ME/CFS for 18 years, recently diagnosed with D-Lactic acidosis as cause of symptoms and illness.

Avenger

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Hi bread, Kanga Sue, Archie, Michael M, Pearshaped, Howard, SamB, I hope I have not forgot any in this thread;


I have had a good holiday from 'D-Lactic ME' , but I have crashed again after trying protocols including Naltrexone and Probiotics to fully reverse the illness and I am back on the exclusion diet. I am getting close, but I expect that a Fecal Transplant my be the best way after a heavy antibiotics to destroy bacteria and candida infections. I have used my time to make further attacks on Somatization in ME by the NHS and psychiatrists becuause I believe that Somatization stands as a Human Rights abuse because it causes vulnerability to patients who have illness that takes longer that 2 years to diagnose, vulnerable to psychiatrists and such a dangerous diagnosis that if placed in your records will act as a warning that all of your symptoms are psychological and do not need investigation. I believe that the diagnosis of Somatization to be sheer ignorance and the poorest thinking from those who we expect the highest level and in opposition to the hypocratic oath.

Cort Johnson at Health Rising has also taken a stance against Somatiztion 'Ending the Somatization Myth, Who's Deluded Now'.

https://www.healthrising.org/blog/2019/11/11/somatization-myth-chronic-fatigue-syndrome/

Sorry not to get back to you for so long, but have continued my NHS fight by taking it to the EU Human Rights Courts, while still fighting other aspects though the Ombudsman. It has taken a lot out of me and I had ended up using alcohol to be able to cope with the stress and then fell ill again. I do not believe that I will get a fair hearing in the UK and the Ombudsman have refused to investigate anything to do with Somatization disorder which is routinely diagnosed for ME/CFS.

Excerpt of my EU Human Rights Complaint below;

My application to the European Court of Human Rights concerns 18 years of abuse of my Human Rights that started in 2001 (two years after I became ill in 1999); when I was misdiagnosed with a psychological illness (Somatization) after a two year delay in diagnosis of illness which has recently been related
to D-Lactic acidosis that was delayed in diagnosis until 2017, because of inherent discrimination caused by the Somatization diagnosis that was placed prejudicially in my records and NHS summery documents including A&E and my 'Significant Medical History' to cause further stigmatization, because Somatization has influenced all treating Doctors and Services including A&E. I cannot obtain a fair or impartial investigation from the NHS or Ombudsman; I am still unwell and this has caused three years of fighting for investigation.


I need to take my Human Rights complaint concerning Somatization disorder diagnosis and other Human Rights abuse to the European Court of Human Rights before it is too late. The Tory Government according to Liberty plan to stop fundamental Human Rights after Brexit. I have only one chance to make an appeal to the court of Human Rights. Please read my reasons below; because the NHS Trust has tried to cover up that I was diagnosed with Somatization or that it was placed in my most influential summery documents, which they are stating they now cannot find in my records as though it does not exist, so that it cannot be realized; and due to a number of replies from the Ombudsman I suspect collusion.

I now believe that the psychological diagnosis of 'Somatization disorder' stands as a Human Rights abuse in its own right, because it is unreasonable and unethical; because the parameters for diagnosis of Somatization by a Psychiatrist is based upon a lack of evidence or clinical diagnosis within 2 years; which means that a number of illnesses including MS, Bechet's disease, Systemic Lupus and D-Lactic acidosis that take on average over two years to diagnose would be negatively and prejudicially influenced by such a psychological diagnosis as Somatization; which will cause further delay in obtaining the correct diagnosis and will only add to the stress and psychological trauma of patients with such a misdiagnosis, which happened to me when I was left with traumatic symptoms and pain after the Somatization diagnosis acted to cause me long term discrimination, because it became my diagnosis for all of my systemic symptoms and illness caused by infection and D-Lactic acidosis since 2001; there is evidence that illness was caused by prescription drugs and then dismissed as Somatic.

'Somatization disorder' was placed in my clinical record and a number of summery documents for all Doctors to see as a warning that my symptoms were psychological and I was frequently dismissed without investigation or refused attendance; and I have had to make a number of complaints to the Parliamentary and Health Service Ombudsman which all relate to the Somatization diagnosis causing discrimination, which has caused Doctors to dismiss my illness and not to attend during exacerbations of D-Lactic acidosis which can cause fatality and has caused me frequent illness including breathing difficulty like suffocation, drunk like confusion, abdominal and systemic pain, muscle weakness, tachyarrhythms and systemic neurological symptoms; which were dismissed by Doctors in A&E as psychological and Somatization caused them not to make requested Blood Gas investigations, even after a number of Doctors who had got to know me had made statements that my symptoms were in fact not Somatic from 2002 (just a year after Somatization diagnosis).

I cannot afford a solicitor because the issues have become more complex due to the dishonesty of the NHS replies to my Hospital Complaints. I need urgent help because the abuse has continued from the NHS Chief Executive who have dishonestly tried to cover up the Somatization diagnosis as though it has never happened and the Ombudsman have refused to investigate any of the issues concerning Somatization; and after so many years of continued abuse is causing me further depression and making me unwell. I feel that I can no longer live under such conditions in the UK. I cannot endure any further abuse.

I have tried to reasonably make complaints to my local NHS Trust and Health Service Ombudsman for the past 3 years, but the Ombudsman has closed my case based on the dishonesty of a number of NHS Complaint Replies; for which I have only recently found evidence of misrepresentation, dishonesty and hiding information to prevent it being realized. I also cannot afford a Solicitor because the delay in diagnosis has caused me debt because I have been too unwell to work as a Sculptor; and the simple complaint about the delay in diagnosis of D-Lactic acidosis and misdiagnois of Somatization, has now become abnormally complicated due to the dishonesty employed by the NHS stop my information being realized.

I believe that the Ombudsman was complicit in leaving the Somatization diagnosis active in 2005 to cause discrimination and further delay in my diagnosis for another 12 years, because they had not taken the evidence into account of real illness in 2005 and evidence from Doctors that I was not Somatizing. They have covered this up by not investigating my Hospital Complaints concerning Somatization in 2017, after I finally gained a diagnosis. I did not feel that I would be treated and differently by the Ombudsman until I had gained a full diagnosis, but made 4 Complaints which I had asked to be seen together as evidence of the effects of Somatization, but the Ombudsman refused and investigated them separately, without investigating the effects of the Somatization diagnosis. Prior to the Somatization diagnosis I had been diagnosed with ME. which has similar neurological symptoms to D-Lactic acidosis and it is possible that a Subset of ME is caused by D-Lactic acidosis; and I had also asked for investigation of D-Lactic acidosis on behalf of many other patients with ME in the UK, but had been refused. I had also evidenced to the Ombudsman Somatization as a Human Rights abuse .



Paul.
 
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How do you find a gastro who will entertain such theories of functional conditions being caused by the gut? Who will run the proper tests and try various treatments?
 

Avenger

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There are very few Gastroenterologists who understand these issues because a number of Consultants are telling me that they are not trained to; or the NHS are putting up the front that they do not understand these issues.

You will need to find an expert in Small Bowel Bacterial Overgrowth first. There are a number who can diagnose this condition and test for it. But they may not test for Methane producing Bacteria, only Hydrogen producing. If you have Gastrointestinal Symptoms, reflux, bloating, dyspepsia, abdominal pain etc. then you need to have this diagnosed. The Gastrointestinal symptoms although uncomfortable are mild compared with side effects of the production of Organic Acids including D-Lactic acid. My belief is that there are a number of Bacteria causing ME/CFS symptoms in at least a Subset.

I would go privately, and also do a MOAT test for other Organic Acids that will evidence Bacterial Overgrowth and possibly identify the type of Bacteria, eg. Candida etc. (although it will not identify D-Lactic Organic Acids). This is £110 from Biolab. Have this simple urine test done when your symptoms are at worst for the best results.

From the way that I have been treated by the NHS, they do not want to allow the probability that there may many others with such Gastrointestinal problems after the way that they have been treating patients as though they have psychological problems for so long. The backlash from so many patients would be disastrous for the NHS.

I am still finding it impossible to have a D-Lactic assay performed by the NHS when I have an exacerbation of symptoms, despite it being requested by my Consultant. I believe that even though I have a diagnosis, that the NHS do not want to allow this to happen.

There has been a quantum change in understanding and many diseases are now being treated with Fecal Transplants including MS, Autism and ME outside of the UK, although in the early stages, the results are encouraging.

My own belief is that along with environmental changes we have also damaged many thousands of years of evolutionary symbiotic bacteria through the use of antibiotics, because we have not understood or overlooked the importance of Gastrointestinal Bacteria that not only digest out food, but take part in our immune system and the production of neurotransmitters such as Seratonin.

The NHS has been making absolute statements concerning ME as a psychological problem, treatable through cognitive behavioral therapy and graded exercise, based upon false statistical data; when they have little understanding of the underlying Gastrointestinal issues and prescribed treatments by the NHS such as Antibiotics, Probiotics and Proton Pump Inhibitors have been implicated in different forms of Bacterial Overgrowth.


Paul.
 

Avenger

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Hi all who have followed this post.

I am asking for some help passing my message to anyone who may be able to help or is supportive of ME/CFS.

I am going to have to force the issue and have the investigations done privately prior to trying for funding to have a Fecal Transplant. I will try to identify the Bacteria concerned in Overgrowth and then prove that this condition is reversible, which may force the NHS to provide treatment for others with similar Gastrointestinal issues causing symptoms of ME/CFS in a Subset.

I have been turned down for a Fecal Transplant by the NHS despite being close to total resistance to antibiotics (which is unethical). I am certain that a Fecal Transplant may offer reversal of D-Lactic acidosis and SIBO and my Consultant agrees. I also have evidence that a Fecal Transplant may also reverse or eliminate resistant species of bacteria.

I have gone to gofundme for help.

Statement for gofundme;

I have been unwell for 18 years with a rare illness (D-Lactic Acidosis) which has the same symptoms as ME.

I want to pioneer a Fecal Transplant and or Phage Therapy to reverse the condition which can be life threatening.

I believe that a Subset of ME/CFS patients may have the same or similar illness that could be reversed by a Fecal Transplant.

I am facing total antibiotic resistance without a Fecal Transplant and denied one from the NHS (it is treated with cyclical antibiotics).

This would save my life and be ground breaking at the same time and could help the lives of many thousands with ME who may have similar forms of this illness.

I am possibly the first to gain a diagnosis and to trial a Fecal Transplant to reverse D-Lactic acidosis if i can gain funding. I am also in contact with many others who have similar Gastrointestinal illness who are being denied treatment.

I also believe that we have created ME, which seems to have started around the same time as we started using antibiotics in the 1950's (paradoxically treated with antibiotics). Some Probiotics including those used by the NHS may be implicated, but this is all still controversial as there is still not enough evidence.

Antibiotics can cause Overgrowth's of Bacteria that act like a hidden infection (through the resistance of some species and decimation of more vulnerable species; and altering immune response). This is a form of evolution that we have aided; chance selection at the cost of symbiosis.

I was a Sculptor before I became ill. My greatest desire would be to regain my health and be able to share my life with my daughters and grandchildren and to make sculpture again.

I may have little time before total resistance occurs. There is now evidence that a Fecal Transplant from a healthy donor may also reverse antibiotic resistance.

https://www.gofundme.com/f/rare-ill...dium=copy_link&utm_campaign=p_cf+share-flow-1
 
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JES

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FMT as a treatment holds a lot of promise, as there is now a long list of diseases that are associated with abnormal microbiome. FMT is even trialed for diseases like ALS now.

The main problems with FMTs are availability, cost and safety. I can't see it becoming a mainstream treatment in the near future for other than life threatening conditions. There is also the problem that for most people, FMTs need to be redone periodically to maintain remission, one is rarely going to be curative. Without a good donor this treatment is also a no-go, so in order to get a good response people are looking for so called super donors. If the donor is not good or happens to carry some pathogenic antibiotic resistant bacteria, there is a real risk of death following FMT.

There is a thread here highlighting this problematic and what needs to be done for FMT to become mainstream treatment.
 

Avenger

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Hi Archie, sb4 and all following the D-Lactic/Bacterial Overgrowth threads; you will definitely like this!

SamB, sent this to me; amazingly similar symptoms to out own!!!!

Wed 25/12/2019 20:00

https://www.rollingstone.com/music/music-features/boy-bear-dave-hosking-fecal-transplant-919384/


A Medical Mystery Almost Ended His Band. Then He Found a 'Poo Roadie'
Boy & Bear’s Dave Hosking was doubled-over, disoriented and depressed until fecal transplants gave him his health and his music back
www.rollingstone.com
 
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Avenger

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Hi dyllanmurphey, Archie, sb4 and all following the D-Lactic/Bacterial Overgrowth threads; you will definitely like this!

SamB, sent this to me; amazingly similar symptoms to out own!!!!

Wed 25/12/2019 20:06

https://www.rollingstone.com/music/music-features/boy-bear-dave-hosking-fecal-transplant-919384/



A Medical Mystery Almost Ended His Band. Then He Found a 'Poo Roadie'
Boy & Bear’s Dave Hosking was doubled-over, disoriented and depressed until fecal transplants gave him his health and his music back
www.rollingstone.com
 
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Avenger

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Hi Archie, sb4, KangaSue, Jimbo and all following the D-Lactic/Bacterial Overgrowth threads; you will definitely like this!

SamB, sent this to me; amazingly similar symptoms to out own!!!!


Wed 25/12/2019 20:06
  • Paul Smith
https://www.rollingstone.com/music/music-features/boy-bear-dave-hosking-fecal-transplant-919384/



A Medical Mystery Almost Ended His Band. Then He Found a 'Poo Roadie'
Boy & Bear’s Dave Hosking was doubled-over, disoriented and depressed until fecal transplants gave him his health and his music back
www.rollingstone.com

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Yesterday at 1:53 PM
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Avenger

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Hi Archie;
SamB found this thread on HealthRising, which also has a lot of excellent articles;
My belief is that this is further evidence of different forms of Gastrointstial Bacterial Overgrowth, which may be both similar and different in all of us; SamB is doing a lot of similar research and turning up some very interesting articles and more and more people with direct Gastrointestinal related illness or ME/CFS.


I think the article below is of great interest and a story similar to my own; Bacteria, Parasites, Archaea and Viruses are all overlapping possibilities; I think that this is another 'variation on a theme'.

healthrising.org/forums/threads/antiparasitic-treatment-is-working.6250/
Pgrovetom is Member of Health Rising.

Nov 6, 2019
I posted this in the general forum but now that I'm near symptom free or greatly reduced for almost 2 months, I thought it was time to post under recovery. I hope this doesn't jinx me but I think its important for others to read. Its possible all the parasites were not killed and it will return but then I will know what to do. The changes are miraculous. NO MORE FM-like pain!


My previously posted story:

I've been on a quest to unravel my own CFS/ME and FMS. I initially relied on doctors thinking they should be able to diagnose my condition. But after seeing dozens of local, integrative, Stanford, John Hopkins, UCSF and Mayo Clinic doctors, I realized they weren't like the doctors who's papers I read on PubMed. I'm now doing the thinking and doctors occasionally offer good ideas and run tests I can't get on my own. After going down many dead ends and curing some unrelated problems, I'm getting close to what is going on. It might be something seen in others so I thought I would share what I've discovered and see what people think.

From the early days of my problems over 10 years ago, I kept seeing evidence implicating my gut. But I was pulled off into many other possibilities such as Lyme disease, Gluten sensitivity, SIBO, Spinal stenosis, vasculitis, MS, myositis, Fungi, autoimmune, hormonal, toxins and a variety of infections. I returned to investigating my gut since antibiotics, diet and especially sugars definitely modulate my symptoms and have done so for over 10 years. I had significant remission from key symptoms due to treatment with Flagyl, Bactrim and a few obscure anti-microbials. My high IgE, IL-5, IL-4, eosinophillia was suggestive of a parasitic infection or related gut based problem. My IBS-C fluctuated in severity along with other broader symptoms. I could eat something with a sugar such as milk, a candy bar or ice cream and I had severe asthma within 30-60 minutes. An early hypothesis to which I have returned was that something "living" in my gut was "stirred up" by the sugar causing a gut immune reaction which in turn found its way into my circulatory system and stimulated a body-wide immune reaction. That reaction seemed to vary but seemed behind all my extra-intestinal symptoms ( i.e. pain, fatigue, neurological etc..). So I finally found a marker that shows what is happening to my intestines that leads to the immune response bleeding into my greater circulatory system. I've always heard about leaky gut but its such a vague description of the complex intestinal permeability problem. That marker is F-Actin IgA antibody. It indicates damage to the intestinal Actin.

Severe Celiac Disease if allowed to go for years can mimic all the symptoms I experience. But I tried going gluten free plus thorough and repeated testing suggested I did not have Celiac Disease. But it was noticed that I had a very high F-Actin IgA antibody. That is used to monitor Celiac patients for being gluten free.

The Celiac story. Think Celiac-like damage but not caused by gluten. Something living in your gut is doing the same type of damage as gluten which is leading to symptoms that mimic the Celiac extraintestinal symptoms. Since these are immune mediated, they can cause a wide variety of symptoms due to the pervasive nature of a varying over active innate and adaptive immune system.

https://arup.utah.edu/media/celiac_disease/Celiac disease Final 19.8.12.pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809109/

https://www.inovadx.com/sites/default/files/2018-07/690418 - Celiac Brochure.pdf

This is because the gluten immune reaction in the intestines damages the intestinal smooth muscle Actin. Actin is a key structural protein of the cytoskeleton network that is particularly abundant in intestinal microvilli. But Gluten is not the only thing that damages the intestinal Actin. So the F-Actin IgA antibody test is useful for detecting this particular damage to the intestines which if severe can cause all the symptoms of Celiac but has nothing to do with gluten. Going gluten free does modify your intake of sugars and carbohydrates so may give the impression its having an impact via microbiome alterations. The problem involves the microbiome driven gut immune activity altered when the microbiome is changed that bleeds out into the body via increased permeability due to Actin damage. Just like Celiac.

Cytoskeletal Regulation of Epithelial Barrier Function During Inflammation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913378

So my F-Actin IgA antibody was quite high on the 2 recent tests and being gluten free made no difference. So that suggests something in my gut is damaging my intestinal Actin and causing increased permeability such that my gut immune reactions are bleeding into my system. By avoiding sugar 99.99%, I'm able to decrease my overall symptoms but that's only one factor. So I've been on a search for what's in my gut that is known or believed to damage Actin. And what is in my gut that is known to damage Actin. So far I've been able to identify a few organisms in my gut using DNA stool testing that are suspect. They include a parasitic worm, blastocystis, Clostridium difficile and Clostridium perfringens. There are many other possibilities but organisms are potentially treatable and it can be tested with empiric treatment.

Clostridium difficile Toxins A and B: Insights into Pathogenic Properties and Extraintestinal Effects

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4885049/

The treatment of the parasitic worm is fairly easy but given its a 10 year plus infection, the maximum treatment is suggested. So I was given 1200mg of Praziquantel twice day and 400mg of Albendazole also twice a day for 14 days. I then waited 2 weeks and repeated the treatment. As of this writing, all my pain is gone and many other symptoms are at an all time low. This is promising but then I moved on and am now treating the blastocystis with Nitazoxanide ( Alinia) with 500mg twice a day for 14 days. I will then treat the blastocystis one more time with Flagyl at 400mg twice a day for 10 days. So far things look quite promising. I've yet to get any doctor to consider any of this as realistic. They are so rigid and seem unable to think outside a very small box and fear curiosity and generally don't really care. I was given the drug Nucala for the severe Asthma symptoms which is seriously contraindicated for someone with a parasitic infection. When I mentioned my very high IgE, IL-5, IL-4 and eosinophillia which strongly suggest a parasite, they looked at me like I was crazy. When I also mentioned that DNA meta-genetic sequencing found a parasitic worm, they asked what meta-genetic sequencing was and how did I get it done - being suspicious rather then curious.

Since Clostridium difficile and Clostridium perfringens cannot be treated, the only strategies to control the problem would be using a aluminosilicate toxin binder. Hopefully the Clostridium perfringens toxin will bind to an aluminosilicate binder. By taking the binder 3 times a day, as it passes through my intestines unabsorbed, the toxins bind to it and they pass with the stool. This won't eliminate all the toxins but will reduce the quantity. Some strains of Clostridium difficile are known to have a toxin B that is 100 times more toxic than typical strains. Clostridium difficile toxins are known to cause extra-intestinal effects similar to Celiac. I've been taking the binder along with the parasitic treatment. I will see if I can reduce or eliminate most of my symptoms and then recheck the F-Actin IgA antibody test to see if my gut lining is healing.

Effective Sequestration of Clostridium difficile Protein Toxins by Calcium Aluminosilicate
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4649210/

So to summarize my hypothesis, I'm thinking I have a Celiac-like condition that is damaging my smooth muscle F-Actin in my intestines which is leading to Celiac-like extra-intestinal symptoms. I am testing 3 different possible organism based causes through empiric treatment. I suspect organisms are involved due to the effects of diet and anti-microbials. I would recommend anyone with CFS/ME and FMS with IBS-like symptoms that seem to be modulated with diet to ask your doctor for the F-Actin IgA antibody test. You can learn more about it below. If you are positive, you should investigate the cause and try and "treat" it down to normal. I suspect this might be a common problem not yet widely understood. Its mentioned in many research papers but the condition is not widely known like IBS or IBDs.

F-Actin IgA antibody Labs:
http://ltd.aruplab.com/Tests/Pub/0051724
http://www.rdlinc.com/test_menu/anti-f-actin-ab-iga/
https://www.cyrexlabs.com/CyrexTestsArrays - Intestinal Antigenic Permeability Screen Actomyosin IgA

Test developer brochure
https://www.inovadx.com/sites/default/files/2018-07/690418 - Celiac Brochure.pdf

Pgrovetom made this statement on Health Rising; ''let me know what you think! Sound familiar? Think I'm crazy? Anybody had the same experience with doctors?'' This does sound familiar, and he is most certainly not crazy. He has found another possible part of the puzzle and possibly other possible pathogens and ways of treating them. The pathogens causing my D-Lactic symptoms have not been identified. I may try the Parasite treatment, because it may still affect my Bacterial Overgrowth.

Pgrovetom from Health Rising has also used Flagyl (Metronidazole) as I had with success, and has IgA abnormalities. I was also found to have high IgM and eosinophilia. This may be a similar story with a slight variation of causation or understanding. I will have to contact him.

(Archaea domain contains single-celled organisms. Archaea have genes that are similar to both bacteria and eukaryotes. Because they are very similar to bacteria in appearance, they were originally mistaken for bacteria. Like bacteria, archaea are prokaryotic organisms and do not have a membrane-bound nucleus).

It is articles like this that will break the back of this illness.


Paul.
 

Avenger

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Gut instinct leads EnteroBiotix scientists to a microbiome wonder drug.
A Special One For the New Year! May all of your ills be healed and your chains broken!

There is a new Fecal derived 'drug' that may reset those with a damaged Gut Microbiome in the near future. This is further evidence that the Gut Microbiome may be to blame for at least a Subset of ME/CFS and many other diseases.


Hi Archie,
Sb4, Kanga Sue, Jimbo and SamB and anyone interested in the Gut Microbiome as the cause of ME/CFS, IBS and other forms of illness; There may be a happy ending in sight!

Please read The Times report by Tom Whipple Science Editor on Dr. James Mcllroy; Fecal Transplant may now be a thing of the past, because a new process that will bring a pill form of 'filtered' dried and Gut Bacteria from a super donor may be available to all of us in the near future.


On top of this there is recognition that the Microbiome can cause a range of diseases, bowel conditions and Chronic Fatigue Syndrome; and that a Fecal Transplant can be life changing. The idea that a Fecal Transplant breaks the cycle and patients get better.

https://www.thetimes.co.uk/article/...entists-to-a-microbiome-wonder-drug-8fw8k0t3d
Gut instinct leads EnteroBiotix scientists to a microbiome wonder drug
Tom Whipple, Science Editor
December 10 2019, 12:01am, The Times

The microbiome, the diverse populations of microbes in our guts, has been linked to diseases ranging from bowel conditions to chronic fatigue syndromeALAMY
Never has a wonder drug had such a PR challenge. Yes, this treatment can cure a disease that otherwise ruins lives and even leads to death. Yes, it has the potential to produce results in other conditions ranging from diabetes to multiple sclerosis. There is, however, a significant and understandable barrier to its wider acceptance: it generally involves ingesting faeces.
Now a Scottish company believes it has a solution that could make faecal transplants more palatable: by drying the healthy bacteria found in poo and putting it in a pill.
“We want to expand access, maximise patient safety and reduce the ick and yuck factor,” James McIlroy, from EnteroBiotix, said. “What.....

Happy New Year to You All!

Paul.
 

Avenger

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Hi Archie,
Sb4, Kanga Sue, Jimbo and SamB and anyone interested in the Gut Microbiome as the cause of ME/CFS, IBS and other forms of illness;
Here is another that is now theorized as down to Gut Microbiome;
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6241162/

2018; 9: 2627.
Published online 2018 Nov 9. doi: 10.3389/fmicb.2018.02627
PMCID: PMC6241162
PMID: 30483222
Altered Gut Microbiota in Myasthenia Gravis
Dongxu Qiu,1,2 Zhiwei Xia,1,2 Xiao Jiao,1,2 Jun Deng,1,2 Lei Zhang,1 and Jing Li1,2,*
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.

Associated Data
Supplementary Materials
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Abstract
Myasthenia gravis (MG) is an autoimmune-mediated disorder, the etiology of which involves both environmental factors and genetics. While the exact factors responsible for predisposition to MG remain elusive, it is hypothesized that gut microbiota play a critical role in the pathogenesis of MG. This study investigated whether gut microbiota are altered in MG patients by comparing the fecal microbiota profiles of MG patients to those of age- and sex-matched healthy controls. Phylotype profiles of gut microbial populations were generated using hypervariable tag sequencing of the V4 region of the 16S ribosomal RNA gene. Fecal short-chain fatty acids (SCFAs) were assessed by gas chromatographic analyses. The results demonstrated that, compared to the healthy cohort, the gut microbiota of the MG group was changed in terms of the relative abundances of bacterial taxa, with sharply reduced microbial richness, particularly in the genus Clostridium. The fecal SCFA content was significantly lower in the MG group. Furthermore, microbial dysbiosis was closely related to the levels of inflammatory biomarkers in the sera of MG patients.
Keywords: myasthenia gravis, 16S rRNA, gut microbiota, Clostridium, short-chain fatty acids
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Introduction
Myasthenia gravis (MG) is an antibody-mediated, T cell-dependent autoimmune disease. It is characterized by fluctuating weakness of skeletal muscles, mainly caused by autoantibodies directed against the acetylcholine receptor (AChR) located in the postsynaptic membrane at the neuromuscular junction. The pathogenesis of MG is closely correlated with high levels of circulating AChR antibodies (Pestronk et al., 1985). Several studies have revealed that the production of AChR antibodies is associated with the disequilibrium of Th1, B cells, and Foxp3+ T regulatory (Treg) cells (Mu et al., 2009; Aricha et al., 2011). Among them, Foxp3+ CD4+ Treg cells play a critical role in maintaining self-tolerance and immune homeostasis in the prevention of the development of MG. Foxp3+ CD4+ Treg cells regulate the production of AChR antibodies by influencing the amount of autoreactive T cells and suppressing the activity of autoreactive B cells, leading to the reduction of disease severity and progression(Shin et al., 2014). In patients with MG, the frequency of Foxp3+ CD4+ Treg cells is significantly deficient and has become the major focus of many studies on the pathogenesis of MG (Fattorossi et al., 2005; Li et al., 2008; Masuda et al., 2010). Therefore, novel approaches that can restore the defects in Foxp3+ CD4+ Treg cell numbers will be valuable for the treatment of MG disease.
Foxp3+ CD4+ Treg cells are the most prominent regulatory cells in the body. The frequency of Foxp3+ CD4+ Treg cells is notably higher in colonic lamina propria than in any other organ (Atarashi et al., 2011). Furthermore, the Foxp3+ CD4+Treg cells in intestinal lamina propria have unique characteristics, which are markedly affected by the composition of gut microbiota (Nagano et al., 2012). For instance, the colonization of germ-free mice with a mix of Clostridium strains increases the frequency of Foxp3+ CD4+Treg cells in colonic lamina propria. In addition, a mixture of 17 strains of Clostridium isolated from a healthy person strongly induces Foxp3+ CD4+Treg cells in the human colon. These data provide new insights indicating that Foxp3+ CD4+Treg cells in the intestine maintain homeostasis of the gut microbiota (Nagano et al., 2012; Atarashi et al., 2013). Indeed, the gut microbiota could affect the number and T-cell receptor (TCR) repertoire of Foxp3+ CD4+ Treg cells. The TCRs on Foxp3+ CD4+ Treg cells can recognize subsets of commensal bacteria, inducing naive CD4+ T cells to differentiate into antigen-specific Foxp3+ CD4+Treg cells, leading to an increased amount of Foxp3+ CD4+ Treg cells (Cong et al., 2009; Lathrop et al., 2011). Remarkably, the frequency of Foxp3+ CD4+ Treg cells is significantly deficient in MG patients and has become the major focus of interpreting the pathogenesis of MG. Therefore, we hypothesized that perturbations in the composition of gut microbial communities may be associated with intestinal bacteria-induced Foxp3+ CD4+Treg cell deficiency. Modifying the intestinal microbiome could be crucial for the design of therapeutic interventions toward MG. However, to date, no studies have evaluated the microbiota profiles of MG patients. To address this issue, we report a case-control study and analyses of the gut microbial communities in MG patients. We also measured fecal short-chain fatty acids (SCFAs) to investigate whether specific changes in microbial composition may affect the production of microbial metabolites, which may play critical roles in regulating Treg differentiation through epigenetic modifications. According to our data, changes in microbial composition, diversity, and metabolites seem to have far-reaching effects on MG disease.


Discussion
The gut microbiome may be a factor responsible for the precipitation of disease in genetically susceptible individuals (Abegunde et al., 2016; Alverdy and Luo, 2017). Our results provide the first evidence that MG disease features a dysbiotic microbiota with an overall depletion of microbial diversity, as well as an altered structure of the microbial community. Specifically, levels of commensal microbe-derived SCFAs were significantly lower in MG patients. Our results provide novel insights into MG-relevant host–microorganism interactions.

The human gut is considered a bioreactor with a high diversity of bacterial taxa, predominantly belonging to the Firmicutes and Bacteroidetes (Haro et al., 2016), that is shaped by different environmental parameters. We observed that Bacteroidetes and Firmicutes are the main bacterial phyla involved in changes in the microbiota, and the ratio of Firmicutes/Bacteroidetes (F/B ratio) in the MG patients was significantly lower than that in HC individuals. Indeed, the F/B ratio can describe a pro-inflammatory environment, the inflammatory microbiota of which might cause damage to the intestinal epithelium, subsequently triggering an immune response that contributes to the immunological imbalance characteristic of autoimmune disorders. Our results are in line with the fact that there is a shift toward a decreased F/B ratio in inflammatory bowel disease and Crohn’s disease (Andoh et al., 2011; Walker et al., 2011). Taken together, these findings lend support to the notion that changes in the F/B ratio are linked to a range of autoimmune-mediated disorders. However, its impact on the balance of anti- and pro-inflammatory forces might be more complex.

Changes in the microbial community can influence a multitude of physiological functions by regulating the host’s autoimmune system. In our study, differences between the microbiota of the HC and MG groups were identified in terms of the relative abundance of specific genera. We revealed that the richness of genera such as Clostridium and Lactobacillus were sharply decreased in the MG group. Among them, the genus Clostridium, a member of the Firmicutes, was the most depleted (T-test, p < 0.001). Furthermore, qPCR analyses confirmed this finding and showed that the absolute amount of Clostridium was approximately threefold greater in HC subjects than in MG patients. It is now well documented that specific changes in microbial composition, particularly the proportion of Clostridium strains, have profound effects on the number and TCR repertoire of Foxp3+ CD4+ Treg cells. Indeed, TCRs on Foxp3+ CD4+ Treg cells recognize subsets of commensal bacteria, inducing or expanding in response to bacterial stimuli. Although Clostridia do not adhere to intestinal epithelial cells (IECs), they colonize the mucus layer near the epithelium and have a powerful influence on IECs (Atarashi et al., 2011), increasing the expression of 2,3-dioxygenase and TGF-β1, which may promote the differentiation of naive CD4+ T cells into antigen-specific colonic Foxp3+ CD4+ Treg cells, consequently leading to an increased frequency of Foxp3+ CD4+ Treg cells (Cong et al., 2009; Kuhn and Stappenbeck, 2013). As an autoimmune disease, MG is characterized by the overproduction of AChR antibodies (Lindstrom et al., 1976; Engel et al., 1977); the disequilibrium of B cells and Foxp3+ CD4+ Treg cells is involved in the overproduction of AChR antibodies. Remarkably, Foxp3+ CD4+ Treg cells suppress autoreactive B cells as well as anti-AChR auto-antibody production, leading to a reduction in the severity of MG disease (Shin et al., 2014). Thus, the abundance of Foxp3+ CD4+ Treg cells is critical for the prevention of MG disease. However, the frequency of Foxp3+ CD4+ Treg cells in the peripheral blood lymphocytes is significantly deficient in MG patients. Therefore, therapeutic interventions that could restore depleted Clostridia, consequently leading to an increase in the number of Foxp3+ CD4+ Treg cells, will be novel therapeutic strategies against MG disease.

Of particular significance is the dramatically increased level of Streptococcus in the MG cohort. Recent studies have revealed that Streptococcus have a direct impact on the peroxisome proliferator-activated receptor (PPARγ) (Jones, 1988). PPARγ is involved in the regulation of immune cell proliferation and differentiation (Couvigny et al., 2015). For instance, PPARγ induces the differentiation of Foxp3+ CD4+ Treg cells, which indicates that PPARγ could lead to greater numbers of Foxp3+ CD4+ Treg cells (Nettleford and Prabhu, 2018). Streptococcus have been shown to regulate both PPARγ and its ligand 15d-PGJ2; the mechanism is through activation of PPARγ by inhibiting certain pathways or immune cell functions (Nettleford and Prabhu, 2018). A sharply greater abundance of Streptococcus has also been observed to ameliorate rheumatoid arthritis, experimental IBD, and eosinophilic airway inflammation (Kawahito et al., 2000; Hammad et al., 2004; Kim et al., 2014); our results are in line with these findings. Taken together, these findings highlight the notion that the relative abundance of Streptococcus can affect transcriptional regulation through factors such as PPARγ, leading to a tightly tuned balance in the immune system response (Nettleford and Prabhu, 2018).

The precise mechanism through which Clostridia regulate the differentiation and activation of immune cells remains unclear. One possible mechanism is the cooperative generation of SCFAs (Furusawa et al., 2013; Narushima et al., 2014). Microbes such as Clostridia are well-known producers of SCFAs as fermentation end-products of proteins and carbohydrates (Cummings and Macfarlane, 1991; Duncan et al., 2004). SCFAs have profound effects on T cells and directly regulate their differentiation into Foxp3+ CD4+ Treg cells (Maslowski et al., 2009; Atarashi et al., 2013). SCFAs facilitate Foxp3+ CD4+ Treg cell differentiation by at least two different mechanisms. First, exposing naive CD4+ T cells to SCFAs enhances the acetylation status of histone H3 in the promoter and CNS3 enhancer regions of the Foxp3 gene loci, leading to the differentiation of Foxp3+ CD4+ Treg cells (Furusawa et al., 2015). Second, SCFAs alter the phenotype of dendritic cells (DCs), inducing Raldh1 expression in DCs to promote the production of RA, inducing the differentiation of Foxp3+ CD4+ Treg cells (Atarashi et al., 2013). Therefore, changes in the specific microbial composition changes the production of microbial metabolites, which seem to have far-reaching effects on immunity and may be particularly relevant in the context of MG disease. Here, we observed that the levels of SCFAs were significantly lower in MG individuals. Furthermore, the abundance of Clostridia, identified as the main producers of SCFAs (Cummings and Macfarlane, 1991), was also lower in that cohort. Taken together, these results indicate that it is certainly plausible that depletion of Clostridia leads to a decrease in microbial metabolites (SCFAs), which are partly associated with deficiencies of Foxp3+ CD4+ Treg cells.

It is becoming clear that dysbiosis may drive chronic inflammation, which has the greatest influence on systemic immune responses (Forsythe et al., 2007; Karimi et al., 2009). Hence, changes in certain members of gut microbial communities are always involved in biomarkers of autoimmune inflammation. One of the mechanisms proposed to explain this pro-inflammation status is microbe translocation (MT) from an inflamed gut. To date, a widely used measure of MT is the serum concentration of lipopolysaccharide (LPS) and endotoxin core antibody immunoglobulin M (EndoCAb-IgM). Both reflect MT-associated immune activation (Monnig et al., 2016). Previous studies have reported that MT is an exclusive pathogenic characteristics in IBD/IBS (Abdul et al., 2016), graft-versus-host disease (Eriguchi et al., 2012) and HIV disease (Yim et al., 2009), which feature increased levels of LPS-sCD14 and EndoCAb-IgM. Indeed, the commensal flora operate synergistically with the intestinal barrier, and interact with the innate immune system well. Once the specific microbial composition changes, microbes as well as their metabolites are able to invade and pass through the intestinal barrier, evade immune intervention, and egress into circulation, consequently leading to immune activation and chronic system inflammation (Yim et al., 2009). In contrast to previously published data, we found that the concentrations of LPS-sCD14 and EndoCAb-IgM were significantly lower in the MG cohort, which indicates little causality between MT and the related inflammation in those patients. However, other inflammatory biomarkers, such as TNF-α and IL-6, were detected at higher levels in MG individuals. In summary, changes in the microbial communities in MG might amplify systemic inflammation by driving the expression of inflammatory mediators rather than the pathogenesis of MT.

This study had several limitations. First, the numbers of MG patients and control cases were small, limiting the ability to analyze potential confounding factors. Second, we added potassium dichromate to the collected fecal samples. Potassium dichromate is an antiseptic and effectively kills most microbial taxa. It is a strong oxidizing agent. As facultative anaerobes are more resistant to oxidation than strict anaerobes, potassium dichromate might have selective effects on the obligate anaerobes. Therefore, our results might have been affected by a relevant bias. Finally, our study, like others conducted on humans, does not answer the question of whether dysbiosis is the consequence or cause, or both, associated with MG disease. Future work to establish the causal relationship between them is needed.

Paul.
 
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Hi all who have followed this post.

I am asking for some help passing my message to anyone who may be able to help or is supportive of ME/CFS.

I am going to have to force the issue and have the investigations done privately prior to trying for funding to have a Fecal Transplant. I will try to identify the Bacteria concerned in Overgrowth and then prove that this condition is reversible, which may force the NHS to provide treatment for others with similar Gastrointestinal issues causing symptoms of ME/CFS in a Subset.

I have been turned down for a Fecal Transplant by the NHS despite being close to total resistance to antibiotics (which is unethical). I am certain that a Fecal Transplant may offer reversal of D-Lactic acidosis and SIBO and my Consultant agrees. I also have evidence that a Fecal Transplant may also reverse or eliminate resistant species of bacteria.

I have gone to gofundme for help.

Statement for gofundme;

I have been unwell for 18 years with a rare illness (D-Lactic Acidosis) which has the same symptoms as ME.

I want to pioneer a Fecal Transplant and or Phage Therapy to reverse the condition which can be life threatening.

I believe that a Subset of ME/CFS patients may have the same or similar illness that could be reversed by a Fecal Transplant.

I am facing total antibiotic resistance without a Fecal Transplant and denied one from the NHS (it is treated with cyclical antibiotics).

This would save my life and be ground breaking at the same time and could help the lives of many thousands with ME who may have similar forms of this illness.

I am possibly the first to gain a diagnosis and to trial a Fecal Transplant to reverse D-Lactic acidosis if i can gain funding. I am also in contact with many others who have similar Gastrointestinal illness who are being denied treatment.

I also believe that we have created ME, which seems to have started around the same time as we started using antibiotics in the 1950's (paradoxically treated with antibiotics). Some Probiotics including those used by the NHS may be implicated, but this is all still controversial as there is still not enough evidence.

Antibiotics can cause Overgrowth's of Bacteria that act like a hidden infection (through the resistance of some species and decimation of more vulnerable species; and altering immune response). This is a form of evolution that we have aided; chance selection at the cost of symbiosis.

I was a Sculptor before I became ill. My greatest desire would be to regain my health and be able to share my life with my daughters and grandchildren and to make sculpture again.

I may have little time before total resistance occurs. There is now evidence that a Fecal Transplant from a healthy donor may also reverse antibiotic resistance.

https://www.gofundme.com/f/rare-ill...dium=copy_link&utm_campaign=p_cf+share-flow-1
Hey my friend. Why don't you find someone who's close to you and do it yourself?


These are some of the things openbiome screens for.

Just pick someone trustworthy who's your age, healthy, and has a low-risk lifestyle.

Screen for just a couple things like C Diff and maybe Rotavirus.

Just a thought - you have to make your own decision of course.
 

Avenger

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Hi dyllanmurphey,
I have already considered this, and it may be my only choice in the future; But it is important to do this through accepted channels and with a properly screened donor as there have been a few recorded fatalities; and it is more important that this is done for the benefit of all, properly recorded after the Bacteria have been quantified and possibly identified so that a path can be established for others with forms of ME/CFS/Bacterial Overgrowth.


I am very suspicious that the NHS are not interested in investigating any possibility that ME/CFS may be caused by Bacterial Overgrowth or abnormal microbiota. I think that they may be more worried about repercussions, which is the only explanation that I can find for their actions in the face of increasing evidence. They cannot be totally vacant to such a logical possibility.

The ancient Greek Father of Medicine, Hippocrates penned that “all diseases begin in the gut

I am finding more and more disease processes that have recently been related to abnormal Gut microbiota composition. I do not believe that these are all secondary abnormalities. It is looking as though we have completely misunderstood the importance of Gastrointestinal Bacteria, which still remain an undiscovered continent. We still need to map the Genetic differences to compare healthy and unhealthy compositions.


Cystic Fibrosis;
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0198457

Altered intestinal microbiota composition, antibiotic therapy and intestinal inflammation in children and adolescents with cystic fibrosis
  • Maiara Brusco de Freitas,
  • Emilia Addison Machado Moreira ,
  • Camila Tomio,
  • Yara Maria Franco Moreno,
  • Felipe Perozzo Daltoe,
  • Eliana Barbosa,
  • Norberto Ludwig Neto,
  • Vittoria Buccigrossi,
  • Alfredo Guarino
Altered intestinal microbiota composition, antibiotic therapy and intestinal inflammation in children and adolescents with cystic fibrosis
  • Maiara Brusco de Freitas,
  • Emilia Addison Machado Moreira,
  • Camila Tomio,
  • Yara Maria Franco Moreno,
  • Felipe Perozzo Daltoe, …x
  • Abstract
    The aim of the present study was to evaluate the effect of cystic fibrosis and antibiotic therapy on intestinal microbiota composition and intestinal inflammation in children and adolescents. A cross-sectional controlled study was conducted with 36 children and adolescents: 19 in the cystic fibrosis group (CFG) and 17 in the control group (CG) matched for age and sex. The CFG was subdivided based on the use of antibiotic therapy (CFAB group) and non-use of antibiotic therapy (CFnAB group). The following data were evaluated: colonization, antibiotic therapy, mutation, breastfeeding, use of infant formula, type of delivery, introduction of solid foods, body mass index, fecal calprotectin and intestinal microbiota composition (fluorescence in situ hybridization). Intestinal inflammation evaluated by fecal calprotectin was significantly higher in the CFG (median: 40.80 µg/g, IQR: 19.80–87.10, p = 0.040) and CFAB group (median: 62.95 µg/g, IQR: 21.80–136.62, p = 0.045) compared to the CG (median: 20.15 µg/g, IQR: 16.20–31.00), and the Bacteroides, Firmicutes, Eubacterium rectale and Faecalibacterium prausnitzii were significantly decreased (p < 0.05) in the CFG compared to the CG, whereas the bacteria Clostridium difficile, Escherichia coli and Pseudomonas aeruginosa were significantly increased in the CFG (p < 0.05). The main differences were found between the CG and CFAB group for Eubacterium rectale (p = 0.006), Bifidobacterium (p = 0.017), Escherichia coli (p = 0.030), Firmicutes (p = 0.002), Pseudomonas aeruginosa (p < 0.001) and Clostridium difficile (p = 0.006). The results of this study confirm intestinal inflammation in patients with CF, which may be related to changes in the composition of the intestinal microbiota.

Figures














Citation: de Freitas MB, Moreira EAM, Tomio C, Moreno YMF, Daltoe FP, Barbosa E, et al. (2018) Altered intestinal microbiota composition, antibiotic therapy and intestinal inflammation in children and adolescents with cystic fibrosis. PLoS ONE 13(6): e0198457. https://doi.org/10.1371/journal.pone.0198457
Editor: Nades Palaniyar, Hospital for Sick Children, CANADA
Received: November 6, 2017; Accepted: May 18, 2018; Published: June 22, 2018
Copyright: © 2018 de Freitas et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: All relevant data are within the paper and its Supporting Information file.
Funding: We thank the National Council for Scientific and Technological Development (CNPq) - Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) for their financial support (#471197/2013-0) and scholarships for EAMM (#304281/2012-3); Programa de Bolsas de Estudo da Educação Superior de Santa Catarina (UNIEDU) for scholarships to MBF.
Competing interests: The authors have declared that no competing interests exist.
Introduction
Microbiome acquisition begins in the uterus and progresses during childhood. The composition of the microbiota is influenced by the type of delivery, feeding, exposure to antibiotics in the perinatal period and maternal physical contact [1, 2]. An increase in the diversity of the intestinal microbiota occurs beginning at birth and children one to three years of age have a pattern similar to that found in adults. However, the occurrence of infection results in a lower diversity of microbiota [3, 4]. In addition to being associated with health promotion, breast milk provides significant amounts of Bifidobacterium and Lactobacillus [5] and the ingestion of solid foods may or may not exert a positive influence on the microbiome, depending on the type of food [6].
The defect in the cystic fibrosis transmembrane regulator in patients with cystic fibrosis (CF) can have manifestations in the gastrointestinal tract, such as gastroesophageal reflux, viscous intestinal mucus due to dehydration, acidification of the medium, altered mucosal glycosylation [7], distal intestinal obstruction, inflammation, bacterial overgrowth in the small intestine, slow transit time, inflammatory bowel disease [8] and dysbiosis [9], the latter of which can trigger the overgrowth of opportunistic pathogens and contribute to the development of diseases [10, 11].
The mechanism underlying the inflammatory bowel process remains unclear, but inflammation in evidenced by the increase in inflammatory markers, such as calprotectin and rectal nitric oxide, in patients with CF [6, 12]. The use of antibiotics, such as tobramycin and erythromycin, is another factor that may influence the microbiota of the gastrointestinal tract [11]. While the ecological balance is normally restored within a few weeks after antibiotic ingestion, there is evidence that antibiotic-associated disorders may persist for a long time after treatment. Thus, prolonged exposure to antibiotics may result in the overgrowth of antibiotic-resistant bacteria [13], as Clostridium difficile (C. difficile), which can cause severe diarrhea and/or pseudomembranous colitis [14].
Studies have shown that patients with CF typically have decreased amounts of Bifidobacterium spp. [6], the Bacteroides-Prevotella group [12], Clostridium cluster XIVa [15], Faecalibacterium prausnitzii (F. prausnitzii) [6] and Eubacterium rectale (E. rectale) [6], whereas Enterobacteriaceae and Clostridia [14] are increased.
The clinical relevance of the change in intestinal microorganisms is not well established, but the microflora of the gastrointestinal tract is known to be related to metabolic functions, such as the regulation of host immune response. Thus, the frequent use of antibiotics can have a negative cumulative effect on the metabolism and immune system in this population [16].
The aim of the present study was to evaluate the effect of CF and antibiotic therapy on intestinal microbiota composition and intestinal inflammation in children and adolescents.
Methods and subjects
Study design
A cross-sectional study was conducted between March and December 2016 at the Joana de Gusmão Children’s Hospital in the city of Florianópolis, Brazil. This study received approval from the Human Research Ethics Committees of the hospital and the Federal University of Santa Catarina (certificate number: 48959715.2.1001.0121). The legal guardians of the children and adolescents signed a statement of informed consent.
Subjects
The required sample size calculated by the difference in means was 18 for each group (OpenEpi® program, 1:1 proportion of exposed to non-exposed, 80% power and 95% confidence level). Thus, the overall sample was composed of 36 children and adolescents. The control group (CG) was composed of 17 individuals with a median age of 3.00 years [interquartile range (IQR): 0.60–7.00 years] and cystic fibrosis group (CFG) was composed of 19 individuals with a median age of 4.00 years (IQR: 1.10–9.50 years). Moreover, the CFG was subdivided based on the use of antibiotic therapy (CFAB group) and non-use of antibiotic therapy (CFnAB group).
The inclusion criteria for the CFG were a diagnosis of CF (chloride sweat test ≥ 60 mmol/L) and clinical stability for at least 30 days prior to the data collection process [17]. The individuals in the CG were recruited from children’s care clinic of the hospital and matched to the CFG for age and sex, with a body mass index (BMI) in the ideal range and the absence of CF [17]. The following were the exclusion criteria for the CG: fever, trauma, diseases (celiac, respiratory, inflammatory, intestinal, rheumatic, psychiatric, degenerative, cardiovascular, diabetes mellitus, renal, primary or secondary immunodeficiency and glucose/lactose intolerance) and use of antibiotics, hormones, non-hormonal anti-inflammatory drugs, proton pump inhibitors, oral, inhaled and intravenous corticosteroids, ranitidine hydrochloride, immunosuppressants and antihistamines 30 days prior to the data collection. The exclusion criteria for the CFG were the same as those for the CG, except for the use of antibiotics. Patients taking antibiotics (colimycin, azithromycin, tobramycin, cefuroxime, ciprofloxacin, oxacillin and ceftazidime) for the treatment of lung disease were admitted to the study. Daily supplementation as part of the protocol was taken into account and supplement intake was determined on the basis of patient reports. The hospital medical protocol prescribed the following supplements: SourceCF® vitamin supplement (Eurand Pharmaceuticals, Huntsville, AL, USA) for those aged ≥ 1 year to < 4 years, 2 mL/day; ADEK® (Axcan Pharma, Birmingham, AL, USA) at a dose of one tablet/day for those aged ≥ 4 to < 10 years and two tablets/day for those aged ≥ 10 years [18]; CREON® (Solvay Pharmaceuticals, GmbH, Germany) for older children and adults, who require 500 to 4000 lipase units per gram of fat ingested (mean = 1800 lipase units/g of fat) [19].
Assessment of clinical characteristics, BMI, lung function and disease severity
Data on age, sex, date of birth, date of diagnosis of CF, colonization, antibiotic treatment and mutation were collected from the patients’ medical records. Information on breastfeeding, the use of an infant formula, type of delivery and the introduction of solid foods was based on parental reports. Anthropometric data (height and weight) were collected using the method described by Pereira [17]. BMI was classified based on the World Health Organization criteria [20] using the Anthro and AnthroPlus programs (WHO, Geneva, Switzerland). Bacteriological findings and lung function [assessed based on forced expiratory volume in one second (FEV1)] were determined as described by Pereira [17]. Disease severity was determined based on the Shwachman-Kulczycki (S-K) score [17].
Analysis of intestinal inflammation
For the analysis of fecal calprotectin, feces were collected in plastic containers and delivered directly to the hospital. Intestinal inflammation was assessed based on fecal calprotectin, which was measured using the RIDASCREEN® Calprotectin (R-biopharm-AG) immunoenzyme test. Samples with a calprotectin concentration of 0 to 50 µg/g were considered normal, values between 50 to 100 µg/g were considered intermediate and values higher than 100 µg/g were considered indicative of intestinal inflammation [21].
 

Avenger

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Hi @Avenger , how much could stand and walk when you were sick?
How was your energy level?
Hi RIman, sorry I do not know how I missed your post.

I was very unwell, my symptoms fluctuated from day to day, hour to hour. I was expecting to die or have to commit suicide. The symptoms were like being tortured; and at worst breathing difficulty like suffocation and confusion and even a seizure. Milder symptoms of dizziness, pain and generally feeling unwell, so fatigued that I could barely stand at times, but also remissions and periods of feeling almost normal except for abnormal fatigue after any form of activity. I could not recover from any activity and fatigue would be compounded by forcing myself to try again before i had recovered; which would result in being bed bound for days to weeks thinking that I was going to die.

I would also have periods of abnormal abdominal pain, hypoglycemia, ectopic heartbeats and tachyarrhythms and headaches and zig zags at the periphery of vision which was also often blurred when ill.

I had kept fit from the age of 16, taking part in power lifting and thought at one point that I could just force my way through the illness, to my detriment and had to stop any form of exercise within weeks of falling ill; but I tried again and again to do different activities only to fall ill, often with breathing difficulty after almost every attempt.

My energy and muscle strength would also vary with periods fatigue for days, weeks or months on end.
 

Avenger

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Fecal Transplant Refused; The great Probiotic debate;

Hi Guys and Gals,
I have just been turned down for a Fecal Transplant. They have told me that they are not licensed for D-Lactic acidosis.
I will obviously fight this as a Human Rights issue; it would be unethical for me not to be allowed a Fecal Transplant in the face of antibiotic resistance after being given long term cyclical antibiotics.

Anyway back to Probiotics for now; a Consultant from Birmingham and a Dietitian from Bristol have told me to use Symprove Probiotics; I do understand that they contain D-Lactic Bacteria including Lactobascillus acidophilus, but I had to try the brand and blend as they were recommended.

I have also been using a number of other Probiotics including L. Rhasmosus and Bifidobacterium intermittently on top.

I had been unwell again for some months with pretty bad symptoms after another experimental failure to reverse the Overgrowth; and I must admit that I am feeling a lot better again using Symprove. I had stopped my symptoms with Erythromycin and then started Symprove with no ill effects so far.

It may be that the blend stops imbalance or overgrowth occurring?, but again I cannot be sure until it is put fully to the test going back on FODMAP Carbohydrates and Complex Sugars without developing D-Lactic symptoms again.

But... I am still unable to recover from any form of activity without often delayed muscle problems and fatigue that compounds with further activity. That I can live with.

Sheedy et al expected there to be other Bacteria involved in D-Lactic Overgrowth, and that could explain the ongoing problems after activity; and it may be that we all have different combinations of Bacterial Overgrowths, so that the same Probiotics may not fit all and will come down to experimentation. But I have read that L. Rhasmosus (recommended by Dr. Myhill) and Bifidobacterium Longum can be used in cases of Sepsis to attenuate systemic inflammaory response; But L. Rhasmosus has also have been cited as a cause of Sepsis in immune suppressed patients, so you will need to read as much as possible before making any decisions and FMT from a properly screened donor may be a better option.


Paul.



 

Avenger

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Eosinophils, probiotics, and the microbiome;
Eosinophils as a marker for Gut Dysbiosis;
This is an important report and I will evidence why in my next message.


Probably one of the most important reports that I have seen for a long time and fills in a lot of the gaps including Policing of Gut Microflora through the immune system; and why a Fecal Transplant may be better than using Probiotics for some (Some Probiotics have also been blamed for Gut Dysbiosis and Disease; possibly the real reason that the NHS have stopped using Probiotics such as VSL-3, rather than lack of efficacy; before possible litigation.)

Probiotics have also been associated with Eosinophilia, which is an autoimmune response that causes a syndrome similar to M.E. But Low Eosinophils are also associated with Gut Dysbiosis (I have had frequently low Eosinophils, for which their importance has only recently been understood and there is still a long way to go).

Read the Full Abstract;https://jlb.onlinelibrary.wiley.com/doi/pdf/10.1189/jlb.3RI0416-202R

This may be important in understanding why Probiotics may not suit everyone or be a 'one size fits all', and why Fecal Transplants may be better or not at controlling abnormal Gut Microbiota, because FMT transfer not only Bacterial Species but also Immune Products such as Eosinophils that may possibly contribute to recolonization....and there are so many implications; We have not fully understood the implications of Antibiotics or Probiotics on the Gut or the complexity of immune components such as Eosinophils. I am guessing that Gut Microbiota may be 'genetically' more similar in close relatives for FMT purposes in both Bacteria and Immune components. The issues are hugely complex.

Report;
Eosinophils, probiotics, and the microbiome Helene F. Rosenberg,*,1 Joanne C. Masterson,†,‡ and Glenn T. Furuta†,‡ *Inflammation Immunobiology Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA; † Section of Pediatric Gastroenterology, Hepatology and Nutrition, Gastrointestinal Eosinophilic Diseases Program, Department of Pediatrics and Digestive Health Institute, Children’s Hospital Colorado, Aurora, Colorado, USA; and ‡ Department of Medicine, Mucosal Inflammation Program, University of Colorado School of Medicine, University of Colorado School of Medicine, Aurora, Colorado, USA RECEIVED APRIL 26, 2016; REVISED JULY 24, 2016; ACCEPTED JULY 26, 2016. DOI: 10.1189/jlb.3RI0416-202R

ABSTRACT; There is currently substantial interest in the therapeutic properties of probiotic microorganisms as recent research suggests that oral administration of specific bacterial strains may reduce inflammation and alter the nature of endogenous microflora in the gastrointestinal tract.

Eosinophils are multifunctional tissue leukocytes, prominent among the resident cells of the gastrointestinal mucosa that promote local immunity. Recent studies with genetically altered mice indicate that eosinophils not only participate in maintaining gut homeostasis, but that the absence of eosinophils may have significant impact on the nature of the endogenous gut microflora and responses to gut pathogens, notably Clostridium difficile. Furthermore, in human subjects, there is an intriguing relationship between eosinophils, allergic inflammation, and the nature of the lung microflora, notably a distinct association between eosinophil infiltration and detection of bacteria of the phylum Actinobacteria. Among topics for future research, it will be important to determine whether homeostatic mechanisms involve direct interactions between eosinophils and bacteria or whether they involve primarily eosinophil-mediated responses to cytokine signaling in the local microenvironment.

One cannot see eosinophils in tissue and state a priori that the outcome will be positive or negative; eosinophil responses to their environment are clearly highly nuanced and context dependent [22, 23]. Toward this end, we are still seeking a clearer understanding of the way in which eosinophils modulate the nature of the microbiome.

Likewise, although is it clear that eosinophils can and do interact with bacteria in vivo, their ability to discern between pathogenic and probiotic species in various settings remains to be explored. J. Leukoc. Biol. 100: 881–888; 2016. Introduction There is a large and growing interest in the promise of probiotic microorganisms, defined by the World Health Organization as “live micro-organisms which, when administered in adequate amounts, confer a health benefit on the host” [1]. Probiotics, which are typically select species from the genera Lactobacillus or Bifidobacterium, currently represent a multibillion dollar commercial component of the dietary supplements industry. Nonetheless, at this time, the health benefits conferred by probiotic supplements are not completely clear, nor are they universally substantiated upon review of multiple clinical trials ([2–11]).

Probiotics are typically administered orally, and most of our current understanding and information comes from mouse model studies and clinical evaluation of their mechanisms of action at the gastrointestinal tract. Among these mechanisms, probiotic bacteria may restore balance to the endogenous gut microflora [12–14], the community of microbes known as the gut microbiome. Other, related mechanisms under exploration include interactions between probiotic bacteria and the epithelial cells lining the small intestines, as well as direct and indirect interactions with macrophages, DCs, and T and B lymphocytes present in the gut mucosa (reviews in [15–18]). Interestingly, and frequently overlooked, eosinophils are also among the resident cells of the gut mucosa [19–21] (Fig. 1). Although eosinophils circulate in small numbers in the bloodstream and can be recruited to somatic tissues, largely in response to the eosinophil chemoattractant eotaxin-1 (CCL11), working in concert with Th2 cytokine provocation [22, 23], eosinophils are present in the gut at homeostasis [24, 25]. As such, they are poised to interact with both endogenous microflora and exogenous probiotic bacteria alone or in concert with other resident leukocytes.

Much of the literature on probiotics and their relationship with eosinophils focuses on amelioration of allergic disease, notably allergic inflammation of the respiratory tract and skin. Among the confounding issues, there is no clear understanding of what features of probiotic organisms are crucial to elicit the desired response (e.g., bacterial species or strain that is most efficacious, use as prevention vs. therapy, duration of application, mix and composition of specific strains, length of therapy, and/or mechanism of action). Although the World Allergy Organization (WAO) has recently presented recommendations on probiotics for the prevention and therapy of eczema [26], there remains no consensus opinion on the impact of probiotics in allergic disease. The intent of this review is to examine more closely our current understanding of the relationship between eosinophils, 1. Correspondence: Inflammation Immunobiology Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 9000 Rockville Pike, MSC 1883, Building 10, Room 11C215, Bethesda, MD 20892, USA. E-mail: hrosenberg@niaid.nih.gov Abbreviations: COPD = chronic obstructive pulmonary disease, DC = dendritic cell, EET = eosinophil extracellular trap, EoE = eosinophilic esophagitis, GRAS = generally recognized as safe, NOD = nucleotidebinding oligomerization domain, PRR = pattern recognition receptor, SAMP = senescence-accelerated mouse prone, WAO = World Allergy Organization 0741-5400/16/0100-881 © Society for Leukocyte Biology Volume 100, November 2016 Journal of Leukocyte Biology 881......

EOSINOPHILS AND MICROFLORA IN THE GASTROINTESTINAL TRACT There is evidence from experimental mouse models indicating that eosinophils have an influence on the nature of the normal resident gastrointestinal microflora. Gastrointestinal eosinophils emerge during fetal life, before the acquisition of gut microflora [19, 20], and are maintained in the tissue by homeostatic levels of eotaxin-1 and cytokines from type 2 innate lymphoid cells [19–21, 24, 25]. Among the most interesting data in support of a role for eosinophils modulating microbial disease in the gut are recent findings from Buonomo et al. [50], who demonstrated a significant role for eosinophils in lethal infection with Clostridium difficile. Specifically, mice treated with the microbiota-regulated cytokine IL-25 were protected from lethal infection, an effect that was dependent on the influx of CD11b+ SiglecF+ eosinophils to the gut.

Eosinophil-deficient PHIL mice [51] were not protected from C. difficile infection by IL-25. Interestingly, mice lacking eosinophils suffered profound epithelial destruction, unrelated to levels of IL-4, mucin, or IgA. The results suggested that eosinophils maintained epithelial barrier function via mechanisms yet to be clarified. An intriguing counterpoint to these findings are those of DeSalvo et al. [52], who explored the interplay of IL-33, eosinophils, and normal microflora in colitis-prone SAMP mice. The SAMP strain featured in this study (SAMP1/YitFc [53]) carries a spontaneous mutation and has elevated levels of intestinal IL-33. In this study, IL-33–mediated eosinophil infiltration contributed to intestinal pathology, including profound loss of intact villous structure. Furthermore, minimal levels of IL-33 were detected in intestinal tissue of germ-free SAMP mice; introduction of normal microflora via fecal transplant resulted in induction of IL-33, Th2 cytokine production, eosinophil infiltration, and inflammatory pathology. Although there are many differences that can be accounted for between these 2 studies, among the most prominent is the fact that the responses, actions, and impact of eosinophils were clearly distinct and were influenced by the nature of the local microenvironment. One cannot see eosinophils in tissue and state a priori that the outcome will be positive or negative; eosinophil responses to their environment are clearly highly nuanced and context dependent [22, 23]. Toward this end, we are still seeking a clearer understanding of the way in which eosinophils modulate the nature of the microbiome.

In their study featuring mice devoid of eosinophils (DdblGATA), Chu et al. [54] found that the gut microflora in these mice was highly irregular, including more bacteria per milligram of feces, along with a skewed ratio favoring gramnegative to gram-positive species, with more bacteria of the phylum Bacteroidetes and fewer Firmicutes than in their wildtype BALB/c counterparts. Interestingly, Jung et al. [55] reported the reverse; in a series of experiments with the same mouse strains (BALB/c and eosinophil-deficient DdblGATA) under similar conditions (cohoused for at least 3 wk), the completely opposite results were observed, including a profound decrease in the proportion of Bacteroidetes and an increase in the fraction of Firmicutes in the same strain. As we begin to understand more about factors that may have a profound impact on the results from any individual microbiome study, it would be helpful as we move forward to have specific information on the diet provided to these mice, the specific age and gender, the frequency of cage changes [56], and factors such as temperature and dark–light cycles in the vivarium [57]. Apart from the opposite results, it is not clear whether eosinophils had a direct impact (e.g., via their granule proteins and cytokines) on the nature of the microbiome or whether the differences observed were more indirect, (i.e., eosinophils modulating survival of IgA+ plasma cells, the latter having a direct impact on gut homeostasis [54] or via support of Peyer’s patches and production of IL-7 [55]). Indeed, as DdblGATA mice are fully devoid of eosinophils, it cannot be said for certain that the gut eosinophils per se were the only cells of this lineage contributing to this response. Other studies suggest that the gut microbiome may have an impact on eosinophils at sites beyond the immediate gut microenvironment. Specifically, Suarez-Zamorano et al. [58] reported that elimination of the endogenous microflora using either antibiotic treatment or generation of germ-free mice resulted in expression of Th2 cytokines (IL-4, IL-5, and IL-13) and recruitment of eosinophils and macrophages to inguinal subcutaneous (s.c.) tissue in association with the development of functional beige-fat, a process known to be dependent on eosinophil-mediated macrophage polarization [59, 60]. The larger mechanisms linking microflora depletion and eosinophil accumulation at this more distant site remain unclear. Moving beyond the small intestines, Fillon et al. [61–63] explored the microbiome of the esophagus in healthy individuals and in patients with EoE and gastroesophageal reflux disease, the latter 2 disorders associated with increased numbers of eosinophils in the esophagus, a tissue ordinarily devoid of these cells......... 884 Journal of Leukocyte Biology Volume 100, November 2016


In the light of such limited understanding of the Microbiome and associated Immune interaction for so long by Doctors; I find their response to ME and similar illness to be beyond unreasonable and unethical; They have no right to be taking a stance against those with ME and I would go as far as to say that those who do so, must have psychological problems to believe such nonsense or to have such pathological lack of empathy, unless they are under pressure to act in this way; because they cannot possibly believe what they are saying or what they are trying to make us believe; as in Shamanism, because they must understand the limitations of medicine and their own understanding; when they are not trained or have little understanding of these issues and do not seem to be keeping up with the research. They are simply not trained to understand these issues and have no right to make such judgments. How can they, when they do not have all of the facts that are only slowly unwinding?
 
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Avenger

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For Sam and those terrorized by Ignorant Psychiatric Misunderstanding;
ME/Bacterial Overgrowth/D-Lactic acidosis & Somatization disorder!


One of the key parameters for Somatization disorder after being diagnosed by a Psychiatrist is Gastrointestinal Complaints!

Somatization disorder is regularly diagnosed for the symptoms of ME and Chronic Fatigue Syndrome and was also diagnosed for the symptoms of D-Lactic acidosis when I first fell ill 18 years ago.

One of the main symptoms of D-Lactic acidosis is Abdominal Pain and Motility issues (Constipation or Diarrhea) along with a host of Fluctuating Neurological Symptoms!

ME, Chronic Fatigue syndrome and even Fibromyalgia may be related to Gastrointestinal Conditions such as Bacterial Overgrowth and D-Lactic acidosis recorded . IBS has also been related to Bacterial Overgrowth is known to cause Chronic Fatigue, Abdominal Pain and Motility problems.

Somatization diagnosis and defenitions from The Internet;

Patients with somatization disorder (also known as Briquet's syndrome) present with unexplained physical symptoms, lasting several years, and including at least two gastrointestinal complaints, four pain symptoms, one pseudoneurologic problem, and one sexual symptom (Table 2).1 Nov
2007 ..

https://www.google.com/search?q=Som...ome..69i57.30700j1j8&sourceid=chrome&ie=UTF-8

https://familydoctor.org/condition/somatic-symptom-and-related-disorders/
How is somatoform disorder diagnosed?


Web results
www.ncbi.nlm.nih.gov › pmc › articles › PMC5798205
Diagnosis and treatment of somatoform disorders - NCBI


by JK Smith - ‎2012 - ‎Cited by 5 - ‎Related articles
Somatization may be suspected when the panoply of dysfunctional organ systems is belied by the patient's apparent health. A constellation of pain complaints and gastrointestinal, sexual, and pseudoneurologic symptoms is required for a DSM-IV diagnosis of somatization disorder.
Summary · ‎CONCLUSIONS

www.cghjournal.org › article › fulltext
High Somatic Symptom Burdens and Functional ...



by GS Sayuk - ‎2007 - ‎Cited by 27 - ‎Related articles
High Somatic Symptom Burdens and Functional Gastrointestinal Disorders ... more somatization state symptoms, had more somatization trait diagnoses, and had greater ... of an FGID in outpatients presenting with gastrointestinal complaints.
familydoctor.org › condition › somatic-symptom-and-related-disorders
Somatic Symptom and Related Disorders - familydoctor.org


24 Jan 2018 - To a person who has hypochondriasis, a grumbling stomach may ... Even with treatment, he or she may still have some pain or other symptoms.


There has been a basic misunderstanding of these conditions as mental illness due to the lack of basic understanding of Gastrointestinal conditions that are most likely due to a lack of the most basic knowledge or training (Ignorance). The most basic understanding is that there are a number of underlying causes of these Gastrointestinal Issues including Diabetes due to the increased use of Starches in the West; but also that Antibiotics may also be one of the contributory factors because they can select for different forms of Bacterial Overgrowth. It may also be that in treating infections (including Helicobacter), we may exchange infection for Bacterial Overgrowth in a subset. Every Antibiotic we take orally affects out Gut Bacteria and there is still no full understanding of Gut Symbiosis, immune Bacterial interactions, so this absolutism in Psychology is ignorant presumptive nonsense, that is a result of poor thinking.

To create such a belief system in such a vacuum of knowledge, is a pretense of knowledge and should qualify as dysfunctional thought, which equates to a psychiatric disorder. But to impose that thought on so many thousands of people who have become vulnerable because they are unwell is criminal!

How dangerous and absurd. I am both Angry and Terrified of this Ignorant abuse of power and understanding by Psychiatrists! If we who are unwell persist in out beliefs due to significant illness we could be locked up for our mistaken belief that we are unwell when the mistaken beliefs are due to !

This is what we are up against; Know your Enemy! Your Enemy is Ignorance, lack of Emapthy, Lack of Training and a Totalitarian NHS Regime based upon a fictional Psychiatric understanding of these issues. For those of us with Gastrointestinal related conditions, this could so easily be diagnosed and treated. This is not our fault but we are being blamed and abused for being unwell!

Paul.
 
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Sorry if this has been posted before, but this study is interesting. Seems that it's all about permeability, not the d-lactate itself.

Intestinal microbial and metabolic alterations following successful fecal microbiota transplant for D-lactic acidosis

https://www.ncbi.nlm.nih.gov/pubmed/29901551
What is Known

 D-lactic acidosis (D-LA) is a rare complication of short bowel syndrome, characterized by elevated plasma D-lactate and encephalopathy.
 Present therapies focus on reducing gut bacteria (antibiotics) and eliminating the substrate for D-lactate production (dietary carbohydrate restriction).
 Despite these treatments, a subset of patients have recurrent D-LA episodes.

What is New

 FMT was safe and effective for recurrent D-LA in the patient described in this study.
 FMT resulted in changes to the composition and metabolism of the intestinal microbiota.
 Increased fecal D-lactate (despite reduced plasma D-lactate) after FMT suggests intestinal permeability could play a role in D-LA pathogenesis.
 

Avenger

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Dear Pechias,
Thank you for the most interesting report. This will help me put pressure on for FMT, because I have recurring D-Lactric acidosis and increasing antibiotic resistance.

Most forms of Bacterial Overgrowth are related to Gut Permeability, but I do not understand the suggested role in pathogenesis, because there is no raise in temperature as in a normal infection that enters the bloodstream. This is why my illness remained undetected for so long, because I was frequently checked for temperature when I told Doctors that it felt like an infection. In D-La it feels like an infection, but there is no raise in temperature because the immune system is not activated by the production of Organic Acids. This will all need further research before much of this is fully understood.

But there are a number of Medications that can cause Bacterial Overgrowth including Antibiotics which can Select for different forms of Overgrowth including D-Lactic. My belief is that this is an environmental issue cause by our overuse of Antibiotics including battery farming techniques and early weening of piglets which have caused Bacterial Resistance and Overgrowth through decimation of other Bacterial Colonies. ME/CFS had been increasing since we first started using Antibiotics in the 1940's. I believe that ME/CFS may have been one of the first signs of Antibiotic Resistance caused illness. C.Diff is also known to be caused by Antibiotics. My belief is that we have caused an unnatural form of Selection giving a hand up to some species of Bactria in an attempt to control our environment through the new god of science; and have unwittingly added so many other chemicals and environmental toxins that it would not be possible to even consider the variables.

I had been guessing that FMT for D-La was possible since I was diagnosed with D-La without short bowel syndrome in 2017. I believe that what is known is not necessarily the whole truth. That D-La is caused primarily in short bowel does not mean that it cannot be caused in other situations. Motility issues can act to cause similar problems and Bacterial overgrowth can also self maintain through controlling motility; through the production of Hydrogen and Methane which act upon the Gastrointestinal Tract to alter motility, and there may be many other ways in which D-La can be caused.

Read Gastroenterologist Luke White; NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #145 Luke White, D.O. Department of Critical Care Medicine, Memorial Hospital, South Bend, IN D-Lactic Acidosis: More Prevalent Than We Think? https://med.virginia.edu/ginutrition/wp-content/uploads/sites/199/2014/06/Parrish-September-15.pdf

I think that the main point is that; D-La has been believed to be a rare disorder. This may be why it has evaded detection for so long. Have you seen the in depth study below that shows increased D-Lactic producing Bacteria in CFS patients.

My belief is that there are a number of forms of Bacterial Overgrowth and combinations that produce Oraganic Acid Metabolites that act as neurotoxins. But all forms of Bacterial Overgrowth cause Gut Permeability.

2009 Jul-Aug;23(4):621-8.
Increased d-lactic Acid intestinal bacteria in patients with chronic fatigue syndrome.
Sheedy JR1, Wettenhall RE, Scanlon D, Gooley PR, Lewis DP, McGregor N, Stapleton DI, Butt HL, DE Meirleir KL.
Author information

Abstract
Patients with chronic fatigue syndrome (CFS) are affected by symptoms of cognitive dysfunction and neurological impairment, the cause of which has yet to be elucidated. However, these symptoms are strikingly similar to those of patients presented with D-lactic acidosis. A significant increase of Gram positive facultative anaerobic faecal microorganisms in 108 CFS patients as compared to 177 control subjects (p<0.01) is presented in this report. The viable count of D-lactic acid producing Enterococcus and Streptococcus spp. in the faecal samples from the CFS group (3.5 x 10(7) cfu/L and 9.8 x 10(7) cfu/L respectively) were significantly higher than those for the control group (5.0 x 10(6) cfu/L and 8.9 x 10(4) cfu/L respectively). Analysis of exometabolic profiles of Enterococcus faecalis and Streptococcus sanguinis, representatives of Enterococcus and Streptococcus spp. respectively, by NMR and HPLC showed that these organisms produced significantly more lactic acid (p<0.01) from (13)C-labeled glucose, than the Gram negative Escherichia coli. Further, both E. faecalis and S. sanguinis secrete more D-lactic acid than E. coli. This study suggests a probable link between intestinal colonization of Gram positive facultative anaerobic D-lactic acid bacteria and symptom expressions in a subgroup of patients with CFS. Given the fact that this might explain not only neurocognitive dysfunction in CFS patients but also mitochondrial dysfunction, these findings may have important clinical implications.
PMID: 19567398
[Indexed for MEDLINE] Free full text