D-Lactic Acidosis in CFS


I don't disagree with what you are saying. I was mostly making an expansive philosophical comment about the new paradigm we are entering. I have only skimmed it but if you haven't check out Khun's "Structure of Scientific Revolutions" or some summaries of it. We've been doing this stuff for a looong time.

I think with what may end up being called "the microbiome model of health" or something, lots of things will have to be reframed, including the idea of inheritance.

In the same way that somatisation is used to explain away confusing things, inheritance is also used to explain how habits and behaviours and health are passed on. But the framing is always in the context of genetic inheritance. "It's just in my genes / it's in my DNA". I also get the feeling inheritance was a trending explanation once the genome started to be mapped. It was a hot topic, so at the front of people's minds (easy to access/lazy thinking - which is normal human behaviour). Same goes for using somatisation. Everyone learns about placebo and psycho somatic. When you see someone in distress complaining about their health, it's very easy to access that as an explanation. "Thinking, Fast and Slow" by Khanemann does a great job of explaining why and what sort of thinking habits we perpetuate to our detriment.

As a side note, I have Gilbert's Syndrome. They explain it away as "genetic inheritance" but they don't know. I actually first developed jaundice and was told I had Gilbert's after being given an anti anxiety medication that has since been discontinued because it caused liver failure.... "inheritance" indeed.

People with alcohol or drug addiction have a lot of emotional problems, and inheritance is often used to explain addiction. When we start to reframe mental health with a microbiome model we start to understand people with poor microbiome's also have various imbalances in neurotransmitters and using drugs and alcohol can be a form of treatment for the emotional state that leaves one in. Addiction is a symptom of a traumatised emotional state, which is a symptom of poor health, which can be due to "the microbiome model".

Probably a lot of things will be reframed in the end, but it could take decades and with the way things are, probably with a lot of pushback. Especially from drugs companies that have never thought about how their drugs affect the gut and have no research or investment in the space.

I can't find the link right now but my friend who works in mental health shared a story with me about how anti-psychotic medication was linked to multi year weight gain that didn't stop after use. They realised it was due to altered microbiome. I'm sure you know all this, but basically stuff that that will cause big headaches for the drug companies so we can expect push back for sure, especially in the US.

Let me know if you want me to dig out the article. There are papers on the same topic anyways.

By the way, I get the feeling we are preaching to the converted here, but interesting to talk this stuff out anyways.
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Senior Member
Hi Michael, I think that you have a lot of very good points. We have a lot in common, sorry, I was not disagreeing. I have a report below concerning Antibiotics and Gut Bacteria, I have also seen similar reports that indicate that the effects of antibiotics on Gut Bacteria also affect the production of Seratonin.

Microbes Help Produce Serotonin in Gut | www.caltech.edu

https://www.caltech.edu › about › news › microbes-help-produce-serotoni...

9 Apr 2015 - Although serotonin is well known as a brain neurotransmitter, it is estimated that 90 percent of the body's serotonin is made in the digestive tract. ... Peripheral serotonin is produced in the digestive tract by enterochromaffin (EC) cells and also by particular types of immune cells and neurons.

Study shows how serotonin and a popular anti-depressant affect the gut's microbiota
Date:September 6, 2019Source:University of California - Los AngelesSummary:A new study in mice strongly suggests that serotonin and drugs that target serotonin, such as anti-depressants, can have a major effect on the gut's microbiota -- the 100 trillion or so bacteria and other microbes that live in the human body's intestines.Share:

A new study in mice led by UCLA biologists strongly suggests that serotonin and drugs that target serotonin, such as anti-depressants, can have a major effect on the gut's microbiota -- the 100 trillion or so bacteria and other microbes that live in the human body's intestines.

Serotonin -- a neurotransmitter, or chemical messenger that sends messages among cells -- serves many functions in the human body, including playing a role in emotions and happiness. An estimated 90% of the body's serotonin is produced in the gut, where it influences gut immunity.

The team -- led by senior author Elaine Hsiao and lead author Thomas Fung, a postdoctoral fellow -- identified a specific gut bacterium that can detect and transport serotonin into bacterial cells. When mice were given the antidepressant fluoxetine, or Prozac, the biologists found this reduced the transport of serotonin into their cells. This bacterium, about which little is known, is called Turicibacter sanguinis. The study is published this week in the journal Nature Microbiology.

"Our previous work showed that particular gut bacteria help the gut produce serotonin. In this study, we were interested in finding out why they might do so," said Hsiao, UCLA assistant professor of integrative biology and physiology, and of microbiology, immunology and molecular genetics in the UCLA College; and of digestive diseases in the David Geffen School of Medicine at UCLA.

Hsiao and her research group reported in the journal Cell in 2015 that in mice, a specific mixture of bacteria, consisting mainly of Turicibacter sanguinis and Clostridia, produces molecules that signal to gut cells to increase production of serotonin. When Hsiao's team raised mice without the bacteria, more than 50% of their gut serotonin was missing. The researchers then added the bacteria mixture of mainly Turicibacter and Clostridia, and their serotonin increased to a normal level.

That study got the team wondering why bacteria signal to our gut cells to make serotonin. Do microbes use serotonin, and if so, for what?

In this new study, the researchers added serotonin to the drinking water of some mice and raised others with a mutation (created by altering a specific serotonin transporter gene) that increased the levels of serotonin in their guts. After studying the microbiota of the mice, the researchers discovered that the bacteria Turicibacter and Clostridia increased significantly when there was more serotonin in the gut.

If these bacteria increase in the presence of serotonin, perhaps they have some cellular machinery to detect serotonin, the researchers speculated. Together with study co-author Lucy Forrest and her team at the National Institutes of Health's National Institute of Neurological Disorders and Stroke, the researchers found a protein in multiple species of Turicibacter that has some structural similarity to a protein that transports serotonin in mammals. When they grew Turicibacter sanguinis in the lab, they found that the bacterium imports serotonin into the cell.

In another experiment, the researchers added the antidepressant fluoxetine, which normally blocks the mammalian serotonin transporter, to a tube containing Turicibacter sanguinis. They found the bacterium transported significantly less serotonin.

The team found that exposing Turicibacter sanguinis to serotonin or fluoxetine influenced how well the bacterium could thrive in the gastrointestinal tract. In the presence of serotonin, the bacterium grew to high levels in mice, but when exposed to fluoxetine, the bacterium grew to only low levels in mice.

"Previous studies from our lab and others showed that specific bacteria promote serotonin levels in the gut," Fung said. "Our new study tells us that certain gut bacteria can respond to serotonin and drugs that influence serotonin, like anti-depressants. This is a unique form of communication between bacteria and our own cells through molecules traditionally recognized as neurotransmitters."

The team's research on Turicibacter aligns with a growing number of studies reporting that anti-depressants can alter the gut microbiota. "For the future," Hsiao said, "we want to learn whether microbial interactions with antidepressants have consequences for health and disease." Hsiao wrote a blog post for the journal about the new research.

I am just angry that many Doctors pretend to fully understand all of the issues that are clearly extremely complex and still unexplored yet pontificate in areas such as ME/CFS. We are at their mercy when we fall ill, yet many Doctors make absolutist statements of assured authority, when they have no understanding. But I am most angry because of Psychologists who have created diagnoses that have no scientific foundation, yet Doctors accept their authority and instead of helping, Somatization in ME/CFS stand as an act of aggression.

A philosopher (Ludwig Whitgenstein) once said 'whereof one cannot speak, one must remain silent'. He used this in the context of limitation of language. The statement should be applied to the limitation of knowledge and the arrogance of Psychology and Medicine. But they speak and act when they have no understanding.

I was also given medication that causes Liver Damage.

I was given a drug called Fenbfen (a non-steroidal anti-inflammatory analgesic) for a lower back pain at high dosage for several years before falling ill. Fenbufen was later taken off the market due to causing liver damage in 2010;

I had signs of Liver damage with raised ALT and raised CK levels when I was given the Somatization diagnosis to explain my D-Lactic symptoms and my Doctor and Laboratory Consultant had written to warn that raised ALT may be due to underlying pathology and causing my illness. But the Pain Clinic went ahead and diagnosed Somatization, which influenced my care for the next 18 years.

It is looking as though a lot of medications including antibiotics have serious side effects. SSRI's are known to influence weight gain and a number of antidepressants also influence the Gut and the production of Seratonin.

Antibiotics, gut microbiota, and Alzheimer’s disease
Alzheimer’s disease (AD) is a neurodegenerative disease whose various pathophysiological aspects are still being investigated. Recently, it has been hypothesized that AD may be associated with a dysbiosis of microbes in the intestine. In fact, the intestinal flora is able to influence the activity of the brain and cause its dysfunctions.

Given the growing interest in this topic, the purpose of this review is to analyze the role of antibiotics in relation to the gut microbiota and AD. In the first part of the review, we briefly review the role of gut microbiota in the brain and the various theories supporting the hypothesis that dysbiosis can be associated with AD pathophysiology. In the second part, we analyze the possible role of antibiotics in these events. Antibiotics are normally used to remove or prevent bacterial colonization in the human body, without targeting specific types of bacteria. As a result, broad-spectrum antibiotics can greatly affect the composition of the gut microbiota, reduce its biodiversity, and delay colonization for a long period after administration. Thus, the action of antibiotics in AD could be wide and even opposite, depending on the type of antibiotic and on the specific role of the microbiome in AD pathogenesis.

Alteration of the gut microbiota can induce changes in brain activity, which raise the possibility of therapeutic manipulation of the microbiome in AD and other neurological disorders. This field of research is currently undergoing great development, but therapeutic applications are still far away. Whether a therapeutic manipulation of gut microbiota in AD could be achieved using antibiotics is still not known. The future of antibiotics in AD depends on the research progresses in the role of gut bacteria. We must first understand how and when gut bacteria act to promote AD. Once the role of gut microbiota in AD is well established, one can think to induce modifications of the gut microbiota with the use of pre-, pro-, or antibiotics to produce therapeutic effects.



Senior Member
United States, New Hampshire
I still suffer insomnia, but I do not think that this is all about inheritance.
I agree. I actually feel that genetic inheritance has a much smaller role in chronic disease than the gut microbiome. I do think many of us get a dysbiotic microbiome from our mothers at birth. Which then gets made worse, often by antibiotics.

Take a look at the reports below my message. Antibiotics may have a profound effect not only on our immune systems, but also on our brains. These are new studies and need further corroboration, but the implications are profound.

Antibiotics are also able to select for Overgrowth through some Species gaining resistance and others being decimated and Overgrowth occurring.

Coupled with the direct effects of antibiotics upon the Gut Microbiome, it is no wonder that we have ME/CFS or other forms of disease.
I completely agree. I took dozens courses of antibiotics before I developed CFS. I'm convinced antibiotics were the main cause of my CFS.

If antibiotics are to blame, you can imagine that subsequent generations since the 1950's would have increasing alterations to the Gut Microbiome passed on from mother to mother, which means that we are
de-evolving our Gut Microbiome, generation by generation, that has evolved symbiotically over hundreds of thousands of years, so in that sense it is linked to inheritance.
BINGO!! I have said this for years now and believe it to my core. I use to have a graph that showed the dramatic increase in chronic disease since the 1950's. When they started using antibiotics worldwide.

Every generation is getting sicker and sicker because of this dysbiotic microbiome being passed on.

It's good to exchange posts with you and Michael. Knowing that you guys really "get it"!!


Senior Member
Hi Jimbo and MichaelM,
if antibiotics have such effects upon the immune system and natural symbiotic bacteria, biochemistry and brain, then antibiotics may also be causing or contributing to the increases in Cancer, which incidentally have been found to increase since the 1950's (Statistics below). I think that a paradigm shift in thinking is definitely under way, if we are not killed off by the old one first! The 'new' God of Science is as flawed as the old god's.

Cancer incidence in the American population has skyrocketed--up 48% from 1950 through 1990, according to National Cancer Institute statistics. These statistics are adjusted for an aging population and exclude lung and stomach cancers where the causes are generally well-understood. (See Note 2).

Those who say cancer rates are decreasing focus on cancer death rates because the cancer death rate overall is stable, despite increasing incidence. While cancer kills the same percentage of people that it always has, far more people are getting the disease. See Table 1.

Table 1: Cancer incidence in the American population has increased by 48 percent since 1950 (excluding cancers of the lung and stomach and adjusted for an aging population).

Source: National Cancer Institute. SEER Cancer Statistics Review (Miller, et al. 1994).

Framing the debate in terms of death rates is particularly cold-hearted toward children. It intentionally obscures the fact that a greater percentage of children get cancer than ever before in our history. The incidence of childhood brain cancer and childhood leukemia has increased 33 percent since 1973 (Ries et al. 1993). Cancer kills more children under the age of 14 than any other disease.

Focusing on childhood death rates further minimizes the pain and suffering of these children, the higher incidence of subsequent cancers that these people face as adults, and the costs of maintaining a growing number of childhood cancer wards.

Since 1950, cancer rates for the general population (excluding lung and stomach cancer) have risen at a rate of about 1.2 percent per year, with extraordinary increases in certain cancers, including cancers of male and female sexual organs, notably the breast (up 52%), prostate (up 134%), and testis (up 125%) (Miller et al. 1993).

Other organs exhibiting huge cancer increases during the past 40 years -- which are also shown in lab tests to be prone to tumors from carcinogenic chemicals--are the kidney (up 116%), liver (up 88%), brain (up 74%), and thyroid (up 102%), as well as non-Hodgkin's lymphomas (up 172%) and multiple myelomas (up 183%) (Miller et al. 1993). Farmers, otherwise healthier than the average population, have elevated rates of several types of cancer that are associated with chemical exposure (see farmer reference, Appendix 2). Although some of these higher cancer rates could be due to better detection, detection alone does not account for such enormous increases (Miller et al. 1993).


Senior Member
Reposting what I wrote in the PM:

A little bit of a negative opening here:

Yes, sadly I actually think that the NHS caused my friends mum to die in their care. She was grossly obese with many psych issues. On a lot of drugs.

She was an in patient but ready to be discharged, they gave her an antibiotic for a "suspected infection".... She suffocated. Could be allergic, but given what we are talking about, could just as well be lactic acidosis triggered by the antibiotic. She was a massive sugar addict and clearly had major gut issues from years of overeating.

The NHS will do anything to protect themselves. I don't think they took any reponsibility in my friends mum's case, and I never really pushed him on it because it was a hard time for him. NHS is under attack in many ways. It's so very far from perfect but we are also lucky. Other areas of the world are not entitled to such health care, as bad as it can be.

In the end I try to take a middle ground. Humans are humans, we are often stupid. I can't get too upset because I get hurt myself, but I really feel your pain and I have experienced similar myself. I just can't engage in the fight as such, but I will try my best to educate others and change perspective where I can, and discuss this.

In my case re SMH in some ways I am lucky because my only A&E trip got me a bed for 3 days due to mixed drugs toxicity and opiate withdrawal. They took me seriously. Gastroenteritis is on record too.

I also have MRI scans that show lesions, and they consider me an "almost MS" diagnosis case.

That said, I have a history of mental health on record, and it clearly isn't helping when I talk about acidosis or any of the nervous issues. I will look into my SMH. Most of my consultant letters are pretty clear there is at least something going on, and I've seen neuro psychiatry and while they have been ambiguous at times, they haven't put me in the shit.

To be balanced, we have to remember that interally triggered nervous disorder probably looks exactly the same on the outside as psychological trauma. I've had a hard time sharing with my family even that what I experience isn't panic... but to them they see mood issues and panic because during an episode, our bodies are in panic mode. I'm also lucky they haven't seen me slurring during an episode, or stumbling. They would think I was on drugs first due to my history.
Dear MichaelM,
I thought that you would like this email from Professor Malcolm Hooper. We are all being conned by he NHS and GOV,T. Someone has to engage them. I believe that there is a vast difference between Humans and Human beings. There is an inherent ugliness in the way that we are being treated. Suppression at all costs!

Dear Paul,
This is excellent but would be strengthened by referring to he abject failure of the PACE trial that clearly showed that the treatment of ME/CFS with psychiatric techniques CBT/GET is ineffective despite the study being established at great cost >£6 million to demonstrate its efficacy.
CBT/GET have become the cornerstone of treatment for a number of complex chronic multisystem conditions which have been labelled as somatoforrm disorders due to laziness/ igorance/or the mindless embrace of cheap medicine. ME as a biomedical disorder has been clearly vindicated along with others such as Gulf War Syndrome, Aerotoxic Syndrome, and Sheep dip poisoning which can no longer be dismissed but must be investigated. Government Policy including the NHS England, DWP, MRc, Insurance Companies can no longer rely on CBT/GET or somatisation as a creditable “treatment” for these illnesses or resist payment of benefits and financial and clinical support for people suffering from them.
Well done with your persistence in exposing the roots of your illness.
With best wishes
Malcolm Hooper
On 9 Jul 2017, at 02:12, Paul Smith​


Senior Member
Hi, I have added an addition to my other possible causes of damage to our 'natural' Microbiome, Flora and Fauna and Gut Mucosa;

There have been many changes to what we eat and consume in terms of Chemicals, Medication, Antibiotics, Pesticides since the 1950's; My conclusion is that we have prematurely introduced too many multiple variables now acting simultaneously since the 1950's and have barely accounted for individual problems, let alone multiple variables which may affect each other;

Fluoride in water in the western world is another;

Karen Spenser, M.A. from Lesley University (1993)
Answered Jun 8, 2017
1- Fluoride is an inflammatory drug. Gastrointestinal effects are common.
2- Fluoride is also an adjuvant, a substance that intensifies the immune response. The gut is full of immune system censors which can become inflamed from exposure.
3- Fluoride is an enzyme poison. It inhibits and even kills cells.
It is a common ploy of the fluoridationists to make fun of those who oppose fluoridation. Making fun of statements that “fluoride causes gas” is one of their standbys. However, given the different impacts on gut health, gas is symptomatic of any number of ill effects.



It is well established that fluoride ingestion can cause a range of gastrointestinal (“GI”) symptoms, including nausea, pain, and vomiting. It is not yet understood, however, what level of fluoride in the stomach is necessary to cause these symptoms, and how much this level varies based on the sensitivity of the individual. In 2006, the National Research Council called for more research to explore these issues.
Individuals with High Exposures to Fluoride
It is well known that humans with high levels of fluoride ingestion can suffer significant and persistent gastric problems. Humans suffering from skeletal fluorosis, for example, have been repeatedly observed to suffer high rates of GI disorders. When fluoride intake is reduced among these patients, the gastrointestinal problems are among the first symptoms to disappear. Similarly, when high doses of fluoride (18-34 mg/day) have been used as an experimental drug to treat osteoporosis, gastric disturbances are one of the two main side effects consistently encountered.

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HI Paul/All,

Thanks for the last 2 posts, interesting.

FYI I did message one of our family friends who is married to an enthusiastic hiker with many healthy friends - to ask for stool donations to try a transplant. She's a nurse on the NHS. She's very kind and understanding, but when my mum emailed in advance to brief her that I was going to message about a medical issue, my mum mentioned CFS. She said "I was discussing similar issues around mental health at work recently". Probably the worst response I could see to begin with. I have since sent the email asking for stool donations, and been met with silence so far. Sad times, but also understandable if her training has been on the mental health angle.

So I did 2 SIBO tests this week. Hydrogen breath tests. I was actually in one of my "near remission" or more manageable phases, coming out of the 6 weeks+ of acidosis type symptoms since my last intake of probiotics (which led me here). Then I realised I had the lactulose test coming up so furiously started eating sugars for a couple of days. It ended up taking me nearly a week to get quite ill.

The literal icing on the cake is that I drank 70g of glucose yesterday for a home breath test. After 3 hours got very disoriented, followed by creeping relapse into gait issues, cognition issues, nervous issues etc. No real heart issues apart from feeling fluttery in the chest zone.... typing is very hard. You know the score. It's pretty key here, near remission, then some sugars and it comes back, then 70g of sugars and BAM - it's horrible! Today is actually worse than yesterday, prickly skin, wonky pounding heart beats etc. Looks like this is here to stay for a while.

Next is d-lactate testing. Pushing for plasma somewhere but may have to fork out for the Genova urine test.... And... probably will have to break some near remission after I get myself back on my feet with another dose of sugars just to get the test. So frustrating, but I'm doing it, for science!

After that it's probably antibiotics (Rifamaxin - which I'm terrified of btw), then I did manage to find the money for a Taymount FMT, but I still would like to find a single donor to work with.

Will post back progress.

Best wishes


Senior Member
Hopefully some good news for ME/CFS with Gastrointesinal symptoms! Biolab Organic Profile Tests below (Metabolites of Fungal (Candida) and Bacterial Overgrowth);

Hi Michael,
I did exactly the same thing before a Hydrogen Breath Test and fell so incredibly ill that I was forced to take antibiotics to stop the symptoms. If I have the symptoms of Bacterial Overgrowth, I am unwell.

Remember that you can have either Hydrogen or Methane production depending upon the bacteria concerned, and it is possible that Methane producing Bacteria live off the bi-products of Hydrogen producing. You need both Hydrogen and Methane Breath tests (hydrogen causes diarrhea and Methane constipation. You can have either with D-Lactic acidosis).

It is also likely that mood including depression is influenced by Seratonin manufacture in the Gut by Bacteria. The NHS have little understanding of these issues and are living in the medical 'middle ages' where mental health is a Freudian concept of Somatic illness being caused due to life trauma. They can do nothing but make things worse with Cognitive Behavioral Therapy and Graded Exercise, because someone suffering the traumatic and painful symptoms of ME/CFS, like us will be terrified that their traumatic symptoms are being blamed on their mental state (where mental changes are often secondary to serious illness, especially if it is not taken seriously; due to ignorance).

Your Donor should come from a healthy family member if possible, but any healthy individual should be OK. Dr. Myhill's site shows you how to DIY FMT. It has been practiced for thousands of years. The only question is whether to use Oral rout or Colonic rout.

Rifaximin are a good antibiotic because only a small % of this antibiotic exits the Gut. But it should be used at 1400 to 1600mg per day. Metronidazole also works very well. Antibiotics and exclusion diet is a good way to diagnose Bacterial Overgroth cheaply; seeing if you respond to these antibiotics or diet. But it is better not to use antibiotics once diagnosed unless there is no other way (eg. Varied Non-D-Lactic Probiotics, Naltrexone or finding the underlying cause of Overgrowth, Diabetes etc.........).

But more imortatly;

I may have some good news for you and many others on this site; Bilolab are now doing Organic Acid Tests! For Metabolites found in any Fungal or Bacterial Overgrowth! Biolab have stated as the cause of fatigue and immune dysfunction etc.

Organic Acids Profile - Biolab Medical Unit London UK - Tests;

https://www.biolab.co.uk › index.php › cmsid__biolab_test › Organic_Aci...

  1. The Organic Acids Test (OAT) provides an accurate evaluation of intestinal yeast and bacteria. Abnormally high levels of these microorganisms can cause or worsen behaviour disorders, hyperactivity, movement disorders, fatigue and immune function. ... A profile of 73 organic acids (including 20 microbial organic acids).

The Organic Acids Test (OAT) provides an accurate evaluation of intestinal yeast and bacteria. Abnormally high levels of these microorganisms can cause or worsen behaviour disorders, hyperactivity, movement disorders, fatigue and immune function. Many people with chronic illnesses and neurological disorders often excrete several abnormal organic acids. The cause of these high levels may include: oral antibiotic use, high sugar diets, immune deficiencies, and genetic factors. If abnormalities are detected using the OAT, treatments can include supplements, such as vitamins and antioxidants, or dietary modification.

A profile of 73 organic acids (including 20 microbial organic acids). These profiles are referred to Great Plains Laboratory in the USA - please contact us for further details.

NOTE: Samples for this test are referred to the Great Plains Laboratory in the USA.
Patient Instructions:
Early morning urine (before eating or drinking) - avoid apples, grapes, pears and cranberries (and their juices) for 24 hours beforehand. Also abstain from vitamin and mineral containing supplements for 24 hours prior to providing a specimen.
Sample should be frozen if there is a delay before submitting to Biolab.
organicacidsds.pdf (Click to Download)
Sample Report:
organicacidsrep.pdf (Click to Download)
Sample Requirements:
Mid-stream early morning urine.

We are many minds; we can reverse this together, Paul.

Thanks Paul,

It seems my version of d-lactate producing SIBO may be slightly less sensitive than yours. I did get quite ill but because I was in a remission phase and I had lots of B1 and other coping strategies to hand I have managed to get stable since without antibiotics. Maybe 1 day of hell and confusion but then gradually back to moderately bad. I'm staying this way until I get a d-lactate test, so more sugars to come! :(

But yeah, every time: gut problems = neuro problems and acute phases = acidosis symptoms. When gut problems subside the whole world becomes clear again.

I assume that Biolab had been doing that for a while, but I'm new to these labs.

Genova offer a similar test (I have not been through the whole list of measurements but the name is almost the same), but the Genova test also measures d-lactate:


the American site has the full list of metabolites, the EU site is not showing them for some reason;


I'm going to stick with antibiotics into probiotics before taking FMT seriously. Just because I have some reservations about Taymount, plus the cost.

I like the idea of trying a "synbiotic" treatment.

Apart from Mutaflor what other species can I introduce after antibiotics to try to colonise and compete with LAB?


Senior Member
Hi Michael,
I have not seen the list yet. But D-Lactic acid is an Organic acid. It is likely not to be the only Organic acid in ME/CFS patients who have Gastrointestinal problems.

Sheedy et al. believe that there may be a number of Organic acids involved due to continued fatigue after treatment of D-Lactic acidosis.

I have used Multiflor myself, which may have contribute to my ongoing remission (this was a generous donation by another member as was Myarisan; and Naltrexone which is now fully prescribed and I am most grateful).

I am guessing Naltrexone plus different probiotics (Multiflor, Myarisan, Rhasmosus etc.) have greatly helped me. I am no longer dependent on antibiotics or facing Resistance.

This has shown me that Fecal Transplant may most probably reverse D-Lactic acidosis; but that the underlying problem, motility in my case, may need to be continuously controlled (unless the change in motility is solely due to the effects of Gasses and Metabolites produced by the Overgrowth upon the Gastrointestinal tract).

I have been able to return to Carbohydrates for the first time in many years! I could and still may crash, but I am definitely on the right track!!! I am an ongoing experiment! but I am certain that if i stop the treatments that I will fall ill again.



Senior Member
Hi, I had forgotten to include that Fecal Transplant is looking promising in Autism;

It looks as though Gut Bacteria is still an unchartered continent and may hold a lot of surprises as the cause of many disease processes....

The Mail Online reports: “Autism symptoms can be reduced 50% in children who received faecal transplants.” But further research on a much larger group of people is needed to show if the treatment works.

Faecal transplants, originally designed to treat C.diff infections, involve receiving a transplant of gut microbes taken from a donor with healthy gut bacteria. This procedure has been found to improve gut health and digestive symptoms.

While autism is mainly associated with difficulty with communicating and interacting with others, autistic people can also experience digestive problems such as diarrhoea and constipation.

This small US study involved 18 autistic children. Researchers found an improvement in digestive symptoms and signs of autism 2 years after receiving a faecal transplant - 8 children no longer fitted the criteria for a diagnosis of autism and there was a 58% reduction in gut symptoms overall.

This is very early-stage research involving just a small sample of children.

The results of this study could also have been affected by the fact 12 of the children had changed their usual medication, supplements or diet during the course of the 2-year follow up. This means we cannot be certain that improvements in symptoms were down to the transplant.

Previous studies have shown an association between gut problems, such as constipation and diarrhoea, and autism but this is not the case for all autistic children. So even if this treatment is shown to be effective, it may just be for a select group of children.


Senior Member
It is beginning to look as though we have taken a first step in gaining a fuller understanding of important chains concerning Gastrointesinal Bacteria; This makes very interesting reading!

dinavian Journal of Gastroenterology
Informa Healthcare
Scand J Gastroenterol. 2014 Dec; 49(12): 1493–1498.
Published online 2014 Jul 8. doi: 10.3109/00365521.2014.936034
PMCID: PMC4266036
PMID: 25000845
Tryptophan: ‘essential’ for the pathogenesis of irritable bowel syndrome?
Arnold Berstad,
Jan Raa, and Jørgen Valeur
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.

Go to:
Tryptophan is an ‘essential’ amino acid: humans cannot make it themselves, but must obtain it in the form of food. In addition to being a building block in the biosynthesis of proteins, this aromatic substance can be converted into a number of metabolites of great clinical importance. The best known is the enzymatic conversion to serotonin. However, in recent years, attention has increasingly focused on the medical significance of the enzymatic oxidation of tryptophan to form indole compounds collectively known as kynurenines. Both excessive kynurenine production and an accompanying deficiency of the substrate, tryptophan, may be the cause of a number of pathological conditions. In addition, the oxidation itself may affect the body’s redox balance. In this article, we hypothesize that tryptophan is ‘essential’ in the pathogenesis of irritable bowel syndrome (IBS).
Go to:
Indolamine dioxygenase
Indolamine dioxygenase (IDO) is the key enzyme involved in the conversion of tryptophan in the intestine. The enzyme catalyses oxidation of tryptophan to kynurenine in a reaction that produces peroxide and gives rise to highly reactive and potentially harmful oxygen and hydroxyl radicals. The IDO reaction may therefore contribute to what is generally called oxidative stress [1,2]. Oxygen and hydroxyl radicals formed as a result of the IDO reaction will accelerate the oxidation of nitrogen monoxide (NO) to nitrite (NO2) and of ferrous iron compounds to ferric iron compounds. The reactive oxygen products have an antimicrobial effect, but may also harm mitochondria and lead to increased production of inflammatory cytokines (TNF-α, IL-6) [3,4] and be causally related to fatigue and pain hypersensitivity [5,6].
The harmful effects of the IDO reaction may be counteracted by ascorbic acid (vitamin C) and by antioxidants that occur naturally in plants. Most antioxidants in plants are members of the main groups polyphenols, carotenoids and flavonoids. The best known are curcumin in turmeric, catechines in green tea, resveratrol in red wine and epigallocatechins in cocoa. In addition to phenol antioxidants, edible plants in the Brassica family, such as cabbage and broccoli, contain glucosinolates that are broken down in the stomach to thiocyanates. These compounds help to control the redox balance in the intestine, for example, by activating the redox-regulating transcription factor Nrf2 [7]. Glucosinolates also give rise to indole products that are identical to some of those formed by enzymatic breakdown of tryptophan in the intestine, for example, indole-3-carbinol and 3,3-di-indolylmethane [7].
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Increased production of peroxide and reactive oxygen as a result of IDO activation may conceivably disrupt the finely tuned interaction between oxidants and antioxidants, concurrently with a change in the tryptophan and kynurenine levels. Perhaps such disruptions in the redox and tryptophan–kynurenine balance, and alterations in levels of tryptophan and tryptophan metabolites can ‘explain’ the abdominal and systemic symptoms of IBS? If this is the case, tryptophan is indeed essential, also in IBS pathogenesis.
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The kynurenine pathway
Up to the present, interest in tryptophan from a medical perspective has focused mainly on its role in serotonin metabolism. Serotonin is an important neurotransmitter in the enteric and central nervous system. In the bowel, it regulates secretion, motility and sensibility, while in the central nervous system it modulates mood, cognition and sleep. Neuropsychiatric problems have been attributed to too much or too little serotonin. For example, it has been demonstrated that a temporary tryptophan deficiency causes memory failure in healthy individuals [8]. In recent years, the focus has been more on tryptophan metabolism via kynurenine (the kynurenine pathway), where most of the tryptophan is catabolised by the IDO in the gastrointestinal tract. Tryptophan ‘surplus’ is catabolised in the liver, but by a different dioxygenase from IDO: tryptophan-2,3-dioxygenase. Only 1% of tryptophan intake is metabolised into serotonin, and the two metabolic pathways (serotonin and kynurenine) compete for the substrate (tryptophan) [9]. Increased consumption of tryptophan via the kynurenine pathway may result in too little tryptophan and serotonin in both the central nervous system and the gastrointestinal tract. It has been clearly shown to cause symptoms of anxiety and low mood in mice [10]. This may also be relevant for humans, because people vulnerable to stress may benefit from tryptophan supplements, for example, in the form of tryptophan-rich albumin or whey protein hydrolysates [11].
Most of the serotonin in the body (95%) is found to be in the gastrointestinal tract. Interestingly, studies have demonstrated that patients with IBS have low serotonin concentrations [12] and small numbers of serotonin-containing neuroendocrine cells in the small intestine [13]. Acting on mucosal and submocosal neurons in a paracrine fashion, serotonin is highly important for regulation of motility of the gastrointestinal tract. Impaired small intestinal motor function, as observed in patients with IBS [14], may thus be a consequence of too low serotonin levels within the intestinal wall. The end product of serotonin catabolism, 5-hydroxy indole acetic acid, is excreted in urine. In patients with IBS this excretion is low, indicating low production of serotonin as well [15]. Serotonin is inactivated by reuptake to enterocytes, neurons and platelets, and this serotonin transport function is reduced in patients with IBS, possibly a result of increased production of interferon gamma (INFγ) [16,17].
Immunoactivation that results in increased production of INFγ will also increase IDO activity [1]. IDO oxidation stimulated by tryptophan has proved to be of great significance for such diverse diseases as myocardial infarction, Alzheimer’s disease and mental retardation [8,18,19], and tryptophan is used in some therapeutic combinations for cognitive impairment in the elderly [20]. Activation of the kynurenine pathway also has an immunomodulatory effect, and is of significance for the development of multiple allergies and autoimmune diseases [21,22]. Both local tryptophan deficiency and systemic metabolites from the kynurenine pathway are considered to play an important part in this interaction. Thus, local tryptophan depletion in and around infected mucosal cells may impair microbial growth [23]. Intestinal malabsorption may also contribute. Patients with IBS and chronic fatigue often have signs of low-grade malabsorption with deficiencies of iron, vitamin B12, folic acid and vitamin D, and we have previously demonstrated that about 30% of IBS patients have fat malabsorption [24]. Ledochowski et al. demonstrated as early as in 2001 that an excessively high fructose level in the colon may reduce the availability of tryptophan as a substrate for biosynthesis of serotonin, and that serotonin deficiency and depression may be associated with fructose malabsorption [25].
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Microbial IDO activation?
A high kynurenine/tryptophan ratio is the result of a high level of activity in the kynurenine pathway, and this may be the closest one comes to a biomarker for IBS [26,27]. But this ratio is also high in a number of other inflammatory conditions and types of cancer where there is a high INFγ, either locally or systemically [26,28]. Low tryptophan and a high kynurenine/tryptophan ratio are therefore not specific to IBS, but may indicate an underlying low-grade inflammatory process. This immunoactivation and subsequent high IDO activity may conceivably have a microbial cause. Brottveit et al. recently described an INFγ increase in duodenal biopsies after intake of gluten-containing bread by gluten-sensitive patients without coeliac disease [29]. The mechanisms and consequences of this INFγ increase have not been determined. Gluten is only partly digestible by human enzymes, and remains semi-digested and unabsorbed in the small intestine. Undigested gluten peptides may be directly toxic [30], antimicrobial and immunomodulatory [31]. INFγ activation is an important part of the innate immune system and may be induced by microbes [32,33]. As soon as the undigested gluten peptides reach the large intestine, they become food for the intestinal bacteria [34], and the question is whether it is this gluten-stimulated intestinal flora that causes IBS-like symptoms in patients with non-coeliac gluten-sensitivity. Our hypothesis is that INFγ activation and subsequent IDO oxidation of tryptophan is a pathogenetic mechanism of IBS and that the initial stimulus may be of microbial origin also in the case of non-coeliac gluten-sensitivity.
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Does tryptophan act via aryl hydrocarbon receptor?
The receptor protein aryl hydrocarbon receptor (AhR) has been preserved in phylogenesis of vertebrates for several hundred million years. It used to be believed that its primary significance was in the inactivation of environmental toxins such as xenobiotics, by stimulating the activity of cytochrome P (CYP) enzymes. However, activated AhR also functions as an intracellular transcription factor that governs a number of vital functions [35] and is necessary inter alia for normal intestinal immune function. Of particular interest to us is the fact that AhR regulates the barrier function of the intestinal mucous membrane, apparently in a system whereby the mucous membrane ‘tastes’ the contents of the intestine and regulates its defences accordingly. AhR activation of lymphoid cells produces cytokines (IL-22), which regulate the immune system and development of tolerance. These innate lymphoid cells (ILC) form part of the innate immune system. In other words, the ‘old’ receptor (AhR) acts on cells that are ready to function already at birth, and we are clearly dealing with an innate immune system here. A number of studies have revealed that AhR ligands regulate the number of intraepithelial and regulatory T cells, cytotoxic T cells, antibody-producing B cells and mast cells. Failure of this immune system may result in autoimmunity and allergy [36].
Since AhR is an innate receptor in a number of cells, it is reasonable to assume that endogenous ligands may exist – and they do. New AhR ligands are constantly being found, and many of them actually prove to be tryptophan metabolites [37]. INFγ-induced tryptophan degradation may induce antimicrobial and immunomodulatory effects in epithelial cells [31]. Little research has been conducted on the importance of the intestinal flora in this regard, but the microbes can metabolise tryptophan and give rise to AhR ligands, which in turn affect the mucous membrane defence. The lactic acid bacteria (i.e., Lactobacillus reuteri in the intestine and L. acidophilus in the vagina) eat tryptophan as a source of energy and produce indole-3-aldehyde (IAld), an AhR ligand that activates ILC and releases IL-22, which stimulates the production of antimicrobial peptides, curbs the growth of Candida albicans, but boosts the growth of lactic acid bacteria. Given the choice, bacteria eat sugar rather than amino acids – and without tryptophan in their ‘diet’ they do not produce IAld – which will mean less lactobacilli and more Candida [33], which is typical of IBS.
It was also shown recently that kynurenine activates mast cells via AhR [38] and that AhR is upregulated in allergic rhinitis [39] and can be inhibited by another (non-toxic) tryptophan metabolite (abbreviated to ITE) [40]. These metabolites present very interesting possibilities for developing new treatments for allergies. However, there are a number of AhR ligands that are much more readily available and that may be equally interesting: the Brassica family, for example, contains tryptophan derivatives (glucosinolates) which convert gastric acid into potent AhR ligands that contribute to a favourable microbial environment in the stomach [41]. A relevant question is therefore: How much and in what manner is this regulatory system affected by our daily diet?
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Therapeutic possibilities for IBS
If IBS and associated health problems like fibromyalgia and fatigue [42] are an IDO-stimulated consequence of an abnormal intestinal flora, one might imagine that the problems could be treated with antibiotics. Interestingly, we sometimes see astonishing results due to antibiotics, but in our experience, unfortunately, the patients subsequently become sicker than ever. We suspect that the guilty microbes are facultative anaerobes, and that they are mucous-producing and possibly ‘conceal themselves’ in a biofilm of mucus [43]. Lipopolysaccharide (LPS) from Gram-negative bacteria may stimulate IDO [44], but LPS and CD14 in blood appear to be normal (unpublished data), even though the LPS receptor TLR4 may appear upregulated in the colon of a subgroup of IBS patients [45]. We therefore believe that the undesirable intestinal flora is not Gram-negative.
When antibiotics do not work, we must find other options. Dietary treatment (low FODMAP diet) to ‘starve’ the bacteria has proved useful [46], but hardly curative. The alternative, bacteriotherapy, is increasingly in fashion. Following the publication of a study of such therapy for patients with post-giardiasis IBS [47], we have noticed great interest in faecal bacteriotherapy (a variant of faecal microbiota transplantations). The effect was transitory, unfortunately, but perhaps better, nonetheless, than the effect of rifaximin, a non-absorbable antibiotic that was recently described in the New England Journal of Medicine [48]. However, getting the installed flora to establish themselves in a new host is a major problem that may be due to changes in the environment of the host’s ‘fermentation chamber’ – the coecum. The contents of the coecum should normally be slightly acidic, with a pH of between 5 and 6, and the acidity in the coecum is related to the redox potential [49]. If the redox potential is not low enough (not sufficiently anoxic), there will be excessive growth of facultative anaerobic bacteria, and the fermentation process will be incomplete [50]. With too high oxygen tension in the coecum, reactive oxygen species will be generated, which can oxidise NO to NO2 leaving an NO deficiency, while NO2 (and other oxidation products) may become ‘food’ for a non-benign bacterial flora [51]. If the host coecum does not have the correct redox potential, this may be sufficient to prevent new flora establishing themselves – until something is first done with the host redox environment. This is a challenge that has not yet been solved.
Exogenic addition of tryptophan may increase levels of serotonin and benign AhR ligands. However, this gives rise to the fear that one may be ‘adding fuel to the flames,’ because tryptophan oxidation will give rise to more reactive oxygen compounds. This is where the combination with antioxidants comes in. If we can curb the oxidative stress with antioxidants, the favourable effects of increased levels of serotonin and AhR ligands may make the overall effect of administering tryptophan positive. Thiocyanates formed by the breakdown in the stomach of glucosinolates in Brassica plants may be of special interest because they activate the Nrf2 receptor and have a regulatory effect on the redox level [7]. A diet high in Brassica vegetables is associated with reduced risk of chronic diseases [7], and constitutes an uninvestigated possibility of reducing pain and pain hypersensitivity in IBS and fibromyalgia [5,6]. In the past, we probably consumed much larger quantities than we do now, because hybridisation of Brassica plants has led to a reduction in their glucosinolate levels [52].
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Concluding remarks
IBS may be related to disrupted tryptophan metabolism with increased oxidative stress and deficiencies of tryptophan and tryptophan-derived AhR ligands [36]. The cause may be dysbiosis [53] due to high intake of carbohydrates [46]. If the microbes get their preferred food (sugar), they do not produce AhR ligands that strengthen the defences of and barrier presented by the mucous membranes. Without these AhR ligands, the ratio between the lactic acid bacteria and C. albicans is reduced and the immunobalance skewed in favour of the development of IBS, allergies and autoimmune diseases. When we say ‘You AhR what you eat’ [54], it means that a number of disorders, including IBS, fibromyalgia and fatigue, may be indirect consequences of diet, mediated by the essential amino acid tryptophan and its microbial metabolites. So perhaps it is more correct to say ‘You AhR what your microbiota eat?’
So this paper is kind of bothering me before I take Rifaximin:


More recently, Xu et al[79] demonstrated that Lactobacilli could grow in response to rifaximin administration.
Stool samples were analyzed before, at the end and 1 mo after the end of rifaximin treatment. Lactobacillus abundance was increased at the end of treatment with rifaximin and 1 mo thereafter, while no modification of the overall composition of the gut microbiota was observed, even stratifying patients according to treatment timepoints and considering the original disease.
originally came from this site:


So should I expect just short term relief from Rifaximin? Should I take Mutaflor etc immediately after? I'm confused at this stage whether I should even bother with antibiotics if SIBO just grows back... Luke White's paper says antibiotics are pretty much just to treat acute episodes of DLA.

I do believe I have general dysbiosis and probably other inflammation causing metabolites, but the lactate is the number one priority here.

@Avenger where do you get your Miyarisan from? I want to be sure I get the real thing. What was your inspiration to take it?
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ooooh, looky here, not only is this a d-lactate free multi strain probiotic, it's made by serious people who have even written their own paper on treating d-lactic acidosis with it:



The 2 others I've found are either obscure about what exact strains they contain, and have no studies like this. It also contains Rhamnosus GG which has been studied quite a lot.

other 2 here:




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and in the end we may learn in the coming years/decades it's the primary cause for many things.

My mum has depression, arthritis, some cardiac issues and now has some cognitive issues. Inflammation is clearly present. She also talks about developing anxiety when she moved to Singapore. I wonder how her microbiome changed. She lives a pretty healthy life in general, but something else is going on.

We probably inherit all this stuff, not necessarily from genes. Inheritance or "runs in the family" might be mistakenly attributed to genes because it was a hot topic and it's easy.

I also think the ideas of a healthy diet or any other therapeutic interventions are not honed to how it changes your gut yet.

e.g. we know losing sleep alters the gut. We also know losing sleep is bad for you. But those 2 things never seem to be framed together because our models are outdated. But, things are clearly evolving here, it will just take time.

also when people talk about strategies for insomnia, they put everything on mental and practical tips (meditate, do something X, do something Y, turn off lights...) But it's clear to me that the insomnia I have is entirely microbebiome linked. No practical strategy will help beyond just managing when it's really bad. Overthinking while lying awake is just a side effect in the end, but we always blame ourselves for "thinking ourselves awake"
I tried every mental strategy known to man to help me sleep more but none worked. Probiotics on the other hand give me an extra 2hrs sleep guaranteed.
I tried every mental strategy known to man to help me sleep more but none worked. Probiotics on the other hand give me an extra 2hrs sleep guaranteed.
I just read "The Second Sleep" by Robert Harris. Not pleasant reading but I really liked the basis for the title.

Back pre industrialisation we used to naturally sleep twice a night, with a little period of awake time in the middle. I always get annoyed when I wake in the night... now I know it's natural! If I could only get my minimum 2 or 3 wakes down to 1, with 2 quality sleeps, oh that will be the day ;)

Talking on a similar note. I tried mutaflor today. I really noticed a change in mood. Then later I was wondering why and I found this: https://www.nature.com/articles/srep17324

I also wonder if I will get a better nights sleep. This is the first day, but sadly I haven't noticed any effect on the d-lactate specific symptoms. But because my mood is better, I'm not too fussed. I have other probiotics coming next week which I feel comfortable about.

RE acidosis plan:

I have found positive anecdotes and also asked Mandi from Mandi mart if she knows of anyone who had treated acidosis with this: https://www.mandimart.co.uk/custom-...wder-50-grams-by-custom-probiotics-1296-p.asp

She had one customer give her positive feedback on exactly this for a 9 yo (customers rarely actually give feedback). Also many autistic children have benefitted from the product (I developed autistic tendancies as I developed chronic anxiety and IBS 6 years ago). I'm waiting til next week for the owner of Custom Probiotics to reply to similar questions. Did you or have you had autistic tendancies @Avenger ?

Will post updates here and in the other thread on lactic acidosis. I decided to hold off on Rifaximin while I sample the probiotics, and wait for test results. Maybe this could be enough if I'm lucky. Or I can try blasting later with antibiotics once I've established the probiotics that work.

Also have you tried Bimuno @Avenger from my preliminary understanding it should feed the bifidos and not the lactos. Also looking at S. Boulardi + MOS.