In an earlier post, I had illustrate the problem of whether L.Reuteri produced histamine. The answer is “Not sufficient information to answer” — why is shown below. It depends on which strain you have! The source (human/not human) is not sufficient. In general, the probiotic species is insufficient to answer the histamine question.

• Individual strains of Lactobacillus paracasei differentially inhibit human basophil and mouse mast cell activation [2016] “Thus, L. paracasei CNCM I‐1518 could not only inhibit mouse mast cell and human basophil activation 19, but also protect mice from Salmonella Typhimurium infection 31, induce regulatory T cells in skin inflammation model 32, and improve allergic rhinitis in children 33. These studies, which focused on one or a few strains of bacteria, did not permit an accurate comparison of the effects of different bacterial strains.“

Lactobacillus Casei and Paracasei

On many studies, this is reported to reduce hay fever and allergies. If you check the web, you will find that it is also reported as a histamine producer. How can this be true since increased histamines would make allergies worst. The answer is simple. BOTH ARE CORRECT when you look at the fine print… (and you need the fine print that may be missing on the probiotic label).

• “histamine production were found in … Lactobacillus casei 18, isolated from cider)” [2013]
• “According to the results,  Lactobacillus casei CCDM 198 exhibited the best degradation abilities…. significantly (P < 0.05) reduced BAs (putrescine, histamine, tyramine, cadaverine), up to 25% decline in 48 h.” [2020]
• ” Lb. paracasei subsp. paracasei CB9CT and another strain (CACIO6CT) of the same species that was able to degrade all the BAs were singly used as adjunct starters for decreasing the concentration of histamine ” [2016]
• “Seventeen isolates were found that were able to degrade tyramine and histamine in broth culture. All 17 isolates were identified by 16S rRNA sequencing as belonging to Lactobacillus casei.” [2012]

For Lb Casei and Paracasei, most of the studies suggests that it degrades histamine.

Worked Example

We use L. Casi and L. Paracasei from Custom Probiotics, for two main reasons, they are the cheapest per BCFU, they have no fillers, pre-biotics, etc so we do not have to deal with counter-indicated formulation that often happens with commercial probiotics blends (often using a marketing-driven formulation).

So looking up the strains, I see Lc-11 and Lpc-37, Time to search for information on these:

On LPC-37

• Lacticaseibacillus paracasei Lpc-37® improves psychological and physiological markers of stress and anxiety in healthy adults: a randomized, double-blind, placebo-controlled and parallel clinical trial (the Sisu study) [2020]
• The immune system in healthy adults and patients with atopic dermatitis seems to be affected differently by a probiotic intervention [2008] use Lpc-37
• The influence of Lactobacillus Paracasei LPC-37 on selected properties of fermented sausages [2015]

On Lc-11

• Obesity and gut microbiome: review of potential role of probiotics [2021] “In obese women, the administration of a probiotic mix composed of L acidophilus LA-14, L casei LC-11, L lactis LL-23, and B bifidum BB–06, improved BW composition after an 8-week supplementation period. A”
• Title: Enumeration of probiotic strain Lactobacillus casei Lc-11 using viability real time PCR [2019]
• I also found this table that is helpful for those taking antibiotics.
  

Bottom Line

IMHO, you need to:

• Know every strain in your probiotics (not just species!)
• You need to be able to locate studies using that strains (Lb. Casei Snakeoild may be just a marketing name to hide that fact that the manufacturer/packager does not know the strain)
  • I have seen some product literature claiming benefits from a different strain because they were the same species —FALSE LOGIC.
• Ideally, you will find some relevant studies using these strains — ideally on humans!

If you are using antibiotics, you may wish to search for the probiotics antibiogram. Ideally, the manufacturer/seller would provide all of that information with a simple email requesting it.

This is an area that I became aware of a decade ago and used this knowledge to discard some suggestions and take other suggestions based on the physical characteristics of the brain. This has major implication for brain fog, autism, ME/CFS, depression, Alzheimer’s, Long Haul Covid and many many more conditions.

The literature

“Research on disease-modifying treatments for  central nervous system  [CNS] diseases have generated a cemetery of failed drugs, rejected in part because of their incapacity to cross the BBB” [3,4,5,6,7]. 

The Molecular Weight [MW] threshold of BBB drug transport of small molecules has been demonstrated previously in studies of drug penetration into the brain.^33, 34 Blood–brain barrier permeation decreases 100-fold when the size of the drug is increased from an MW of 300 Da, which corresponds to a surface area of 50 square angstroms, to an MW of 450 Da, which corresponds to a surface area of 100 square angstroms.³⁵

Drug transport across the blood–brain barrier [2012]

• Disease-Induced Modulation of Drug Transporters at the Blood–Brain Barrier Level [2021] Hints that some infections/conditions may drop the threshold lower.
• Low Molecular Weight (poly)Phenol Metabolites Across the Blood-Brain Barrier: The Underexplored Journey [2021]

I remember that for my treatment of ME/CFS back in 2000, Low Molecular Weight Heparin was what was advocated. It was found far more effective than normal heparin (and costed 30+time more!!)

Getting information on Molecular Weight

What is Da? It’s Dalton — “Measure of molecular weight or molecular mass. One molecular hydrogen molecular atom has molecular mass of 1 Da, so 1 Da = 1 g/mol.” This information is often available on Wikipedia in the left hand column as molecular mass. i.e. 457.483 g·mol⁻¹ –> 457 Da

Information is also available at https://pubchem.ncbi.nlm.nih.gov/

If there is a choice, you want the smallest number. Remember we are talking 100x LESS getting thru with an increase of weight by 50%! Some examples:

• Piracetam: 142.16 g/mol – this has always been an excellent removal of brain fog for me!
• Niacin: 123.11 g/mol — also helps me with brain fog
• Vitamin C: 176.12 g/mol
• alpha-Lipoic acid: 206.3 g/mol
• Quercetin: 302.23 g/mol
• Curcumin: 368.4 g/mol
• Vitamin D: 384.6 g/mol
• Rutin: 610g/mol
• Heparin (compound): 1134.9 g/mol – hence why low molecular weight heparin worked better!
• Cyanocobalamin (Vitamin B12): 1355.4 g/mol — would not expect any impact on cognitive issues
• Antibiotics:
  • Tetracycline: 444.4 g.mol
  • Doxycycline: 444.4 g.mol
  • Minocycline: 457.5 g/mol
  • Azithromycin: 749 g/mol
  • Vancomycin 1449.2 g/mol

Bottom Line

The concept of “needing to take anti-inflammatories for brain inflammation” is correct — the gotcha is that many of the items you may take will never reach the brain because they are too big! Go thru your lists (and suggestions from others) and trim them down to the light molecular weight ones. You will likely get much better success — I did!

I’ve recently added computations for Methane and Hydrogen using KEGG data to Microbiome Prescription. Checking the contributed symptoms, I had over 120 samples with SIBO indicated. So it was time to test the hypothesis.

Charts

What about the old Methane?

The old computation was done on adhoc gathered associations from the literature. It also did not show any patterns.

Bottom Line

With the obvious path being unsuccessful, then time to examine where we did find associations.

ProductName	Pattern
(4R,5S)-4,5,6-trihydroxy-2,3-dioxohexanoate	Between 33%ile to 66%ile
cob(II)yrinate a,c diamide	Between 66%ile to 100%ile
D-tagatose	Between 0%ile to 33%ile
undecaprenyl phosphate	Between 0%ile to 33%ile

EndProduct	Pattern
Vitamin B9 (Folic Acid/Folate)	Between 66%ile to 100%ile
Lactic acid	Between 0%ile to 33%ile
2-Butanone	Between 66%ile to 100%ile
Hydrogen cyanide	Between 66%ile to 100%ile
Methyl thiocyanide	Between 66%ile to 100%ile
Propionate	Between 66%ile to 100%ile
Vitamin K	Between 66%ile to 100%ile
Vitamin B7 (biotin)	Between 66%ile to 100%ile
Sialic acid	Between 66%ile to 100%ile
Norepinephrine	Between 66%ile to 100%ile

EnzymeName	Pattern
succinyl-CoA:acetate CoA-transferase	Between 33%ile to 66%ile
phosphoenolpyruvate carboxykinase (GTP)	Between 33%ile to 66%ile

Definition	Pattern
Pentose phosphate pathway (Pentose phosphate cycle)	Between 75%ile to 100%ile
Pentose phosphate pathway, oxidative phase, glucose 6P => ribulose 5P	Between 75%ile to 100%ile
Pentose phosphate pathway, non-oxidative phase, fructose 6P => ribose 5P	Between 75%ile to 100%ile
Serine biosynthesis, glycerate-3P => serine	Between 75%ile to 100%ile
Histidine degradation, histidine => N-formiminoglutamate => glutamate	Between 75%ile to 100%ile
Riboflavin biosynthesis, plants and bacteria, GTP => riboflavin/FMN/FAD	Between 75%ile to 100%ile
Tetrahydrofolate biosynthesis, GTP => THF	Between 75%ile to 100%ile
CAM (Crassulacean acid metabolism), light	Between 75%ile to 100%ile
Lysine biosynthesis, DAP dehydrogenase pathway, aspartate => lysine	Between 75%ile to 100%ile

tax_name	tax_rank	Pattern
Blautia hansenii	species	Between 33%ile to 66%ile
Filifactor alocis	species	Between 66%ile to 100%ile
Bacteroidia	class	Between 66%ile to 100%ile
Bacteroides gallinarum	species	Between 66%ile to 100%ile

Last, we look at what studies reported

Tax Rank	Tax Name	Shift	Distribution	Citation Link
genus	Enterococcus (NCBI:1350 )	High	Distribution	📚 PubMed
genus	Klebsiella (NCBI:570 )	High	Distribution	📚 PubMed
genus	Prevotella (NCBI:838 )	High	Distribution	📚 PubMed
genus	Salmonella (NCBI:590 )	High	Distribution	📚 PubMed
genus	Staphylococcus (NCBI:1279 )	High	Distribution	📚 PubMed
genus	Streptococcus (NCBI:1301 )	High	Distribution	📚 PubMed
phylum	Firmicutes (NCBI:1239 )	Low	Distribution	📚 PubMed
species	Acinetobacter baumannii (NCBI:470 )	High	Distribution	📚 PubMed
species	Bacteroides fragilis (NCBI:573 )	High	Distribution	📚 PubMed
species	Bifidobacterium longum (NCBI:216816 )	Low	Distribution	📚 PubMed
species	Enterococcus faecalis (NCBI:1351 )	High	Distribution	📚 PubMed
species	Enterococcus faecalis (NCBI:1351 )	Low	Distribution	📚 PubMed
species	Enterococcus faecium (NCBI:1352 )	High	Distribution	📚 PubMed
species	Escherichia coli (NCBI:562 )	High	Distribution	📚 PubMed
species	Escherichia coli (NCBI:562 )	High	Distribution	📚 PubMed
species	Methanobrevibacter smithii (NCBI:2173 )	High	Distribution	📚 PubMed
species	Methanobrevibacter smithii (NCBI:2173 )	High	Distribution	📚 PubMed
species	Pseudomonas aeruginosa (NCBI:287 )	High	Distribution	📚 PubMed

Looking at the “usual suspect” for SIBO, Methanobrevibacter smithii, a methane producer, we found only 23 samples with any (and all of the labs associated with these samples reports this bacteria so over 100 (80%) of the people reporting SIBO had none appearing)

Tentatively conclusion, SIBO does not leave any clear tracks in a 16s Sample.

It is that season again — and some areas are reporting much higher levels than usual (with predictions for it getting worst). Some people will load themselves up daily on antihistamine, for example, Diphenhydramine HCl , which impacts over 800 different bacteria. We do have a profile of the bacteria shifts seen on Microbiome Prescription.

Supplements

The bad news is that we have lots of studies, but no good studies — all of them have problems…

” A total of 57 062 articles were derived from searching seven online databases and evidence from 48 RCTs and 10 observational studies were reviewed for methodological quality and risk of bias. No qualitative studies meeting the inclusion criteria could be found, therefore only a quantitative review was performed. ”

Health supplements for allergic rhinitis: A mixed-methods systematic review [2020]

• Association of Serum Vitamin D and Immunoglobulin E Levels With Severity of Allergic Rhinitis [2021] ” vitamin D deficiency is associated with increasing severity of allergic rhinitis symptoms.” [2021 ]
  • “This MR study found no evidence supporting a causal association between serum 25(OH)D levels and risk of AR, AS and NAR in European-ancestry population. ” [2021]
• Effects of vitamin E and selenium on allergic rhinitis and asthma pathophysiology [2021]
  “Our results indicated that vit E could attenuate allergic rhinitis and asthma symptoms; nevertheless, treatment with Se alone was not effective in controlling allergic symptoms. ” [2021]

Probiotics?

Lactobacillus

“Probiotics may be beneficial in improving symptoms and quality of life in patients with allergic rhinitis; however, current evidence remains limited due to study heterogeneity and variable outcome measures. Additional high-quality studies are needed to establish appropriate recommendations.”

A systematic review and meta-analysis of probiotics for the treatment of allergic rhinitis [2015]

Probiotic Potential of Lactobacillus Species in Allergic Rhinitis [2021 – full text] is a recent review with two appearing to be most likely effective (to some extent): Lactobacillus Casei and the closely related Lactobacillus Paracasei with dosages up to 30 billion CFU/day. These happen to be less than the suggested dosages from Custom Probiotic.

Bifidobacterium

If we look at Nat.Lib.of Medicine studies at Microbiome Prescription, we do not see any reports of low Lactobacillus. What we do see is low Bifidobacterium) ( Bifidobacterium longum , Bifidobacterium adolescentis, Bifidobacterium catenulatum) and Clostridium butyricum. Logically those seem better candidates!

• Probiotic NVP-1703 Alleviates Allergic Rhinitis by Inducing IL-10 Expression: A Four-week Clinical Trial[2020], a mixture of Bifidobacterium longum and Lactobacillus plantarum… ” Therefore, NVP-1703 can be treatment option for perennial AR.” [2019]
• [Allergic rhinitis management:environment control and patient education].[2017], combined clostridium and bifidobacterium capsules(called Changlekang) – good results
• Probiotics ( Lactobacillus gasseri KS-13, Bifidobacterium bifidum G9-1, and Bifidobacterium longum MM-2) improve rhinoconjunctivitis-specific quality of life in individuals with seasonal allergies: a double-blind, placebo-controlled, randomized trial [2017] “This combination probiotic improved rhinoconjunctivitis-specific quality of life during allergy season for healthy individuals with self-reported seasonal allergies; however, the associated mechanism is still unclear. “
• Bifidobacterium mixture (B longum BB536, B infantis M-63, B breve M-16V) treatment in children with seasonal allergic rhinitis and intermittent asthma [2017] “Children treated with probiotic mixture achieved a significant improvement of symptoms “

Bifidobacterium longum produces a rich collection of end products (1,380), the absence of which may account for hay fever.

Bottom Line

I suspect Placebo effect and poor study construction has resulted in the fuzziness for supplements and lactobacillus probiotics. The Nat.Lib.of Medicine profiles points to some specific bacteria that are low and the available studies, appear to suggest that taking those bacteria as probiotics will significantly improve hay fever. The list is:

• Bifidobacterium longum ,
• Bifidobacterium adolescentis,
• Bifidobacterium catenulatum) and
• Clostridium butyricum i.e. Miyarisan

Adequate Vitamins D and E supplementation may also help. I use the word adequate because often the dosages suggested in some studies are insufficient to alter blood level by any reasonable amount in a month (see this post for a formula ) – hence “no effect”.

There is one more path to consider, getting suggestions explicit for the shifts reports.

The results are shown below

We see L.Casei, L. Paracasei and Clostridium butyricum on the recommended list — in agreement with the above. Further down, we see Selenium (cited above) also listed

The above is evidence based on the microbiome shifts seen with hay fever.

This morning I chatted 90 minutes with another data scientist about the microbiome. After the video chat he sent me a link to this recent article: From IBS to ME – The dysbiotic march hypothesis [2020]

” The pathogenesis of the relationship is unknown. Intestinal dysbiosis may be a common abnormality, but based on 1100 consecutive IBS patients examined over a nine years period, we hypothesize that the development of the disease, often from IBS to ME, actually manifests a “dysbiotic march”. In analogy with “the atopic march” in allergic diseases, we suggest “a dysbiotic march” in IBS; initiated by extensive use of antibiotics during childhood, often before school age. Various abdominal complaints including IBS may develop soon thereafter, while systemic symptom like CFS, fibromyalgia and ME may appear years later.”

Related to the above:

• How Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) Progresses: The Natural History of ME/CFS [2020]
• Can You Trust Your Gut? Implicating a Disrupted Intestinal Microbiome in the Progression of NAFLD/NASH [2020]
• Microbial transitions from health to disease [2021] “dysbiotic microbial populations may be important in the development of approaches to prevent the progression of disease and to restore health in diseased individuals.”

Personally, I have seen someone progress from GERDs to IBS to Chronic Fatigue Syndrome to atypical Crohn’s disease. The progression is not deterministic, with DNA being a significant factor.

I have had on my todo list, creating a microbiome progression map. I have just added it (based solely on gold-standards PubMed studies). It can be seen via https://microbiomeprescription.com/Library/PubMed

When you click the crystal ball . you will be taken to a new page. For example, IBS

Bottom Line

This is based on PubMed studies which are often hit and miss for depth of analysis and reporting shifts. Over time, I expect data to improve and the forecasts on this page to improve.

A Periodic Review of PubMed for COVID Fecal Microbiome finally found some studies:

One paper reported very very good results!

The optimal eight oral microbial markers (seven faecal microbial markers) were selected by fivefold cross-validation
on a random forest model, and the classifier based on the optimal microbial markers was constructed and achieved an area under the curve (AUC) of 98.06% (99.74% in the faecal microbiome).”

Alterations in the human oral and gut microbiomes and lipidomics in COVID-19 [2020]

“The heatmap showed that the faecal microbial community in CPRs (Confirmed Patients Recovered) was different from that in CPs (Confirmed Patients) and HCs,(Healthy Controls)” [SP is suspected Patient, SPR is suspected Patient recovered] which appears to confirm my hypothesis that most infections will leave a “garbage state” in the microbiome which will generally shift slowly back to the healthy state. This return to a healthy state is not certain and when it fails to happen, then we have diagnosis such as long haul covid, chronic fatigue syndrome, and post-infection syndrome.

More coming…

This month (Feb 2021) there as a major article Structural and Functional Dysbiosis of Fecal Microbiota in Chinese Patients With Alzheimer’s Disease released. I have updated my list of bacteria (with links to source studies),

This post is for caregivers that are interest in low risk treatment that theoretically have a high probability of success and low cost.

Short Summary of Approach

The microbiome produces some 4000+ different chemicals. For many conditions, especially “untreatable”, it appears that imbalances in these chemical mixtures result in cells, including brain cells, malfunctioning.

Some drugs help — and often those drugs were seen to alter the microbiome, correcting some of these shifts. The stupid question is this, if we know the bacteria that are involved — then why not starve or feed to put it into better balance.

IMHO It works! In my 50’s I had a sudden onset of cognitive issues, including memory. A SPECT scan was read as Early Onset Alzheimer’s. I also had another diagnosis. That other diagnosis has a bacteria shift pattern reported in 1998 in Australia. Making changes to alter that pattern caused the cognitive issues to fade and disappear.

Steps

You need to have a microbiome sample (done by taking a little bit of a stool and sending it to a lab). Then the data need to be upload to the free citizen science site, Microbiome Prescription. Not all labs are supported (i.e. they do not make their data available in a suitable format); those that are supported are listed here (with discount codes).

Once the data is uploaded, there are two Quick Suggestions links that generates suggestions using Fuzzy Logic Artificial Intelligence techniques.

There is a demo logic that show all of the features…. BiomeSight Example Login

There are a lot of tools there, depending on you skill sets and devotion to seeking improvement.

There is a YouTube Channel showing how to use this site and discussion of issues.

A reader contacted me about a disagreement and the cause was a bug in the code for Kaltoft-Moltrup — subsequently fixed. This post looks at the bacteria selected by each for similarities and differences — so people can better understand the difference (which is a little abstract).

I am going to use one the demo samples from BiomeSight (BiomeSight:2019-06-10 Self).

• Extreme 3% picked 29 bacteria
• KM picked 24 bacteria

I sorted their selections below in alphabetical order, 13 are in common (just over 50% of the KM choices).

Kaltoft-Moltrup	Extreme 3%
Actinomyces : Too High	Actinomyces : Too High
Actinomyces naturae : Too High
	Anaerofilum : Too High
Actinomycetaceae : Too High
Bacillales Family X. Incertae Sedis : Too High	Bacillales Family X. Incertae Sedis : Too High
Bacteroides cellulosilyticus : Too High
Bacteroides denticanum : Too High
	Bacteroides dorei : Too Low
Bacteroides intestinalis : Too Low	Bacteroides intestinalis : Too Low
Bacteroides rodentium : Too High	Bacteroides rodentium : Too High
Bacteroides sartorii : Too High	Bacteroides sartorii : Too High
	Bacteroides thetaiotaomicron : Too High
Bacteroides vulgatus : Too Low	Bacteroides vulgatus : Too Low
Blautia : Too High
Blautia obeum : Too Low	Blautia obeum : Too Low
	Brochothrix : Too High
	Brochothrix thermosphacta : Too High
	Chitinophagaceae : Too High
Clostridium paradoxum : Too High	Clostridium paradoxum : Too High
Coprobacillus : Too High
Coprococcus : Too High	Coprococcus : Too High
cunicula : Too Low
	Dehalogenimonas : Too High
Desulfovibrio vietnamensis : Too Low
Johnsonella : Too High	Johnsonella : Too High
Johnsonella ignava : Too High	Johnsonella ignava : Too High
	Lachnospira : Too High
Lactococcus : Too High	Lactococcus : Too High
	Leuconostoc : Too High
	Listeriaceae : Too High
	Micrococcaceae : Too High
Oscillospira : Too High
	Prevotellaceae : Too Low
Streptococcaceae : Too High
Streptococcus vestibularis : Too High	Streptococcus vestibularis : Too High
Sutterella : Too Low
	Syntrophobacteraceae : Too High
	Tetragenococcus : Too High
	Thiothrix : Too High
	Turicibacter sanguinis : Too Low

Looking at a chart of Prevotellaceae, we see that KM low is 2.25%, thus be this sample being between 2.25 and 3 resulted it being excluded on one and included on another. For Listeriaceae : Too High, KM used 95.6% instead of 97%.

For Sutterella, KM uses 22% for low, hence it included. This is reasonable because there is a distinctive drop off around that!

For Coprobacillus, it looks like I need to do some adjustments of the KM, a chunk of unusual data caused a “step” that incorrectly triggered the high computation.

Bottom Line

We have good overlap with the differences being due to the curves being different. With the extreme 3% approach, we are insensitive to the difference of shapes. With KM we are sensitive (and some parameters to the algorithm needs a little adjustment).

This is an analysis using a standard flow that I tend to use… The analysis was done using data from Thryve and uploaded to Microbiome Prescription.

Microbiome Functional Abnormalities

With the recent addition of KEGG information, my focus has shifted from a naive “this bacteria is too high or too low” to this enzyme or end-product is too high or too low. Why? Bacteria can substitute for each other.

Consider building a wall on a house. If you grow up in the US. Northwest, it will be 90% wood and 10% gypsum board. But walls may be built with steel framing, concrete siding, bricks, stones, logs, concrete blocks etc. Is a wall not built of 90% wood unsafe? No, the question should be how does the wall function for structure strength, insulation etc. It is the same with bacteria.

Three Functional Checks

End Product Abnormalities

At this point, the reader should copy and google information about each end product.

• “Indole may act as an interspecies signaling compound.” [src] translation: the bacteria internet is flaky
• Biogenic amines – these are neurotransmitters
• Bacteriocin: Lasso peptide – “It has varieties of biological activities, among which the most important one is its antibacterial efficacy.” [src] in other words is suppresses other bacteria

So the story appears to be bad communications between bacteria and the microbiome being bias towards those that tolerate the natural antibioitic, Bacteriocin: Lasso peptide.

Clicking thru to the bacteria involved, we find that the antibiotic effect is due to one bacteria, shown below. The Indole appears to be due to low Alistipes level (most common source, and has a low value)

I dropped filtering to 90% and only the enzymes show issue.

Core Supplements

The purpose of this is to identify items that may compensate for low amounts. There were none.

Predicted Symptoms

There was only one item that had strong likelihood:

 Impaired Memory & concentration|Neurological-Vision: Blurred Vision|

Pub Med Microbiome Reports

Cerebral palsy is not in my existing list of medical conditions, so I did a pub med search and found just two studies.

• The effect of different dietary structure on gastrointestinal dysfunction in children with cerebral palsy and epilepsy based on gut microbiota [2021]
  • “The gut microbiota of children with CP and epilepsy consuming a liquid diet had elevated levels of symbiotic pathogens and diminished intestinal barrier protection bacteria, relative to a general diet group. These differences in bacterial microbiota were associated with GI dysfunction symptoms.”

“The increased risk of “Neurodegenerative diseases” in CPE patients was probably attributed to Streptococcus, Parabacteroides, and Bacteroides ” [2019]

I added CP to the database with the bacteria shifts reported. And then ran for matches to the reported patterns

The top results for probiotics are shown below

In terms of diet additions:

As well as:

And diet avoidance

We note that some species of lactobacillus are on the to take and others to avoid. Different species produce different bacteriocins (natural antibiotics against other bacteria)

Bottom Line

The above changes will likely have a positive impact and should slow neurodegeneration. As always, these suggestions should be review by knowledgeable medical professional before starting. These are machine learning suggestions that is blinkered in terms of factors considered.

This set of tools is designed for two scenarios:

• One person who has had many samples of time. Typically that person is looking for outliers to reduce or disappear
• A family with samples from different members. Typically one person is challenged and since the family group has shared DNA and diet — the hope is that the bacteria grouping causing the challenge will be identified. Once identified, it may be actionable.
  • This scenario will have more tools added over the next weeks.

I have used them in these prior posts:

• New Features – Autism Children
• A family case study: DNA + Microbiome

If you have two or more samples uploaded, you will see the top two items on the Available Samples page. These may be collapsed into one over the next few weeks.

Clicking the right button of these two will take you to a sample selection page.

The program will list all items below that matches all samples OR all samples except 1 (but at least two).

I selected a group of 5 samples from when I was having a ME/CFS flare.

IMHO, it correctly identified what was wrong with me.

Doing some research, I found “. L-tryptophan is produced in the shikimate pathway from chorismate” Which lead to many ME/CFS articles on PubMed.

Again, it may take some research to understand what this is.

The cause of ME/CFS flare was stress and a quick search on PubMed found several articles where this genus increased with stress, the latest was “Gut Microbiota Are Associated With Psychological Stress-Induced Defections in Intestinal and Blood–Brain Barriers“[2020]

Bottom Line

This set of tools does not give immediate answers; it gives you leads to investigate. For myself, the findings plus the use of PubMed studies weaved a story of what happened that agrees with the literature. This is very important because ME/CFS contains dozens of subsets. Often I have seen that what is helpful for one subset is harmful for another. I suspect this also applies to other conditions, such as ASD/Autism.

In this case, it identified one key family to reduce. Identified enzymes that I was short on. Lead to a possible supplements that I should consider because of the dysruption.