Overview of this Blog and the Microbiome

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

Notes to Treating Physicians     Quick Self Start on treating CFS

Analysis of Microbiome/stool with recommendations

Site: has moved to http://microbiomeprescription.azurewebsites.net

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

Microbiome Definition of CFS/FM/IBS

A coarse condition that results from:

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

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

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

Replace the metabolites produced by the missing bacteria

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

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

Other Supplements Reported to Help

Bootstrapping Bifidobacterium and Lactobacillus

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

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

Bootstrapping E.Coli

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

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

Dealing with the other microbiome shifts

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

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

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

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

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


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.

Ozone Therapy – A Review

A reader forwarded me a link to: “Ozone therapy is an effective therapy in chronic fatigue syndrome:result of an Italian study in 65 patient” My initial take was that I was not surprised — why? Ozone kills some bacteria… but we need to dig deeper. Note: both Ozone and Hydrogen peroxide have one abnormal Oxygen atom that easily reacts. Hydrogen peroxide does wonders for killing bacteria on wounds.

First this study

What was done: “therapeutic shock of ozone autohemotherapy”

What was the result: “> 50% improvement in symptoms”

  • No one went into remission.
  • “symptoms” is way too subjective
  • “The practice of autohemotherapy carries significant risks without any health benefit. Patients have died. Plus, autohemotherapy has been an illegal practice in Germany since 1984, but you will find naturopaths advertising ozone therapy as “commonly used in Europe.” [www.naturopathicdiaries.com] – a very good read on legality in the US.

On PubMed

There are some 70 articles on ozone autohemotherapy many of them are from China.

Bottom Line

I would recommend a pass on this approach for three reasons:

  • No studies suggesting remission, just symptom improvement (whatever that means — especially given the placebo risk)
  • Real significant risks of adverse effects
  • Those offering it are likely violating laws or naive in understanding the full picture.

” Ozone as a medical therapy has been used in many medical conditions; unfortunately, however, like every other therapy, ozone therapy has side effects. The literature concerning ozone therapy supports possible strong vasoconstrictor and prothrombotic effects of ozone therapy, further supporting our suggestion that ozone can lead to acute coronary syndromes in human beings. In conclusion, to our knowledge, our case report reveals a possible complication of ozone therapy that has never been reported before. We think that this article will raise the awareness of the possibility of thrombotic complications after ozonated autohemotherapy. ” [2015]

Blood Type: Microbiome and Diet

One of my favorite sources for information on the microbiome is run by Dr. Peter J. D’Adamo. For many years he has advocated eating for your blood type. In this week’s issue of New Scientist. an article “Your gut bacteria may match your blood group – but we don’t know why

The difference between many blood types are sugars. [PDF]

These sugars are called antigens and help tell your immune system that your blood cells belong to you and shouldn’t be attacked. If an A person were to accidentally receive a transfusion of B blood, antibodies made by their immune system would react with the B sugar and flag these cells for destruction. ..
The team found that blood type wasn’t linked to any differences in the kinds of bacteria a person had. However, they noticed that bacteria seemed to be recognised by antibodies from different blood types, in a similar way to when antibodies detect incompatible blood cells.
This suggests that gut bacteria make sugars that match their host’s blood type. “We were very surprised to see this,” says Yin.

While some bacteria are already known to carry molecules that are similar to B antigens, this is the first indirect evidence that bacteria can have sugars that behave like A antigens too.

Gut microbiota have blood types as human
A blood antigen (GMA) and B blood antigen (GMB)

You can help build Blood Type Profiles of Microbiomes

Microbiome site is updated with the ability to record blood type with your microbiome. http://microbiomeprescription.azurewebsites.net

  • Login to see your uploaded sample.
  • Click on Analysis for your microbiome sample.
  • Click the item highlighted below

You will now see the ability to associate your blood type to your sample.

Remember to do this for each of your samples.

Bottom Line

Consider reading Peter’s eating for your blood type. Food impacts bacteria. I will be looking at the effort of filtering some suggestions by blood type in the next few weeks.

KEGGs and Inflammatory Bowel Disease

I often have attended the yearly talks of futurist/predictionist
Mark Anderson. This year there was talk about Mark’s new company, Pattern Computer.On that site I saw this interesting item

Insights in Inflammatory Bowel Disease

Using the Pattern Discovery Engine™ coupled with a hypothesis-free approach, we analyzed a large dataset of 50 human microbiome samples, each with the relative abundance of the ~10,000 KEGG protein families. We identified 39 KEGGs that were significant in differentiating the disease states from each other and from healthy, with 9 of the KEGGs (out of 10K total) being most associated with a dynamic path from disease to health in the human-gut microbiome. Using our approach we were able to reduce the size of the dataset to be analyzed by three orders of magnitude.

What is a KEGG?

KEGG (Kyoto Encyclopedia of Genes and Genomes) is a knowledge base for systematic analysis of gene functions, linking genomic information with higher order functional information. The genomic information is stored in the GENES database, which is a collection of gene catalogs for all the completely sequenced genomes and some partial genomes with up-to-date annotation of gene functions. The higher order functional information is stored in the PATHWAY database, which contains graphical representations of cellular processes, such as metabolism, membrane transport, signal transduction and cell cycle.

KEGG: Kyoto Encyclopedia of Genes and Genomes [2000]

Or in plain english, it is show what produces, consumes or influence processing of chemicals in nature (including the human body and the microbome in your gut).

We are getting into complex areas which makes a Gordian knot look like a straight piece of rope.

Their Draft Paper

Read the paper here. A chart from it is very interesting:

Further research into these nine KEGG protein families revealed that six of the nine KEGG protein families identified are related to oxidative phosphorylation. IBD, like other inflammatory diseases, may be associated with abnormal oxidative phosphorylation or oxidative stress [10]. Oxidative phosphorylation produces reactive oxygen species (ROS) in both prokaryotes and in the mitochondria of eukaryotes. Microbial ROS production affects the innate immune response, influencing the integrity of the intestinal epithelial barrier (2) which is compromised in IBD.

Path ways: K00330, K00348, K00351, K00434, K00604, K00607, K00609, K00633, K03671.

Bottom Line

While the sample sizes were small (and likely not widely distributed geographically), the results are definitely interesting. It does point to reducing oxidative phosphorylation and inhibiting reactive oxygen species as desired paths forward (and likely topics for future posts).

For people interested in watching the talk:

Mark Anderson’s 2019 Predictions

Lecithin: Friend, Foe or Neutral

I received several questions about Lecithin on Facebook and this blog after my last post on Emulsifiers. I cited one study that I found for illustration purposes:

Dietary carnitine (present predominately in red meat) and lecithin (phosphatidyl choline) are shown to be metabolized by gut microbes to trimethylamine (TMA), which in turn is metabolized by liver flavin monoxygenases (especially FMO3 and FMO1) to form trimethylamine-N-oxide (TMAO). High levels of TMAO in the blood strongly correlate with cardiovascular disease and associated acute clinical events.

Dietary modification of the microbiome affects risk for cardiovascular disease.[2013]

Many of the questions came from the belief that lecithin helps heal the gut. My goal is to see what has been found in studies listed on PubMed – my gold standard for separating urban-(medical)-legend from reasonable facts. I first look at conditions: There was nothing for Chronic Fatigue Syndrome.

Irritable Bowel Syndrome

There are no studies except with boswellia where it was used as a delivery mechanism.

Crohn’s Disease

“The most promising approach in UC seems to be the use of probiotics or the natural compound lecithin as a stabilizer of mucus structure to enhance the barrier…. ongoing phase III study … “

Improvement of a ‘Leaky’ Intestinal Barrier. [2017]

Note: that we have an “or” and “seems to be” — so no concrete results yet.

“Children with CD frequently consume food additives, and the impact on disease course needs further study. ( Mean exposures per day for xanthan gum was 0.96 ± 0.72, carrageenan 0.58 ± 0.63, maltodextrin 0.95 ± 0.77, and soy lecithin 0.90 ± 0.74.  )”

Children with Crohn‘s Disease Frequently Consume Select Food Additives. [2018]

Note: The authors are stating concerns about all of these food additives for Crohn’s Disease children

Ulcerative Colitis

In randomized controlled studies, delayed-release lecithin [phosphatidylcholine (PC)]  was proven to be clinically and endoscopically effective, which now awaits a phase III authority approval trial.

Lecithin as a therapeutic agent in ulcerative colitis. [2013]

Note: There were no results published for the phrase III study. If there are old studies indicating positive results and plans for more studies, but nothing is published, THEN most researchers would conclude that no positive results were obtained and thus the study was not published because it failed to produce intended results.

Issues Associated with Lecithin

 lecithin, choline, and carnitine) are converted by closely related gut bacterial TMA lyases to TMA, which is absorbed and converted predominantly by flavin mono-oxygenase 3 to the toxic trimethylamine N-oxide (TMAO). TMAO causes atherosclerosis in animals and is elevated in patients with coronary heart disease

New Insight into the Dietary Cause of Atherosclerosis: Implications for Pharmacology. [2016]

 No scientifically valid clinical studies exist on the safety and efficacy of high-dose lecithin supplementation in nursing mothers or infants. 

Lecithin. Drugs and Lactation Database (LactMed) [Internet]. Bethesda (MD): National Library of Medicine (US)

Bottom Line

It appears that some early studies saw improvement when a delayed- release dosage of lecithin was used (no information on the dosage). As these studies were on what appear to be a potential commercial product, the missing phrase III studies suggest that positive results were not found. What is more interesting to infer is the decision to use delayed release — it implies there were issues seen with direct lecithin (which likely were not published but known to the researchers).

There are reports of lecithin overdose and drug interference. There are no safety studies to determine what dosage is beneficial (and what level is harmful).

I conclude that current published evidence does not support the use of lecithin supplements.

Emulsifiers – making autoimmune flare again!

My eye caught a news story today Common food additive may impact gut bacteria, increase anxiety.

Earlier studies have shown that emulsifiers can alter the microbiome of mice, causing low-grade inflammation and increasing the risk of obesity and metabolic disorders.

study in humans concluded that gut bacteria “can be directly impacted by these commonly used food additives, in a manner that subsequently drives intestinal inflammation.”

The scientists showed that the emulsifiers did impact gut bacteria, but in different ways for male and female mice. They also showed that the changes in behavior were different between the sexes.

Specifically, they saw an increase in anxious behavior, particularly in male mice. In female mice, there was a reduction in social behavior.

A common one is polysorbate 80, which I have a page on the bacteria that it is known to change, here. It is often found in ice cream and cottage cheese. It is also in some vaccines.

Another one, cited above is carboxymethylcellulose (CMC)

Other emulsifers used in the US include [2017]:

  • lecithin [phosphatidylcholine (PC)]  ,
  • mono- and diglycerides (MDGs),
  • stearoyl lactylates,
  • sucrose esters, and
  • polyglycerol polyricinoleate.

For lecithin, we read:

Dietary carnitine (present predominately in red meat) and lecithin (phosphatidyl choline) are shown to be metabolized by gut microbes to trimethylamine (TMA), which in turn is metabolized by liver flavin monoxygenases (especially FMO3 and FMO1) to form trimethylamine-N-oxide (TMAO). High levels of TMAO in the blood strongly correlate with cardiovascular disease and associated acute clinical events

Dietary modification of the microbiome affects risk for cardiovascular disease.[2013]

Bottom Line

Checking products for any emulsifiers before buying (and asking your waiter when eating out, which menu items contains no emulsifiers) is strongly recommended — especially if you have any gut or anxiety issues.

Foods commonly containing emulsifiers are:

  • almost every processed food, from ice cream, to low fat cookies and salad dressing contains a wide range of emulsifiers that keep ingredients from separating, improve the texture and taste especially of low-fat foods, and increase shelf life. ” [src]
  • salad oils
  • some cottage cheese, some cheese (especially processed) and many yogurts [src]
  • ice cream
  • bread
  • chocolate
  • margarine
  • processed meat

Some of this list from an article entitled “The perfect mixture: emulsifiers make our food enjoyable” . IMHO, it needs a subtitle, “and do a number on your microbiome!’

A list of various names that may be on products [src]:

  •  Soya Lecithin Granules G
  • Soya Lecithin Powder P
  • (Ultralec® P & G)
  • Soya Lesithin-Powder,Granulate,Liquid
  • Distilled Glycerin Monostearate(D…
  • Potassium Stearate
  • Calcium Stearoyl Lactylate(CSL)
  • Glyceryl Monostearate
  • Mono Propylene Glycol
  • SPAN 80
  • Sodium stearoyl lactylate(SSL)
  • Tween
  • Sodium Stearate
  • Glycerol Triacetate
  • Sugar Esters
  • Polyglycerol Esters of Fatty Acid…
  • Non dairy creamer
  • Calcium Stearate
  • Polyglycerol Polyricinoleate (PGPR)
  • E No: E476
  • Soya Lecithin Liquid (Yelkin® TS)

Bottom line: Use the raw ingredients to prepare meals. Beware of all processed foods.

Intrinsic Factor and low Vitamin B-12 levels Cognitive Impact

What is Intrinsic Factor?

Intrinsic factor (IF), also known as gastric intrinsic factor (GIF), is a glycoprotein produced by the parietal cells of the stomach. It is necessary for the absorption of vitamin B12 later on in the ileum of the small intestine.[5] In humans, the gastric intrinsic factor protein is encoded by the GIFgene.[6]:989


With CFS/ME, Lyme and other conditions being low in Vitamin B12, suggests that an issue with GIF could have developed. This may be due to an epigenetic event. The incidence of defects in the GIF Gene is very low.

However, wikipedia is incomplete, because it is not only parietal cells.

These findings demonstrate a potential for cellular expression of human intrinsic factor in nonparietal cells. Because such expression occurs normally at the margins of anatomical gastric regions, it suggests that local factors may influence expression of intrinsic factor.

Human gastric intrinsic factor expression is not restricted to parietal cells. [1996]

These data in humans with and without gastritis are consistent with the hypothesis that local factors influence ectopic gastric IF expression, arising from either the anatomical location, the focal inflammation, or both.

Production of ectopic gastric intrinsic factor in gastric mucosa of humans with chronic gastritis [2011]

The earliest recorded history of autoimmune gastritis can be traced to 1849 in London, when Thomas Addison described “a very remarkable form of anemia” later called pernicious (fatal) anemia (PA). This was followed by the recognition of a gastric mucosal defect suspected to have a nutritional basis, the discovery of the megaloblast that characterized the anemia, the insufficiency of a dietary extrinsic factor characterized as vitamin B12 (cobalamin), and a gastric-secreted intrinsic factor. Treatment with vitamin B12 proved curative. The link between PA and gastritis and atrophy was first confirmed histologically after immediate fixation of the stomach postmortem and later, in the 1940s, by peroral tube biopsy. The causes of gastritis remained enigmatic until the era of autoimmunity, when autoantibodies were detected first to gastric intrinsic factor and then to gastric parietal cells. Hints of a dichotomy in pathogenesis of gastritis were crystallized by the description in 1973 of Type A (Autoimmune) and Type B (later, Bacterial) gastritis.

Autoimmune gastritis: historical antecedents, outstanding discoveries, and unresolved problems. [2005]

Proton pump inhibitors also reduce the absorption of vitamin B(12) probably by inhibiting intragastric proteolysis 

Effect of proton pump inhibitors on vitamins and iron [2009]

 The results suggest that IF insufficiency may occur during cimetidine treatment in patients 

Effect of cimetidine on intrinsic factor secretion stimulated by different doses of pentagastrin in patients with impaired renal function. [1983]

Issues reported in the literature with low B12, includes:

  • “The most common psychiatric symptoms were depression, mania, psychotic symptoms, cognitive impairment and obsessive compulsive disorder. Neurological involvement includes mainly combined spinal sclerosis, peripheral neuropathy and dementia. ” [2015]
  • “These symptoms seem to fall into several clinically separate categories: slow cerebration; confusion; memory changes; delirium, with or without hallucinations and/or delusions; depression; acute psychotic states; and (more rarely) reversible manic and schizophreniform states. ” [1988]

Bottom Line

From the literature, it is well established that one bacteria influences GIF, Helicobacter pylori. In terms of drugs that reduces GIF, we see these drugs impact a lot of bacteria families (linked to from drug below):

It appears that GIF production is influenced by the local environment/factors. An important factor for this is the microbiome – bacteria involved.


First choice is always to stop drugs that reduces GIF. Second choice, is to eliminate any known bacteria that reduces GIF, explicitly, testing for
Helicobacter pylori (you may lack symptoms and still have it). Third choice is supplementing with Vitamin B12.

Fourth choice (which may also impact the 2nd choice), probiotics that produces or processes B12.

Update on Parkinson’s and the Microbiome

A reader asked me to update my earlier posts (as well as

Blautia coccoides and Clostridium leptum produced the largest amount of hydrogen. Escherichia coli and Bacteroides fragilis constituted the second group that produced hydrogen 34- to 93-fold lower than B. coccoides. Bifidobacterium pseudocatenulatum and Atopobium parvulum constituted the third group that produced hydrogen 559- to 2164-fold lower than B. coccoides. Lactobacillus casei produced no detectable hydrogen. Assuming that taxonomically neighboring strains have similar hydrogen production, we simulated hydrogen production using intestinal microbiota that we previously reported, and found that PD patients produce a 2.2-fold lower amount of intestinal hydrogen compared to controls. 

Quantification of hydrogen production by intestinal bacteria that are specifically dysregulated in Parkinson’s disease [2018]

For what increases Blautia coccoides see this summary. In short:
arabinoxylan oligosaccharides (prebiotic) with rosemary, bernine, and cholic acid! No more red wine, smoking or walnuts!

Changes of Colonic Bacterial Composition in Parkinson’s Disease and Other Neurodegenerative Diseases. Several studies showed an increase of LactobacillusBifidobacterium, Verrucomicrobiaceae and Akkermansia in PD. A decrease of Faecalibacterium spp., Coprococcusspp., Blautia spp., Prevotella spp. and Prevotellaceae was observed in PD. 

Changes of Colonic Bacterial Composition in Parkinson’s Disease and Other Neurodegenerative Diseases. [2018]

Chronic stress-induced gut dysfunction exacerbates Parkinson’s disease phenotype and pathology in a rotenone-induced mouse model of Parkinson’s disease[2018].

Gut microbiome-based secondary metabolite biosynthetic gene clusters detection in Parkinson’s disease.[2018]

Although most of these differences were associated with disease duration, lower abundance in Lachnospiraceae was the only difference between de novo PD and HC (remaining lower across almost all PD duration strata). Decreased Lachnospiraceae and increased Lactobacillaceae and Christensenellaceae were associated with a worse clinical profile, including higher frequencies of cognitive impairment, gait disturbances, and postural instability. When compared with HC, MSA and PSP patients shared the changes in PD, with a few exceptions: in MSA, Lachnospiraceae were not lower, and Prevotellaceae were reduced; in PSP, Lactobacillaceae were similar, and Streptococcaceae were reduced.

Unraveling gut microbiota in Parkinson’s disease and atypical parkinsonism.

The following genera were enriched in the blood of PD patients: IsoptericolaCloacibacteriumEnhydrobacter and Microbacterium; whereas genus Limnobacter was enriched in the healthy controls after adjusting for age, gender, body mass index (BMI) and constipation. Additionally, the findings regarding these genera were validated in another independent group of 58 PD patients and 57 healthy controls using real-time PCR targeting genus-specific 16S rRNA genes. Furthermore, not only the genera Cloacibacterium and Isoptericola (which were identified as enriched in PD patients) but also the genera Paludibacter and Saccharofermentans were positively associated with disease duration. Some specific genera in the blood were related to mood disorders. We believe this is the first report to provide direct evidence to support the hypothesis that the identified microbiota in the blood are associated with PD. 

Detection of Microbial 16S rRNA Gene in the Blood of Patients With Parkinson’s Disease. [2018]

 In conclusion, the present meta-analysis revealed a higher prevalence of H. pylori infection in PD patients suggesting that H. pylori may contribute to PD pathophysiology. In addition, the significantly lower UPDRS scores in non-infected PD patients and in patients after H. pylori eradication therapy demonstrate that the infection may deteriorate the clinical severity of the disease.

H. pylori and Parkinson’s disease: Meta-analyses including clinical severity. [2018]

Caution: The treatment for H. pylori will also impact the microbiome and the changes may be due to side-effects on other bacteria.

Side Note on Suggestions from MicrobiomePrescription site vs Literature

However, it is not yet clear whether a specific dietary concept or the effects of the intestinal microbiota on the human metabolism could play a role in the course of the disease. Given the lack of prospective nutrition studies, only general recommendations can be given: a “balanced” seasonal regional diet with emphasis on vegetables, fruits, nuts, fish, low amount of red meat, and non-processed foods with a low level of simple carbohydrates may be helpful. 

[Nutritional aspects in Parkinson’s disease: disease risk, dietary therapy and treatment of digestive tract dysfunction] 2018.

From MicrobiomePrescription, based on bacteria shifts alone, we have very similar results, even on non-processed food:


Adherence to the Mediterranean diet is associated with lower probability of prodromal PD in older people. Further studies are needed to elucidate the potential causality of this association, potential relation of the Mediterranean diet to delayed onset or lower incidence of PD, as well as the underlying neurobiological mechanisms

Mediterranean diet adherence is related to reduced probability of prodromal Parkinson’s disease.

In terms of the analysis site, the Mediterranean diet has many plus and many minus. See Explaining Suggestions post for understanding why this may have occurred.

Bottom Line

Microbiome dysfunction and Parkinson’s is getting better and better established. There is a bit of a chicken and the egg situation between infections such as H. pylori or fungus [2017]. Did those pathogens triggered the microbiome dysfunction that lead to Parkinson’s OR did the Parkinson’s microbiome make it easier for those pathogen to occur?

Blind use of antibiotics or other drugs may make things worst. The following ones adversely impacts at least 50% of the microbiome shifts reported:

With literally dozens of drugs of antibiotics impacting 35% of the microbiome shifts adversely.

At the supplement level, we find that B vitamins adversely impact more microbiome shifts than they help:

  • Vitamin B3: Adverse 9, Helps 6
  • Vitamin B1: Adverse 9, Helps 5
  • Vitamin B7: Adverse 7, helps 4
  • Vitamin B6: Adverse 7, helps 4
  • Vitamin B9: Adverse 7, Helps 4

There was not a single clear “you should take” in the list of vitamins generated. At the amino acid and similar, melatonin had a 11 Adverse to 4 Helps. Proline was the exception: 4 increases and 1 adverse.

In terms of food: Whey, sesame cakemeal, red meat all were clean avoids, having adverse shifts for 25% of the known shifts and nothing known to help. (i.e. in the low protein diet above — exclude red meat)

Harsh bottomline: It seems that most of the things that helps CFS and many other conditions — may actually make Parkinson’s worst. “Cook book recipe for healthy living” may make things worst.