Gut microbes-pathogenesis of CFS

[MeSci]

Hi MeSci

It may not be the case that you must LOOK the same as Scandinavians in order to predispose you to CFS. It may be a gene or set of genes that are inherited.

Like most people I am probably VERY ethnically mixed, with Scandinavian, sub-Saharan African, Asian and even Neanderthal DNA. I almost-certainly have Spanish ancestry on one side, and a grandfather was blond and blue-eyed.

I haven't read the links on evidence that there is a disproportionate propensity to ME in people of Scandinavian origin, but in another thread some time ago I posted evidence of high incidence in non-Scandinavian countries and also probable under-reporting/under-diagnosis for a range of reasons. I can't find it at the moment.

 

[Vegas]

Yes I've long thought the same. I, and all my family are blonde/brown hair with blue eyes and 3 of us with CFS. Even though we are not Scandinavian. I bet many others on this forum have the same features too.

Anyway, I've always wondered why and always attributed it to an evolutionary trait but never thought of Vitamin D.

Stranger things have occurred...

Well, like others have said, this fact certainly cannot offer much in the way of explaining disease susceptibility, but I have seen some data to believe that those who originated from the North Atlantic are disproportionately likely to suffer from a handful of conditions that would impair detoxification, I have also read that those whose ancestors originated from Scandinavia are over-represented among ME/CFS, this was an anecdotal report from a specialist hardly proof of the propensity. I do know that pernicious anemia is much more common in blue-eyed humans; there is disease susceptibility. With regard to what I would generically term as "poor detoxifiers," I think you there may be an over-representation of a combination of blue-eyes and Type O blood, just an association. There is also a complementary theory with respect to malarial susceptibility and folate availability. Again, I wasn't looking for this, or seeking to explain susceptibility, I just kept seeing these associations.

The melanin connection with VDR was interesting to me with regard to the detoxification of bacterial organisms, but I thought it was also curious because humans with blue eyes, which of course is a consequence of decreased melanin production in the iris, all originate from a single ancestor, and a very recent one at that, dating back to 8000 years ago or so. So it looks like you and me are related much more closely than our friends with green or brown eyes. Everyone in my household has blue eyes, and my mother has PA.

 

[Vegas]

Like most people I am probably VERY ethnically mixed, with Scandinavian, sub-Saharan African, Asian and even Neanderthal DNA. I almost-certainly have Spanish ancestry on one side, and a grandfather was blond and blue-eyed.

I haven't read the links on evidence that there is a disproportionate propensity to ME in people of Scandinavian origin, but in another thread some time ago I posted evidence of high incidence in non-Scandinavian countries and also probable under-reporting/under-diagnosis for a range of reasons. I can't find it at the moment.

I would think the same, under-reporting/diagnosis from other non-industrialized regions; I think you would have to look at these characteristics in a particular region on country and control for those things that would affect reporting, diagnosis, social issues leading to treatment, etc.

 

[MeSci]

Well, like others have said, this fact certainly cannot offer much in the way of explaining disease susceptibility, but I have seen some data to believe that those who originated from the North Atlantic are disproportionately likely to suffer from a handful of conditions that would impair detoxification, I have also read that those whose ancestors originated from Scandinavia are over-represented among ME/CFS, this was an anecdotal report from a specialist hardly proof of the propensity. I do know that pernicious anemia is much more common in blue-eyed humans; there is disease susceptibility. With regard to what I would generically term as "poor detoxifiers," I think you there may be an over-representation of a combination of blue-eyes and Type O blood, just an association. There is also a complementary theory with respect to malarial susceptibility and folate availability. Again, I wasn't looking for this, or seeking to explain susceptibility, I just kept seeing these associations.

The melanin connection with VDR was interesting to me with regard to the detoxification of bacterial organisms, but I thought it was also curious because humans with blue eyes, which of course is a consequence of decreased melanin production in the iris, all originate from a single ancestor, and a very recent one at that, dating back to 8000 years ago or so. So it looks like you and me are related much more closely than our friends with green or brown eyes. Everyone in my household has blue eyes, and my mother has PA.

There was a poll on blood type here. It showed a very wide spread of blood groups among people with ME, but it really needed more participants, and then the results would need to be compared with the prevalence of different blood types in the general population.

Re VDR, I have 3 genetic polymorphisms that affect the Vitamin D receptor, e.g. see here.

 

[Jon_Tradicionali]

How do we kill things lodged in the dendritic cells?

That's the next step.

A former user of PR (I forget the name) did it using a mixture of high dose oral and IV ABX.
The mixture and dose was enough for him to recover within the next two weeks.
His story is on the net somewhere but I can't recall.

KDM is almost there. He has shown HERV expressions but cannot find the offender.
He has also shown Strp/Entero over-representations in PWCFS.

Therefore, its a viable explanation to believe Strep/Entero are in the dendritic cells of the small intestinal lining.

What I can say is, we are closer than we have ever been to solving this.

 

[Jon_Tradicionali]

Gene sharing between bacteria and susceptibility to phages.
Conclusion below:

"Analysis of spacer sequences suggest that these pathogens may be susceptible to a limited range of phages and provide further evidence of cross-species exchange of genetic material among Streptococcus pyogenes, Streptococcusagalactiae and Streptococcus dysgalactiae."

http://www.ncbi.nlm.nih.gov/pubmed/24256234

Although the above study was on horses, the findings are based on the Strep pathogens themselves
which do stand regardless. Bacteria has been well known to exchange genetic material between
one another in order to survive the bodies immune system. This is one way bacteria can evolve
to evade the immune system. However, it does show that the correct phage made specifically the
pathogen can be effective in destroying it.

Onwards

 

[Jon_Tradicionali]

Pathogenic bacteria activates pDC's, which in turn detects the bacteria and summons formation of macrophages to deal with the pathogen. However, Non-pathogenic bacteria does not activate pDC's as its not classed as a threat in order to activate it.

"L. lactis strains also stimulated expression of immunoregulatory receptors on pDC (ICOS-L and PD-L1), and accordingly augmented pDC induction of CD4(+)CD25(+)FoxP3(+) Treg compared to the Lactobacillus strain. Oral administration of L. lactis JCM5805 induced significant activation of pDC resident in the intestinal draining mesenteric lymph nodes, but not in a remote lymphoid site (spleen). Taken together, certain non-pathogenic spherical LAB in wide dietary use has potent and diverse immunomodulatory effects on pDC potentially relevant to anti-viral immunity and chronic inflammatory disease."

http://www.ncbi.nlm.nih.gov/pubmed/22505996

LAB (Lactic Acid Bacteria) is shown to not activate pDC's. Although, it can do quite the opposite in that it has immunomodulatory effects on pDC's which may be useful in certain scenarios. One such example would be in the case of an infection which activates the immune system but the immune system is not able to locate and destroy it (for various reasons that I have outlined in previous posts) which will leave the immune system in a chronic 'fight' state.
Therefore, non pathogenic LAB's can reduce inflammation by way of its immunomodulatory effects on pDC's and decrease intensity of bodies "fight" state as shown in this study.

Onwards

 

[Jon_Tradicionali]

Bacteria causes CFS. Or does it? Here is a few ways to find out:

"Based on Kirby-Bauer antimicrobial susceptibility data, streptococci were found to be generally susceptible to cephalothin, erythromycin, nitrofurantoin, penicillin, and ticarcillin and clavulanate. Resistance to antimicrobials has not developed over the years, except for gentamicin and tetracycline against S. equisimilis."

http://www.ncbi.nlm.nih.gov/pubmed/22362945

The above antimicrobials are effective against Strep which KDM found an abnormal representation in all PWCFS in comparison with controls. Some of the effective antimicrobials listed above are intravenous which are generally more potent than oral variants.

Onwards

 

[tdog333]

I'm curious to know whether anyone has tried a fecal transplant? I think there are a ton of different ways CFS is caused, but there are probably a lot less reasons why it doesn't go away. Maybe we are lacking a(or quite a few) certain strain of bacteria that is especially good at preventing these microbes from wreaking havoc. I'm sure the great majority of people here have taken at least one, if not MANY courses of abx. The studies I have read show that there are a massive amount of unknown strains of bacteria in a healthy body.

If you look at C.Difficile for example- Fecal transplant works almost 100% of the time. This could be due to the sheer amount of bacteria competing or a certain strain we have no isolated. What's interesting is that some fecal donors stool samples are completely ineffective, while others work incredibly well. We are in the dark ages when it comes to the gut flora unfortunately.

I read one study where after a single course of abx the gut flora was completely crippled for 9 months, and after 5 years it didn't even look remotely the same in terms of species and amounts- complete balance shift. The gut flora also makes up a significant portion of our immune activity.

Combine this fact with some unknown(or known) viruses/infections, genetic defects, environmental toxins and heavy metals in our every day lives, oxidative stress, poor diet, I can go on and on with causes.

Cell mediated immunity is also often compromised as we hit on earlier a bit. So I think it's important to correct all of these things since we may not know exactly what is wrong with each individual. I've learned a holistic view is much more effective than spending 100% of energy and time focusing on only one step.

 

[Sushi]

@tdog333

Try a google site search. There is a lot of discussion of fecal transplants on this site.

Best,
Sushi

 

[Jon_Tradicionali]

Considering the findings from the conference yesterday bracketing CFS as an inflammatory disorder, I have decided to share the following article linking inflammation with bacteria:


------------------------------------------------------
Meconium microbiome analysis identifies bacteria correlated with premature birth.
Authors
Ardissone AN, et al. Show all
Journal
PLoS One. 2014 Mar 10;9(3):e90784. doi: 10.1371/journal.pone.0090784.

Affiliation
Abstract
BACKGROUND: Preterm birth is the second leading cause of death in children under the age of five years worldwide, but the etiology of many cases remains enigmatic. The dogma that the fetus resides in a sterile environment is being challenged by recent findings and the question has arisen whether microbes that colonize the fetus may be related to preterm birth. It has been posited that meconium reflects the in-utero microbial environment. In this study, correlations between fetal intestinal bacteria from meconium and gestational age were examined in order to suggest underlying mechanisms that may contribute to preterm birth.

METHODS: Meconium from 52 infants ranging in gestational age from 23 to 41 weeks was collected, the DNA extracted, and 16S rRNA analysis performed. Resulting taxa of microbes were correlated to clinical variables and also compared to previous studies of amniotic fluid and other human microbiome niches.

FINDINGS: Increased detection of bacterial 16S rRNA in meconium of infants of <33 weeks gestational age was observed. Approximately 61·1% of reads sequenced were classified to genera that have been reported in amniotic fluid. Gestational age had the largest influence on microbial community structure (R = 0·161; p = 0·029), while mode of delivery (C-section versus vaginal delivery) had an effect as well (R = 0·100; p = 0·044). Enterobacter, Enterococcus, Lactobacillus, Photorhabdus, and Tannerella, were negatively correlated with gestational age and have been reported to incite inflammatory responses, suggesting a causative role in premature birth.

INTERPRETATION: This provides the first evidence to support the hypothesis that the fetal intestinal microbiome derived from swallowed amniotic fluid may be involved in the inflammatory response that leads to premature birth.

http://www.ncbi.nlm.nih.gov/m/pubmed/24614698/?i=2&from=bacteria fetus
------------------------------------------------------

Bacteria infects humans earlier than previously thought, triggering inflammation.

Would also like to point out 2 findings revealed at the conference:

-PWCFS have delta waves whilst awake, in comparison to controls that have them during sleep only

-Gene comparison show CFS to be most closely linked to an inflammatory disorder, followed by parasitic and bacterial infection.

Delta waves whilst awake is no surprise considering how disconnected from our surroundings we feel.

Gene comparison showed very interesting results. Most closely linked to inflammatory disorder which points us to a trigger and followed closely by parasitic and bacterial infections which have comparable genes to PWCFS.

Everything consistently points at a chronic inflammatory state in PWCFS. Triggered and maintained by a bacterial infection.

 

[Radio]

Considering the findings from the conference yesterday bracketing CFS as an inflammatory disorder, I have decided to share the following article linking inflammation with bacteria:


------------------------------------------------------
Meconium microbiome analysis identifies bacteria correlated with premature birth.
Authors
Ardissone AN, et al. Show all
Journal
PLoS One. 2014 Mar 10;9(3):e90784. doi: 10.1371/journal.pone.0090784.

Affiliation
Abstract
BACKGROUND: Preterm birth is the second leading cause of death in children under the age of five years worldwide, but the etiology of many cases remains enigmatic. The dogma that the fetus resides in a sterile environment is being challenged by recent findings and the question has arisen whether microbes that colonize the fetus may be related to preterm birth. It has been posited that meconium reflects the in-utero microbial environment. In this study, correlations between fetal intestinal bacteria from meconium and gestational age were examined in order to suggest underlying mechanisms that may contribute to preterm birth.

METHODS: Meconium from 52 infants ranging in gestational age from 23 to 41 weeks was collected, the DNA extracted, and 16S rRNA analysis performed. Resulting taxa of microbes were correlated to clinical variables and also compared to previous studies of amniotic fluid and other human microbiome niches.

FINDINGS: Increased detection of bacterial 16S rRNA in meconium of infants of <33 weeks gestational age was observed. Approximately 61·1% of reads sequenced were classified to genera that have been reported in amniotic fluid. Gestational age had the largest influence on microbial community structure (R = 0·161; p = 0·029), while mode of delivery (C-section versus vaginal delivery) had an effect as well (R = 0·100; p = 0·044). Enterobacter, Enterococcus, Lactobacillus, Photorhabdus, and Tannerella, were negatively correlated with gestational age and have been reported to incite inflammatory responses, suggesting a causative role in premature birth.

INTERPRETATION: This provides the first evidence to support the hypothesis that the fetal intestinal microbiome derived from swallowed amniotic fluid may be involved in the inflammatory response that leads to premature birth.

http://www.ncbi.nlm.nih.gov/m/pubmed/24614698/?i=2&from=bacteria fetus
------------------------------------------------------

Bacteria infects humans earlier than previously thought, triggering inflammation.

Would also like to point out 2 findings revealed at the conference:

-PWCFS have delta waves whilst awake, in comparison to controls that have them during sleep only

-Gene comparison show CFS to be most closely linked to an inflammatory disorder, followed by parasitic and bacterial infection.

Delta waves whilst awake is no surprise considering how disconnected from our surroundings we feel.

Gene comparison showed very interesting results. Most closely linked to inflammatory disorder which points us to a trigger and followed closely by parasitic and bacterial infections which have comparable genes to PWCFS.



Everything consistently points at a chronic inflammatory state in PWCFS. Triggered and maintained by a bacterial infection.

We need to challenge are comprehension of the facts and ask the right questions to have full understanding of disease.


What is the main contributing factors in acquiring these chronic inflammatory bacterial infections?

The liver insufficiency is a contributing factor in detoxifying the toxic microbiota waste created by the dysbiosis imbalances. The root cause of this conundrum in my opinion is inflammation of the stomach lining that develops into hypochlorhydria that deplete the stomach ability to produce hydrochloric acid. We need the correct gut pH to have balance in are gut flora. We need HCL to achieve homeostasis in the body. Please research Dr. Alex Vasquez per-review work on dysbiosis, inflammation and chronic health problems. Also, these chronic inflammatory bacterial infections can damages the mitochondria cells and affects the kidney, brain and liver as well.


Hypochlorhydria + Dysbiosis + Chronic inflammation = Acquired Mitochondrial Disease



Alex Vasquez, D.C., N.D.
http://www.academia.edu/3862817/Nut...etal_Inflammation_and_Chronic_Health_Problems

H.pylori-Hypochlorhydria-Dysbiosis-Liver-CFS/ME-Connection
http://forums.phoenixrising.me/inde...dria-dysbiosis-liver-cfs-me-connection.28937/

 

[snowathlete]

Not sure where I stand on what the cause is; I guess a pathogen is likely to be the trigger, but probably doesn't need to stick around.
I don't think it's gut bacteria for instance, even though there is clearly gut dysbiosis. I think that's a secondary effect, along with lots of other secondary effects, as a result of autoimmunity/faulty immune tollerance.

 

[Jon_Tradicionali]

Created a thread with reference to a study which I believe deserved special mention:

http://forums.phoenixrising.me/index.php?threads/one-theory-to-prove-them-all.29336/