A reader forwarded me their report and asked me to do an analysis and asked some specific questions about what can be done for some items. I had done an earlier post on another patients KyberKompakt Pro report — the results are very similar, consistent with what appears to be the usual shift away from normal seen in CFS patients. I would expect at least 90% of CFS patients to have very similar results (IMHO, this specific test is a good validation of a CFS diagnosis OR if dissimilar, suggests other issues may be occurring.

Each line means 10x, so E.Coli is 3 lines below the bottom of the normal range, or 10 x 10 x 10 – 1000 times less (not a little decrease).

How do the 2 sample compare?

• E.Coli: < 1 x 10⁴, < 2 x 10⁴ – 100x less
• Bifidobactrium:  7 x 10⁶, 4 x 10⁶ – 500x less
• Lactobacillus: 2 x 10⁶ (Normal), 2 x 10⁴ – 10x less
• Hydrogen Peroxide producing Lactobacillus: 2 x 10⁴ (Normal), 2 x 10⁴ – 5x less
• Enterococcus spp: 2 x 10⁵, 1 x 10⁴ – 100x less
• Akkermansis muciniphia:  5 x 10⁴ , 8 x 10⁴ – 10000x less
• Faecalibacterium prausnitzi: 1 x 10⁷ (100x less),1 x 10^{9 (Normal)}

Lactobacillus is always a problem because patients may be taking it as probiotics or yogurt before the testing. Also, the magnitude is much less than the other ones.

We also see that the pH is off significantly.

Addressing Akkermansis muciniphia shortage

• Preparation and preservation of viable Akkermansia muciniphila cells for therapeutic interventions[2017]. “The anaerobic gut bacterium Akkermansia muciniphila is a well-characterised member of the mucosal microbiota and has shown to be a gut symbiont in human…A. muciniphila cells reversed highfat diet-induced obesity and its associated metabolic disorders in mouse models…A. muciniphila cells with high yields and very high stability, with up to 97.9±4.5% survival for a time period of 1 year at -80 °C in glycerol-amended medium.”
  • So work is ongoing to develop a probiotic (therapeutic) use!
• Intestinal Microbiome, <i>Akkermansia muciniphila</i>, and Medical Nutrition Therapy[2016].
• “an increase of Enterobacteriaceae, Desulfovibrio sp., and mainly Akkermansia muciniphila in Constipated-predominant IBS patients compared to healthy individuals.” [2016]
  • So an overgrowth has a distinct symptom — C-IBD! (this may be why this was being tested for)
• Pomegranate ellagitannins stimulate the growth of Akkermansia muciniphila in vivo [2017].
  • Pomegranate extract induces ellagitannin metabolite formation and changes stool microbiota in healthy volunteers[2015]. “1000 mg of POM extract daily for four weeks….Verrucomicrobia (Akkermansia muciniphila) was 33 and 47-fold higher in stool samples of UA producers compared to non-producers” — 25% were non responders.
• “vitamin D deficient high fat feeding (HFD+VDD), … Akkermansia muciniphila, a beneficial symbiotic, is diminished.” [2016]
  • Vitamin D supplements (my own “normal” is always the top of the Vitamin D range — typically requiring 15,000 IU/day)
• Aguamiel concentrate from Agave salmiana and its extracted saponins attenuated obesity and hepatic steatosis and increased Akkermansia muciniphila in C57BL6 mice[2016].
• ” Flax Seed diet altered the fecal microbial community structure (16S rRNA gene profiling), including … a 30-fold reduction in Akkermansia muciniphila abundance.” [2016] – Avoid flaxseed!!!
• Akkermansia muciniphila inversely correlates with the onset of inflammation, altered adipose tissue metabolism and metabolic disorders during obesity in mice[2015]. i.e. it decreases as inflammation increases.
• “supplying a gluten-free diet to mice increased fecal levels of Akkermansia species (32).” [2015]
• Low relative abundances of the mucolytic bacterium Akkermansia muciniphila and Bifidobacterium spp. in feces of children with autism [2011].

A reader wrote to me and stated that he had “harsh Multiple Chemical Sensitivities” and this improved it greatly. While this is an anecdotal report, I do like following up on such (to see if there is logic to it via the model that I am working from).

On MCS sites and books, it is often sited as being needed, for example:

But in “University of Toronto case–control study of multiple chemical sensitivity-3: intra-erythrocytic mineral levels [2006]”  Molybdenum was detected in only 7% of the MCS suffers (and only 7% of the controls!) with both groups being 200 people. The level was much lower for this 7% (0.021 vs 0.077) but for 93 percent of each group, it was not detectable.

There was very few hits on PubMed,

• “Results of this study suggest that Cu from CuGly may be more available than CuSO(4) when supplemented to diets high in S and Mo.” [2008]
• “molybdenum-induced secondary copper deficiency… illness and subsequent death of cows was observed. ” [1989] – do NOT overdose on this supplement!!!!!!!! More is not better, more may be deadly!

Thus supplementation could reduce copper levels — unfortunately, the studies that I found had MCS and CFS having normal copper levels (as a population) compared to controls, so this is unlikely to be the mechanism of action for MCS relief.

The microbiome dimension

• “Intakes of copper, magnesium, manganese, and molybdenum were positively associated with Firmicutes (r = 0.33, 0.38, 0.44, and 0.51, respectively; P ≤ 0.01) and negatively associated with Bacteroidetes (r = -0.38, -0.44, -0.48, and -0.53, respectively; P ≤ 0.01).” [2015]  Note: molybdenum had the greatest effect of the four minerals.
  • ” In contrast, in the stool samples there was a higher relative abundance of Bacteroidetes and lower abundance of Firmicutes observed in ME/CFS patients compared to healthy controls.” [2015]
• “In certain gastrointestinal disorders, however, extensive fecal losses may occur. Balance data obtained in our laboratory from two subjects with Crohn’s enterocolitis demonstrated that during active disease, gastrointestinal losses of molybdenum may exceed 400 ,ug/day.” [1984]

Bottom Line

The traditional rationalization of for taking molybdenum (low levels) does not stand up to studies. There are no studies of molydbenum with IBS/FM/CFS (which is always my gold standard).

According to the model, molybdenum should help shift ME/CFS microbiome in the right direction. All of this literature is from 2015.

If you take it, keep to the recommended dosages and consult with your knowledgeable medical professional.

As a further FYI: he used Thorne Research – Molybdenum Glycinate – Trace Mineral Cofactor – $9 for 60 capsules

I have yet to find the magical ideal — I do know the characteristics that it should have.

• Human sourced with evidence of taking up residency.
  • Best documented to date is Symbioflor-2
• Does not produce histamine (implicated in a subset of CFS), ideally converts histamine to other chemicals
• Does not produce d-lactic acid (implicated in a subset of CFS), ideally converts d-lactic acid aggressively
  1. Best documented to date is Miyarisan
• Resistant to many antibiotics
  • Best documented is Lactobacillus Fermentum ME3
• Effective against Candida
  • Best documented is Lactobacillus Fermentum ME3
• Encourages microbiome diversity
• Create toxins against bad bacteria strains but not their good cousins
  • Best documented is Lactobacillus Fermentum ME3
• Produces B12
  • Best documented is L.Reuteri — but human strains produce histamines and lactic acid also!
• Produces chemicals that are anticoagulants
  • “Strong acidification and coagulation activities of Lactic acid bacteria strains were recorded.” [2009] i.e. Lactobacillus in general encourages coagulation! There are exceptions

Problem with most commercial probiotics

• The source is never identified (i.e. a chicken strain is very unlikely to take up residency)
• The strain is rarely identified, i.e.
  • Lactobacillus Casei — is a family
  • Lactobacillus Casei Shirota — is the strain
• Often the family is incorrect (especially for Bifidobacteria) if no strain is given
• There is no independent certification agency for the content of probiotics
• Even with strains that have PubMed studies published, only a few answers to the above questions are found. The rest is guessing!
• Often health professional will make up answers about it being “high quality” etc and there is zero evidence based research supporting the benefits they claim.

People with those diagnosis are ill, often very ill. The name is what is very incorrect. In some cases, doctors and patients cling to the name for reasons such as “Lyme can be treated, but Chronic Fatigue cannot!” – just as they will say “You will be all right (when they know the odds are that the patient will not live)”.

A year ago, I did a review of Chronic Lyme, and stated ” I believe that Post Infection Fatigue Syndrome is a better approach for treatment success.” The key factor is there is no ability to tell these different ascribed names  via lab tests — especially with long term patients.

“This post-infective fatigue syndrome phenotype was stereotyped and occurred at a similar incidence after each infection. The syndrome was predicted largely by the severity of the acute illness rather than by demographic, psychological, or microbiological factors.”  [2006] Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: prospective cohort study.

This has been in the literature since at least 1987 Post-infectious fatigue. “an illness characterized by persisting fatigue and disability after apparent acute infections. In most cases the illness is attributed to a chronic Epstein-Barr virus infection.”

In the literature on PubMed you will find:

• Post-giardiasis chronic fatigue syndrome [2017] “cases that developed CFS after Giardia infection compared to cases that recovered well.”
• Post-mononucleosis[EBV] chronic fatigue [2012] “Chronic Fatigue Syndrome (CFS) has been known to follow Epstein-Bar virus (EBV) and other systemic infections;”
  • Active Epstein-Barr virus infection in post-viral fatigue syndrome [1989].
• “the role of the herpesviruses EBV, CMV and HHV-6 in post-infective fatigue syndrome [2012].
• [Post-Lyme disease syndrome] 2016.
• Chronic fatigue syndrome following a toxic exposure [2001]. – five patients
• Q fever: persistence of antigenic non-viable cell residues of Coxiella burnetii in the host–implications for post Q fever infection fatigue syndrome and other chronic sequelae [2009].
  • Chronic fatigue syndrome after Q fever [2007].
  • “These results suggest the possibility of direct involvement of C. burnetii in the pathological state of CFS to be low, despite the C. burnetii infection rate being high in CFS patients” [2005]
• Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: prospective cohort study [2006].
• Post-infectious fatigue syndrome in dengue infection [2007].
• Chronic fatigue syndrome (CFS) associated with Staphylococcus spp. bacteremia, responsive to potassium arsenite 0.5% in a veterinary surgeon and his coworking wife, handling with CFS animal cases [2001].

I have personally met a post-leprosy chronic fatigue patient (leprosy is cause by the same family of bacteria as lyme).

Retreating Treatment rarely has success

• “Despite treatment with doxycycline, he continued to have markedly elevated Coxiella burnetii phase I antibody titers for 10 years after the initial diagnosis.” [2006]
• http://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2571617
• 
  • Point: antibiotic therapy is not the answer for patients with persisting symptoms attributable to lyme disease [2007].

With so many different diseases — what is in common?

The answer is simple — the diseases alter the microbiome. This alteration causes many of the symptoms. If this alteration get ‘stuck’, the symptoms will continue.

” However, the altered microbiome, in turn, may aggravate the disease, as it has the potential to overproduce toxic substances such as ammoniac and GABA, and to impact manganese metabolism; all three are thought to play a role in hepatic encephalopathy [11]. Interestingly, treatments that are currently used, laxatives, antibiotics, and enemas, actually target the microbiome. The benefits are only temporary, likely because they do not prevent the reconstitution of the harmful microbiome; a more permanent modulation could be sought as a novel way to treat this disease.” [2016]

Microbiome-wide association studies link dynamic microbial consortia to disease [2016]

Shifts of the microbiome also happens with stress.

So what is the right name?

• Post-infection… is not correct, because it excludes those that slipped into CFS from stress…
• Chronic Fatigue .. this name is already problematic.
• “Off-stomach” .. while better, people will not the persistent aspect
• Microbiome Dysfunction Disease .. unfortunately, Crohn’s, IBD would be included.
• “Bell-Cheney Disease” — after Dr. Bell and Dr.Cheney!  This is my favorite suggestion.

The microbiome shift seen in CFS can result in prior health issue becoming active. Candida issues as well as EBV, CMV and other virus may be come active. The unfortunate side effect is that these infections often reinforce the microbiome dysfunction making CFS even harder to treat. In my prior posts on Valganciclovir and Valacyclovir, we looked at antivirals.

A reader contacted me because of severe issues with candida and asked about probiotics that could help. The following is what I found:

• “The sparsity of currently available antifungals and the plethora of proposed anti-candidal therapies is a distinct indication of the urgent necessity to develop efficacious therapies for candidal infections. Alternative drug delivery approaches, such as probiotics, reviewed here is likely to be a reality in clinical settings in the not too distant future.” [2016]
• ” prevalence of Candida species was 69.2% in children with decayed teeth and 5% in caries-free subjects.” [2016] – dental health is essential!!
• Increased number of Candida albicans in the faecal microflora of chronic fatigue syndrome patients during the acute phase of illness.[2007]
•  Yeast metabolic products, yeast antigens and yeasts as possible triggers for irritable bowel syndrome[2005].
  • “The change in mean log₁₀ colony-forming unit (CFU)/ ml of C. albicans in
    • A) probiotics was 0.43 ± 0.72,
    • B) 0.2% chlorhexidine digluconate oral rinse. 0.68 ± 1.05 and
    •  C) herbal oral rinse(neem etc) 0.22 ± 0.66 CFU/ml respectively.”
    • 
• Inhibitory effects of Lactobacillus rhamnosus and Lactobacillus casei on Candida biofilm of denture surface[2016].
  • “The results suggest that Lact. rhamnosus is able to influence the expression of virulence factors by C. albicans and can alter its antifungal sensitivity profile.” [2016]
• “All Lactobacillus fermentum strains tested, namely LF5, LF09, LF10, and LF11, have the ability to significantly inhibit the growth of the five species of Candida of at least 4 logarithms (10000x). Furthermore, the best result obtained with miconazole on C. parapsilosis is still 2 logarithms lower.(100)” [2016] See this post about this very special probiotic type.
  • “Furthermore, L. fermentum LF5 showed a significant activity after both 24 and 48 hours ….A significant dose-dependent growth inhibition was recorded in particular after 48 hours of incubation [of L. Fermentum], even achieving a 80% inhibition of G. vaginalis growth.” [2016]
• “Bacillus subtilis exhibited clear zones of inhibition for Candida albicans and Candida parapsilosis but not for Candida krusei.” [2016]
• “Bifidobacterium animalis subsp. lactis (DSM 10140) and Lactobacillus spp. (Lactobacillus casei R-215 and Lactobacillus acidophilus R-52)..were only affected by TTO concentration ≥ 4% v/v, while, at concentrations < 2% v/v, they remained viable.” [2015] – i.e. high dosages are required.
• “Thus, daily use of probiotic lozenges(Lactobacillus reuteri (DSM 17938 and ATCC PTA 5289) may reduce the prevalence of high oral Candida counts in frail elderly nursing homes residents” [2015]

Bottom Line

Lactobacillus Fermentum inhibits by a logarithm 4 fold while the tested alternative best was just 0.68 — very minor in comparison. I would suggest taking Bacillus subtilis with it — while not effective against all species, it is effective against many. Both of these are available in the US.

As always consult with your knowledgable medical professional first.