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

Avenger

Senior Member
Messages
323
Avenger, I had a Cancer scare last January they removed a Cancer tumor in my terminal ileum I lost some of my right side bowel l am told I am Cancer free now. I wonder how could this area play a role in D-lactate Acidosis testing?

My symptoms have not changed at all before or after the Surgery with ME/CFS the Tumor was found in an early stage, I am worried about the fact my Father died from bowel Cancer he had it twice

Hi Aidan, have been offline or a while; please see the report in my last message;
The report below may be of relevance if your Cancer had caused damage to the Mucosal lining and intestinal injury. My problems were cause by long term, high dose NSAID's.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4806238/

World J Gastroenterol. 1997 Dec 15; 3(4): 225–227.
logo-wjg.gif


Published online 1997 Dec 15. doi: 10.3748/wjg.v3.i4.225
PMCID: PMC4806238
PMID: 27053870
Plasma D (-)-lactate as a new marker for diagnosis of acute intestinal injury following ischemia-reperfusion
Yong-Ming Yao, Yan Yu, Ye Wu, Lian-Rong Lu, and Zhi-Yong Sheng
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
 
Messages
8

Avenger

Senior Member
Messages
323

Thank you so much MouseGraft,
I have wondered for some time exactly what 'Julia Flora' is. It is an important article. And there are a number of equally interesing related articles such as ''Effectiveness of fecal-derived microbiota transfer using orally administered capsules for recurrent Clostridium difficile infection''.

My own belief is that there are many diseases including ME/CFS that would benefit from Faecal Transplantation and I am looking forward to a time when Faecal Derived Microbiota Capsules may be available; My own belief that we have created these disease 'monsters' through antibiotics such as cephalosporins mentioned below causing C.Difficilile. My own problem being that I have to keep using antibiotics, but can never replace the necessary bacteria for permanent recolonisation with long term species (that are able to stop the return of opportunistic species) before the opportunistic bacteria that are causing me to be ill return as the dominant species in Overgrowth to act as an infection due to the production of organic acid neurotoxins. It will be Groundhog day for me untill I either break the chain or become totally resistant.

I am not sure that this is a perfect or full explanation, because many of the Bacteria that go into Overgrowth are often found naturally within the Gastointestinal Tract and only act opportunistically under certain conditions including other underlying problems such as Diabetes etc. But Faecal Transplant does work to stop the overcolonisation of opportunistic Bacteria. But we may not know the full mechanisms for decades; because there is a co-operation between species and our own immune system and signalling between these species to maintain the microbiome that we have evolved over millions of years (and I believe that we are devolving through the use of antibiotics and antimicrobrials such as Chlorine and Fluoride, to mention but a few; and we educate opportunistic Bacteria through giving them a taste of low level antibiotics used in Farming over the past decades, where different Bacteria can gain early resistance. We have used our most recent and important antibiotics on farm animals to our detriment. I have often wondered if 'fresh' chicken that we make contact with in supermarkets can pass resistant forms untill cooked?)

Report;
''.. In another study in the Amsterdam Medical Centre, a three-arm study was set up where 42 recurrent CDI patients either received vancomycin, vancomycin and a bowel lavage, or all these treatments followed by duodenal infusion of healthy donor faeces . After an interim evaluation, the study was stopped by the medical- Heidt et al. (1983) The number (N) of described cases is indicated as are the different modes of delivery (D, duodenal; C, colonic or caecal; O, Oral). Studies with the largest number of patients reported are listed. ...
... The generated microbiota was termed first J.F. flora, and later named Julia Flora (see above and Table 2) and also Human Donor Flora (HDF). Remarkably, during the maintenance in mice, E. coli was lost as a major component of the microbiota and mainly consisted of anaerobic bacteria (Heidt et al., 1983). We now know from various studies that the human microbiota in germ-free animals may change rapidly in structure and function (El Aidy et al., 2012). ...

A method to prevent endogenous infections in patients and laboratory animals with an impaired immune capacity is the total decontamination of the gastrointestinal tract. This is performed by oral administration of nonabsorbable antibiotics. One of the disadvantages of total decontamination is the fact that especially after termination of this treatment the decontaminated individual is easily colonized with organisms from the environment. This is the result of the elimination of the anaerobic part of the microflora, which is responsible for the so-called colonization resistance (CR). This CR is the resistance against exogenous microorganisms to colonize the gastrointestinal tract. In the absence of an anaerobic flora, the colonizing microorganisms can reach abnormally high faecal concentrations, thus increasing the risk for infection. In mice, the implantation of an anaerobic, mouse-derived flora after termination of total decontamination resulted in the restoration of a good CR, as could be shown by orally challenging the animals with a strain of Escherichia coli. Therefore, an anaerobic microflora, free of potentially pathogenic microorganisms, which was isolated from a healthy human volunteer was administered to monkeys and patients after a decontamination period in an attempt to restore CR. In the monkeys, this human donor flora (HDF) did not reduce the faecal concentration of microorganisms that had colonized the gastrointestinal tract before the donor microflora had been established, in contrast to the findings in some of the patients. Qualitative analysis of the microflora of patients which were contaminated with the human donor flora showed that the CR is not of the same quality as is found in healthy individuals. This can be the result of the impaired immune capacity of the patients at the time of HDF implantation. However, the results obtained show that implantation of the HDF in monkeys and patients after a decontamination period allows reconventionalization without an undue risk of microbial infection.''

Fame and future of faecal transplantations--developing next-generation therapies with synthetic microbiomes
Article
Full-text available
  • Apr 2013


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... Total GID was successful in 57 (51%) of the 112 evaluable graft recipients. After discontinuation of the antibiotics for total decontamination, the patients were reconventionalized on posttransplant day 40 by oral administration of strictly anaerobic intestinal enteric flora from an unrelated human donor [59]. The number of patients who developed GvHD was small: 9 of 112 (8%). ...

History of Graft-versus-Host Disease
Article
Full-text available


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... [245][246][247] Bacteriotherapy Bacteriotherapy (fecal microbiota transplantation) to restore normal gut microflora is experiencing a resurgence of interest. [248][249][250][251][252] This interest has been driven largely by the increased incidence of severe C difficile associated diarrhea and colitis, 253 254 and by the recognition of opportunities for intervention in other diseases. 255 Certain antibiotics such as third generation cephalosporins have long been known to be associated with colonization and infection by opportunistic and antibiotic resistant pathogens including C difficile. ...

Early versus late surgical intervention or medical management for infective endocarditis: A systematic review and meta-analysis
Article
Full-text available


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... [245][246][247] Bacteriotherapy Bacteriotherapy (fecal microbiota transplantation) to restore normal gut microflora is experiencing a resurgence of interest. [248][249][250][251][252] This interest has been driven largely by the increased incidence of severe C difficile associated diarrhea and colitis, 253 254 and by the recognition of opportunities for intervention in other diseases. 255 Certain antibiotics such as third generation cephalosporins have long been known to be associated with colonization and infection by opportunistic and antibiotic resistant pathogens including C difficile. ...

Antibiotic resistance in Enterobacteriaceae: Mechanisms and clinical implications
Article
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... The role of the microbiota in antibiotic-induced diarrhea was recognized long before the identification of specific pathogens responsible for this condition. This understanding has stimulated significant interest in fecal-derived microbiota transfer (FMT): the transplantation of fecal-derived bacteria from a healthy individual into the GI tract of the affected patient [21][22][23][24][25]. This strategy, which utilizes the complex fecal microbiota of a healthy donor to reconstitute the normal microbiota, is an effective and appropriate treatment for recurrent CDI or pseudomembranous colitis, as supported by many case series reports [11,22, and a randomized trial [52]. ...

Effectiveness of fecal-derived microbiota transfer using orally administered capsules for recurrent Clostridium difficile infection
Article
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The Impact of Gut Microbiota on the Immune Response to Vaccination
Chapter
  • Jan 2021
 
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kangaSue

Senior Member
Messages
1,851
Location
Brisbane, Australia
"Julia flora" was derived from a human donor
I have wondered for some time exactly what 'Julia Flora' is.
They're doing something somewhat similar with stem cell transplants nowadays, but using the patients' own stool (autologous fecal microbiota transplant; a-FMT), taken and frozen prior to doing the stem cell transplant.

Interestingly, some FMT studies into IBS and IBD have included patients doing a-FMT as the comparative placebo control treatment to the donor FMT group and in some cases, a good percent of the autologous FMT group have also achieved some of the study end point goals.

Presumably, stool samples were collected from these 'a-FMT control' patients at time of the trial, so also presumably when the patient is sick and their stool composition could be far from ideal. There's scant detail about this in the few study results I have been able to find though.

I'm finding the whole topic of autologous FMT to be an engrossing read, particularly this latest paper;
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7308243/
 

Avenger

Senior Member
Messages
323
Rheumatoid arthritis: New ‘highly effective’ treatment on the way after scientific breakthrough
EXCLUSIVEResearchers have found, for the first time, that damage to the lining of the gut plays a key role in disease by making it leaky

This report was passed to me by SamB;

https://inews.co.uk/news/science/rh...ghly-effective-treatment-breakthrough-1185281

Report;

''And the researchers have identified existing stomach-repairing drugs used for the digestive disorders, coeliac disease and Crohn’s disease that could be used treat rheumatoid arthritis, which affects about 400,000 people in the UK – a third of whom gain very little benefit from current therapies.

Laboratory tests on human tissue and mice samples found a drug currently in clinical trials for Coeliac disease – known as AT1001 – was effective at mending the gut and relieving symptoms while vercirnon, a treatment already being used on the NHS to treat Crohn’s is another potential candidate.

The researchers are now working towards a clinical trial involving one or more of these drugs in humans for rheumatoid arthritis.

“Our findings are exciting. They suggest that the stomach lining is a therapeutic target. Importantly, we found that using existing drugs that restore the gut-barrier integrity, could reduce the severity of arthritis,” says Professor Claudia Mauri, of University College London.


In a best case scenario, an existing drug will be found to be effective and become available for rheumatoid arthritis patients on the NHS within three to four years, Prof Mauri said – while stressing that it could be much longer and may never happen.

Experts not involved in the study said the findings significantly increase our understanding of disease that could lead to effective new treatments.

“This is an exciting study [that] may help to identify new ways to treat arthritis in some patients,” said Professor Simon Milling, of the University of Glasgow who edits the British Society for Immunology’s journal Immunology.

The study is published in the journal Med and was funded by the Versus Arthritis charity and government bodies UK Research and Innovation and the Medical Research Council.

Dr Neha Issar-Brown, Director of Research at Versus Arthritis said: “The findings are exciting on many fronts. Not only do they demonstrate a link between damage to the gut lining, its microbiome and rheumatoid arthritis, but they also show how it might be triggering the immune system and contributing to inflammation and the onset of RA. This research is truly impactful in opening new avenues for exploration.”

“This new research looks promising but it is still very early days,” added Arthritis Action’s medical advisor Wendy Holden.

The researchers found that, compared to healthy people, gut damage was greater even at the earliest stages of arthritis, and that the damage got higher the more the disease progressed. They were also surprised to find distinct signs of inflammation.''

I think that many of us already understand Leaky Gut;
it just shows what we are dealing with. Hippocrates was right (2,500 years ago); to believe that ''all disease is begins in the Gut''.
 
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Avenger

Senior Member
Messages
323
They're doing something somewhat similar with stem cell transplants nowadays, but using the patients' own stool (autologous fecal microbiota transplant; a-FMT), taken and frozen prior to doing the stem cell transplant.

Interestingly, some FMT studies into IBS and IBD have included patients doing a-FMT as the comparative placebo control treatment to the donor FMT group and in some cases, a good percent of the autologous FMT group have also achieved some of the study end point goals.

Presumably, stool samples were collected from these 'a-FMT control' patients at time of the trial, so also presumably when the patient is sick and their stool composition could be far from ideal. There's scant detail about this in the few study results I have been able to find though.

I'm finding the whole topic of autologous FMT to be an engrossing read, particularly this latest paper;
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7308243/

This is really interesring; rather like keeping a clone of oneself, but storing a good copy of your own Feacal matter to reset illness after some form of interruption. It would be so interesting to understand fully what those interruptions are; but Viruses like Covid-19 seem to be able to be one possibility; endowing some species with resistant Bacteria with copies of the Virus attached and capable of reinfection or reactivation; The main drive of a Virus is to reproduce and enter any cells available causing Overgrowth through advantaging some species of Bacteria.

This is obviously too late for me; but it would be a good insurance policy for anyone to maintain copies of their healthy Gut Microbiome from an earlier period. But adding Stem Cells to help restore the microbiome and possibly immune funcion in the Gut.
 

kangaSue

Senior Member
Messages
1,851
Location
Brisbane, Australia
This is obviously too late for me; but it would be a good insurance policy for anyone to maintain copies of their healthy Gut Microbiome from an earlier period.
No, I don't think it's too late for anyone as it's suggested by the research that in some cases, even using your own 'unhealthy' stool sample can induce a period of remission in some conditions, such as IBS and IBD.

The science around FMT still doesn't know what aspect of it confers the most benefit either so it's not necessarily just from the transfer of 'beneficial' bacteria. It could also be coming from the transfer of the viral lode (natural phages?), or the fungal composition of the stool.

Even with doing just a colonoscopy without following up with FMT, some people get significant GI symptom relief benefit just from doing the bowel wash out in preparation for the examination, and this is known to be able to change a SIBO breath test result from positive to negative, but does not always improve the GI symptoms.

Bearing all that in mind, and especially where doing autologous FMT with the upper GI delivery ('top down') route, it could be that a combination of all these factors are involved in transferring stool from the large bowel back into the small bowel.

About the only way to do autologous FMT 'top down' on a d.i.y. basis would be to make your own capsules though, and that may be problematic for people who have an issue with delayed gastric emptying (gastroparesis) at the more severe end of the scale.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6602784/
The Effect of Allogenic Versus Autologous Fecal Microbiota Transfer on Symptoms, Visceral Perception and Fecal and Mucosal Microbiota in Irritable Bowel Syndrome: A Randomized Controlled Study (2019)
[ Conclusions: This study showed that a single FMT by colonoscopy may have beneficial effects in IBS; however, the allogenic fecal material was not superior to the autologous fecal material. This suggests that bowel cleansing prior to the colonoscopy and/or processing of the fecal material as part of the FMT routine contribute to symptoms and gut microbiota composition changes in IBS. ]

https://pubmed.ncbi.nlm.nih.gov/29100842/
Faecal microbiota transplantation versus placebo for moderate-to-severe irritable bowel syndrome: a double-blind, randomised, placebo-controlled, parallel-group, single-centre trial
[ Three participants did not undergo FMT and four were excluded after diagnosis of microscopic colitis, leaving 83 for final modified intention-to-treat analysis (55 in the active treatment group and 28 in the placebo group). 36 (65%) of 55 participants receiving active treatment versus 12 (43%) of 28 receiving the placebo showed response at 3 months ]
 

Avenger

Senior Member
Messages
323
Major Study Links Gut Bacteria to Fatigue in Chronic Fatigue Syndrome (ME/CFS)
by Cort Johnson | Nov 10, 2021 | Gut, Homepage, Microbiome | 87 comments

Emailed to me By SamB;

Led by Cheng Guo (lead author) and Brent L. Williams (senior author) this big NIH-funded study from Ian Lipkin’s Columbia team at the “Center for Solutions for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (CfS for ME/CFS)” set out to fix some of the problems found in prior gut studies. The study “Deficient butyrate-producing capacity in the gut microbiome of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome patients is associated with fatigue symptoms” was bigger (n=200), more rigorous, and used better bacterial sequencing techniques than past studies.
Lactobacillus_paracasei-Dr.-Horst-Neve-Max-Rubner-Institut-CC-BY-SA-3.gif

A lactobacillus gut bacteria (Dr.-Horst-Neve-Max-Rubner-Institut-CC-BY-SA-3.gif). This study found a reduced diversity of gut bacteria in ME/CFS.
Ian Lipkin’s team involved seemingly everyone possible (Mady Hornig, Anthony Komaroff, Susan Levine, Lucinda Bateman, Suzanne Vernon, Nancy Klimas, Jose Montoya, Dan Peterson) in this big NIH-funded study. The study was not just big – it was long as well. Study participants provided stool samples 4x’s over a year and completed a multidimensional fatigue inventory each time to boot.
Plus, following past studies from this group – the study assessed the effect irritable bowel syndrome – a common but certainly not universal comorbid condition found in ME/CFS – has on gut flora. Finally, as it did in a past study, this new study added metabolomics to the mix as well.
The study also used a technique that appears to be new to ME/CFS gut studies called “shotgun metagenomics sequencing” which allows researchers to comprehensively sample all the genes in all the organisms found in a complex environment. This technique allows researchers to detect bacterial species that other methods are likely to miss.
This study provides us clearly our best look yet at the gut bacteria in chronic fatigue syndrome (ME/CFS).
The Irritable Bowel Syndrome (IBS) Connection
“Both our current and prior fecal shotgun metagenomic study support the notion that IBS morbidity must be carefully considered in future ME/CFS microbiome studies”. The authors​
Irritable bowel syndrome (IBS) is characterized by symptoms like abdominal pain, cramping or bloating usually associated with a bowel movement, changes in the appearance of bowel movements (ranging from hard-packed feces to diarrhea), and changes in how often you’re having a bowel movement. About a third of the ME/CFS patients in the study had IBS.
A Less Diverse Ecosystem
Having IBS made a real difference. Specifically, the differences in the alpha diversity of the gut bacteria largely reflected whether one had IBS or not. Alpha diversity is a term borrowed from ecology that measures the richness or diversity of complex ecosystems (like a forest or a gut). Like a forest, the higher the species richness or alpha diversity of the bacteria in the gut the more resilient, healthy, and productive the gut should be
The bacteria in our guts form an ecosystem. This study suggests that some ME/CFS patients’ gut ecosystems are less diverse and less resilient (“Wild Garden of the gut bacteria” – from Wikimedia Commons”)
Alpha diversity isn’t the only measure of gut health but it is an important one. One Ph.D. student reported that “High gut alpha diversity has been linked to a healthy state in so many studies that it has become common knowledge in microbiome circles.”
Having IBS had a dramatic influence on alpha diversity with only the ME/CFS +IBS having a reduced alpha diversity compared to healthy controls.
Beta diversity can also be used to assess gut health. The beta diversity test compared the difference between the microbiome species found in the presumably healthier guts of the healthy controls with the ME/CFS patients with and without IBS. In contrast to the alpha diversity finding, both ME/CFS cohorts (those with and without IBS), had altered beta diversity; i.e. whether they had IBS or not, the flora in the ME/CFS patients’ guts was markedly different than the flora found in the healthy controls’ guts.
“A Potential Biosensor of Human Health” Reduced
The study found that the relative abundance of two species (E. rectale and Faecalibacterium prausnitzii ) and six genera (Eubacterium, Faecalibacterium, Dorea, Roseburia, Gemmiger ) differed in relative abundance in ME/CFS compared to healthy control subjects.
F. prausnitizi stood out because it’s been found reduced in at least one fibromyalgia and two ME/CFS studies. This odd bacterium, which does not produce spores, and moves around very little, makes up a full 5% of the bacteria found in our guts. Through its fermentation of dietary fiber, F. prausnitizi produces butyrate and other short-chain fatty acids, and an important anti-inflammatory product. It’s been called “a potential biosensor of human health”.
The authors noted that low fecal F. prausnitzii levels have been found in inflammatory bowel disease (IBD), IBS, celiac disease, colorectal cancer, obesity, in people with COVID, and in long COVID. The Flemish gut project found that Faecalibacterium and Coprococcus bacteria were associated with higher quality of life scores, and reduced levels of F prausnitizii have been associated with fatigue in inflammatory bowel disease.
Reduced Butyrate Levels – A Seminal Gut Finding in ME/CFS
Fatigue was certainly the byword in this study as lower butyrate levels were associated with more fatigue and both general and/or physical fatigue were particularly associated with reduced levels of F. prausnitz, Coprococcus, and a few other bacteria.
Butyrate’s becoming a pretty big deal in ME/CFS gut studies. It’s the primary energy source for the endothelial cells lining the gut – an interesting finding given all the focus on the endothelial cells lining the blood vessels in ME/CFS and long COVID. Given the strong possibility that leaky gut is present in ME/CFS, it’s intriguing that butyrate protects the gut lining. Its support of regulatory T-cells and its anti-inflammatory activity helps keep the immune system in check as well.
Butyrate_Levels_ME_CFS_Lipkin_2021.gif

Dramatically reduced butyrate levels (middle column) in ME/CFS patients (with IBS – green; without IBS – violet) compared to healthy controls.
Reduced butyrate levels in ME/CFS then, could result in an inflammatory state in the gut and a weakened gut barrier to boot; which is perhaps just the right combination to spark an inflammatory response that ranges from the gut all the way to the brain.
The deeper the researchers dug, the more solid the low butyrate finding became. A metagenomic analysis snagged one source of the butyrate problem when it found that people with ME/CFS tended to be deficient in one of the two genes (the “but” gene) used to produce butyrate using the acetyl-CoA pathway gene. A functional analysis then indicated that the bacteria using that gene were the same bacteria that people with ME/CFS were missing.
The butyrate connection got even stronger when the authors found reduced levels of a substance called acetate. Because butyrate-producing bacteria need acetate to produce butyrate, the acetate deficiency fit the bill.
The Gist
  • Ian Lipkin’s group presented the findings of the largest gut study ever done in ME/CFS.
  • The study found that having ME/CFS and irritable bowel syndrome – reduced the “alpha diversity” or richness of their gut flora – resulting presumably in less productivity and resilience. Just having ME/CFS, on the other hand, did not.
  • As several other studies have found the bacteria that produce butyrate – an anti-inflammatory that provides essential energy resources to the endothelial cells linking the gut wall – were deficient in ME/CFS. Low levels of butyrate were associated with greater fatigue as well.
  • With this study, three different methodological approaches have identified low butyrate levels in ME/CFS patients’ guts – making it one of the more solid findings in all of ME/CFS.
  • Low levels of butyrate could result in inflammation, weakened gut linings, and leaky gut – potentially producing systemic inflammation that reaches all the way to the central nervous system.
  • This also makes this study the third to find reductions of a specific butyrate producer called F. prausnitizi. Low levels of F. prausnitizi , which has been called a potential biosensor of health, have been found in a number of chronic diseases including IBS, IBD, and fibromyalgia.
  • Because acetate is needed to produce butyrate, the reduced acetate levels found made sense as well.
  • What was causing the higher-than-normal levels of bacteria in ME/CFS patients’ feces was unclear.
  • Recent studies which have shown that reduced activity levels are associated with reduced levels of butyrate bacteria suggest one reason why butyrate-producing bacteria may be low in ME/CFS.
  • People with ME/CFS could be caught in a kind of low butyrate “loop” where low butyrate levels spark inflammation, which produces fatigue thus reducing activity levels, reducing butyrate levels further, etc.
  • GIven that, it’s possible that increasing gut butyrate levels in ME/CFS could reduce inflammation, reduce fatigue, increase activity levels, etc.
  • An upcoming blog will focus on increasing butyrate levels.

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Digging even further into the butyrate mystery, the authors found that one of the four butyrate-producing pathways – the dominant one called the CoA pathway – was responsible for the butyrate deficiency found.

The fact that three different techniques (qPCR, metabolomics, metagenomics) have now found low butyrate-producing bacteria in ME/CFS makes the butyrate gut finding possibly one of the most solid findings in ME/CFS.
The fact that more people with ME/CFS than healthy controls (10%-2%) were taking supplements (prebiotic fiber) which should have enhanced their levels of butyrate-producing bacteria present only increased the mystery about the low butyrate levels studies have consistently found in ME/CFS.
Bacteria Packed Feces
Another interesting finding concerned the fact that the feces of the ME/CFS patients were packed with more bacteria than normal. The authors discarded antibiotic use, acute malnutrition, and inflammatory bowel diseases as possible causes and suggested several possibilities: low levels of FODMAPs (fermentable oligo-, di-,539 mono-saccharides, and polyols) foods, small intestinal bacterial overgrowth (SIBO), greater bacterial “washout” or the loss of bacteria that adhere to the mucosal walls.
FODMAPS diets can be helpful in IBS and SIBO appears to be common in ME/CFS. (The idea of malnutrition was intriguing – at least to this layman’s mind – given that the metabolomic findings in ME/CFS mirror those found in starvation and the possibility that the cells of ME/CFS patients may be starving in the midst of plenty. Could people with ME/CFS also not be utilizing all the nutrients in their food?)
The Activity Question
We don’t know why the butyrate-producing bacteria are so low in ME/CFS but low levels of physical activity may come into play. Recent studies (mostly done on rodents) indicate that physical exercise stimulates the same butyrate-producing bacteria that are deficient in ME/CFS.

It’s not clear why this is so but numerous possibilities (reduced gut motility, reduced blood flows to the gut, circulation of bile acids, etc.) exist. The association this study found between reduced butyrate levels and fatigue could, then, be caused by the lower activity levels that more fatigued people with ME/CFS engage in. Clearly, we need gut studies that also assess activity levels to address this issue.
It’s clear to me personally, though, that low activity levels are not responsible for all the gut perturbations in ME/CFS as I am not deconditioned (and have the Oura stats to prove it), yet I still intermittently suffer from irritable bowel syndrome.
In a sense, the activity question doesn’t matter. Given that the guts of people with ME/CFS and perhaps fibromyalgia and long-COVID patients have low butyrate levels which could result in gut inflammation, leaky gut problems, and perhaps even systemic and neuroinflammation – the question is what to do about them?
It’s possible that people with these diseases are caught in a kind of low butyrate loop: their lowered activity levels (or something else) resulted in reduced levels of butyrate-producing bacteria – which then produced inflammation and leaky gut (particularly as a result of exercise), which resulted in more fatigue and less exercise, which further reduced their butyrate levels, and on and on.
One way out of this loop might be to increase butyrate levels, thus reducing the inflammation and leaky gut (particularly after exercise) allowing people with ME/CFS to be more active, resulting in more butyrate production, higher activity levels, and on and on.
  • Coming up – increasing acetate and butyrate levels in the gut for better health
 
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kangaSue

Senior Member
Messages
1,851
Location
Brisbane, Australia
@Avenger There is a discussion thread on that paper;
https://forums.phoenixrising.me/threads/study-butyrate-and-bacteria-levels-cfs-nov-2021.86131/

You'll be interested in another Cort article that makes mention of d-lactic acidosis and a possible connection with increased Streptococus bacteria in those with ME/CFS. An antibiotic treatment is suggested for addressing this bacteria and I believe there is a phage therapies available for treating this bacteria as well.
https://www.healthrising.org/blog/2016/03/01/lactate-fibromyalgia-chronic-fatigue-syndrome/
 

Avenger

Senior Member
Messages
323
Hi kangaSue,
thanks again; not well today, exhausted after spinal surgery, having some night sweats and headaches and still back pain and feel dopey (the sweats are definitely not to do with D-Lactic acidosis because I do not develop a temperature during episodes).

The Butyrate and Bacteria levels for CFS are interesting. I have copied out the only study performed for myself for Hypoglycemia, with all 3 low, Acetate and Propionate; but Butyrate very low; This may relate to D-Lactic acidosis.

From Cort Johnsons blog; 'whether they had IBS or not, the flora in the ME/CFS patients’ guts was markedly different than the flora found in the healthy controls’ guts'.

I am wondering if it is the Organic Acids themselves; produced through overgrowth that may cause the dysfunction leading to other key Bacteria remaining low. D-Lactate can influence the production of immunosuppressive proteins, causing immune dysfunction, damaging intestinal epithelial cells, and affecting energy metabolism; but this is a chicken before the egg situation; so what was the initial break in the chain that led to this dysfunction? For me this may have been the use of NSAID's during a period of stress, possibly also Helicobacter and Epstein Barr Virus, because I had been fit prior to onset.

I have been interested in Phage Therapy for a long time, so will look at the costs of getting this done. I know someone on this site who's father was very ill and had successful Phage Therapy in Georgia. But Phage Therapy should be far better than Antibiotic Therapy and should target Bacteria that they can identify.

Do you know of any well established Phage Therapy Centers in Europe that are affordable?

DSC02301.JPG
 

kangaSue

Senior Member
Messages
1,851
Location
Brisbane, Australia
Do you know of any well established Phage Therapy Centers in Europe that are affordable?
I haven't delved into phage therapy very much myself, Hip posted an updated and informative thread on it just recently though;
https://forums.phoenixrising.me/threads/phage-therapy-to-treat-me-cfs-and-bacterial-dysbiosis.85467/
The Butyrate and Bacteria levels for CFS are interesting. I have copied out the only study performed for myself for Hypoglycemia, with all 3 low, Acetate and Propionate; but Butyrate very low; This may relate to D-Lactic acidosis.
Lactate is supposed to be fermented to butyrate (I asume that goes for both the l and d isomers but don't know for sure) and it looks like the acetyl-CoA pathway could be the weak link in this process.
https://pubmed.ncbi.nlm.nih.gov/15960680/
I am wondering if it is the Organic Acids themselves; produced through overgrowth that may cause the dysfunction leading to other key Bacteria remaining low.
There may be something of interest to you about (urinary) organic acids in this article;
https://musculoskeletalkey.com/urin...ient-deficiencies-gut-dysbiosis-and-toxicity/
The Butyrate and Bacteria levels for CFS are interesting. I have copied out the only study performed for myself for Hypoglycemia, with all 3 low, Acetate and Propionate; but Butyrate very low; This may relate to D-Lactic acidosis.
I didn't know that low level of butyrate could be implicated with hypoglycemia. Have you looked into supplemeting taurine or TUDCA for hypoglycemia? Or maybe even UDCA which interestingly, is said to be used as a treatment for SIBO so might be restorative of the balance of your gut bacteria. I have no idea if either has any beneficial effect on butyrate or d-lactic acidosis though.
 

Avenger

Senior Member
Messages
323
Sub Clinical Effects of D-Lactate;

Hi kangaSue,
have not been too good so have only just been able to look at your most interesting reports.



I had been off antibiotics for some months to have a D-Lactic assay performed to have FMT. I has been very hard, but I believed that it would be worth the effort to have a possible permanent cure from a tested donor;

I was tested for D-Lactate on the 7th May while unwell and with encephalopathy, but the D-Lactate test was taken long after the worst symptoms had stopped (D-Lactate is known to be transient, much like ME/CFS symptoms can change through the day). I fell ill around 10.00 and was tested at 2.30; It took over an hour waiting for an Ambulance and 3/4 hour just to wait for Covid tests and have the blood test performed on a ward; but I still had a subclinical result of 0.8mmol/litre that shows production of D-Lactate (I now need to have the symptoms properly induced in hospital because I have to achieve the full 3mmol/litre for FMT for licensing reasons).

I was also using the FODMAP diet because I was not sure that I could cope using the worst fermenting foods if symptoms spiralled too far out of controll (wheat products, bread and pasta etc.) Symptoms are reduced using the FODMAP diet, but can still be bad enough.

But even after the worst symptoms had stopped, I still felt achy, weak and unwell at the point my blood was taken; which made me wonder if others would have similar effects at a subclinical level. In fact the more I read, the more that I realise that there is no absolute surety of the plasma concentration ranges because so few D-Lactic assays have been performed; and they do not take into account individual reaction to the neurotoxin or allergy and there may be other Organic Acids compounding the problem which may go undetected;

''The pathophysiological mechanism is not fully known,7 but plasma D-lactate levels do not correlate to symptom severity, so that other organic acids may act as false neurotransmitters.4 ''

Can you or anyone corroborate what the normal production of D-Lactate Blood Plasma is; I have found at least 2 different possible answers? I have 11 to 70 nmol/L normal and Sub-Clinical 50micromol to 2.0mmol/litre. 3mmol/litre or over as acidosis.

There is now some interest in Sub-Clinical D-Lactate; with reports that D-Lactate is a cause of Sleep Apnoea and intermittent Hypoxia which would cause abnormal fatigue, even after a nights sleep (I was also diagnosed with sleep apnoea when my symptoms first began. I did eventually find a cure for my Sleep Apnoeas; Nightly Oxygen recommended by Dr. Myhill, used for over a year has stopped the symptoms for good, but I also had some control over the D-Lactic symptoms at that point).

Serum D-lactate concentration in healthy adults ranges from 11 to 70 nmol/L (5,7–9). Urine excretion is ∼0.1 μmol/h (10).

Examining clinical similarities between myalgic encephalomyelitis/chronic fatigue syndrome and d-lactic acidosis: a systematic review

''We stress that d-lactate theory may be relevant for a select subgroup and if not causative, may be a factor that perpetuates or exacerbates neurological symptoms. To date, there is no research that has measured d-lactate levels in ME/CFS. Improved efciency and availability of d-lactate measurement in urine and blood samples is needed. Measurement of d-lactate will clarify its role of d-lactate in this population and may generate an avenue for alternative treatments. Subclinical levels of d-lactate in diverse populations suggest that this may be Wallis et al. J Transl Med (2017) 15:129 Page 19 of 22 extended to other conditions. The proposed continuum is relevant for general physicians, gastroenterologists, psychiatrists and psychologists alike. Awareness of gastrointestinal origins for neurological presentations may hasten diagnostic accuracy, prevent misdiagnosis and improve treatment outcomes.''

L-lactate and D-lactate - clinical significance of the difference;
https://acutecaretesting.org/en/art...tate-clinical-significance-of-the-difference/

The current relative lack of availability of D-lactate assays might change now that there is growing research interest in the clinical significance of subclinical elevation of plasma D-lactate concentration [8], i.e. plasma D-lactate concentration in the approximate range (50 µmol/L - 2.0 mmol/L).

It was once supposed that the relatively very small amount of D-lactate normally present in the blood of humans (concentration 5-20 µmol/L in healthy adults [3] compared to 1000 µmol/L, i.e. 1.0 mmol/L for L-lactate) is solely derived from exogenous sources (diet and the carbohydrate-fermenting bacteria normally present in the gastrointestinal tract).

However, it is now clear that despite the absence of D-LDH, D-lactate is both produced and metabolized within human cells, albeit in tiny amounts compared to that of L-lactate. Metabolic production of D-lactate in human cells is the result of the methylgloxal pathway, a minor off-shoot pathway of glycolysis that results in nanomolar production of methylgloxal, a toxic product that is converted to D-lactate [4,5].

In the absence of D-LDH, human cells can metabolize D-lactate to pyruvate by the action of the mitochondrial enzyme D-2-hydroxyacid-dehydroganse [4,5].

In summary, the small amount of D-lactate normally present in blood is derived from three sources:

  • cellular production by the methylgloxal pathway
  • diet (foods containing D-lactate, e.g. yoghurts, soured cream, cheese)
  • lactate-producing bacterial species normally resident in the large intestine (colon).
Overgrowth of bacteria in the colon is a feature of short-bowel syndrome, the only pathology associated with increase in plasma D-lactate concentration of sufficient severity to cause acidosis (D-lactic acidosis).
 
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kangaSue

Senior Member
Messages
1,851
Location
Brisbane, Australia
Can you or anyone corroborate what the normal production of D-Lactate Blood Plasma is; I have found at least 2 different possible answers? I have 11 to 70 nmol/L normal and Sub-Clinical 50micromol to 2.0mmol/litre. 3mmol/litre or over as acidosis.
You're mixing up the measurements and comparing millimolar, micromolar and nanomolar values. Sub-clinical d-lactate of 50umol/litre (or 0.5mmol/litre) is equal to 500nmol/L - or about 7 times the upper normal range for d-lactate (2.0mmol/litre equals 2000nmol/L)
 

Avenger

Senior Member
Messages
323
Autoimmune Disease, the Gut and Sibo;

Still exhausted and have new symptoms other than D-lactic since I came off the FODMAP diet and antibiotics for a few months last year to produce a D-Lactic assay for FMT; then spinal surgery and reacted to the Covid Booster soon after surgery, then getting worse flares; but this may have started a few years ago when I developed intermittent flares of abnormal fatigue even when D-Lactic symptoms had been controlled with antibiotics; and I now have new symptoms including trigger finger, hand stiffness, joint pains that come and go even in my hips and knees, abnormal fatigue, periods of collapsing and weak knees; flu like symptoms and possible lymph swellings (hard to tell difference between D-lactic systems at times, but many of the symptoms are new, for the first time in 20 years).

Which is why I have taken new interest in Autoimmune disease and now sending the report below that further reinforces that much disease has a common root in the Gut; 80 different Autoimmune diseases already identified and 40 illnesses susspected to have an Autoimmune component; SIBO is believed to have a strong connection to Autoimmune disease and IBS; and could easily turn out to be one cause of ME/CFS.

There is evidence in the report below from a family who all changed to a Gluten Free diet who have all beneffitted; A number of high Gluten yielding foods are also high fermenting and cause me the worst D-lactic symptoms. ''gluten grains are high in starches and sugars that can be easily fermented by intestinal bacteria. This can cause bloating, cramping and/or diarrhea.'' In fact Celiac sufferers may also benefit from a FODMAP diet; ''Studies have shown that a low FODMAP diet may be an effective treatment for celiac patients who continue to experience IBS-like symptoms.'' These conditions all seem to be related and possibly reversible.


Gut Health and Autoimmune Disease — Research Suggests Digestive Abnormalities May Be the Underlying Cause
By Aglaée Jacob, MS, RD
Today’s Dietitian
Vol. 15 No. 2 P. 38
February 2013 Issue


Research from nearly a decade ago shows that most autoimmune conditions may share a common root hiding in the intestinal lining of individuals with autoimmune diseases, even years before the symptoms manifest.

A Peril on the Rise
To date, at least 80 different autoimmune diseases have been identified, and an additional 40 illnesses are suspected to have an autoimmune component, according to the American Autoimmune Related Diseases Association (AARDA), a nonprofit health agency increasing the awareness of autoimmune diseases. Autoimmune conditions are chronic and can affect every organ in the body, crossing almost all medical specialties, including gastroenterology, cardiology, neurology, rheumatology, gynecology, dermatology, and endocrinology.

The prevalence of autoimmune disorders is rapidly rising and now affects an estimated 23.5 million Americans, 75% of them women.1 In fact, autoimmune diseases are now among the top 10 leading causes of death in American women under the age of 65.

Emerging research shows that most autoimmune conditions may share a common root hiding in the intestinal lining of individuals with autoimmune diseases, even years before the symptoms manifest.

Inside the Gut
The intestines are the largest mucosal interface between the environment and us. A single layer of epithelial cells is all that separates the bloodstream and the contents of the intestines. The small intestine has the complex and crucial role of allowing nutrients inside the body while keeping bacteria, toxins, and wastes outside. The tight junctions separating the intestinal cells assume some of these functions.

The tight junctions aren’t cemented as previously thought but rather are dynamic structures. Incompetent tight junctions cause increased intestinal permeability, commonly referred to as leaky gut, and can result in the absorption of incompletely digested protein and antigens that overstimulate the immune system through the bloodstream.

Autoimmune Triad
Alessio Fasano, MD, a world-renowned pediatric gastroenterologist, research scientist, and founder of the University of Maryland Center for Celiac Research, believes all autoimmune conditions have three factors in common: a genetic susceptibility, antigen exposure, and increased intestinal permeability.2

“Besides celiac disease, several other autoimmune diseases, including type 1 diabetes, multiple sclerosis, and rheumatoid arthritis, are characterized by increased intestinal permeability secondary to non-competent tight junctions that allow the passage of antigens from the intestinal flora, challenging the immune system to produce an immune response that can target any organ or tissue in genetically predisposed individuals,” Fasano wrote in the February 2012 issue of Clinical Reviews in Allergy and Immunology.2

While it was previously believed that the autoimmune process remained ongoing once activated, this recent evidence indicates that the process could be modulated and possibly reversed by interrupting one of the modifiable factors involved in the autoimmune triad.

Tiffany, 31, transitioned her whole family to a 100% gluten-free diet when her 3-year-old daughter was diagnosed with celiac disease. To Tiffany’s surprise, her daughter wasn’t the only one to benefit from eliminating wheat and other gluten grains from her diet.

At Tiffany’s follow-up visit with her rheumatologist, the doctor was impressed by the marked reduction in her C-reactive protein and erythrocyte sedimentation rate levels, two inflammatory markers indicating disease activity in rheumatoid arthritis (RA), a common autoimmune condition. Tiffany now feels better than she has in years and is excited to wake up pain free every day since changing her way of eating.

Autoimmune conditions such as RA tend to run in families, and many of these conditions seem to start in the gut.

Diagnostic Testing
As dietitians, requesting additional testing for patients suffering from autoimmune conditions can help determine whether their intestinal health is associated with their symptoms.

Considering that many people have more than one autoimmune condition, testing for celiac disease is a good place to start. Positive results can help motivate clients to embrace a gluten-free diet to normalize their intestinal permeability. Dietitians should be aware that only about one-half of celiac patients demonstrate the condition’s “classic” symptoms at diagnosis, according to a study published in the February 2001 issue of Gastroenterology. It’s important to remember that celiac disease testing isn’t reliable if clients haven’t been consuming sufficient quantities of gluten in the previous weeks.

Testing for SIBO is appropriate for clients presenting with any type of gastrointestinal complaints mimicking IBS, considering SIBO’s strong connection with autoimmune diseases. A simple and noninvasive lactulose or glucose breath test can reveal whether SIBO could be altering patients’ intestinal permeability and therefore contributing to the autoimmune process.

The lactulose/mannitol test used to monitor intestinal permeability is reserved mostly for clinical research, but it’s available in some commercial labs and can be a useful tool to track the impact of dietary and lifestyle changes over time. If taken at home, the procedures for this test must be followed carefully to receive accurate results. A zonulin ELISA assay, predicted to be available in the near future, also could be a tool dietitians use to detect and monitor intestinal permeability in patients affected by autoimmune conditions.


Happy New Year, wishing you all find peace and health this coming year!
 

Avenger

Senior Member
Messages
323
Understanding the causes of ME/CFS

I have just found an exciting study fron Dr. Karl Morten from the University of Oxford for those of you who have not already seen this; but there are a number of existing and new studies underway;

The existing studies already show specific differences between healthy and ME/CFS cohorts with evidence of a number of biological differences with studies on the Microbiome, L-Forms found in Bloods and much evidence that ME/CFS is an organic problem; and already Faecal Transplants performed on ME/CFS trials with successfull outcomes in some patients who had abnormalities with the Microbiome.

Please look at the short film on the page below;

https://www.development.ox.ac.uk/mecfs
 

Husband of

Senior Member
Messages
313
@Avenger if someone were to try changing their diet for three days to see if it made a difference, how would you suggest they do it without crashing due to low energy? Also I don’t really understand what you mean by zero carbs? Does that mean zero vegetables? Thanks.
 

Husband of

Senior Member
Messages
313
Actually, my layman’s understanding is that even amino acids and fat can be converted to glucose. So it seems the only way to starve the lactic acidosis producing bacteria, without starving yourself of energy, is to go into ketosis??
 

Avenger

Senior Member
Messages
323
Hi 'Husband of',
sorry not to get back sooner; you need to go back to the beginning of my post; Ketosis is not exactly the aim and would be dangerous, but a Ketogenic or Palao diet, best explained on Dr. Sarah Myhills web page https://drmyhill.co.uk/wiki/The_Paleo_Ketogenic_Diet_-_this_is_a_diet_which_we_all_should_follow

The aim is to find alternative food sources to avoid, what to all intents and purposes, is a hidden Gut 'infection' due to the abnormal increase of naturally occurring Bacterial in Overgrowth causing fermentation of Simple Carbohydrates; that will not allow you to process many of the 'normal' foods to energy that we have been using since we started Farming and using grains around 40,000 years ago; the very low Carbohydrate diet is a return to a more primitive diet that would have been used pre-farming; but FODMAPS diets utilize starches (complex Carbohydrates) that your body takes longer to break down and will not ferment easily, especially in the small intestine (very simple explanation). You could start with Dr. Myhills Stoneage or Palao diet to see if your symptoms improve. Many ME/CFS have related gastrointestinal symptoms.

This is about reducing abnormal levels of D-Lactic producing Bacteria and reducing abnormal fermentation of D-Lactic producing Bacteria, or other Organic acids produced by other Bacterial Overgrowth; by reducing Simple Sugars and using Low Fermenting Carbohydrates so that the Bacteria cannot produce high levels of D-Lactate (it is now believed that we can process a small ammount of D-Lactate unless that ability is missing, which is another possible cause of D-Lactic acidosis). The FODMAP diet is similar to diets used for IBS, Diabetes and other forms of SIBO with low Fruit Sugars https://thefoodtreatmentclinic.com/low-fermentation-diet/; I now use a FODMAP diet, but used a very Low Carbohydrate diet for a year or so after diagnosis in 2017.

ME/CFS has been related to altered and less diverse microbiome with decreases of Firmicutes and increase of Bacteroidetes (Gram positive bacteria). Firmicutes are more effective in extracting energy from foods.

Low fermenting diets will also assist with other forms of Bacterial Overgrowths or SIBO, causing the production of Organic acids with similar neurotoxicity that may be associated with ME/CFS.

In D-Lactic acidosis diet needs to reduce any abnormal fermentation of certain Carbohydratres to D-Lactate instead of L-lactate (which is our normal source of energy when converted to Glucose and Energy in the Pyruvate/Glucose Chain). ''l-lactate formation occurs via the reduction of pyruvate catalyzed by lactate dehydrogenase. l-lactate removal takes place via its oxidation into pyruvate, which may be oxidized or converted into glucose. ... Enzymes of the gluconeogenesis pathway sequentially convert pyruvate into glucose.'' ''By digesting food, you break it down into smaller and smaller parts. Carbohydrates turn into glucose. Protein becomes amino acids. Fat breaks down to triglycerides and fatty acids. All these smaller parts of food can be used for energy. '' So we can also get energy from proteins and fats as we did pre farming.

You have to cut out all simple sugars and alcohol such as Lager and Beers which are high in Carbohydrates; The worst Carbohydrates for me are Bread, Pasta or wheat based products that ferment easily eg. Pizza.

I used a very low close to non-Carbohydrate Diet at first; mainly Meats, Fish, Eggs, Hard Cheese, some Veg and low sugar fruits such as Blueberries and Cranberries; This diet was the best for me, but I found it very hard to stick to permanently and it takes great imagination to create meals (Dr. Myhill has produced a Palao Ketogenic Cook Book); but would be a good place to start (after checking with your health professionals first). But I was later offered a FODMAP diet that allows low fermenting Carbohydrates and use this coupled with antibiotics that only temporarily stop the symptoms by reducing the Overgrowth, but I have found that symptoms still come back gradually even though reduced, there must still be some fermentation, enough to cause me symptoms.

Antibiotics can also make things worse but give me temporary reprieve; and long term use has already caused resistance in several antibiotics, and antibiotics have been implicated in causing other heath ptoblems due to the effect on other microbiome species, including low or lack of significant species; but there may be some light at the end of the tunnel, because Phage Therapy for Superbugs is already being tested in Belgium and it may eventually become an acceptble treatment for these forms of Microbiome disorders;
https://www.newscientist.com/articl...nfections-are-being-tested-in-belgium/https:/

The only other alternatives for me is Probiotics or Faecal Transplant; FMT although successful in some patients (and has been used for C.diff infections, MS, ME etc.) may not work for all and may also need more than one treatment.https://neurosciencenews.com/microbiota-transplants-19966/

I have found specific Non-D-Lactic producing Probiotics in combinations that will stop my symptoms, but they are expensive and hit and miss in terms of quality and quantity needed (the NHS will no longer fund Probiotics because they state that they are deemed to have low efficacy) ; but there is interest in Micobiome replacement therapy at the Dove Clinic; GFRT - Gut Flora Replacement Therapy - The Dove Clinic
although D-Lactic producing Bacteria would need to be avoided for a Subset of patients who have D-Lactic producing Overgrowths.

You can also have a Microbiome test performed at Atlas The Atlas Microbiome Test shows how gut bacteria impact your health (atlasbiomed.com).

You may have missed this report at the beginning of my posts; Increased D-Lactic Acid Intestinal Bacteria in Patients with Chronic Fatigue Syndrome; https://iv.iiarjournals.org/content/23/4/621.short?ssource=mfr&rss=1.

D-Lactate is an unwanted abnormal fermentation to the Organic acid; D-Lactate, which is a Neurotoxin and Poison; directly related to lack of energy, because D-Lactate causes fluctuating acidosis and greatly affects Mitochondrial Function and Neurological symptoms are caused when the Neurotoxin enters the Blood Stream and Spinal Fluid to cause abnormal fatigue, encephalopathy and multiple symptoms including pain (as in Myalgic Encephalitis).

It is possible to have more than one form of Bacterial Overgrowth once the microbiome becomes compromised; In D-Lactic acidosis there are often at least two different competing species and possibly other Overgrowths. It is what is driving these changes that is important; you could also try drinking water that is not Chlorinated or contain Fluoride; because these chemicals also affect the microbiome. We have most probably caused these problems that allow other competing elements such as Virus in Covid-19 to make changes to our microbiome similar to ME/CFS https://www.bmj.com/company/newsroom/make-up-of-gut-microbiome-may-be-linked-to-long-covid-risk/

We are all different and it may take some experimentatioin!
 
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gregh286

Senior Member
Messages
976
Location
Londonderry, Northern Ireland.
Hi @Avenger
Amazing
I had a reading of 2.8 mmol at kdm for d lactate.

Funy when I go without food start to feel better until tipping point when glucose dries up then energy crash....its hard to get the balance.

Sorry for ignorance....Will anaerobic cellular production make l lactate ?
Are these 2 different beasts?

Can d lactate only come from gut bacteria?
I read over 4 is almost fatal. Gees.

Seen this strain specially designed
https://www.customprobiotics.com/d-lactate-free-probiotics.html
 

Avenger

Senior Member
Messages
323
Hi @Avenger
Amazing
I had a reading of 2.8 mmol at kdm for d lactate.

Funy when I go without food start to feel better until tipping point when glucose dries up then energy crash....its hard to get the balance.

Sorry for ignorance....Will anaerobic cellular production make l lactate ?
Are these 2 different beasts?

Can d lactate only come from gut bacteria?
I read over 4 is almost fatal. Gees.

Seen this strain specially designed
https://www.customprobiotics.com/d-lactate-free-probiotics.html

Hi gregh286,
I am off antibiotics and eating normal food again to become unwell to have a D-Lactic assay induced at Birmingham QE Hospital; I started feeling unwell last night and symptoms are escalating and already affecting my thinking, so please forgive any mistakes (I have been able to stop the symptoms with combinations of Probiotics in the past, but they are expensive and not permanent acting indicating that they do not take up residence and when last used my symptoms returned after just a few days of forgetting to take the Probiotics; Customprobiotics look good but I am seeking a permanent cure if at all possible).

I do not think it fair to rely on one D-Lactate test alone, especially if it was not perofmed while you were at the peak of an exacerbation because production of D-Lactate is known to be transient. 2.8mmol Plasma D-Lactae is very close; and shows abnormal production; because 0.0033 mM, as far as I am aware, is normal production in humans (although varies with different researchers).

Plasma D-Lactate far less than yours has been seen in Gastrointestinal Ischemia, Appendicitis and Chrones disease (eg. ''phlegmonous and perforated appendicitis of 0.72 mM, 0.72 mM and 0.42 mM, respectively'') and D-Lactate is being researched as a new biomarker for these problems. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7490090/

The best way to obtain a true D-Lactic assay if you are that close to 3mmol; Is to be taken into hospital and be given fermenting Carbohydrates while in Hospital and have acidosis induced to get a true picture of what you are producing at worst and for Doctors to witness how unwell you become. How unwell did you feel at 2.8mmol and what were your sympoms? In another D-Lactic patient, it was believed that there were other Organic acids involved contributing to the symptoms. None of this is simple but you need to speak to the Geatroenterologist involved in your care.

To properly understand this illness; Assays would have to be taken in the early stages as symptoms begin (eg. Fatigue, Memory difficulty and Dizziness prior to an exacerbation), but no one has done this so far. At the moment there is just a set magic limit for having D-Lactic acidosis as if symptoms appear only after this point ; But the point at which D-Lactate causes systmic symptoms may not be the same for all of us and there may also be differences in how we detoxify these Organic acids. I am certain that I have specific low level symptoms long before encephalopathy starting with fatigue, dizziness, memory difficulty, pain and often gastrointestinal symptoms of reflux, difficulty emptying my stomach and bringing up food.

Symptoms are Transient; even at worst and I have been ill in Hospital in the years prior to diagnosis; had bad symptoms, but had to wait often over two hours to see a Doctor (because my symptoms has earlier been deemd CFS or Somatic) and the symptoms would often abate or reduce temporarily only to recur again later after being sent home.

An assay has to be taken quickly and then seperated to plasma and frozen within an hour or the D-Lactate will degrade. Hopefully your assay was frozen quickly.

The production of D-Lactate is not fixed; the microbiome is a dynamic system that changes with every meal and other influences including bacteria, motility, infection and underlying health problems such as diabetes.

Not enough research has been done on how low level production of D-Lactate affects us; Dr. Sarah Myhill also talks of allergies due to the waste products of Bacteria that could be another cause illness. Researchers have confirmed that there is no guaranteed absolute set level for D-Lactate, because there have not been enough Assays carried out because the illness has been deemed rare, so there is little research into setting the over 3mmol.

It has been hypothesised that D-Lactate may effect a percentage of the population causing illness at lower levels; or because they are unable to detoxify D-Lactate. There is still so little research, but hopefully that is now changing.

Around 70 to 90% L-Lactate is produced in the Gut from fermentation. Lactate (L-lactate) is an organic compound also produced during anaerobic energy metabolism, but is again converted back to Glucose. It’s constantly being formed, even when we are at rest, but is formed in higher quantities when ATP levels are low and anaerobic energy metabolism is high. Apparently several forms of lactate are produced by anaerobic bacteria in the gut.

But all comes down to personal experiment and trying methods proven successful so far, such as diet and Non-D-Lactic producing Probiotics, but Probiotics are expensive especially for those in this situation and I have found that high quality and quantity are needed to work. Have you tried the 'customprobiotics' and had any results?
 
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