: Trimethylaminuria
    • Ideally with a positive test
  • Comorbid: Proximity triggered Malodor
  • Comorbid: Chronic Halitosis
    • A differentiation (see [2007])
  • Autonomic Manifestations: Chemical Smelling Urine (atypical)

If the CFS diagnosis masked reporting malodor, please update your symptoms.

For new Malodor readers with uBiome




A post from a reader on microbiome mechanism

Ben posted this on an earlier post, I thought that it should be presented as a reader post.

This article may be of interest:

The researchers identified a new mechanism where repeated exposure to typical food poisoning pathogens lead to a chronic disease state that did not resolve by itself, even after the pathogens were cleared, and even if the levels of pathogen were less than is needed to produce acute food poisoning symptoms (so the hosts may not have been aware).
The mechanism is to do with an acquired deficiency of an important gut inflammation mediating enzyme – called Intestinal Alkaline Phosphatase ( IAP)

Without this enzyme, the host is unable to deal with normal bacterial toxins from even beneficial microbes in the gut, and a cascade of damaging inflammation is created in a self-perpetuating cycle.

  • This leads to a big list of symptoms that are a pretty good match to much of what is described in CFS
    •  Inflammation of Colon and Small Intestine
    • Leaky Gut (small intestine membrane permeability)
    • Weight loss (likely indicates malabsorption)
    • diahrea (or altered bowel habit)
    • faecal blood – and prolapsed anus
    • colon shortening
    • systemic inflammation (host of inflammatory cytokines are increased by up to 26 fold)
  • It’s pretty easy to see this might lead to further symptoms in a chain of events
    • disrupted metabolism (due to systemic inflammation, oxidation etc )
    •  fatigue ( due to malabsorption, leaky gut or systemic inflammation etc)
    •  allergy / food sensitivity ( due to gut permeability)
    •  systemic cell aging – neuraminidases are known to regulate the aging of various enzymes and cells in the body
    •  hormonal / sympathetic nervous system disorders – again from systemic inflammation (dysregulated sleep, blood pressure, temperature, mood, etc
    •  neurological disorders – again from inflammation, dysbiois (memory, cognitive function, etc etc )
    •  clotting disorders – Neuraminidases are known to interfere with both cell membrane and clotting mechanisms

I mention it here as it’s a possible explanation or underlying model describing the experiences discussed here.

The fit seems very good.

Interestingly the condition also causes the host to lose control of the gut microbiota population resulting in imbalance in the proportions of beneficial and pathogenic strains. Further re-enforcing the cycle – and would match many of the gut symptoms reported by sufferers. And echo the Ubiome reports of people here.

Neuraminidases are also known to cause disruption of the clotting mechanisms in humans – so this could explain the link to red blood cell morphology in CFS sufferers and sticky blood as discussed here.

It would also explain the prolonged ‘Herx’ reactions that many sufferers report. When the mainstream view is that any true Herxheimer reaction lasts only a few days as microbes in the blood are killed. But, if an overactive immune response to the LPS toxins of microbes in the gut is responsible then we would indeed expect a long-term reaction as it is just not practical to kill all bacteria in the gut with these treatments.

Also – in another interesting avenue; Neuraminidases are used by viruses to multiply their infection rate in the host cells. In fact, Anti-viral drugs for Flu e.g. Tamiflu are neuraminidase inhibitors. This could potentially therefore be an explanation for CFS sufferers becoming susceptible to infection with and developing chronic forms of viruses such as EBV, CMV, Herpes Simplex etc. that other people clear (as described by many Physicians specialising in CFS, Eg Myhill, Cheney etc.). As higher circulating neuraminidases may benefit viruses and hamper the human immune system.

Finally, CFS is common, at over 1% of the population by most counts, so whatever causes it is more likely to be something that lots of people are exposed to like mild food borne pathogen exposure – rather than some rare pathogen that few people will be exposed to. So, it fits with the epidemiology.

The researchers prevented the condition developing with co-commutant supplementation with additional IAP – or a neuraminidase inhibitor. Both worked well, leading to the question of whether neuraminidase inhibitors – either natural forms (btw. I think turmeric may include them) – or pharmaceutical, could be useful in reversing CFS with gut symptoms in humans. Or IAP for that matter – there are some human trials of it in IBD already.

There is a summary here http://science.sciencemag.org/content/358/6370/eaao5610
Or the full study text here http://nizetlab.ucsd.edu/Publications/Gut-Inflammation.pdf

The study is in mice – so the usual provisos apply.

I wasn’t sure where was best to post this – but since Giardia is a gut pathogen i thought this would work – but feel free to move it.

I would be interested in others thoughts.

Intestinal Alkaline Phosphatase

  • ” IAP is an endogenous protein expressed by the intestinal epithelium that is believed to play a vital role in maintaining gut homeostasis. Loss of IAP expression or function is associated with increased intestinal inflammation, dysbiosis, bacterial translocation and subsequently systemic inflammation. As these events are a cornerstone of the pathophysiology of many diseases relevant to surgeons,” [2016]
  • “The present review analyzes the earlier literature on the dietary factors modulating IAP activity in light of these new findings. IAP regulates lipid absorption across the apical membrane of enterocytes, participates in the regulation of bicarbonate secretion and of duodenal surface pH, limits bacterial transepithelial passage, and finally controls bacterial endotoxin-induced inflammation by dephosphorylation, thus detoxifying intestinal lipopolysaccharide. Many dietary components, including fat, protein, and carbohydrate, modulate IAP expression or activity and may be combined to sustain a high level of IAP activity. In conclusion, IAP has a pivotal role in intestinal homeostasis and its activity could be increased through the diet. This is especially true in pathological situations (e.g., inflammatory bowel diseases) in which the involvement of commensal bacteria is suspected and when intestinal AP is too low to detoxify a sufficient amount of bacterial lipopolysaccharide.” [2010]
  • “Intestinal alkaline phosphatase (IAP) plays an essential role in intestinal homeostasis and health through interactions with the resident microbiota, diet and the gut. IAP’s role in the intestine is to dephosphorylate toxic microbial ligands such as lipopolysaccharides, unmethylated cytosine-guanosine dinucleotides and flagellin as well as extracellular nucleotides such as uridine diphosphate. IAP’s ability to detoxify these ligands is essential in protecting the host from sepsis during acute inflammation and chronic inflammatory conditions such as inflammatory bowel disease. Also important in these complications is IAP’s ability to regulate the microbial ecosystem by forming a complex relationship between microbiota, diet and the intestinal mucosal surface. Evidence reveals that diet alters IAP expression and activity and this in turn can influence the gut microbiota and homeostasis. IAP’s ability to maintain a healthy gastrointestinal tract has accelerated research on its potential use as a therapeutic agent against a multitude of diseases. Exogenous IAP has been shown to have beneficial effects when administered during ulcerative colitis, coronary bypass surgery and sepsis. There are currently a handful of human clinical trials underway investigating the effects of exogenous IAP during sepsis, rheumatoid arthritis and heart surgery.” [2014]

SelfHacked.Com has an interesting post on this.