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.

ME/CFS Symptom List

CFS/ME is not understood by most medical professionals because it lacks:

  • Definitive Tests
  • Definitive Treatment Plans
  • Consistency of presentation from patient to patient for those assigned to this group

One major challenge for front line physicians is they have three patients with similar symptoms, when a fourth one arrives with different symptoms – it throws them into a loop. The CDC and health providers like Kaiser Permanente are slowly working to re-educate physicians (remember it tooks 30 years to re-educate physicians that stomach ulcers were caused by H. Pylori (a bacteria) and not because the person worried too much!). This issue has been made worst from evangelism to MDs of bad science. I like it that the Centers for Disease Control is now emphasising ” Myalgic encephalomyelitis”[pain with inflammation of central nervous system] which should help with changing perceptions. It is matching the neurological classification of ME in the World Health Organization’s International Classification of Diseases (ICD G93.3). 

This is even worst with the general with common misconceptions such as “yuppie flu” and “I get tired too”. In some cases, it has been deemed to be burnout, although a 2019 study found this to be false.

The most common peri-onset events reported by subjects were infection-related episodes (64%), stressful incidents (39%), and exposure to environmental toxins (20%)… At the time of survey, 47% were unable to work and only 4% felt their condition was improving steadily with the majority (59%) describing a fluctuating course. Ninety-seven percent suffered from at least one other illness: anxiety (48%), depression (43%), fibromyalgia (39%), irritable bowel syndrome (38%), and migraine headaches (37%) were the most diagnosed conditions. 

Rates of unemployment can be as high as 81% (7) while ~25% of patients may be homebound or bedridden … the median rate of full recovery is only 5%

Onset Patterns and Course of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. [2019]

The results indicated that chronic fatigue and burnout should be perceived as 2 distinguishable constructs in the academic context. “


Last Wednesday, I attended a lunch with the Seattle CFS/ME group. Despite some of the people having had the conditions for over 30 years, now being confined to wheel chairs – the conversation revealed that they were not aware of all of the symptoms (they had some classic CFS symptoms and were not aware that they were CFS associated).

Symptom List

This list (with references) is associated with chronic fatigue syndrome a.k.a.
Myalgic encephalomyelitis. My view is that these diagnosis is a reflection of a microbiome dysfunction. Many CFS patients have gone into temporal full remission from a fecal matter transplant. With this view, we also have a list of symptoms that may be associated with a microbiome dysfunction. This is only a partial list.

Sources: [2015] , [2011] ,[2011] [1987] [1993] [2009]

  • ‘small heart’ with small left ventricular chamber and poor cardiac performance in patient subsets
  • 10% reduction in grey matter volume
  • abdominal pain,
  • abnormal growth factor profiles,
  • air hunger,
  • altered control and reduced cortisol production
  • arthralgias and ‘gelling’ (stiffness),
  • ataxia
  • auditory learning reduced
  • autonomic dysfunction
  • awaken feeling exhausted regardless of duration of sleep,
  • awaking much earlier than before illness onset,
  • bloating,
  • brain stem hypometabolism
  • cardiac and left ventricular dysfunction 
  • cerebrospinal fluid proteomes distinguish patients from healthy controls
  • cervical and/or axillary lymph nodes may enlarge or be tender on palpitation
  • chronic cough(40%),
  • cognitive dysfunction
  • cold extremities
  • day-time sleepiness
  • decreased cortical blood flow
  • decreased natural killer cell signalling and function,
  • decreased neutrophil respiratory bursts and Th1,
  • depression,
  • difficulty processing information
  • extreme pallor or Raynaud’s Phenomenon
  • fatigue of chest wall muscles
  • faucial injection and crimson crescents may be seen in the tonsillar fossae, which are an indication of immune activation.
  • feeling unsteady on feet,
  • Fibromyalgia
  • frequent awakenings,
  • headaches
  • hypoperfusion 
  • immediate recall reduced
  • immune dysfunction
  • impaired depth perception
  • impairment in attention and motor functioning (50%)
  • impairment in speed information processing and executive functioning (40%)
  • inability to focus vision,
  • inability to tolerate an upright position – orthostatic intolerance, neurally mediated hypotension,
  • increases in inflammatory cytokines,
  • insomnia,
  • irritable bowel syndrome
  • Joint hypermobility
  • laboured breathing,
  • light-headedness/dizziness
  • low blood pressure and exaggerated diurnal variation
  • low threshold of physical and mental fatigability (lack of stamina) results in a substantial reduction in pre-illness activity level.
  • marked diurnal fluctuations;
  • marked, rapid physical and/or cognitive fatigability in response to exertion,
  • moons of finger nails may recede.
  • mottling of extremities,
  • muscle weakness,
  • nausea,
  • neuroendocrine and immune symptoms
  • neuroimaging studies report irreversible punctuate lesions
  • neuroinflammation of the dorsal root ganglia
  • nocturia
  • pain,
  • palpitations with or without cardiac arrhythmias,
  • pathological fatigue and malaise that is worse after exertion,
  • photophobia
  • Poor attentional capacity and working memory 
  • poor coordination,
  • postural orthostatic tachycardia syndrome, 
  • pro-inflammatory alleles
  • prolonged sleep including naps,
  • recurrent adenopathy (33%),
  • recurrent feelings of feverishness with or without low grade fever,
  • recurrent low-grade fevers (28%). 
  • recurrent rash (47%), 
  • recurrent sore throat (54%),
  • sensitivity to light, noise, vibration, odor, taste and touch;
  • shift towards a Th2 profile
  • short-term memory loss
  • significant pain can be experienced in muscles, muscle-tendon junctions, joints, abdomen or chest
  • sinusitis,
  • sleeping most of the day and being awake most of the night,
  • slow processing of information 
  • sore throat,
  • subnormal body temperature,
  • susceptibility to viral infections with prolonged recovery periods
  • sustained/switching/divided attention reduced
  • sweating episodes,
  • twitching,
  • unrefreshing sleep
  • urinary urgency or frequency,
  • vivid dreams/nightmares

The COMPASS 31 indicated that 50% have symptoms consistent with orthostatic intolerance. About 43/69 (62%) had Epworth sleepiness scores ≥10, ie, consistent with excessive daytime sleepiness, 26/69 (38%) had significant anxiety and 22/69 (32%) depression measured by HADS A & D. Quality of life is significantly impaired in those with Fukuda criteria CFS (QLS score 64±11) with significant negative relationships between quality of life and fatigue (p<0.0001), anxiety (p=0.0009), depression (p<0.0001) and autonomic symptoms (p=0.04).

Prevalence and characteristics of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) in Poland: a cross-sectional study. [2019]

Bottom Line

I am still in a “flare” dealing with a rollercoaster of the symptoms above. Most patients when ask for symptoms will give a list of 3-4 only. If you walk these patients thru the above list, the numbers increase — often to several dozens — the symptoms listed are the worst ones and the other ones tend to be ignored. I do not have just one or two of the above, but a pretty good list when waxes and wanes throughout each day.

For myself, when in a flare, I will enumerate the list and then “cherry pick” active symptoms looking at the audience who will be hearing it. Often patients will just list they dominant symptoms, “tiredness, sore throat” etc which will often be interpreted by others as low significance.

For example, instead of the wordy “Postural orthostatic tachycardia syndrome (POTS)” I would simply say tachycardia (verified by a pulse of 170 on my monitoring smart watch). A simple neurological symptoms usually go over better than “slow mental processing”, “mental fatigue”. If someone presses more, I will respond with I have ”
“hypoperfusion in the brain – my brain is not getting enough oxygen” or more technical “hypoperfusion in the brain according to SPECT Brain Scans”. I know of CFS patients that have had transient ischemic attack (TIA), especially after a stressful event.

Of course, the problem is having diminished executive decision abilities — so patients make poor presentation of their symptoms to others 😦

Another trigger of microbiome shifts: stroke, and ?WiFi?

The model that I am assuming for conditions like CFS, is some event triggers a microbiome shift which persists in a dysfunctional state. A few of these events are well known, or suspected:

  • Infection (viral or bacteria) – best documented example is Bergen Norway – giardiasis
  • Stress:
    • ” an integrative conceptual model is proposed in which stress-induced enteric dysbiosis and intestinal permeability confer risk for negative mental health outcomes through immunoregulatory, endocrinal, and neural pathways.  ” [2017]
    • PTSD (Articles)
  • Vaccinations – in theory should, no studies done on microbiome shifts before and after vaccination (yet!). If the vaccination works, it has been shown that depends on the microbiome being right [2017]
  • Antibiotics or antivirals

In reviewing a news article, The fascinating effect a stroke has on the gut microbiome, reporting on the International Stroke Conference

Prior research from the same team revealed a stroke does have an immediate effect on the microbiome, but how long these effects last for was not known. Using animal models the researchers conducted microbiome examinations three days, two weeks and four weeks following an induced stroke…. A notable decrease was seen in Bifidobacteriaceae, a common bacteria found in probiotics, up to four weeks past the stroke, while increases were seen in Helicobacteraceae across the same observational period.

Another intriguing change in the gut seemingly brought on by the stroke were notable abnormalities in intestinal tissue. Normally in healthy animal models this tissue appears structured in orderly ways, almost like branches of coral. However, close examination up to four weeks post-stroke revealed the villi, structures that project off the intestinal wall, were scrambled and visibly quite different from the healthy models.

The fascinating effect a stroke has on the gut microbiome,

The real interesting aspect of the article was:

Another compelling study from 2017 suggested magnetic simulation to specific areas in the brain can affect the composition of a person’s gut microbiome.

The fascinating effect a stroke has on the gut microbiome,

The question is then — do cell phones create magnetic fields (that could potentially stimulate the brain). The answer is yes:

Among the valves tested, the settings of the Strata valve, the Hakim valve, and the Sophy valve were affected by magnetic flux densities of 6.0, 17.5, and, 40.0 mT, respectively. Cell phones produce a magnetic flux density of 3.0 to 40.0 mT. 

Effect of cell phone magnetic fields on adjustable cerebrospinal fluid shunt valves [2005]

And for Wifi, the evidence is cleaner still:

The pure cultures of Listeria monocytogenes and Escherichia coli were exposed to RF-EMFs generated either by a GSM 900 MHz mobile phone simulator and a common 2.4 GHz Wi-Fi router. It is also shown that exposure to RF-EMFs within a narrow level of irradiation (an exposure window) makes microorganisms resistant to antibiotics

Evaluation of the Effect of Radiofrequency Radiation Emitted From Wi-Fi Router and Mobile Phone Simulator on the Antibacterial Susceptibility of Pathogenic Bacteria Listeria monocytogenes and Escherichia coli. [2017]

Bottom Line

While we know that all of the above can cause microbiome shifts, most people microbiome returns to normal. Most people. As a statistician, I know that as the number of low risk events increases, the chance of a significant event cumulates.

We cannot say: Wifi, vaccination etc causes any specific long term autoimmune conditions, it just increases the risk — like smoking does. There are people who seem immune to the effects of smoking (like the Comedian George Burns who lived to 100 and love smoking cigars).

Workplace Stress – Case Study

subtitle: A probiotic that is giving me a nice herx

One aspect of chronic fatigue syndrome is having stress intolerance [US Gov Job Accommodation Site], this is also an aspect of autism spectrum [US Gov Job Accomodation site]. I have both. I was very fortunate back in high school being part of a very gifted child program which included research psychologists evaluation of the selected students (only 0.3% of the students were selected. Mensa is 2%). These psychologists noticed and remarked to me, something that was very unusual for this population — I was stress-dysfunctional. Autism Spectrum was largely unknown in those days. This simple observation altered my behavior for school and subsequently for work.

The unfortunate aspect is when you provide literature to your supervisors (for example the above two links) — some do not get stress intolerance — especially in IT with individuals that function best with stress. They expect everyone to be like themselves.

I have been trying to exit such a situation for a month — especially when a neurological symptom appeared, which disappeared once I got a few days away from work. This symptom was a new one for me, but a sweet one for early warning. The symptom is nicely described as “Some patients will experience paralysis of the lower half of the face leading to drooling, change in speech quality, sagging of the corner of the mouth.” [Src]. With my model it means that metabolites being produced from the stress are impacting my neurological system.

Last Friday, the supervisor went into panic mode and hit me with too much stress (and unrelated to my actual code/work). At 10AM, I could feel a state change in the body and booked off sick for the rest of the day (and still off sick). The usual roller coaster of symptoms seen when leaving remission: difficulty understanding, quick mental fatigue, circulation issues, over a dozen bowel movements a day, tachycardia, dysregulation of blood pressure (POTS etc), atypical spells of depression, problems with sentence construction, etc.

A question arises on interventions — especially given a recent study in Cell finding that intervention after antibiotics is counter productive — how much do you attempt to fix things? I did my usual stress herb — Ashwagandha which appears to impact stress related bacteria (see this list of what it impacts). I happen to recall a recent post on human sourced probiotic mixtures — one of which contained Lactobacillus Fermentum (Post#1 and Post#2 on it) – which happens to be available at my local co-op.

I am trying to keep to few interventions – so not looking for the usual high dosages of antibiotics that I have needed in the past.

I am on day 2, I must say that I am impressed because I am experiencing the classic herx pattern for a few hours after taking it. That’s it — just sharing an observation. Every strain is human sourced, so there is some chance of some taking up residency – but regardless, it seems to be effecting change.


For a man, the above is not expected — but I wanted to have the lactobacillus fermentum.

As for myself, I have lots of sick time and unused vacation, emailed some key people on the issue, so I expect things to be healthy resolved. If not, then time to move on (putting up with stress is not a viable option).

Bottom Line

Enduring stress is not a viable option with stress intolerant conditions.

Coagulation Issues – Testing and Literature

A reader asked me to assemble a list of known DNA mutations. In my post on Multiple Chemical Sensitivity we see that the MTHFR gene is associated with abnormal blood clotting ( US National Library of Medicine). Coagulation issues are strongly associated with brain fog.

Since this type of question often leads to “where can I get appropriate testing done?” Coagulation issues are outside of “my wheel house” except for being aware of them and knowing about the specific mutation that I have.

Thrombophilia Mutation Panel seems to be the most detailed all-in-one test:

For general background read:

Multiple Chemical Sensitivity – Current understanding of DNA

In this post, I want to list potential DNA polymorphism (SNPs) associated with MCS and then look at what we know about these polymorphisms.

” There is a significant overlap of MCS, CFS and fibromyalgie.”

Multiple chemical sensitivity syndrome (MCS)–suggestions for an extension of the U.S. MCS-case definition. 2005

Statistically significant differences between patient cases and controls were found with respect to rs1801133 (MTHFR), rs174546 (FADS1) and rs1801282 (PPARγ) polymorphisms…. Specific genetic polymorphisms associated with the syndrome or its pathogenesis were not identified.

Multiple chemical sensitivity: Genotypic characterization, nutritional status and quality of life in 52 patients. [2017]

We observed that high chemical sensitive individuals diagnosed by using Japanese criteria as MCS patients were more significantly associated with SOD2 polymorphisms.

Evaluation of genetic polymorphisms in patients with multiple chemical sensitivity. 2013

demonstrating an increased risk for MCS in Caucasian females homozygous for the CYP2D6 isoform and for the association of CYP2D6 and phase II NAT-2 polymorphisms [98]. Proneness to MCS was connected with NAT-2 polymorphism and homozygous deletions of M1 and T1 GST genes [99].

The Search for Reliable Biomarkers of Disease in Multiple Chemical Sensitivity and Other Environmental Intolerances 2011

A genetic predisposition for MCS may involve altered biotransformation of environmental chemicals. The CYP2D6 enzyme activates and inactivates toxins; the NAT2 enzyme bioactivates arylamines to protein-binding metabolites. A gene-gene interaction between CYP2D6 and NAT2 suggested that rapid metabolism for both enzymes may confer substantially elevated risk (OR = 18.7, P = 0.002)

Case-control study of genotypes in multiple chemical sensitivity: CYP2D6, NAT1, NAT2, PON1, PON2 and MTHFR. 2004

No significant differences of the allelic distribution of geneticpolymorphisms in the genes for 5HTT, NAT1, NAT2, PON1, PON2, and SOD2 were found between cases and controls. The results are in contrast to the study of McKeown-Eyssen and coworkers (2004) but in accordance with the German MCS multicenter study. 

Sequence variations in subjects with self-reported multiple chemical sensitivity (sMCS): a case-control study. 2008

No significant differences in the allelic distribution of genetic polymorphisms in the GSTM1, GSTT1, ALDH2 or PON1 genes were found among the four levels of each subscale, or between cases and controls.

Factors in genetic susceptibility in a chemical sensitive population using QEESI. 2012


  • Clean evidence for
    • MTHFR,
    • FADS1
    • PPARγ
    • CYP2D6
  • Disagreement for
    • SOD2
    • NAT-2
    • 5HTT,
    • NAT1,
    • PON1,
    • PON2



The MTHFR gene provides instructions for making an enzyme called methylenetetrahydrofolate reductase. This enzyme plays a role in processing amino acids, the building blocks of proteins. Methylenetetrahydrofolate reductase is important for a chemical reaction involving forms of the vitamin folate (also called vitamin B9). Specifically, this enzyme converts a molecule called 5,10-methylenetetrahydrofolate to a molecule called 5-methyltetrahydrofolate. This reaction is required for the multistep process that converts the amino acid homocysteine to another amino acid, methionine. The body uses methionine to make proteins and other important compounds.

People with this condition often develop eye problems, abnormal blood clotting, skeletal abnormalities, and cognitive problems

US National Library of Medicine


” These results position Fads1 as an underappreciated regulator of inflammation initiation and resolution, and suggest that endogenously synthesized arachidonic acid and eicosapentaenoic acid are key determinates of inflammatory disease progression and liver X receptor signaling. ”

Δ-5 Fatty Acid Desaturase FADS1 Impacts Metabolic Disease by Balancing Proinflammatory and Proresolving Lipid Mediators

Single nucleotide polymorphisms (SNPs) of FADS1 and FADS2 may affect long-chain polyunsaturatedfatty acids (LC-PUFA) metabolism and have a potential role in the development of atopic (Allergic) diseases.[7] – Wikipedia


Peroxisome proliferator-activated receptor gamma (PPARγ) is a member of the nuclear receptor superfamily of ligand-inducible transcription factors that regulate adipogenesis, lipid metabolism, cell proliferation, inflammation and insulin sensitization. 


PPAR-gamma decreases the inflammatory response of many cardiovascular cells, particularly endothelial cells.[30] PPAR-gamma activates the PON1 gene, increasing synthesis and release of paraoxonase 1 from the liver, reducing atherosclerosis.[31]

Many insulin sensitizing drugs (namely, the thiazolidinediones) used in the treatment of diabetes activate PPARG as a means to lower serum glucose without increasing pancreatic insulin secretion. 


This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein localizes to the endoplasmic reticulum and is known to metabolize as many as 25% of commonly prescribed drugs. Its substrates include antidepressants, antipsychotics, analgesics and antitussives, beta adrenergic blocking agents, antiarrythmics and antiemetics. The gene is highly polymorphic in the human population; certain alleles result in the poor metabolizer phenotype, characterized by a decreased ability to metabolize the enzyme’s substrates. Some individuals with the poor metabolizer phenotype have no functional protein since they carry 2 null alleles whereas in other individuals the gene is absent. This gene can vary in copy number and individuals with the ultrarapid metabolizer phenotype can have 3 or more active copies of the gene. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2014]

US National Library of Medicine

Bottom Line

Using the above information, there seem to be some avenues that should be explore for MCS patients for researchers:

Scanning some MCS discussion groups, at least two of the above avenues appears to help some.

Treatment Status

A search on PubMed shows that modern medical science is still struggling on diagnosis of this condition.

There are many random attempts to treat (usually by people with magic bullets that they are trying to find things to treat):

A randomised, placebo-controlled trial of transcranial pulsed electromagnetic fields in patients with multiple chemical sensitivity. [2017] “PEMF treatment of 6 weeks showed no effect on functional impairments in MCS. ” sometimes with word-smithing to indicate some form of positive effect (which could also be a placebo effect). Two classic phrases:

  • “Significant improvement” – something appears better, but the evidence did not reach statistical significance.
  • “Statistical significant improvement” – maths said something improved, but not remission and may be a very small improvement.

A IT Reader’s Medical Challenges

I usually avoid getting too involved with readers — for a simple reason: this blog and the microbiome analysis site is already a time consuming evening and weekend gig (full time IT day job). I am not a physician or medically trained, so “patient history” is an inappropriate term to use.

This reader came via LinkedIn (where I have started posting items from this blog to confuse all of my technical nerd contacts 😉 ). The number of issues, technical documentation provided, and detail history made if a good review example.

The last time I felt great was in high school, I was eating lots, exercising 2-3 (swimming) hours a day, sleeping well, studying hard. However, even though I was doing well, after a swimming race, I had trouble getting out of the pool and was too tired, no other swimmers were like that. I knew that at age 15 I was sick due to the excessive fatigue.

Ding: typical CFS has a “day-after exhaustion” after exercise. I recall my Stress ECG Test — absolute flying colors. Next morning, horrible. This hints that something else may be in play.

I had mercury fillings since I was about 8 years old and in November 2017 I got them replaced and since then my chelation treatment (DMSA) has been easier in terms of symptoms. My symptoms started when I started college (2006), I wasn’t getting much sleep due to a noisy heating element and had frequent heartburn[GERD –
gastroesophageal reflux disorders ]. I would sometimes be sad but I attributed this to a lack of exercise. Also, I have had misophonia a year after starting university (started 2006, finished 2010).

Partial sleep deprivation is associated with shifts in 4 bacteria families, and 20 genus (list). Sadness is associated with depression in medical terms. It is associated with 13 genus (diagram). Cross comparing the genus lists, there was nothing in common (suggesting that sleep deprivation and depression are not strongly connected). It does imply up to 33 genus may be altered. For GERD, we can add a few more … :

Although far from comprehensive (only approximately 24 clones were sequenced per sample), the study found Veillonella (19%), Prevotella (12%), Neisseria (4%), and Fusobacterium (9%) to be more prevalent in patients than in controls. 

Microbiome in Reflux Disorders and Esophageal Adenocarcinoma [2014]

Reminder that I use: “The microecologic disease theory, or the “Pathogenic Microbial Community” theory, is a new model in which the entire community contributes to pathogenicity, with no individual community members being classified as pathogens.13,14Dysbiosis is a similar concept that refers to an abnormal state of the microbial ecosystem, dividing commensal bacteria into “protective” and “harmful” species. With dysbiosis, the cause of certain chronic diseases is an upset balance between the two groups.13 ” [2014] This model means that AI/Machine Learning is the best tool for analysis.

Reader’s state: ‘sub-clinical dysbiosis’, that is, most gastroenterologists would state “you are fine — I see no issues of concern”.

After university (2011), I went to Asia for a week and a few months after I came back with a duodenal ulcer (found upon endoscopy), it was a stressful experience both emotionally and sleep-wise since I went through 2 12 hour shifts. I presented with fatigue, blood loss, dark stools, coffee ground vomit, collapse, blindness, urinating in bed, sleep loss, pale skin. I then went on to working in one Asian city for about a year (2012), a year after my initial trip to another Asian city , came back to the USA and became very fatigued when I was in my parents home — especially when I was around the carpets (was there for a few months).

Ulcers are usually associated with Helicobacter pylori. (one study found only 27% of these ulcers had H. pylori [2001]). We do see via DataPunk, a large number of bacteria that clusters with (i.e. if you have H. Pylori, you will often find these)

I went back to Asia to a number of cities (after Fukushima) and lived there for 2 years and upon using a new teflon pan, I got a headache, was dizzy, nauseated and got tinnitus (2015).

The carpet scenario with the teflon response implies multiple chemical sensitivity. While teflon is ‘normally considered to be safe’, poorly made or overheated pans are known to release “perfluorooctanoic acid (PFOA) ….
it can stay in the environment and in the human body for long periods of time. “[cancer.org] The table below shows the impact of a very closely related chemical.

Dietary Exposure to the Environmental Chemical, PFOS on the Diversity of Gut Microbiota, Associated With the Development of Metabolic Syndrome [2018]

At this point, my mind go to suggesting an Olestra diet for a few months. YES that ugly horrible synetic fat – Ken, you must be kidding!. Why, see “I would never do this if there was an alternative” in this 2013 post. He is already doing chelation treatment (DMSA) — this is a different form of chelation. I have seen it work for MCS persons after a chemical exposure — they return to normal much faster.

When I came back to the USA and started working in my US office, I started zoning out in the first weeks, then the next week I started having a burning feeling in my tongue, then 2 weeks after I started having headaches, memory loss, and stomach pain. Within 1-2 months, I had short and long term memory loss, I lost sleep, I became fatigued and even though exercise helped in alleviating these symptoms some days I was too tired, then I had nausea, non-blood vomiting, and ulcer symptoms. On a trip to other coast for work, I didn’t sleep well due to some fragrance in the hotel room and being woken by a fire alarm at 3am, I woke up, couldn’t breath, was about to pass out and began losing my vision and ringing in my ears started but I managed to get to some water, prevented passing out, and fell asleep (February 2017).

In fact, a similar set of symptoms appears right before I went to the ER during my first ulcer (2012) but in that case, I lost my sight and hearing and hit a wall, I crawled back to bed based upon feeling my environment.  During the second day of the business trip, I noticed a bloody stool and went to a clinic whereby a rectal exam showed I did have blood in my stool, but the doctor said it wasn’t much and I continued on for a week bleeding. During that week, I had flu-like symptoms and my primary care doctor ran some blood work. I got a call from the doctor the next day to go to the ER immediately since I lost half of my blood/hemoglobin, which explained the extreme fatigue and almost passing out. I did, they found a large duodenal ulcer but it was so big they didn’t cauterize it and they also found a hiatal hernia. I continued on with my work in the office after taking some medical leave. I continued having symptoms and eventually was given work from home, but when I came to the office my tongue felt like it was on fire within 15 minutes.

I think it was due to the carpets and did an air quality test that found the VOC’s were high but not higher than the legal limits, no formaldehyde, almost no mold. I got a diagnosis of multiple chemical sensitivities but was dissatisfied with this since I thought something else was at play. I went to see a naturopath in SF since I found a yelp review of someone whose symptoms mirrored my own and that person claimed she was cured by this particular naturopath. Dr. [withheld] put me on a treatment to fix my gut problems, diagnosed me with heavy metals poisoning, and then put me on treatment for the poisoning. I did that for a while and it helped temporarily but I had the same symptoms again.

I then went to another naturopath who suggested that my phase I liver detox was doing too much and my phase II liver detox wasn’t doing enough and his treatment helped me for a while but it seems to not be doing much now. Everytime after I do chelation, I would feel better initially then usually go back to the way I was before I did the chelation a few days after. I did read Cutler’s “Amalgam Illness” and “Hashimoto’s Protocol” by izabella wentz. I did another treatment with QuickSilver Scientific’s “Deluxe Detox Qube”, once again, it helped for a while but then stopped working.

Many experiments later, I noticed that my tongue was white and when I scrapped it my chemical sensitivities were not as bad. I started scraping my tongue, gargling with baking soda and trisodium phosphate, which helped but didn’t cure my chemical sensitivities. I started consuming 2 tablespoons of food grade diatoms and that got rid of more of my chemical sensitivities but I was still sensitive (burning of tongue, headaches, memory loss, fatigue) to perfume.

I know I haven’t gotten rid of candida completely. I have candida, nystatin helped in getting rid of my chemical sensitivities and tinnitus almost completely for a few days but then my tongue was coated in white and my chemical sensitivities were getting worse.

I try to crowd it out with probiotics but it doesn’t seem to work too well. I got my thyroid tests back and they may indicate autoimmunity but according to some thats a reaction to candida. I took diflucan and then later itraconazole to try to treat the toenail fungus, I did have a history of jock itch but that’s gone and I also have dandruff (some naturopaths think all 3 conditions are connected). The itraconazole seems to be working and the probiotics seem to be working on my unhealing abrasions on my body.

I got tested for EBV, turns out I had it in the past and was actively infected at the time of the test but the only symptoms I had related to EBV was fatigue, I took valganciclovir and had less fatigue after the course of treatment. I took metronidazole, tetracycline for a possible ulcer that occurred recently (sleep deprivation). I tried doxycycline and while being on it in the beginning, I got much more access to my intellect and was able to work/study for 6 hours/day straight and exercise for hours/day. It was similar to when I first started liquid nystatin. I still have high TPO antibodies which we at 51 when I got the mercury diagnosis, went up to 100 after a year of treatment and then after the nystatin treatment, it went down to 70. I suspect that I have multiple conditions still left to treat such as SIBO and parasites but am seeking someone to help me get back to normal.

My hypothesis is that there a bacterial dysbiosis in the brain (interpret that as you may). There may be benefits from trying antibiotics and other substances that will pass easily thru the blood-brain barrier. There is an excellent article on this Characteristics of compounds that cross the blood-brain barrier [2009] One simple take-way is items with LOW Molecular weight. For myself, a SPECT scan was (mis)read as Alzheimer’s during my last major episode.

Ongoing problems

Here are my present problems that I seek help with:

  • toenail fungus
  • memory problems/brain fog
  • insomnia
  • I am frequently too cold
  • Fatigue, still sometimes
  • Infections/scars on my lower legs
  • Tinnitus and sometimes partial deafness of right ear
  • Misophonia
  • Multiple chemical sensitivities such as to perfume, laundry detergent, cleaning solutions, fragrances/air fresheners such as cars.

Suggestions to discuss with your medical professionals

As always, not medical advice, just personal observations that could be relevant.

Brain Fog

This can originate from many causes. For myself, coagulation is a major component.

  • My MD accepted this when I took the maximum dosage of aspirin (per bottle) for 10 days and saw the difference. Subsequently,
    • Deep coagulation testing by a lab that specialized in that only
    • Low dosage heparin (originally injection, but we found sublingual worked just as well)
    • Racetams (Piracetam especially)
    • Other blood thinners or items that reduced viscosity of the blood.
      • At one time, nurses were running out of places to draw blood from me because it was so thick.
  • Get a SPECT scan (not MRI, a SPECT) — my family physician referred me for my last one. A relative got referred to Dr. Daniel Amen from a psychologist that works with him. Both scans were similar results.

Toenail Fungus

I am curious if there was any testing for which particular fungii it is? As well as susceptibility to various treatments. I recall reading that mercury exposure results in reduced susceptibility for many bacteria and suspect it may be the same for fungi.


My first take on this is hypoxia (a.k.a. sea-level altitude sickness). Due to low delivered oxygen level to the brain. ” In the elderly with CVD, SDB mediated by hypoxia can be associated with more insomnia and a worse prognosis. ” [2015] . Brain Fog and hypoxia are associated. Back in 2000, I saw the strong correlation between a subset of CFS symptoms and altitude sickness symptoms.

This issue of poor delivery of oxygen and blood would also account for:

Infections/scars on my lower legs

This one initially stopped me — because I have had a similar issue which I did not get connected to CFS until now. For myself, using Triamcinolone Acetonide ointment reduced it greatly but I still see some ‘rough spots’. I suspect now , as above, that it is an impeded circulation issue which prevents the body naturally addressing issues. As a FYI, over the last 10 years I have had recurrent sepsis on my lower legs. Do you have any foot neuropathy? I have a little on one toe and associated it nerves dying from a lack of oxygen — hypoxia.

Multiple Chemical Sensitivity

There is nothing that I can really add here that I have not covered in prior posts. I do not have it active at the moment, but did experience it for a few months during an acute phrase. My workplace is very saturated with chemicals (although it was suppose to be chemical free a decade ago) – so much so that coming home from work (because my wife has severe MCS)

  • Infrared sauna for 30-45 minutes
  • Repeated showers (occasionally vinegar rinse, and vodka rinse are needed)
  • Clothes go into a plastic bag and often need to be double washed in vinegar.

I do not react physically, but do attempt to avoid fragrances for the sake of my wife.

Only suggestion is OLESTRA chips at least once a day to remove reside chemicals that may be contributing .. Make sure you read about frequent response (toxic smelling stools etc) before you start.

“Ding” revisited

I suspect that the fatigue as a child may be due to impeded circulation. The ability to clear toxins and deliver oxygen was less than other people. If this is correct, then your microbiome would shift to species liking lower oxygen levels. This suggests that increased oxygen levels (oxygen mask or hyperbaric chambers) may assist.

How the microbiome ages

I came across this interesting article currently in peer review (thus may have issues):

Human microbiome aging clocks based on deep learning and tandem of permutation feature importance and accumulated local effects

If the results are correct, then it may give great insight to age-related diseases caused by the microbiome changing. The claim that a healthy’s person’s age can be determined with 4 years from their microbiome (with 95% accuracy) is a surprise, but very likely true.

“Some microbes showed steadily increasing age prediction with increasing abundance (e.g. [Eubacterium] hallii); other microbes were on the opposite, inversely correlating with predicted age (e.g. Bacteroides vulgatus)… certain microbes that were previously identified as important by PFI showed little influence on predicted age (e.g. [Eubacterium] rectale) ”

Among the interesting findings are the following that decreases with age:

  • Bacteroides thetaiotaomicron
  • Bacteroides vulgatus
  • Bifidobacterium bifidum
  • Bifidobacterium longum
  • Odoribacter splanchnicus
  • Streptococcus salivarius

The following increase with age:

  • Lactobacillus reuteri
  • Lactococcus lactis
  • Propionibacterium freudenreichii

Bottom Line

Their AI model is not available on line (I wish it was and could accept ubiome data sets). It presents a significant step forward for determining what should be expected for an individual based on age. There are other factors that should also be included.


Major faecal microbiota shifts in composition and diversity with age in a geographically restricted cohort of mothers and their children (2014)

Age-related changes in gut microbiota composition from newborn to centenarian: a cross-sectional study (2016)