KyberKompakt — Chronic Lyme Diagnosis

A reader who just received a chronic Lyme diagnosis forwarded his KyberKompakt results (done in Spain).  Prior to doing this test he was on Prescript Assist and Equilibrium for  two months.

For reference, see other reports shared — Nov, 2016, Feb 2017Mar 2017

  • E. Coli is low normal range.
  • Entercoccus spp is very low
  • Other proteolytic microorganisms – High
  • Bifidobacterium spp low
  • H202 Lactobacillus low
  • Faecalibacterium prausnitzii low
  • Akkermansia muciniphila low
  • Candida albicans high
  • Lactobacillus spp — low normal

All of these 4 reports have the same pattern for almost all.  Variation are one below the bottom of the normal range, and another is at the bottom of the normal range. Entercoccus spp is the exception with 3 being very low and 1 being very high.

Compare to the other 3 results, this patient had:

  • Highest Bifidobacterium
  • Highest E.Coli
  • 2nd highest Lactobacillus

While there is no direct evidence that this is caused by Prescript Assist and Equilibrium (i.e. we would need to have a before lab results), I favor this as an explanation of the better results.

k1

k2

The patient is about to start with Symbioflor-1 (Enterococcus faecalis) in the hope of raising the low Enterococcus faecalis. Since the E.Coli is in the low normal range, I would suggest discussing taking Symbioflor-2 with Symbioflor-1 with their medical professional. The two appears to amplify each other.

The high other proteolytic microorganisms (Proteolysis is the breakdown of proteins into smaller polypeptides or amino acids [wikipedia]) is likely causing a shift of metabolities (chemicals) which cause symptoms and cascade elsewhere in the body. Neem and Tulsi may be reasonable supplements to experiment with to reduce those.

Concerning low  Akkermansia muciniphila there is just over 100 articles on PubMed. This increases with a high fat diet with Capsaicin (Chili peppers!)  [2017]. It is not available as a probiotic (but being considered) [2016]

Hmm…. Rhubarb and pomegranate pie with chili peppers!!/?!!

Histamines and Antibiotics

There is a subset of CFS/IBS/FM patients that are histamine sensitive.  The probable cause according to the model is overgrowth of histamine producing bacteria, for example, some (not all) strains of Escherichia coli ,Lactobacillus sp., Proteus morganii, Proteus sp. , Pseudomonas reptilivora and Streptococcus sp.   With CFS we see massive overgrown of bacteroidetes — the species that tag-team to cause this to happen, vary from patient to patient.

A reader asked about antibiotics and histamine interactions. That is a good question which I have not attempted to research and very relevant if you have a MD willing to prescribe antibiotics AND have histamine issues.

Drug allergy syndrome may be connected to the drug impact on histamines. “When oral tolerance tests were performed, only doxycycline was tolerated whereas levofloxacin, clarithromycin, nimesulide and tramadol caused mild urticaria [ hives]” [2007]

  • Fosfomycin Tromethamine  – “…suppressed the release of histamine in a dose-dependent manner…We concluded that some antibiotics, particularly fosfomycin, have the capacity to suppress histamine release mediated by various secretagogues, suggesting they may possess an anti-allergic property as well as a bactericidal activity. ” [1987]
  • Polymyxin B  ( derived from the bacterium Bacillus polymyxa.) “…suppressed the release of histamine in a dose-dependent manner. ” [1987]

Tetracyclines

  • Tetracyclines reduces histamines [2005]
  • Minocycline reduces histamine [2011]
    • “…suppressed the release of histamine in a dose-dependent manner. ” [1987]
  • Doxycycline reduces histamine [2014]

Macrolides

Beta-lactams

  • “beta-lactams and aminoglycosides, none had the capacity to enhance antigen-induced histamine release,” [1987]

Aminoglycosides

  • “beta-lactams and aminoglycosides, none had the capacity to enhance antigen-induced histamine release,” [1987]

Cephalosporin

  • Cefaclor etc – appears to increase histamine [2015]

Penicillin

 

Fluoroquinolones

  • “levofloxacin…  induces histamine release from the connective tissue-type mast cells distributed mainly in the liver, somewhat in the cutaneous tissue, through the activation of pertussis toxin-sensitive G proteins.” [2001]

Bottom Line

This is an incomplete list but does cover some common families of antibiotics. If there are additional ones that you wish be to research, just add a comment to this post!

Two of the families of antibiotics (tetracycles and macrolides) that inhibits histamine release are very important in Dr. Jadin’s protocol.

A Microbiome test from Italy

it

A reader forwarded the above test and ask for comments. It is a nice test for the brain fogged because information is presented with graphics and reference controls (CTRL) patients results

it2

The first chart illustrates what many studies report, a major shift of the ratio of bacteroidetes to firmicutes. “patients presented … a decrease in several Firmicutes populations.” [2013][Full Text] This is the general pattern seen with CFS and IBS patients at the highest level. The breakdown under this is where things change with symptoms. Biodiversity decreasing or being normal appears to vary according to how it is calculated.

  • “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]
  • “IBD patients have increased bacteroides, adherent or invasive Escherichia coli, and enterococci, and reduced Bifidobacteria and Lactobacillus species”.[40][Medscape]

CFS is one step towards UC and Crohn’s Disease.. “In chronic fatigue syndrome patients they found bacterial profiles with less diversity. This is similar to those seen in people with two bowel diseases: Crohn’s disease and ulcerative colitis, the researchers said.

The second chart show several families that are overgrowths. This is followed by a chart looking at specific elements. Notice that often one column is 0 and the other is not, that is, what is normal is not there and what is usually not found, is there.[Cornell University]

it3it4

So what should be consider for treatment? It is clear that we want to increase Firmicutes. There are more than 270 genera in it, some of these are LactobacillusBacillusClostridiumStaphylococcus.   The bottom line is that there are no available probiotics for most of these.

There appear to be some relationships to work from:

  • Taking Lactobacillus, increases Lactobacillus and decreases E.Coli and Bifidobacteria in general [2012]
  • Taking Bifidobacteria, increases Lactobacillus and Bifidobacteria, decreases E.Coli slightly [2012]
  • Taking E. Coli, increases Lactobacillus and Bifidobacteria [2016]
  • E.Coli and Enterococcus probiotics taken together cause a bigger effect than E.Coli alone. (i.e. Symbioflor-2 and Symbioflor-1 taken together, or Mutaflor with Bioflorin)

Bacteria inhibit or encourages other families of bacteria. The relationships are complex and poorly understood — hence we need to both research and hope for data; if no data, experiment on ourselves (taking notes and sharing results — such as in the last post)

Results from taking probiotics Symbioflor-1 and -2

One of the people”S”, who shared their ubiome information, forwarded more information about before the sample, and experience after the sample.

“3 weeks before and up to the day I took a sample and sent to uBiome I
did change my eating habits to like they were before I started my GAPS
/ low carb / fiber diet.

For those 3 weeks I ate more or less similar to the food habits before
I got sick.  I wanted my sample to be closer to a my typical “sick
normal”

I intend to do more uBiome samples soon and also after I have gone
through your pulsing program.”

“Abt. 7 years ago I managed to fast for a whole month after I got sick
from ME.  I just drank water, herb teas and fresh juices from
vegetables and fruits.  It was hell but I was determined to do it to
get rid of toxins in my body.  With my poor understanding at the time,
I did this in order to heal myself.  I did NOT CHEAT AT ALL for a
whole month – I did not eat any solid food.    A friend pointed it out
that he had seen research somewhere that fasting has been researched
in mice and it destroys the microflora. I think this was extremely bad
thing to do now.  And this evening I´ve been speculating this might
have killed off some species in my gut.”

exampleB

Response to Probiotics

“Symbioflor2 treatment round justifies on it´s own all the research I
have putten into your work the last months  🙂  In 10 days I worked
up to 5 times recommended dose without difficulties but it always had
an added Herx every time I highered the dose). In those 10 days I
finished a whole small bottle of the probiotic.  I used Symbiflor1 /
enterococcus faecalis with it.  1 drop Symbiflor-1 for every 2 drops
Symbiflor-2.  Half a bottle then for those 10 days. I use raw cacao
(CocoCardio Madre Labs brand – has Beetroot powder in it for Nitric
Oxide),  Resistant Starch (Bobs Red Mill brand) and Apple pectin (Now
brand) with it along with, from time to time,  hazelnuts, figs (last
two for fucose) some Brussels sprouts, Baking soda and D-ribose.
Eating low Carb + rye bread.

Results from all above:  More wet eyes,  lessened anxiety and worries,
less brainfog,  Increased positive mental processes, more clarity and
lovely presence of things in the world around me, a litle bit of lucid
dreaming. more imagination, interest in my studies, and more abilty to
emotionally connect with people. Constructive thoughts can make me
happy and are not as dissociated phenomena as before.  Mobility issues
are gone ( I go to the toilet often twice a day ) and pain in
ascending colon because of stifled feces is non-existent (I look
forward to have it  imaged again to see if its verified).  More
energy for walks and computer work.  Better spiritually aware.

I have now seen your change of emphasis according to uBiome results of
patients experiencing little overgrowth. There are sooo many posts :-)”

Reminder

My focus is on the model, not treating specific people. The model is tested by reports of X making a major difference (for example Tamiflu). If the model is correct, then X should also cause shifts in bacteria to counter the type of shifts seen in CFS. The model also gives the characteristics that you would want to correct the shift, which allows possible candidates to be identified. Whether they work well cannot be determined. They are just items with good odds.

The shifts are NOT all the same. There are a bunch of common characteristics: Low or No for Lactobacillus, Bifidobacteria, E.Coli. Others families may be very low OR very high. Those shifts likely result in specific symptoms — the matching is something that need some major research efforts and dollars.

I do not know how to precisely fix any particular shift. No one does. It is a matter of trial and error — ideally with “loaded dice” (more likely to have good results than bad).

 


Comment from a reader on another post on day after this was posted:

“Hi, I just started taking Symbioflor-2 for my CFS and it has done wonders for my energy levels. The only problem is that I have really bad insomnia now with mild Restless Leg Syndrome. I have tried taking sleeping pills but they don’t work and make me get RLS really bad. I don’t want to stop taking Symbioflor-2 because prior to taking it, I was basically bed ridden. Any ideas on what I could do? I read your post on iron deficiency and it would make sense that the Symbioflor is causing an iron deficiency thus causing me to have RLS and insomnia. I will pick up some iron supplements but I’m not sure this will be enough. Any advice would be great. Thanks.”

Some more ubiome results ..

A few more readers sent in result.

  • “P” Bottom 4% for biodiversity (lowest that I have seen)
  • “Q” 75% for biodiversity
  • “R” 71% for biodiversity
  • “S” 78% for biodiversity

Instead of verbal comparison, see the population charts below for a visual of the various bacteria groups!! Oh boy are there huge shifts!!!!

Example Run of Ubiome Reports

After you log in, you have a menu appear.

choices

Clicking on Compare take you a display like below that shows the relative amount at different levels.

example

Or you can view it visually by volume (Patient “P”)

example1

 

Patient “D”

This is from earlier summary,   D had IBS only and no CFS

Example2

Patient F, CFS only after 20 years

example3

Patient G

exmaple4

Patient J

Latest

example5

A year earlier

example6

Two years earlier

Example7

Patient K

example8

Patient Q

example9

Patient R

exampleA

Patient S

exampleB

Bottom Line

Above you see many different patterns — the shifts are different (and likely match the person symptoms often). “P” is very severe, close to patient J, 2 years earlier (whose profile evolved closer to healthy).

The chart below is from the nature journal[2015]. we have Bacteriodes being the dominate one, nothing comes close!

  • We have some patients with greater Faecalibacterium , Kluyvera in 3 of these parents — definitely a massive overgrowth of these groups!
  • Faecalibacterium and/or Eubacterium are usually #2…  We have three with Blautia being #2. According to the charts, we should not expect more than 1% Blautia

ref

  • -1 ==> 10% of population
  • -2 ==> 1% of the population
  • -3 ==> 0.1 % of the population

What to do?

Most of these bacteria are not available as probiotics. Blautia overgrowth is something that I will research more (because of 3 people having such a high amount). Apart from that, keep to the suggestions of the model. Also, you can see why it is a model — the shifts are not all the same, but the shifts are very noticeable shifts… with the wrong group moving into dominance.

 

 

The CFS Holy Grail: THE biomarker

Over the last 16 years that I have been active dealing with my own CFS and while in remission, trying to understand this horrible puzzle more, I have come across many, many publications about finding a new biomarker for CFS.

IMHO, there is no SINGLE biomarker. The belief that there will be a single biomarker comes from the belief that the cause is a single item. A shift of the microbiome is not a single item. CFS is a a shift of dozen, in some cases, hundreds of relationships between many bacteria. There is no one bacteria or one virus or one DNA mutation responsible. The chemicals produced by these bacteria (metabolites)  may change, with certain ones being common across CFS patients. These same metabolities may also be common with some other diseases. The criteria to be a good biomarker is that it is unique to CFS and not to any other diseases. Almost all of these biomarkers are found by comparing CFS to healthy individuals.

Today, a read forwarded an article about Activin B being a potential biomarker. The article is Activin B is a novel biomarker for chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) diagnosis: a cross sectional study [2017]. “Serum activin B levels for CFS/ME participants were significantly elevated when compared to the study controls, as well as the established reference interval….Elevated activin B levels together with normal activin A levels identified patients with the diagnostic symptoms of CFS/ME, thus providing a novel serum based test. … follistatin levels were significantly lower in the CFS/ME group (p < 0.0001) ”

So what is Activin A and B? There is a wikipedia article on it. In short, it’s a chemical produced by cells.

What do we know from PubMed:

  • “Higher than normal values of these proteins[Activin A and B] were common in patients with H1N1 infection” [2014] So we know that virus can increase…
  • “We also show, for the first time to our knowledge, that IL-1β up-regulates hepcidin by an unexpected mechanism involving increased expression of BMP2 or activin B and consequent activation of the BMP signaling pathway… we found that IL-1β induced a significant increase in expression of activin B in mouse liver… may not apply to humans….Firstly, IL-1β has been implicated in the pathogenesis of IBD by several observations. ” [2015]
  • “Our results correlate and support the previous findings as there was a significant decrease in serum follistatin and significant increase in serum activin-A, activin-B, …  in patients with chronic hepatitis C and who did not receive treatment compared to healthy controls.” [2014] – So this diseases pattern shifts matches 2 of the 3 reported.
  • “Anemia is very common in patients suffering from infections or chronic inflammation and can add substantially to the morbidity of the underlying disease. It is mediated by excessive production of the iron-regulatory peptide hepcidin, but the signaling pathway responsible for hepcidin up-regulation in the inflammatory context is still not understood completely. In the present study, we show that activin B has an unexpected but crucial role in the induction of hepcidin by inflammation.” [2012]
  • “One of the BMP receptor ligands that appears to play a role in the inflammation-induced elevation of hepcidin is activin B.” [2015]
  • “Follistatin is a specific activin-binding protein and blocks the action of activins in most biological systems by preventing the binding of activins to their type II receptors (23).” [2009]

Bottom Line

Activin B is involved with inflammation — CFS has inflammation (as do hundreds of other conditions).  Comparing a group of patients with prolonged inflammation to healthy controls is likely to produce a positive result. Does this result show CFS? No, it shows inflammation — which is already well established by past studies with CFS/FM etc.

The low level of Follistatin reported is far more interesting because it keeps the Activin in control.  Follistatin-like protein has been implicated in Lyme arthritis [2014] . “Whether the associations between fT4 and follistatin levels persist in the whole thyroid function spectrum warrants future investigation.” [2016]

So, will this become a biomarker for CFS — very unlikely. Indirectly, we see that the inflammation chemicals increases Activin B and the decrease of follistatin decrease thyroid function. I would not be surprised to see a study finding high Activin B and low follistatin is associated with thyroid syndromes and thus this biomarker lacks the ability to separate them apart.

Amalgams: Do not go gluten free and other cautions!

I have done prior posts about mercury and MCS. The short form is from Danger of antioxidants (2016) and treating MCS (2016). Why MCS and mercury? “Our data show an increased prevalence of metal allergy and elevation of mercury levels in bioindicators among patients with MCS.” [2013] If a supplement impacts MCS negatively, then it may also impact high mercury in a similar way (this is a fall back approach where there is a lack of studies).

There are some professional ways to remove it, see eMedicine, but these will only be done when it is clear that the level are very high.

Items to reduce mercury levels

“Other than avoiding potential sources of mercury poisoning, there is no major role for self-care at home.” [eMedicine] ” Currently, no chelation agents have been approved for methylmercury or ethylmercury by the U.S. FDA.” [2016]

  • Some forms of mercury will dissolve in olestra [2010] – used for some potato chips
  • “The children and pregnant women in the study were found to have elevated blood levels of lead and mercury compared to age- and sex-matched Canadians. Consumption of probiotic yogurt containing 10(10) CFU Lactobacillus rhamnosus GR-1  had a protective effect against further increases in mercury (3.2 nmol/liter; P = 0.035) and arsenic (2.3 nmol/liter; P = 0.011) blood levels in the pregnant women, but this trend was not statistically significant in the children.” [2014]
  • Lactobacillus Fermentum ME3  [2010] produces glutathione, and per Mercola article “when your glutathione and sulfur levels increase, you’ll typically see higher levels of mercury coming out of your hair… “The core of the detoxification system is the glutathione system,” Dr. Shade says. “Notice that I don’t say, ‘it’s glutathione.’ No, it’s the glutathione system.
  • Effect of Probiotic Bacillus Coagulans and Lactobacillus Plantarum on Alleviation of Mercury Toxicity in Rat [2017]. “Oral administration of either probiotic was found to provide significant protection against mercury toxicity by decreasing the mercury level in the liver and kidney”
  • Taurine: “Results suggested that taurine played a vital role in reducing the mercury toxicity in intoxicated animals.” [2007]

Items to Avoid